cardiac ischemia – ClinCaseQuest https://clincasequest.hospital Medical education in clinical cases Fri, 04 Oct 2024 22:35:21 +0000 en-US hourly 1 https://wordpress.org/?v=6.2.11 https://clincasequest.hospital/wp-content/uploads/sites/7/2020/02/logo-ru-project-90x90.png cardiac ischemia – ClinCaseQuest https://clincasequest.hospital 32 32 Сounseling a patient with suspected Takotsubo-syndrome OSCE guides https://clincasequest.hospital/counseling-a-patient-with-suspected-takotsubo-syndrome-osce-guides/ Sun, 24 Mar 2024 14:21:03 +0000 https://clincasequest.hospital/?p=37665 The onset of the consultation Clarification of the main complaint Comprehensive assessment Medical history History of life Objective examination: Laboratory tests Instrumental diagnostic tests Making…

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Tatyana Zaikina

The onset of the consultation

  1. Wash hands and put on PPE if necessary.
  2. Introduce yourself to the patient by stating your name and role.
  3. Confirm the patient’s last name, first name, and date of birth.
  4. Explain what the examination will involve using language the patient can understand.
  5. Get consent for consultation.
  6. Adequately expose the patient for examination.
  7. Ask the patient if he is in pain before proceeding with the clinical examination.

Clarification of the main complaint

  1. Use open-ended questions to explore the patient’s complaints
  2. Details of the main complaint
  3. Analyze the patient’s thoughts, fears, and expectations
  4. Summarize the patient’s complaints

Comprehensive assessment

  1. Assess other symptoms to get a comprehensive picture

Medical history

  1. Find out when and how the chest pain first appeared; what, according to the patient, could have caused its appearance (pay special attention to psychological or physical stress); specify whether the patient sought medical help, if so, to whom and what was the end of his appeal, if not, then specify why the patient did not seek medical help; whether he took medical drugs on his own or as prescribed by a doctor, if so, whether the nature of complaints changed against the background of treatment 
  2. In the case of hospitalization for chest pain, read the extract from the patient’s medical history, pay attention to the established clinical diagnosis, the results of laboratory or instrumental examinations, the treatment and recommendations after discharge
  1. If the patient has previously undergone laboratory or instrumental examinations for current complaints, analyze their results and indicate important findings
  2. Find out what prompted the patient to contact you
  3. Exclude other causes of chest pain by asking the patient clarifying questions

History of life

  1. The accuracy of the presence of previously diagnosed cardiovascular diseases in the patient, in particular myocardial infarction, stroke, rhythm disorders, cardiomyopathy, angina pectoris, arterial hypertension
  2. Find out whether the patient suffers from mental health disorders, such as depression, anxiety, or schizophrenia, which are risk factors for the development of Takotsubo syndrome
  3. Determine whether the patient has chronic diseases, in particular diabetes, bronchial asthma, and chronic obstructive pulmonary disease, which are risk factors for the development of Takotsubo syndrome
  4. Determine whether the patient is taking medications that stimulate the sympathetic nervous system (eg, beta 2-adrenergic receptor agonists, alpha 1-adrenergic receptor agonists, serotonin and norepinephrine reuptake inhibitors, epinephrine)
  5. Determine whether the patient is abusing psychotropic substances (eg, cannabis, cannabinoids)
  6. Find out whether the menstrual function is preserved; if not, find out the time of menopause and whether the patient is taking hormone replacement therapy
  7. Check whether the patient has undergone surgery
  8. Find out if the patient had any injuries, find out how the recovery period went
  9. Find out whether the patient has a drug intolerance and specify how it manifests itself
  10. Find out whether the patient has bad habits – drinking alcohol, narcotic substances, smoking
  11. Find out the family status of the patient, living conditions, and psychological problems in the family; find out if there were any blood relatives of the patient with cardiovascular diseases
  12. Find out whether the patient works, his profession, conditions, and nature of work, and whether the work is related to physical or psychological overload

Objective examination:

  1. Assessment of the patient’s general condition (satisfactory, moderate, severe, very severe).
  2. General examination of the patient:
  • Consciousness, the position of the patient, gait, and posture.
  • Physique, type of constitution, height, weight, body mass index.
  • Skin and visible mucous membranes (color, rash, scars, scratches), elasticity and moisture of the skin, condition of skin derivatives, and development of subcutaneous adipose tissue.
  • Pastiness, edema.
  • Lymph nodes.
  • Muscular system: development of muscles, their tone, presence of atrophy, soreness.
  • Joints: examination, palpation, measurement of limbs and joints, determination of the degree of joint mobility.
  • Examination of the head, face, and neck with an assessment of the state of the thyroid gland.
  1. Research of organ systems
  • Research of respiratory organs
  • Research of circulatory organs.
  • Research of digestive organs.
  • Examination of the urinary system
  1. Assessment of the probability of Takotsubo syndrome

Laboratory tests

  1. Clinical blood count with leukocyte formula and calculation of ESR (erythrocyte sedimentation rate)
  2. Biochemical blood analysis (total protein, creatinine, urea, alanine aminotransferase, aspartate aminotransferase, glucose, alkaline phosphatase, uric acid, bilirubin with fractions)
  3. Blood electrolytes (K+ and Na+)
  4. Lipid profile
  5. Coagulogram
  6. Blood test for troponin I / T
  7. Blood test for creatine phosphokinase (CK)
  8. Blood analysis for brain natriuretic peptide ( BNP ) or the N-terminal precursor of brain natriuretic peptide ( NT – pro-BNP )
  9. Assessment of thyroid gland function (thyroid-stimulating hormone-TSH) (according to indications)
  10. Urine analysis with sediment microscopy (as indicated)
  11. Pregnancy test for patients of childbearing age (according to indications)

Instrumental diagnostic tests

  1. Electrocardiography
  2. Transthoracic echocardiography
  3. Coronarography
  4. Ventriculography
  5. MRI of the heart
  6. CT angiography of coronary arteries

Making a clinical diagnosis

  1. Carrying out differential diagnosis
  2. Assessment of diagnostic criteria
  3. Determination of the anatomical variant
  4. Definition of complications
  5. Making of clinical diagnosis

Specialist consultations

  1. Cardiologist
  2. Interventional cardiologist
  3. Radiologist
  4. Psychotherapist
  5. Psychiatrist
  6. Endocrinologist
  7. Narcologist
  8. Gynecologist
  9. Doctor of physical and rehabilitation medicine

Purpose of treatment

  1. Supportive therapy
  2. Treatment of complications
  3. Prevention of relapse

Consulting and support

  1. Informing the patient about the disease
  2. Discussion of research results with the patient
  3. Explanation to the patient of the possible cause of the disease
  4. Explanation to the patient of possible symptoms that may occur during the disease
  5. Explanation to the patient of the possible consequences of the disease
  6. Explaining the available treatment methods, informing the patient about the risks and benefits of different treatment methods
  7. Answers to the patient’s questions
  8. Explanation of the scope of monitoring during and after treatment
  9. Appointment of regular checks and controls to assess the effectiveness of treatment and changes in the patient’s condition

End of consultation

  1. Summarize the data and ask the patient if anything important has been missed
  2. Inform the patient about further tactics
  3. Thank the patient
  4. Dispose of PPE properly and wash hands

Key communication skills

  • Active listening
  • Summing up
  • Selection of indicative signs

Join our Simulation Training to gain clinical experience

The onset of the consultation

  1. Wash hands and put on PPE if necessary.
  2. Introduce yourself to the patient by stating your name and role.
  3. Confirm the patient’s last name, first name, and date of birth.
  4. Explain what the examination will involve using language the patient can understand.
  5. Get consent for consultation.
  6. Adequately expose the patient for examination.
  7. Ask the patient if he is in pain before proceeding with the clinical examination.

Examination for Takotsubo syndrome is conducted when characteristic clinical symptoms and objective signs of this condition are present.

Typical clinical symptoms of Takotsubo syndrome include:

  1. Symptoms of myocardial ischemia (chest pain)
  2. Symptoms of heart failure (shortness of breath, sensation of air hunger)
  3. Symptoms of cerebral hypoperfusion (dizziness, loss of consciousness)

Clarification of the main complaint

  1. Use open-ended questions to explore the patient’s complaints
  2. Details of the main complaint
  3. Analyze the patient’s thoughts, fears, and expectations
  4. Summarize the patient’s complaints
  • Use open-ended questions to explore the patient’s complaints
  • Details of the main complaint

The most common complaint of a patient with Takotsubo syndrome is chest pain. To detail this complaint, follow this algorithm:

  • Localization: find out where it hurts
  • Onset: find out how the pain started – suddenly or gradually
  • Nature: Ask the patient to describe how he/she feels the pain.
  • Irradiation: Find out if the pain is spreading
  • Accompanying symptoms: find out if there are other symptoms that accompany the pain
  • Dynamics over time: Determine whether the pain has changed over time
  • Factors that make the pain worse or worse: Find out if there is anything that makes the pain worse or worse

“Can you show me precisely where it hurts?”

“Could you describe this pain?”

Is this pain constant or intermittent?

“How long does the pain typically last?“

“Does the pain radiate to other areas?“

“What typically triggers the onset of this pain?“

“What measures provide relief from this pain?“

“Are there any other symptoms accompanying the pain?”

To detail the complaint of chest pain, we recommend using the SOCRATES questionnaire. An example survey is given below.

SSite (Localization)Ask about the location of the pain“Where does it hurt?”
“Can you tell me precisely where you feel the pain?”
“Can you show me where it hurts?”
“Where is the pain localized?”
OOnsetSpecify how and when the pain occurred“Did the pain come on suddenly or develop gradually?”
“When did the pain first occur?”
“When did the symptoms first appear?”
“Did the pain occur at rest or during physical activity?”
“How long did the pain last?”
“How and when did it start?”
“Did the pain start suddenly, or did it develop gradually?”
“What were you doing precisely when the pain began?”
“What triggers the onset of pain for you?”
“When does the pain typically occur?”
“Under what circumstances does the pain worsen?”

CCharacterAsk about specific characteristics of the pain“How would you describe this pain?”
“Is the pain continuous or does it come and go?”
“Could you describe the pain to me?”
“Can you describe the nature of the pain?”
RRadiation (Irradiation)Ask if the pain is radiating“Does the pain radiate elsewhere?”
“Does it spread or radiate?”
“Where exactly does the pain spread?”
“To which part of the body does the pain radiate?”
AAssociated symptomsAsk if there are any symptoms related to pain“Are there any other symptoms associated with the pain?”
“Do you experience any other symptoms besides pain?”
“What other symptoms are you experiencing?”
“Are there any other symptoms apart from the pain?”
TTime course ( dynamics over time )Find out how the pain has changed over time“Has the pain changed over time?”
EExacerbating or relieving factorsAsk if there is anything that makes the pain worse or worse“Does anything exacerbate the pain?”
“Does anything alleviate the pain?”
SSeverityDetermine the intensity of the pain by asking the patient to rate it on a scale of 0 to 10“How would you rate the pain on a scale of 0 to 10, where 0 is no pain and 10 is the worst pain you have ever felt?”
“Please rate the intensity of the pain on a scale from 0 to 10, where 0 means no pain and 10 represents the most severe pain you have ever experienced.”
“On a scale of 1 to 10, how severe is the pain?”
“Could you rate the intensity of the pain on a scale from 1 to 10?”

Some elements of the SOCRATES acronym can be used to detail a complaint of shortness of breath.

SSite (Localization)––
OOnsetSpecify how and when the shortness of breath occurred“Did the shortness of breath come on suddenly or gradually?”
“When did you first experience shortness of breath?”
“What do you think caused the shortness of breath to start?”
CCharacterAssess the nature of shortness of breath“How would you describe your experience of shortness of breath?”
“Can you describe in detail how you feel when you experience shortness of breath?”
“Could you describe specifically what sensations you feel?”
RRadiation (Irradiation)––
AAssociated symptomsAsk if there are other symptoms associated with shortness of breath“Do you experience any other symptoms alongside the shortness of breath?”
“Have you noticed any coughing along with the shortness of breath?”
“Do you feel any chest pain when experiencing shortness of breath?”
“Have you noticed any blood in your sputum when experiencing shortness of breath?”
TTime course ( dynamics over time )Find out if the shortness of breath has changed over time
“Has the shortness of breath changed over time?”
EExacerbating or relieving factorsAsk if there is anything that makes the shortness of breath worse or worse“What can cause an increase in shortness of breath?” “What exacerbates shortness of breath?”
“What relieves shortness of breath?”
“Under what conditions does shortness of breath increase?”
“Does shortness of breath worsen when lying down?”
“Does shortness of breath increase during physical exertion?”
“Does changing body position affect the severity of shortness of breath?”

SSeverityDetermine the intensity of dyspnea by asking the patient to rate it on a scale of 0 to 10“Estimate the severity of shortness of breath on a scale from 0 to 10, where 0 is the absence of shortness of breath, and 10 is the strongest shortness of breath at rest.”
“Can you describe the intensity of shortness of breath on a scale of 1 to 10?”

Analyze the patient’s thoughts, fears, and expectations

A key component of history taking involves exploring the patient’s thoughts, concerns, and expectations to gain insight into how they currently perceive their condition, their worries, and what they anticipate from the consultation.

The exploration of thoughts, concerns, and expectations should be flexible throughout the consultation, responding to cues from the patient. This approach ensures that your consultation remains patient-oriented rather than formulaic.

It’s important to structure the analysis of thoughts, fears, and expectations in a way that feels natural during your consultation.

ReflectionsExplore the patient’s perception of the current problem“What do you think could have caused these symptoms?”
“Do you have any guesses as to the cause of these symptoms?”
ConcernExplore the patient’s current concerns• “Is there something that bothers you?”
• “How do you cope with everyday activities?”  
“Is there anything you and I haven’t discussed yet?”
ExpectationAsk what the patient hopes to gain from the consultation• “How can I help you today?”
• “What do you expect from today’s consultation?”
• “What do you think would be the best course of action?”

Summarize the patient’s complaints

Summarize what the patient told you about his complaint. This allows you to check how correctly you understood the patient’s complaints and gives the patient the opportunity to correct any inaccurate information.

When you have concluded, ask the patient if there is anything else you missed. Periodically, as the consultation progresses, summarize intermediate results.

Comprehensive assessment

  1. Screen for symptoms of damage to other organs and systems

A comprehensive assessment includes a brief survey of the patient for symptoms of other systems that may or may not be related to the chief complaint. This comprehensive examination also helps identify symptoms that the patient may have forgotten to mention.

Deciding which symptoms to inquire about depends on the presenting complaint and your level of experience.

Here are some examples of symptoms that you might inquire about for each system:

SystemSymptoms
General manifestationsfever, weight change, fatigue, sweating, general weakness
Respiratoryshortness of breath, cough, sputum, wheezing, hemoptysis, pleuritic chest pain
Cardiovascularchest pain, shortness of breath, heart failure, palpitations, swelling of the lower extremities
Gastrointestinaldyspepsia, nausea, vomiting, dysphagia, abdominal pain, stool disorders
Genitourinaryoliguria, polyuria, nocturia, pain during urination
Neurologicalchanges in vision, motor or sensory disturbances, headache
Locomotorpain in the chest wall, bone pain, trauma
Skinrashes, ulcers, hemorrhages, petechiae, bruises, hemorrhages, neoplasms

Medical history

  1. Find out when and how the chest pain first appeared; what, according to the patient, can cause its appearance (pay special attention to psychological or physical stress experienced); specify whether the patient sought medical help, if so, to whom and what was the end of his application, if not, then specify why he did not seek help; whether he took medical drugs on his own or as prescribed by a doctor, if so, whether the nature of the complaints changed against the background of treatment 

“When did the chest pain start for you?”

“What do you think might have caused it to start?”

“Did you seek medical assistance?”

  1. In the case of hospitalization for chest pain, read the extract from the patient’s medical history, pay attention to the established clinical diagnosis, the results of laboratory or instrumental examinations, the treatment and recommendations after discharge
  1. If the patient has previously undergone laboratory or instrumental examinations for current complaints, analyze their results and indicate important findings
  2. Find out what prompted the patient to contact you

“What made you decide to reach out to me?”

  1. Exclude other causes of existing symptoms by asking the patient clarifying questions

“Did you have a fever?”

“Is the chest pain accompanied by nausea or the urge to vomit?”

Other causes of chest pain:

  • Acute coronary syndrome (ACS)

Acute coronary syndrome is characterized by complaints of intense chest pain radiating to the left arm, left shoulder, left scapula, neck, and epigastrium, lasting more than 20 minutes, not relieved by taking nitrates, and often accompanied by shortness of breath, a feeling of fear, and increased sweating. The pain syndrome in ACS is very similar to the pain syndrome in Takotsubo syndrome, which creates significant difficulties for differential diagnosis.

  • Acute myocarditis

Clinical symptoms such as chest pain, shortness of breath, and palpitations are characteristic of both Takotsubo syndrome and myocarditis. The pain syndrome in myocarditis is very similar to the pain syndrome in Takotsubo syndrome, which makes it challenging to differentiate these two conditions based solely on this criterion. However, it should be noted that myocarditis is characterized by the presence of a recently acquired infectious disease, which is not typically associated with Takotsubo syndrome. Conversely, in Takotsubo syndrome, the onset of pain is often preceded by psychological or physical stress.

  • Angina

Angina is characterized by chest pain radiating to the left arm, left shoulder, left shoulder blade, neck, and epigastrium. However, in angina, the pain typically lasts up to 20 minutes and subsides with rest or after taking nitrates. In contrast, in Takotsubo syndrome, the pain persists for a longer duration and is not relieved by nitrates.

  • Thromboembolism of the pulmonary artery

For thromboembolism of the pulmonary artery and Takotsubo syndrome, chest pain often accompanied by shortness of breath and a sensation of breathlessness is characteristic. The nature of the pain in both conditions is anginal, posing a challenge for differential diagnosis. Considering that the primary cause of pulmonary embolism (PE) is typically deep vein thrombosis in the lower extremities, it’s essential to consider typical symptoms such as unilateral pain and swelling of the affected lower limb, along with an increase in its size.

  • Dissecting aneurysm of the aorta

Patients with a dissecting aortic aneurysm typically present with sudden, excruciating, tearing chest pain that radiates to the neck, back, and lower limbs, often in a migratory pattern. While the pain in Takotsubo syndrome can also be intense, it is typically not as severe as in a dissecting aortic aneurysm.

  • Acute pericarditis

The clinical presentation of acute pericarditis shares many similarities with that of Takotsubo syndrome, as both conditions typically involve chest pain and shortness of breath. However, acute pericarditis is distinguished by chest pain that worsens when lying down and improves when sitting, a characteristic not seen in Takotsubo syndrome. Additionally, acute pericarditis often occurs as a complication of an infectious disease, leading to symptoms such as fever and other signs of inflammation.

  • Gastroesophageal reflux

Pain associated with gastroesophageal reflux typically develops gradually and is characterized by a burning sensation localized in the central part of the chest. This discomfort is often accompanied by symptoms such as heartburn, nausea, and a sour taste in the mouth, all of which typically alleviate after taking antacids. Unlike Takotsubo syndrome, dyspeptic symptoms are not a hallmark feature of gastroesophageal reflux.

  • Gastric ulcer disease

In peptic ulcer disease, pain is frequently localized behind the sternum or in the epigastrium, typically occurring approximately 40 minutes after eating. This discomfort tends to diminish or disappear following the administration of antacids and is often accompanied by symptoms such as nausea and a sour taste in the mouth. Such a pain pattern is not characteristic of Takotsubo syndrome.

  • Diseases of the biliary tract

These conditions are typified by the emergence of dull pain behind the sternum or in the epigastrium, typically occurring approximately 1 hour after consuming food, particularly fatty or fried fare. This discomfort is often coupled with nausea, the urge to vomit, and a bitter taste in the mouth. Conversely, chest pain in Takotsubo syndrome is not influenced by dietary intake, and dyspeptic symptoms are generally absent.

  • Spontaneous pneumothorax

In spontaneous pneumothorax, intense chest pain abruptly arises, exacerbating with deep breathing, and is accompanied by pronounced shortness of breath. The aggravation of chest pain during inhalation is not a characteristic feature of Takotsubo syndrome.

  • Diseases of the neuromuscular system and musculoskeletal system

Chest pain resulting from neuromuscular and musculoskeletal system disorders typically worsens with significant body movements such as turning, bending, or raising the arm, a feature not commonly associated with Takotsubo syndrome.

  • Pain in herpes zoster

The pain in herpes zoster typically manifests as a constant burning sensation, often preceding the appearance of a characteristic vesicular rash. It may persist for some time after the rash disappears and is localized along the affected nerve pathway.

Learn more about the specific details of detailing chest pain as the main complaint and taking a patient’s medical history regarding chest pain by visiting the following link:

Chest Pain History Taking / OSCE guide

Other causes of shortness of breath:

  • Bronchial asthma

Shortness of breath in bronchial asthma typically manifests as attack-like episodes with an expiratory character. It is often accompanied by wheezing, a sensation of chest tightness, and coughing, often resulting in the discharge of a small amount of glassy viscous sputum. These episodes tend to occur in the early morning hours and are typically relieved by the inhalation of a short-acting β2-agonist.

  • Chronic obstructive pulmonary disease

Shortness of breath in chronic obstructive pulmonary disease (COPD) typically has a constant and progressive nature. It is often accompanied by a cough productive of mucus or sputum, particularly in the morning upon waking up.

  • Pneumonia

Shortness of breath in pneumonia is often accompanied by an elevated body temperature, symptoms of intoxication, cough with productive sputum, and sometimes chest pain.

  • Lung tumor

Shortness of breath associated with lung tumors typically exhibits a constant and progressive nature, often accompanied by hemoptysis, chest pain, coughing, and symptoms of tumor intoxication such as fatigue, weakness, weight loss, and loss of appetite.

  • Thromboembolism of the pulmonary artery

Shortness of breath associated with pulmonary embolism typically arises suddenly, often without a known cause. It can be so severe that it impedes the patient’s ability to speak. Additionally, it is accompanied by chest pain of a coronary or pleural nature, hemoptysis, dizziness, or even loss of consciousness. Symptoms of deep vein thrombosis of the lower extremities may also be present.

  • Arrhythmia

Tachyarrhythmias, particularly atrial fibrillation, frequently manifest with shortness of breath, palpitations, heart irregularities, and other symptoms indicative of hemodynamic impairment, such as sweating, dizziness, and possibly loss of consciousness. Because rhythm disturbances are typically paroxysmal, shortness of breath also tends to occur in episodes.

  • Anemia

Severe anemia often presents with shortness of breath exacerbated by minimal physical exertion, accompanied by rapid heartbeat, angina pectoris-like pains, dizziness, pronounced weakness, and increased fatigue.

  • Adiposity

Excess weight often leads to shortness of breath due to increased strain on the cardiovascular system, typically manifesting during physical exertion. In cases of significant excess weight, shortness of breath may even occur at rest.

  • Panic attack

Shortness of breath is just one of the symptoms experienced during a panic attack. It typically occurs suddenly and is often accompanied by feelings of fear, anxiety, nausea, palpitations, dry mouth, sweating, and dizziness, which can be unexpected and uncontrollable.

  • Hyperventilation

Shortness of breath is the primary symptom of hyperventilation syndrome. Patients commonly describe it as a sudden sensation of breathing dissatisfaction and a feeling of air deprivation. Due to the underlying cause of hyperventilation syndrome, shortness of breath is often accompanied by feelings of anxiety, panic, numbness, and tingling.

  • Gastroesophageal reflux disease

Shortness of breath is a relatively rare symptom of gastroesophageal reflux disease and arises due to the prolonged exposure of acidic stomach contents to the respiratory tract, typically after eating, while lying down, or when bending forward. Suspect gastroesophageal reflux disease when more specific symptoms are present, such as heartburn, belching, and discomfort when swallowing food.

History of life

  1. The accuracy of the presence of previously diagnosed cardiovascular diseases in the patient, in particular myocardial infarction, stroke, rhythm disorders, cardiomyopathy, angina pectoris, arterial hypertension
  2. Find out whether the patient suffers from mental health disorders, such as depression, anxiety, or schizophrenia, which are risk factors for the development of Takotsubo syndrome
  3. Determine whether the patient has chronic diseases, in particular diabetes, bronchial asthma, and chronic obstructive pulmonary disease, which are risk factors for the development of Takotsubo syndrome
  4. Determine whether the patient is taking medications that stimulate the sympathetic nervous system (eg, beta 2-adrenergic receptor agonists, alpha 1-adrenergic receptor agonists, serotonin and norepinephrine reuptake inhibitors, epinephrine)
  5. Determine whether the patient is abusing psychotropic substances (eg, cannabis, cannabinoids)
  6. Find out whether the menstrual function is preserved; if not, find out the time of menopause and whether the patient is taking hormone replacement therapy
  7. Check whether the patient has undergone surgery
  8. Find out if the patient had any injuries, find out how the recovery period went
  9. Find out whether the patient has a drug intolerance and specify how it manifests itself
  10. Find out whether the patient has bad habits – drinking alcohol, narcotic substances, smoking
  11. Find out the family status of the patient, living conditions, and psychological problems in the family; find out if there were any blood relatives of the patient with cardiovascular diseases
  12. Find out whether the patient works, his profession, conditions, and nature of work, and whether the work is related to physical or psychological overload

Objective examination:

  1. Assessment of the patient’s general condition (satisfactory, moderate, severe, very severe).
  2. General examination of the patient:
  • Consciousness, the position of the patient, gait, and posture.
  • Physique, type of constitution, height, weight, body mass index.
  • Skin and visible mucous membranes (color, rash, scars, scratches), elasticity and moisture of the skin, condition of skin derivatives, and development of subcutaneous adipose tissue.
  • Pastiness, edema.
  • Lymph nodes.
  • Muscular system: development of muscles, their tone, presence of atrophy, soreness.
  • Joints: examination, palpation, measurement of limbs and joints, determination of the degree of joint mobility.
  • Examination of the head, face, and neck with an assessment of the state of the thyroid gland.
  1. Research of organ systems
  • Research of respiratory organs
  • Organs of blood circulation.
  • Research of digestive organs.
  • Examination of the urinary system.

Assess for objects or equipment on or around the patient that may provide useful information about the patient’s medical history and current clinical condition.

It should be noted that physical findings depend on the severity of Takotsubo syndrome.

In patients with a severe course of Takotsubo syndrome, signs of heart failure can be detected, including wet wheezing in the lungs and tachypnea. During auscultation of the heart, tachycardia, an additional pathological third heart sound, as well as a systolic murmur over the apex of the heart due to obstruction of the outflow tract of the left ventricle and mitral regurgitation are often detected. Additionally, patients with Takotsubo syndrome often exhibit a decrease in blood pressure and low pulse pressure.

In patients with a mild course of Takotsubo syndrome, physical findings are typically unchanged.

Assessment of the probability of Takotsubo syndrome

  1. Assessment of the probability of Takotsubo syndrome

The probability of Takotsubo syndrome is assessed in patients presenting with chest pain and/or shortness of breath in the absence of ST-segment elevation on the ECG, particularly those hospitalized in intensive care units.

The InterTAK (The International Takotsubo Diagnostic Criteria) diagnostic scale is utilized to assess the likelihood of Takotsubo syndrome. A score of >70 points on this scale indicates a high probability (approximately 90%) of Takotsubo syndrome, whereas a sum of points ≤70 points suggests a low or moderate probability.

CriteriaPoints
Female gender25
Emotional trigger24
Physical trigger13
Absence of ST segment depression (except AVR)12
Psychiatric disorders11
Neurological disorders9
Prolongation of the corrected QT interval (women > 460 ms, men > 440 ms)6

With a high probability of Takotsubo syndrome, urgent transthoracic echocardiography is recommended. For cases with a low or moderate probability of Takotsubo syndrome, coronary angiography is recommended. This procedure allows for definitive differentiation between Takotsubo syndrome and acute myocardial infarction.

Laboratory tests

  1. Clinical blood count with leukocyte formula and calculation of ESR (erythrocyte sedimentation rate)
  2. Biochemical blood analysis (total protein, creatinine, urea, alanine aminotransferase, aspartate aminotransferase, glucose, alkaline phosphatase, uric acid, bilirubin with fractions)
  3. Blood electrolytes (K+ and Na+)
  4. Lipid profile
  5. Coagulogram
  6. Blood test for troponin I / T
  7. Blood test for creatine phosphokinase (CK)
  8. Blood analysis for brain natriuretic peptide ( BNP ) or the N-terminal precursor of brain natriuretic peptide (NT – pro-BNP )
  9. Assessment of thyroid gland function (thyroid-stimulating hormone-TSH) (according to indications)
  10. Urine analysis with sediment microscopy (as indicated)
  11. Pregnancy test if the patient is of childbearing age (as indicated)
  • Clinical blood count with leukocyte formula and calculation of ESR (erythrocyte sedimentation rate)

Clinical blood count, including the leukocyte count and calculation of the erythrocyte sedimentation rate (ESR), is one of the mandatory laboratory tests conducted in routine clinical practice for somatic patients.

  • Biochemical blood analysis (total protein, creatinine, urea, alanine aminotransferase, aspartate aminotransferase, glucose, alkaline phosphatase, uric acid, total bilirubin with its fractions)

The biochemical analysis of blood, which includes measurements of total protein, creatinine, urea, alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, alkaline phosphatase, uric acid, and total bilirubin with its fractions, is one of the mandatory laboratory examination methods performed in routine clinical practice for somatic patients.

  • Blood electrolytes (K+ and Na+)

Blood analysis for electrolytes (potassium and sodium) is a mandatory laboratory method of examination carried out in routine clinical practice for patients with cardiovascular diseases to diagnose electrolyte disorders.

  • Lipid profile

Lipid profile is a mandatory laboratory test for adult patients with cardiovascular diseases to diagnose lipid metabolism disorders.

  • Coagulogram

Coagulation profile is a mandatory laboratory test for adult patients with cardiovascular diseases to diagnose disorders of the blood coagulation system.

  • Blood test for troponin I / T

“Takotsubo syndrome” is a condition characterized by transient myocardial dysfunction, often triggered by emotional or physical stressors. While troponin levels can be elevated in Takotsubo syndrome, the degree of elevation is typically modest compared to that seen in acute myocardial infarction. It’s important to note that the elevation in troponin levels observed in Takotsubo syndrome is often disproportionate to the extent of regional myocardial dysfunction detected on imaging studies such as echocardiography.

  • Blood test for creatine phosphokinase (CK)

Creatine phosphokinase (CK) is indeed an early marker of myocardial necrosis. In Takotsubo syndrome, its levels may show a moderate elevation, typically disproportionate to the extent of regional myocardial dysfunction detected on echocardiography.

  • Blood analysis for brain natriuretic peptide ( BNP ) or the N-terminal precursor of brain natriuretic peptide (NT–proBNP )

B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are indeed markers of heart failure. In Takotsubo syndrome, their levels are often significantly elevated due to the overstretching of cardiomyocytes caused by the condition’s hemodynamic stress.

Appointment of instrumental methods of examination

  1. Electrocardiography
  2. Transthoracic echocardiography
  3. Coronarography
  4. Ventriculography
  5. MRI of the heart
  6. CT angiography of coronary arteries
  • Electrocardiography

Electrocardiography (ECG) is a mandatory method of examination of patients with suspected Takotsubo syndrome. The most characteristic ECG signs include elevation of the ST segment in the precordial leads, elevation of the ST segment in the AVR lead, diffuse inversion of the T wave, prolongation of the QT interval, rarely depression of the ST segment.

Some experts note that the elevation of the ST segment in the dept. V1-V3 in combination with elevation of the ST segment in the dept. AVR is a characteristic feature of Takotsubo syndrome.

  • Transthoracic echocardiography

Transthoracic echocardiography is a mandatory method of examination of patients with suspected Takotsubo syndrome. Moreover, it is diagnostically significant in patients with a high probability of Takotsubo syndrome according to the InterTAK scale.

Echocardiographic signs of Takotsubo syndrome include a decrease in the ejection fraction of the left ventricle, akinesis of the apical segments of the myocardium of the left ventricle in combination with hyperkinesis of the basal part, apical dilatation of the myocardium of the left ventricle, sometimes obstruction of the outflow tract of the left ventricle.

It should be noted that these signs are transitory in nature.

  • Coronarography

Coronary angiography indeed serves as a vital diagnostic tool to distinguish Takotsubo syndrome from acute myocardial infarction, particularly in patients with a low or moderate probability of Takotsubo syndrome according to the InterTAK scale.

In individuals with Takotsubo syndrome, coronary angiography typically reveals either normal coronary arteries or coronary arteries with non-obstructive stenosis (defined as stenosis <50%). This absence of significant coronary artery disease further supports the diagnosis of Takotsubo syndrome, helping to differentiate it from acute myocardial infarction.

  • Ventriculography

Ventriculography provides an assessment of the morphology and function of the left ventricle. In patients with Takotsubo syndrome, transient dysfunction and dilatation of the mid and apical segments of the left ventricle occur, resulting in a heart shape resembling that of an octopus.

  • MRI of the heart

MRI of the heart is an informative examination method that allows differentiation between Takotsubo syndrome and myocarditis. Characteristic MRI signs of Takotsubo syndrome include transmural edema in regions with reduced local myocardial contractility and myocardial scarring, while the basal parts of the left ventricle remain normal.

  • CT angiography of coronary arteries

CT angiography of the coronary arteries is an alternative examination method for stable patients contraindicated for cardiac MRI. It is performed to rule out significant coronary stenosis.

  • Assessment of thyroid gland function (thyroid-stimulating hormone-TSH) (according to indications)

A blood test for thyroid-stimulating hormone is conducted when there is suspicion of thyroid dysfunction, which can contribute to mental health disorders and potentially act as a trigger for the development of Takotsubo syndrome.

  • General urine analysis with sediment microscopy (as indicated)

A complete urine analysis with sediment microscopy is conducted when there is suspicion of kidney and/or urinary system damage.

  • Pregnancy test if the patient is of childbearing age (as indicated)

It is advisable to conduct a pregnancy test for female patients of childbearing age with Takotsubo syndrome. This helps in selecting appropriate drug therapy tactics, considering that some medications used to treat Takotsubo syndrome are contraindicated during pregnancy due to their teratogenic effects.

Making a clinical diagnosis

  1. Carrying out differential diagnosis

In clinical practice, it is often necessary to differentiate Takotsubo syndrome from acute coronary syndrome (ACS), acute myocarditis, as well as diseases accompanied by chest pain, in particular, angina pectoris, pulmonary embolism, dissecting aortic aneurysm, acute pericarditis, and others.

Clinical symptoms, objective data, ECG signs of Takotsubo syndrome, and acute coronary syndrome have a lot in common, which causes certain difficulties for differential diagnosis.

Both Takotsubo syndrome and acute coronary syndrome are characterized by complaints of intense radiating chest pain lasting more than 20 minutes and often accompanied by shortness of breath.

Levels of markers of myocardial necrosis, in particular troponin I/T and CK, are increased in both cases, but in Takotsubo syndrome this increase is insignificant compared to patients with acute myocardial infarction.

On the ECG of a patient with Takotsubo syndrome and a patient with ACS, ST-segment elevation and T-wave inversion can often be detected.

Echocardiography of a patient with Takotsubo syndrome and a patient with ACS revealed a decrease in the ejection fraction of the left ventricle and a local violation of myocardial contractility. However, patients with Takotsubo syndrome are characterized by akinesis of the apical segments of the myocardium of the left ventricle in combination with hyperkinesis of the basal part, which leads to apical ballooning of the left ventricle. In addition, these changes are transient and disappear within 3 weeks.

Coronary angiography definitively distinguishes Takotsubo syndrome from acute coronary syndrome. In Takotsubo syndrome, coronary arteries typically appear normal, without evidence of stenosis or hemodynamically insignificant stenosis (<50%). In contrast, acute coronary syndrome is characterized by acute occlusion of the arterial lumen.

Takotsubo syndrome develops in 90% of cases in women over the age of 50, whereas acute myocarditis most often affects young people without gender dominance.

Takotsubo syndrome in most cases is preceded by severe stress, while myocarditis is an infectious disease.

Clinical symptoms such as chest pain, shortness of breath, and palpitations are characteristic of both Takotsubo syndrome and myocarditis.

Blood troponin levels are elevated in both Takotsubo syndrome and myocarditis. However, in Takotsubo syndrome, this increase is insignificant and disproportionate to the area of ​​the affected myocardium, while in myocarditis, troponin is usually significantly increased and correlates with the area of ​​myocardial damage.

The level of brain natriuretic peptide is often elevated in Takotsubo syndrome and is usually elevated in myocarditis.

On the ECG of a patient with cardiomyopathy and myocarditis, changes in the ST segment and inversion of the T wave can often be detected. Unlike Takotsubo syndrome, myocarditis is also characterized by conduction disturbances and arrhythmias.

Echocardiography is important for differential diagnosis. Thus, in Takotsubo syndrome, swelling of the apical segments of the myocardium with intact basal sections is determined, which is not characteristic of myocarditis.

Myocardial edema can often be detected on MRI of the heart in Takotsubo syndrome and myocarditis. However, in the acute stage of Takotsubo syndrome, unlike myocarditis, there is no late accumulation of gadolinium.

Both angina and Takotsubo syndrome are characterized by radiating chest pain. However, in angina, the pain typically lasts up to 20 minutes and subsides with rest or after taking nitrates, whereas in Takotsubo syndrome, the pain persists longer and is not alleviated by nitrates.

The ECG of a patient with angina is usually normal or shows ST-segment depression, whereas patients with Takotsubo syndrome often show ST-segment elevation and T-wave inversion.

In patients with angina pectoris, the levels of markers of myocardial necrosis are normal, while in patients with Takotsubo syndrome, they are elevated.

A coronary angiography of a patient with angina usually shows significant stenosis of the coronary arteries, whereas in Takotsubo syndrome the coronary arteries are either intact or with insignificant stenosis.

Chest pain and shortness of breath are characteristic symptoms of both pulmonary embolism and Takotsubo syndrome. The chest pain in both conditions is anginal in nature.

Blood troponin levels may be mildly elevated in both pulmonary embolism and Takotsubo syndrome.

ECG in patients with pulmonary embolism and Takotsubo syndrome often shows sinus tachycardia, T-wave inversion. Pulmonary embolism is characterized by the classic S I Q III T III   pattern, while Takotsubo syndrome is characterized by ST-segment elevation in the precordial leads.

Echocardiography is essential for differential diagnosis. In Takotsubo syndrome, ballooning of the apical segments of the myocardium of the left ventricle with intact basal sections is observed, while in pulmonary artery thromboembolism, akinesia or hypokinesia of the free wall of the right ventricle with preserved contractility of the apex of the right ventricle (McConnell’s sign), 60/60 sign, dilatation and dysfunction of the right ventricle, and acute tricuspid regurgitation may occur.

Patients with a dissecting aortic aneurysm typically describe sudden, excruciating, tearing pain in the chest, which often radiates to the neck, back, and lower limbs and may be migratory. Although the pain in Takotsubo syndrome is intense, it typically does not reach the same level. Physical examination of a patient with a dissecting aortic aneurysm may reveal asymmetry of the pulse and blood pressure in the extremities compared to the other side. In cases where the aortic valve is involved, a diastolic murmur over the aorta and a high pulse pressure may be detected.

On the ECG of a patient with a dissecting aortic aneurysm, as in a patient with Takotsubo syndrome, ST- segment elevation can often be detected, however, in Takotsubo syndrome, ST-segment elevation is visualized in the precordial leads, while in aortic dissection involving the right coronary artery – in leads II, III, AVF.

Echocardiography and chest X-ray have important diagnostic value. On echocardiography and chest X-ray, in the case of aortic arch dissection, dilatation of the affected part of the aorta is revealed, which is not the case with Takotsubo syndrome.

Acute pericarditis is characterized by chest pain that intensifies when lying down and diminishes when sitting up, a feature not typically observed in Takotsubo syndrome. Additionally, patients with acute pericarditis often present with a history or ongoing symptoms of an infectious disease, including fever, respiratory symptoms, and others, which are not commonly associated with Takotsubo syndrome.

Clinical blood analysis of a patient with acute pericarditis reveals signs of an inflammatory process, which is not the case with Takotsubo syndrome.

On the ECG of a patient with acute effusion pericarditis, as in a patient with Takotsubo syndrome, ST -segment elevation, and T-wave inversion can often be detected, however, in Takotsubo syndrome, these changes are visualized in the precordial leads, while in acute pericarditis, ST-segment elevation is diffuse.

Echocardiography is important for differential diagnosis. Thus, in Takotsubo syndrome, ballooning of the apical segments of the myocardium of the left ventricle with intact basal sections is determined, while in pericarditis – thickening and compaction of the pericardial leaves, free fluid in the pericardium, signs of diastolic dysfunction.

  1. Assessment of diagnostic criteria

Diagnostic criteria are used to establish a clinical diagnosis. Among the existing criteria, the diagnostic criteria of the Mayo Clinic are of the greatest practical importance:

  • transient dyskinesia of the middle segments of the left ventricle; local violation of the contractility of the myocardium, which goes beyond the blood supply of one epicardial artery;
  • absence of obstructive coronary artery disease or angiographic signs of acute plaque rupture;
  • the appearance of new changes on the ECG (elevation of the ST segment and/or inversion of the T wave) or a moderate increase in the level of troponins;
  • absence of pheochromocytoma or myocarditis.

In addition to the Mayo Clinic diagnostic criteria, you can use the Takotsubo International Diagnostic Criteria:

  • patients with transient dysfunction of the left ventricle in the form of apical, mid-ventricular, basal or focal dilatation; in some cases, the right ventricle is involved in the process; the area of ​​the affected myocardium goes beyond the area of ​​blood supply by one epicardial artery;
  • an emotional, physically, or combined trigger preceding the onset of symptoms, but not necessarily;
  • neurological disorders (subarachnoid hemorrhage, stroke/transient ischemic attack, convulsions), in particular, pheochromocytoma can serve as a trigger for Takotsubo syndrome;
  • the appearance of new changes on the ECG (elevation/depression of the ST segment, inversion of the T wave, prolongation of the QT interval), in rare cases the ECG remains normal;
  • a moderate increase in the level of cardiac biomarkers (troponin, CPK) in most cases; a significant increase in the level of BNP and NT-proBNP;
  • severe coronary artery disease does not exclude the diagnosis of Takotsubo syndrome;
  • absence of signs of infectious myocarditis;
  • menopausal women are most often affected.

As well as the criteria of the Heart Failure Association and the European Community:

  • transient regional myocardial contractility disorder of the left and right ventricle, which often, but not always, develops as a result of experienced emotional or physical stress;
  • the area of ​​the affected myocardium goes beyond the area of ​​blood supply by one epicardial artery and often leads to circular dysfunction of the involved segments of the ventricles;
  • absence of obstructive coronary artery disease, including acute plaque rupture, thrombus formation, coronary artery dissection, or other diseases that could explain transient left ventricular dysfunction (eg, hypertrophic cardiomyopathy, viral myocarditis);
  • new and reversible changes on the ECG (elevation/depression of the ST segment, inversion of the T wave, prolongation of the QT interval, complete blockade of the left leg of the bundle of His) during the acute phase (3 months);
  • significant increase in the level of BNP and NT-proBNP during the acute phase;
  • moderate increase in the level of cardiac troponin;
  • restoration of the systolic function of the left ventricle, confirmed by MRI of the heart, in dynamics from 3 to 6 months.
  1. Determination of the anatomical variant

To date, there are several anatomical variants of Takotsubo syndrome: apical or typical (75-80%), mid-left ventricular (10-20%), basal or inverted (5%), biventricular (<0.5%), focal (very rarely).

  1. Definition of complications

When formulating a clinical diagnosis, it is necessary to indicate the complications that have arisen in the patient, in particular, arrhythmias, heart failure, thromboembolic complications.

  1. Making of clinical diagnosis

Here is an example of the formulation of the diagnosis in Takotsubo syndrome:

Takotsubo syndrome, apical variant. Ventricular polymorphic polytopic extrasystole, class III according to Laun. ACS-pulmonary edema.

Specialist consultations

  1. Cardiologist

Given that Takotsubo syndrome is a cardiovascular condition, consulting with a cardiologist for timely diagnosis and appropriate treatment is essential.

  1. Interventional cardiologist

Considering that Takotsubo syndrome must be differentiated from acute coronary syndrome, it is recommended to perform coronary angiography, which necessitates the involvement of an interventional cardiologist.

  1. Radiologist

A radiologist is an important member of a multidisciplinary medical team, involved in the implementation of imaging methods of research when Takotsubo syndrome is suspected, particularly magnetic resonance imaging of the heart.

  1. Psychotherapist

Patients with a confirmed diagnosis of Takotsubo syndrome and mental health disorders are recommended to be referred to a psychotherapist, considering that stress, depression, and anxiety are triggers for the development of Takotsubo syndrome.

  1. Psychiatrist

Patients with a confirmed diagnosis of Takotsubo syndrome and symptoms of mental disorders are recommended to be referred to a psychotherapist, considering that some of these disorders, including depression, anxiety disorder, and schizophrenia, are factors in the development of Takotsubo syndrome. Additionally, if a depressed patient is taking serotonin and norepinephrine reuptake inhibitors, a psychiatrist should consider replacing them with other drugs, as serotonin and norepinephrine reuptake inhibitors can also trigger the development of Takotsubo syndrome.

  1. Endocrinologist

Given the established association between hormonal disorders and Takotsubo syndrome, consultation with an endocrinologist is recommended if symptoms of an endocrine disease are present.

  1. Narcologist

If a patient with suspected Takotsubo syndrome is suspected of using psychotropic substances, they should be referred to a narcologist for consultation. This is because some substances, such as cannabis, cannabinoids, and amphetamines, can provoke the development of Takotsubo syndrome.

  1. Gynecologist

Considering that Takotsubo syndrome most often occurs in women during menopause, consulting a gynecologist to determine treatment tactics can be beneficial as part of the comprehensive therapy for such patients.

  1. Doctor of physical and rehabilitation medicine

A physical and rehabilitation medicine physician plays an important role in maintaining the physical well-being of patients with Takotsubo syndrome, assisting them in their recovery process.

Purpose of treatment

  1. Supportive therapy
  2. Treatment of complications
  3. Prevention of relapse
  • Supportive therapy

Patients with Takotsubo syndrome require inpatient treatment, the main goal of which is to maintain hemodynamics until normal left ventricular function is restored and to prevent complications. As a rule, supportive treatment lasts several weeks.

Patients with signs of lung congestion, but without hypotension, are prescribed diuretics and nitrates to reduce venous return to the heart. Additionally, ACE inhibitors, ARB II, and beta-blockers are prescribed to help alleviate congestion, reduce myocardial load, and regulate blood pressure.

Patients with unstable hemodynamics require urgent echocardiography to diagnose obstruction of the left ventricular outflow tract. If signs of obstruction are detected, the administration of beta-blockers and IV fluid infusion is recommended, while inotropic drugs are contraindicated. Inotropes such as dopamine, dobutamine, milrinone, and levosimendan are indicated for patients without signs of left ventricular outflow tract obstruction. In severe cases, mechanical circulatory support is necessary, including extracorporeal membrane oxygenation for patients with left ventricular outflow tract obstruction or intra-aortic balloon counterpulsation for patients without obstruction.

An essential aspect of treating patients with Takotsubo syndrome is the prevention of thromboembolic complications, particularly when there is a large area of akinesis or hypokinesis in the myocardium of the left ventricle. To mitigate this risk, anticoagulant therapy is typically prescribed for a duration of 3 months.

  • Treatment of complications

The most prevalent complications of Takotsubo syndrome include acute heart failure, left ventricular outflow tract obstruction, arrhythmias, and thromboembolic events.

For acute heart failure, refer to the previously outlined therapy. In cases of arrhythmias or thromboembolic complications, treatment should be administered following established guidelines.

  • Prevention of relapse

Considering the high incidence of mental health disorders among Takotsubo syndrome patients, such as depression, anxiety disorders, and substance use, it’s crucial to address these conditions to prevent relapse.

Certain experts advocate for the prolonged use of beta-blockers to mitigate sympathetic nervous system tone, which can serve as adjunctive therapy for anxiety disorders. Retrospective analyses of extensive international registries have shown a beneficial effect of ACE inhibitors, ARBs, and calcium channel antagonists.

Consulting and support:

  1. Informing the patient about the disease
  2. Discussion of research results with the patient
  3. Explanation to the patient of the possible cause of the disease
  4. Explanation to the patient of possible symptoms that may occur during the disease
  5. Explanation to the patient of the possible consequences of the disease
  6. Explaining the available treatment methods, informing the patient about the risks and benefits of different treatment methods
  7. Answers to the patient’s questions
  8. Explanation of the scope of monitoring during and after treatment
  9. Appointment of regular checks and controls to assess the effectiveness of treatment and changes in the patient’s condition
Inform the patient about the disease “Mr./Ms…., I’d like to discuss your diagnosis with you. You’ve been diagnosed with Takotsubo syndrome. This condition occurs when the heart temporarily loses its ability to function normally due to severe emotional stress”.
Explain to the patient the possible causes of the disease “There are several factors that can contribute to the development of Takotsubo syndrome. These include emotional stress, mental health disorders, hormonal imbalances, certain medications, genetic predisposition, among others. Emotional stress is often the primary trigger, leading to the release of large amounts of catecholamines such as adrenaline and norepinephrine. These chemicals can constrict blood vessels and disrupt normal heart function. To determine the exact cause of Takotsubo syndrome, further examinations will be necessary. Once we identify the underlying cause, we can determine the most appropriate treatment approach.”
Inform the patient of the symptoms that may occur with the identified disease “The symptoms of Takotsubo syndrome can resemble those of a heart attack. Typically, patients experience intense chest pain that persists even after taking nitrates, along with shortness of breath. In severe cases, patients may also develop rhythm disturbances and thromboembolic complications.”
Discuss the results of the examinations with the patient“Mr./Ms. [Last Name], I’d like to discuss the results of your examinations with you. During the electrocardiography, we observed changes similar to those seen in myocardial infarction. However, further examinations did not confirm this diagnosis. Coronary angiography showed no evidence of thrombosis in the heart arteries, which would typically indicate a myocardial infarction. Additionally, echocardiography revealed transient heart contractility, characteristic of Takotsubo syndrome rather than myocardial infarction. To confirm the diagnosis, we performed ventriculography, which revealed changes in heart shape during contraction typical of Takotsubo syndrome. Do you have any questions or concerns about what I’ve just explained?”
Explain to the patient the possible consequences of the disease   “The prognosis for Takotsubo syndrome is generally favorable, as heart contractility issues are temporary and typically resolve within 2-3 weeks. However, during this period, it’s crucial to adhere to the doctor’s recommendations aimed at reducing strain on the weakened heart and preventing complications.”
Educate the patient about available treatments “I’d like to discuss the available treatment methods for Takotsubo syndrome, aiming primarily at maintaining blood circulation until the heart’s normal function is restored. The choice of treatment method depends on the severity of the syndrome. Patients without signs of heart failure typically receive beta-blockers, angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers. For those exhibiting lung congestion without low blood pressure, diuretics and nitrates are prescribed to alleviate congestion, reduce cardiac workload, and regulate blood pressure. If there’s unstable circulation, intravenous solutions and/or inotropic drugs may be administered to enhance myocardial contractility. In cases where drug therapy proves ineffective, mechanical circulatory support using various devices may be employed“.
Help the patient understand the risks and benefits of different treatments“Although the medications used to treat Takotsubo syndrome are well-studied, effective, and generally safe, there is a possibility of side effects with therapy. However, I want to assure you that we will take every precaution to minimize these risks.”
Answer the patient’s questions“If you have any further questions regarding the causes of the disease, its symptoms, diagnosis, or treatment, please feel free to ask. It’s crucial that you understand what’s happening and what steps we’ll be taking next.”
Provide an explanation of the extent of monitoring during and after treatment“Monitoring, or observing the main parameters of your body, is crucial for timely assessment of your condition, correction of detected changes, and evaluating the effectiveness of treatment. During monitoring, we will carefully observe your general condition, blood oxygen saturation level, blood pressure, heart rate, and myocardial contractility. Pulse oximetry is performed to determine the level of blood oxygen saturation. A special pulse oximeter device will be worn on your finger to constantly monitor the oxygen level in your blood. Blood pressure monitoring allows us to assess how well your heart is functioning and make corrections if there is a significant decrease or increase in blood pressure. We will use electrocardiography to evaluate heart rhythm by placing special electrodes on the front chest wall to record the electrical activity of your heart. This will enable us to monitor the effect of the treatment. To assess myocardial contractility, we will repeat echocardiography.”
Schedule regular check-ups and follow-up to assess the effectiveness of treatment and changes in the patient’s condition“After discharge from the hospital, it’s important to monitor your well-being and avoid emotional and physical stress. If you experience anxiety, depression, or other mental health disorders, it’s advisable to consult a psychotherapist to determine the appropriate course of action. Your emotional well-being is crucial to prevent the recurrence of Takotsubo syndrome.”

End of consultation

  1. Summarize the data and ask the patient if anything important has been missed
  2. Inform the patient about further tactics

Hospitalization to a specialized cardiology hospital is recommended for a comprehensive examination and selection of optimal treatment tactics. Obtain the patient’s Informed Voluntary Consent for diagnosis and treatment, and agree to the Patient’s Informed Voluntary Consent for processing personal data.

  1. Thank the patient
  2. Dispose of PPE properly and wash hands

Key communication skills

  • Active listening
  • Summing up
  • Selection of indicative signs

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]]> Killip Classification for Heart Failure https://clincasequest.hospital/killip-classification/ Mon, 29 Nov 2021 07:08:00 +0000 https://clincasequest.hospital/?p=31650 Killip Classification for Heart Failure could be used in patients with confirmed acute coronary syndrome in both STEMI and NSTEMI for mortality prediction. Can be…

Сообщение Killip Classification for Heart Failure появились сначала на ClinCaseQuest.

]]> Killip Classification for Heart Failure could be used in patients with confirmed acute coronary syndrome in both STEMI and NSTEMI for mortality prediction.

Can be used as part of the full clinical picture to help decide among treatment options, including reperfusion therapy and intra-aortic balloon pump placement. Predicts mortality in ACS and is validated for both STEMI and NSTEMI.

Killip Classification for Heart Failure

No signs of congestion
S3 and basal rales on auscultation
Acute Pulmonary oedema
Cardiogenic shock




Class 30-day mortality* In-hospital mortality** (historical interest only)
0 0 0

Killip classification:

Class INo signs of congestion
Class IIS3 and basal rales on auscultation
Class IIIAcute pulmonary oedema
Class IVCardiogenic shock

Interpretation:

Class30-day mortality*In-hospital mortality** (historical interest only)
I2-3%<6%
II5-12%<17%
III10-20%38%
IV10-20%81%

*From Khot 2003, which combined class III/IV owing to relatively smaller number of patients in class IV (0.3% of patients).
**From Killip 1967. Killip classification developed in the 1960s, before reperfusion therapy (thrombolytics, PCI); has been shown across several studies since then to still be predictive of mortality. However, mortality rates have declined significantly since the original study.

About the creator

Thomas Killip III, MD, is a professor of medicine and cardiology at Mount Sinai Beth Israel Hospital in New York City. He has published dozens of studies in cardiology since the 1960s. Dr. Killip is best known for the heart failure classification system that bears his name. To view Dr. Thomas Killip III’s publications, visit PubMed

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References:

  1. Thomas Killip III, John T. Kimball Treatment of myocardial infarction in a coronary care unit. Two year experience with 250 patients. Symposium on coronary care unit. 1967, Vol.20(4):P457-464. DOI: https://doi.org/10.1016/0002-9149(67)90023-9
  2. Khot UN, Jia G, Moliterno DJ, Lincoff AM, Khot MB, Harrington RA, Topol EJ. Prognostic importance of physical examination for heart failure in non-ST-elevation acute coronary syndromes: the enduring value of Killip classification. JAMA. 2003 Oct 22;290(16):2174-81. doi: 10.1001/jama.290.16.2174.  PMID: 14570953. https://pubmed.ncbi.nlm.nih.gov/14570953/
  3. DeGeare VS, Boura JA, Grines LL, O’Neill WW, Grines CL. Predictive value of the Killip classification in patients undergoing primary percutaneous coronary intervention for acute myocardial infarction. Am J Cardiol. 2001 May 1;87(9):1035-8. doi: 10.1016/s0002-9149(01)01457-6. PMID: 11348598. https://pubmed.ncbi.nlm.nih.gov/11348598/
  4. Nesković AN, Otasević P, Bojić M, Popović AD. Association of Killip class on admission and left ventricular dilatation after myocardial infarction: a closer look into an old clinical classification. Am Heart J. 1999 Feb;137(2):361-7. doi: 10.1053/hj.1999.v137.89744. PMID: 9924172. https://pubmed.ncbi.nlm.nih.gov/9924172/
GRACE ACS Risk and Mortality Calculator
The Intra-Aortic Balloon Counterpulsation in Acute Myocardial Infarction Complicated by Cardiogenic Shock (IABP-SHOCK II) risk score
SAVE (Survival After Veno-Arterial ECMO) Score

Interactive OSCE Checklist – Emergency care of a patient with chest pain – Acute Coronary Syndrome with ST-segment elevation and equivalents

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• Opening the consultation

• Availability of a defibrillator

• Presenting complaint

• History of presenting complaint

• Past medical history

• Drug history

• Physical examination

• Intravenous access

• Registration of a 12-channel ECG

• Express test for the determination of cardiac troponin, myoglobin, creatine phosphokinase-MB, if possible

• Making preliminary diagnosis

• Drug therapy (basic)

• Evaluation of the door-balloon time (the choice of further reperfusion strategy aimed as soon as possible to restore the coronary blood flow in the infarct-dependent artery)

• Call the nearest reperfusion center

• P2Y12 receptor inhibitor prescription depending on the chosen strategy of reperfusion therapy

• Carrying out thrombolytic therapy as needed

• Transportation to the nearest reperfusion center

Total: 0 / 62
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]]> South Africa Flag sign on ECG https://clincasequest.hospital/south-africa-flag-sign/ Fri, 22 Oct 2021 11:24:40 +0000 https://clincasequest.hospital/?p=30960 South Africa Flag sign on the ECG – a specific ECG pattern that occurs during the development of mid-anterior (high lateral) myocardial infarction (MI) due…

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]]> South Africa Flag sign on the ECG – a specific ECG pattern that occurs during the development of mid-anterior (high lateral) myocardial infarction (MI) due to occlusion of the first diagonal artery – D1 (a branch of the left anterior descending artery (LAD) of the left coronary artery). The first diagonal artery (D1) supplies a part of the anterior wall of the left ventricle (LV) and lesser its basal anterolateral areas (Fig. 1).

Fig. 1. Coronary arteries. First diagonal artery (D1) (pointer – yellow arrow).

Culprit’s arteries

  • Occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) can cause isolated ST elevation in I and aVL.
  • Occlusion of the left circumflex artery can cause ST-segment elevation in I, aVL along with leads V5-6.

Clinical relevance


Very often, high lateral infarctions (STEMI) are not diagnosed on time even by experienced emergency doctors due to the non-contiguous nature of ST-segment elevation on the electrocardiogram (ECG).

Sign of the South African flag on the ECG

With occlusion of D1 (LAD-D1), on the ECG are revealed the following changes (Fig. 2):

  • ST-elevation: leads I, aVL, V2
  • ST depression: Leads III (and inferior leads).


ST-elevation is predominantly localized in leads I, aVL +/- V2, but not in other anterior leads.

Reciprocal ST depression and/or T-wave inversion in inferior leads, most pronounced in lead III.

Fig. 2. South Africa Flag sign on ECG (ST Elevation: Leads I, aVL, V2, ST Depression: Leads III (and inferior leads aVF)).

Algorithm for identifying the feature of the “South Africa Flag sign” on the ECG


Littmann L. offers a simple step-by-step algorithm that can help emergency physicians identify the typical ST-segment abnormalities seen in high lateral STEMI.

The author uses a three-step approach:

Step 1: understand the ST vector in high lateral STEMI.

In high lateral infarction, the ST vector is directed towards the armpit and is usually directed from 0 ° to -90 ° in the frontal plane. 6 ECG leads are grouped in this area, which can inherit a high lateral ST vector. 0 ° corresponds to lead I, -30 ° corresponds to aVL, -60 ° corresponds to a mirror image of lead III, and -90 ° corresponds to a mirror image of lead aVF. Located on the left and above the center of the heart, the projection of lead V2 in the frontal plane is also directed towards the armpit. Therefore, the morphology of complexes in V2 often resembles the morphology in lead aVL. Based on Fig. 3, it is easy to recognize why STEMI-D1 is characterized by ST elevation in leads I, aVL, and V2, and ST depression in leads III and aVF.

Fig. 3. ST-elevation vector in high lateral myocardial infarction with occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) (yellow arrow, blue zone). The ST vector points to leads I, aVL, V2 and forms a mirror image in III and aVF leads.

Therefore, any D1-LAD occlusion causes ST-elevation in lead I, aVL, lead III mirroring, which represents ST depression in lead III and lead V2. Since they are not contiguous in the 4 × 3 12-lead ECG format registration, it is very easy to skip these changes. And since it also causes ST-depression in lead III and aVF, which are adjacent, it is easy to mistake an ST-segment elevation patient for a non-ST-elevated myocardial infarction.

Step 2: recognize the electrocardiographic “South African flag sign”.

Most electrocardiographs record 12-lead ECGs in a 4 × 3 format. With this display, the location of ST-segment deviation resembles the image of the South African flag with ST-elevation in the upper left panel (lead I) and in the two middle panels in the second and third columns (leads aVL and V2, respectively) and ST-depression in the lower-left panel (lead III ).

In fig. 4 shows a case where STEMI can be accurately identified and therefore easier to remember the South African flag pattern. It also demonstrates that the prominent ST-elevation seen in V2 should be a frontal plane rather than a horizontal ST vector reflection because there is absolutely no corresponding ST elevation in leads V1 and V3, the two contiguous chest’s leads.

Fig. 4. The South Africa Flag sign on the ECG. In the most common 12-lead 4×3 ECG format, the most significant ST abnormalities resemble the shape of the South African flag.

The South Africa Flag sign on the ECG has a green middle zone that resembles a “Y”. Leads I and III occupy the upper and lower limb Y. Lead aVL occupies the intersection of two limbs Y, and lead V2 unites the upper and lower parts of Y. Thus, all of these leads coincide, and the elevation ST depression in lead I, aVL, V2, and ST depression in lead III match the South African flag. Therefore, to recognize D1-LAD occlusion, Littmann described one specific 12-lead ECG feature called the flag of South Africa. This flag of South Africa can be easily recognized, which can minimize the chances of missing a D1-LAD occlusion.

Step 3: recognize a more subtle high lateral STEMI.

High lateral STEMI is often not diagnosed early because ST depression seen in leads III and aVF is mistaken for inferior ischemia. However, it should be borne in mind that ST depression in any lead can be a reflection of ST elevation in the mirrored leads. Even when ST elevation is quite mild, if it is localized in leads I, aVL, and V2, ST depression in the inferior leads should probably be considered reciprocal (Fig. 5).

Fig. 5. South Africa Flag sign on the ECG.

Conclusions

Identification of the sign of the South African flag on the ECG can improve the timely diagnosis of high lateral myocardial infarctions that are not diagnosed in time due to the non-contiguous nature of ST segment elevation on the electrocardiogram, which will allow timely reperfusion therapy for this group of patients.

Reference

  1. Durant E., Singh A. Acute first diagonal artery occlusion: a characteristic pattern of ST elevation in noncontiguous leads. Am J Emerg Med. 2015; 33: 1326.e3-5
  2. Littmann L. South African flag sign: a teaching tool for easier ECG recognition of high lateral infarct. The American Journal of Emergency Medicine. 2016;34(1), P107-109.
  3. G Rajendran, S Mahalingam, R Kagne, B Nathan, The South African flag sign—an electrocardiographic sign to predict the culprit artery, QJM: An International Journal of Medicine, 2021.
  4. Monica Monaghan, Shiva Sreenivasa A Red Flag ECG Circulation. 2020;142:1871–1874

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]]> Aslanger’s Pattern https://clincasequest.hospital/aslangers-pattern/ Tue, 19 Oct 2021 16:31:53 +0000 https://clincasequest.hospital/?p=30902 Introduction The fourth universal definition of myocardial infarction (MI) defines ST-segment elevation MI (STEMI) and non-STEMI based on the presence or absence of: 1) J-point…

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]]> Introduction


The fourth universal definition of myocardial infarction (MI) defines ST-segment elevation MI (STEMI) and non-STEMI based on the presence or absence of:

1) J-point elevation in two or more contiguous leads with a cut-off value of ≥0.1 mV (1 mm) in all leads other than V2 and V3;

2) STE in V2 and V3 by age and sex, for which the following cut-off values were applied: 0.2 mV (2 mm) in men ≥40 years old, 0.25 mV (2.5 mm) in men <40 years old, or 0.15 mV (1.5 mm) in women.

However, recently, were described new ECG patterns. This definition should be expanded based on the necessity of the wider implementation of the early reperfusion therapy strategies in this group of patients due to the higher mortality in these patients.

Clinical significance

In April 2020, a group of Turkish scientists Aslanger et al. described an ECG pattern, which was recorded according to their data in approximately 13.3% of cases of lower myocardial infarction. Patients with this pattern on the ECG are often incorrectly regarded in the provision of medical care – as patients with ACS without ST-segment elevation, which deprives them of emergency revascularization, while this ECG pattern is associated with coronary artery occlusion in patients with multivessel coronary disease.

Aslanger et al. analyzed the results of ECG and angiography of 1000 patients with STEMI (without ST-segment elevation), 1000 controls (without myocardial infarction), as well as patients with inferior STEMI (with ST-segment elevation) admitted during the same period (DIFOCCULT Study Protocol – DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial infarction).

Aslanger’s pattern was observed in 6.3% of patients with STEMI and was a predictor of greater heart attack size and higher mortality.

Aslanger pattern

  • Occurs with a combination of lower AMI and critical ischemia of another localization.
  • Larger infarction zone, as evidenced by troponin levels at 24 hours, higher incidence of angiographic injury, and higher incidence of the combined endpoint of acute coronary occlusion compared with patients with AMI without ST-elevation.
  • High mortality, comparable to patients with inferior STEMI, both in-hospital (5% versus 4%, P = 0.675) and one-year mortality (11% versus 8%, respectively; P = 0.311).

Concomitant multivessel coronary artery disease predisposes these patients to poor outcomes if the time to reperfusion is delayed.

Identifying the culprit during angiography can be difficult if there are multiple critical stenoses, and this specimen will help to expose the lesions that supply the lower wall first.

This pattern occurs with a simultaneous combination of inferior MI and diffuse ischemia due to lesions of the anterior interventricular branch of the left coronary artery (left anterior descending artery), the left main coronary artery, or a three-vessel lesion.

ECG criteria:

1) ST elevation in lead III, but in none of the inferior leads, as well as in aVR and V1.

2) Concomitant ST depression in any of V4-V6 with positive / terminally positive T-wave.

3) ST-segment elevation in V1> V2

Aslanger’s Pattern

ST vector in Aslanger pattern

In cases of damage to the inferior wall, the ST vector of inferior myocardial infarction localizes the infarction area and is usually directed downward and to the right (orange arrow). In this case, reciprocal changes will be recorded in leads I and aVL.

ST Vector of injury in the inferior myocardial wall during inferior myocardial infarction (orange arrow)

The ST vector of subendocardial ischemia is not localized to ischemia and, regardless of the coronary region affected, indicates lead aVR (blue arrow). The vector of subendocardial ischemia is directed inward from the left heart, towards avR, in which elevation is determined, and in all opposite directions, respectively, depression is visualized.

ST vector of subendocardial ischemia in lead aVR (blue arrow)

The resulting middle ST vector is directed to the right, causing ST elevation in lead III and aVR only.

Resulting ST vector in the Aslanger pattern (red arrow)

V1 is the rightmost lead on the chest, so ST elevation is also pronounced in V1 in the Aslanger pattern.

ST elevation in the right chest lead V1 in the Aslanger pattern

Considering that the vector of elevation is directed to the right, therefore, ST-elevation will be more pronounced in V1 than in V2, since lead V1 is to the right than V2.

In addition, mirrored depression to aVR cannot occur in lead V2 because the greater proximity of this lead to aVR compared to other chest leads.

ST Elevation V1> V2 in the Aslanger pattern

Limitations

It was found that this ECG pattern is also present in 0.5% of patients without acute MI, which may be the result of chronic changes from previous ischemic injury.

Acute inferior myocardial infarction in the presence of previous infarctions can also change the general orientation of the lesion vector, causing a similar picture.

This is an isolated retrospective study that requires further analysis as a predictor of occlusive MI, in which urgent reperfusion therapy is warranted.

Conclusion

Identification of patients with Aslanger’s ECG pattern can facilitate early revascularization and improve the prognosis in this group of patients.

References:

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]]> Two masks of the same syndrome: Wellens syndrome https://clincasequest.hospital/wellens-syndrome/ Sun, 17 Oct 2021 20:48:33 +0000 https://clincasequest.hospital/?p=30845 Early reperfusion therapy is a gold standard strategy in the management of patients with acute ST-segment elevation coronary syndrome (STEMI-ACS), as elevation on the electrocardiogram…

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]]> Early reperfusion therapy is a gold standard strategy in the management of patients with acute ST-segment elevation coronary syndrome (STEMI-ACS), as elevation on the electrocardiogram (ECG) is recognized as a manifestation of critical stenosis or occlusion of the coronary artery.

At the same time, about 10 – 25% of patients with an acute coronary syndrome without ST-segment elevation, according to coronary angiography, also have critical stenosis or occlusion of a large epicardial artery. A delay in revascularization in this group of patients is associated with worse outcomes. Although the current guidelines briefly mention the criteria for STEMI ACS equivalents, there is still insufficient information on specific ECG patterns.

In this publication, we will consider an electrocardiographic phenomenon – Wellens syndrome.

Introduction

Wellens Syndrome is a clinical syndrome characterised by biphasic or deeply inverted T waves in V2-3, plus a history of recent chest pain now resolved. It is represent highly specific for critical stenosis of the left anterior descending artery (LAD).

Wellens syndrome was firstly described in the early 1980s by de Zwaan, Wellens, and colleagues, who identified a subset of patients with unstable angina who had specific precordial T-wave changes and subsequently developed a large anterior wall myocardial infarction (MI).  Wellens syndrome refers to these specific electrocardiographic (ECG) abnormalities in the precordial T-wave segment, which are associated with critical stenosis of the proximal left anterior descending (LAD) coronary artery.

Wellens syndrome is also referred to as LAD coronary T-wave syndrome.  Syndrome criteria include the following:

  • Characteristic T-wave changes
  • History of anginal chest pain and absence of pain syndrome during identification typical changes on the ECG
  • Normal or minimally elevated cardiac enzyme levels
  • ECG without Q waves, without significant ST-segment elevation, and with normal precordial R-wave progression

Recognition of this ECG abnormality has great significance under this syndrome represents a preinfarction stage of coronary artery disease (CAD) that often progresses to a devastating anterior wall MI.

Pathophysiology

Wellens syndrome represents critical stenosis of the proximal segment of the LAD artery. The LAD arises from the left coronary artery and passes through the interventricular groove along the anterior portion of the heart to the apex. This groove is situated between the right and left ventricles of the heart. The LAD gives rise to 2 main branches, the diagonals, and the septal perforators.

A lesion in the proximal LAD can have severe consequences, as suggested by the common title given to this lesion: “widow maker.” The LAD supplies the anterior wall of the heart, including both ventricles, as well as the septum. An occlusion in this vessel can result in serious ventricular dysfunction, thus placing the patient at serious risk for congestive heart failure (CHF) and death.

Etiology


Wellens syndrome is a preinfarction stage of CAD. The causes of Wellens syndrome are similar to the conditions that cause CAD, including the following:

  • Atherosclerotic plaque
  • Coronary artery vasospasm (cocaine is one possible cause)
  • Increased cardiac demand
  • Generalized hypoxia

Risk factors for Wellens syndrome are essentially those of CAD and include the following:

  • Smoking history
  • Diabetes mellitus
  • Hypertension
  • Increased age
  • Hypercholesterolemia
  • Hyperlipidemia
  • Metabolic syndrome
  • Family history of premature heart disease
  • Occupational stress

Epidemiology and Prognosis


The characteristic ECG pattern of Wellens syndrome is relatively common in patients who have symptoms consistent with unstable angina. Among patients admitted with unstable angina, this ECG pattern is present in 14-18% cases.

Wellens syndrome represents critical proximal segment LAD disease; accordingly, its natural progression leads to anterior wall MI. This progression is so likely that medical management alone is not enough to stop the natural process. Evolution to an anterior wall MI is rapid, with a mean time of 8.5 days from the onset of Wellens syndrome to infarction.

If anterior wall MI occurs, there is the potential for substantial morbidity or mortality. Thus, it is of utmost importance to recognize this pattern early.

Clinical Presentation

Wellens syndrome represents stenosis of the proximal segment of the left anterior descending coronary artery (LAD), and patients typically present with symptoms or complaints consistent with coronary artery disease (CAD). Generally, the history is most consistent with unstable angina. Angina can have varying presentations, but the classic presentation includes the following complaints:

  • Chest pain described as pressure, tightness, or heaviness
  • Pain that is typically induced by activity and relieved by rest
  • Radiation of pain to the jaw, shoulder, or neck

May experience multiple associated symptoms, including diaphoresis, nausea, vomiting, and fatigue.

Elderly, diabetic, and female patients are more likely to present with atypical symptoms.

Physical Examination


Physical examination does not provide any indicators that would give the strong grounds for suspecting Wellens syndrome specifically. However, the results of the patient’s examination may show evidence of ongoing ischemic injury (congestive heart failure).

In addition, most of the electrocardiographic (ECG) changes are recognized when the patient is pain-free, which again underscores the importance of a repeat pain-free ECG in the emergency department.

Diagnostic strategy


Potential diagnostic pitfalls with Wellens syndrome include the following:

  • Failing to recognize Wellens syndrome T-wave changes on electrocardiography
  • Ordering a stress test without recognizing risks (see Workup); this may provoke a large anterior wall myocardial infarction (MI)
  • Underestimating the seriousness of the ECG finding in a pain-free patient
  • Failing to properly admit or consult cardiology on patients with the characteristic ECG changes

Differential Diagnoses

  • Acute Coronary Syndromes
  • Acute Pericarditis
  • Angina Pectoris
  • Atherosclerosis
  • Bacterial Pneumonia
  • Coronary Artery Atherosclerosis
  • Myocardial Infarction
  • Myocarditis
  • Pulmonary Embolism (PE)

In addition to the conditions listed in the differential diagnosis, other conditions to be considered include the following:

  • Central nervous system injury
  • Persistent juvenile T-wave pattern
  • Left ventricular hypertrophy
  • Bundle-branch block
  • Digitalis effect
  • Acute myocarditis
  • Preexcitation syndromes
  • Later stages of pericarditis

Laboratory tests

The following laboratory studies may be indicated as adjunctive tests in patients with suspected coronary artery disease (CAD), acute coronary syndrome (ACS), and Wellens syndrome:

  • Complete blood count (CBC) – To ensure that anemia is not precipitating the angina, red blood cell (RBC) transfusions may be necessary
  • Basic metabolic profile – This includes electrolyte, blood urea nitrogen (BUN), creatinine, and glucose levels
  • D-dimer, international normalized ratio (INR), partial thromboplastin time (PTT) – These are ordered only as medically necessary
  • Cardiac biomarkers – In Wellens syndrome, cardiac biomarkers can be falsely reassuring, in that they are typically normal or only minimally elevated; only 12% of patients with this syndrome have elevated cardiac biomarker levels, and these are always less than twice the upper limit of normal, in the absence of myocardial infarction (MI)

Radiography, CT of Chest


Chest radiography should be performed to look for side effects of ischemia, such as pulmonary edema. In addition, this test should be performed to help exclude other possible causes of chest pain, such as thoracic aneurysm or dissection, pneumonia, and rib fracture.

Computed tomography (CT) of the chest is performed only as indicated to help rule out other causes of chest pain, such as aortic dissection or pulmonary embolus. The value of CT angiography of the chest in the evaluation of chest pain, CAD, and ACS is currently being investigated.

Electrocardiography


ECG should be performed on any patient with a complaint of chest pain if noncardiac causes cannot be diagnosed by other means, including physical examination. It may be helpful to perform ECG both while the pain is present and after the pain has resolved. The ECG changes seen in Wellens syndrome typically are manifested when the patient is pain-free but usually occur in the context of recent anginal chest pain.

In Wellens syndrome, the ECG pattern shows significant involvement of the T wave, with minimal ST-segment alteration. The ST segments themselves are usually isoelectric, but if they are abnormal, there will be less than 1 mm of elevation, with a high takeoff of the ST segment from the QRS complex. The characteristic ECG changes of this syndrome occur in the T-wave and occur in 2 forms.

There are two patterns of T-wave abnormality in Wellens syndrome:

  • Type A – Biphasic, with initial positivity and terminal negativity (24% of cases)
  • Type B – Deeply and symmetrically inverted (76% of cases)

Biphasic T Waves (Type A)

The more common of the 2 forms, which occurs 76% of the time, is deep inversion of the T-wave segment in the precordial leads (see the images below). The ST segment will be straight or concave and will pass into a deep negative T wave at an angle of 60°-90°. The T wave is symmetric. In Wellens syndrome, these changes generally occur in leads V1 -V4 but occasionally may also involve V5 and V6. V1 is involved in approximately 66% of patients, and V4 is involved nearly 75% of the time.

Wellens Pattern A (Type 1)

Deeply Inverted T Waves (Type B)

The less common of the 2 forms of Wellens syndrome, which occurs in 24% of patients, consists of biphasic T waves (see the images below), most commonly in leads V2 and V3 but also, on occasion, in leads V1 through V5 or even V6. The characteristic pattern classically presents only during chest pain–free periods. Noticing this pattern is crucial because it is a sign of LAD disease. This association underscores the importance of serial ECGs and a pain-free ECG on patients with unstable angina. Because the LAD supplies the anterior myocardium, failure to recognize this pattern can result in anterior wall myocardial infarction (MI), significant left ventricular dysfunction, or death.

Wellens Pattern B (Type 2)

Reperfusion of the posterior wall following posterior MI leads to a larger T-wave amplitude in the right precordial leads and an even higher T-wave amplitude in leads V2 and V3.

Wellens T wave evolution


T wave changes can evolve over time from Type A to Type B pattern (Smith et al).

Evolution of T-wave inversion [A-D] after coronary reperfusion in STEMI reperfusion and in Wellens syndrome (NSTEMI). Modified from Smith et al. Evolution of T-wave inversion. The ECG in acute MI, 2002

Diagnostic criteria

Rhinehart et al (2002) describe the following diagnostic criteria for Wellens syndrome:

  • Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
  • ECG pattern present in pain-free state
  • Isoelectric or minimally-elevated ST segment (< 1mm)
  • No precordial Q waves
  • Preserved precordial R wave progression
  • Recent history of angina
  • Normal or slightly elevated serum cardiac markers

Understanding T wave changes

The following sequence of events is thought to occur in patients with Wellens syndrome:

  • A sudden complete occlusion of the LAD causes a transient anterior STEMI, causing chest pain & diaphoresis. This stage may not be successfully captured on an ECG recording
  • Re-perfusion of the LAD (e.g. due to spontaneous clot lysis or prehospital aspirin) leads to resolution of chest pain. ST elevation improves and T waves become biphasic or inverted. The T wave morphology is identical to patients who reperfuse after a successful PCI
  • If the artery remains open, the T waves evolve over time from biphasic to deeply inverted
  • The coronary perfusion is unstable, however, and the LAD can re-occlude at any time. If this happens, the first sign on the ECG is an apparent normalisation of the T waves — so-called “pseudo-normalisation”. The T waves switch from biphasic/inverted to upright and prominent. This is a sign of hyperacute STEMI and is usually accompanied by recurrence of chest pain, although the ECG changes can precede the symptoms
  • If the artery remains occluded, the patient now develops an evolving anterior STEMI
  • Alternatively, a “stuttering” pattern may develop, with intermittent reperfusion and re-occlusion. This would manifest as alternating ECGs demonstrating Wellens and pseudonormalisation/STEMI patterns
  • This sequence of events is not limited to the anterior leads — similar changes may be seen in the inferior or lateral leads, e.g. with RCA or circumflex occlusion.

Also, the inciting event does not necessarily have to be thrombus formation — Wellens syndrome may also occur in normal coronary arteries following an episode of vasospasm, as in this case of cocaine-induced vasospasm. However, it is safer to assume the worst (i.e. critical LAD stenosis) and work the patient up for an angiogram.

Other Tests


Angiography has demonstrated that 100% of patients with Wellens syndrome will have 50% or greater stenosis of the proximal LAD. More specifically, 83% will have the lesion proximal to the second septal perforator.

Stress testing is generally not indicated in patients with this ECG presentation, because it places them at risk for acute anterior wall MI. Ideally, therefore, these patients would bypass stress testing and undergo urgent angiography to determine the extent of disease and potentially provide information about the need for percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), or medical management. If provocative testing is determined to be necessary, it should be done cautiously and only in close conjunction with a cardiologist.

Treatment Approach


A cardiologist should be consulted as early as possible in the management of a patient with Wellens syndrome. If the patient remains pain-free, it is appropriate to admit him or her to an internist on a telemetry floor, but the internist should be notified that the patient is at high risk and should not undergo stress testing unless clearly recommended by cardiologists.

If symptoms persist or electrocardiography shows evolution into ST-segment elevations, an interventional cardiologist should be consulted immediately. Transfer of these patients to institutions with cardiac catheterization capabilities is generally appropriate.

First aid (prehospital stage)

Because Wellens syndrome occurs because of stenosis of the proximal left anterior descending coronary artery, patients typically complain of chest pain presenting as unstable angina. During episodes of pain, they should be treated in the same manner as any patient experiencing chest pain thought to be cardiac in origin.

Immediate arrangements should be made for transport to the nearest hospital. Careful attention should be paid to the ABCs (airway, breathing, and circulation). During transport, efforts should be made to carry out the following:

  • Oxygen supplementation
  • Assessment of vital signs
  • Intravenous (IV) access
  • Administration of aspirin
  • ECG, if available before arrival at the hospital
  • If pain persists, administration of nitroglycerin or morphine, according to local protocols

If Wellens syndrome is identified on an outpatient basis, then arrangements should be made for urgent evaluation. Stress testing should be avoided.

Medical care during hospital stage

Patients presenting with symptoms consistent with unstable angina should generally receive medications and other therapies and measures that may help prevent myocardial infarction (MI). Usually, these would include the following:

  • IV access
  • Supplemental oxygen, when appropriate
  • ECG (initially) – Serial examinations and pain-free tracings may be helpful
  • Telemetry monitoring
  • Chest radiography
  • Laboratory studies (see Laboratory Studies)
  • Aspirin
  • Consideration should be given to providing beta-blocker therapy, nitroglycerin, morphine, heparin, clopidogrel, and glycoprotein (GP) IIb/IIa inhibitors

Once again, the ECG changes in Wellens syndrome are typically only present when the patient is free of chest pain. Thus, obtaining serial ECGs on patients with unstable angina may be helpful.

Even though the ECG changes may be subtle, it is vital to recognize Wellens syndrome because these patients can rarely undergo stress testing safely. Because Wellens syndrome is a sign of a preinfarction stenosis of the LAD, a stress test has the potential to result in acute MI and severe damage to the left ventricle. Therefore, these patients should generally forgo a stress test and instead may undergo angiography to evaluate the need for angioplasty or coronary artery bypass surgery (CABG).

Even with ideal medical management, the natural progression of Wellens syndrome is to acute anterior wall MI. Approximately 75% of patients with Wellens syndrome who receive only medical management and do not undergo revascularization (either through CABG or through angioplasty) will go on to develop extensive anterior wall MI within days. Anterior wall MI carries substantial morbidity and mortality: it will result in left ventricular dysfunction and possibly even death.

Thus, patients generally should be medically stabilized if possible while arrangements are made for urgent angiography and revascularization if appropriate.

The goals of pharmacotherapy are to reduce morbidity and prevent complications. Agents used in the management of Wellens syndrome include salicylates, antihypertensive drugs, antianginal drugs, antiplatelet drugs, analgesics, low-molecular-weight heparins (LMWHs), antiarrhythmic drugs, and anticoagulants.

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References

  1. Mike Cadogan and Robert Buttner  Wellens Syndrome. Ecg library. Sep 2021 https://litfl.com/wellens-syndrome-ecg-library/
  2. de Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr. 103(4 Pt 2):730-6. [Medline].
  3. Nisbet BC, Zlupko G. Repeat Wellens’ syndrome: case report of critical proximal left anterior descending artery restenosis. J Emerg Med. 2010 Sep. 39(3):305-8. [Medline].
  4. Patel K, Alattar F, Koneru J, Shamoon F. ST-elevation myocardial infarction after pharmacologic Persantine stress test in a patient with Wellens’ syndrome. Case Rep Emerg Med. 2014. 2014:530451. [Medline]. [Full Text].
  5. Moore KL, Dalley AF. Thorax. Clinically Oriented Anatomy. 4th ed. Baltimore, Maryland: Lippincott Williams & Wilkins; 1999. 135.
  6. de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J. 1989 Mar. 117(3):657-65. [Medline].
  7. Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. Ann Emerg Med. 1999 Mar. 33(3):347-51. [Medline].
  8. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002 Nov. 20(7):638-43. [Medline].
  9. Driver BE, Shroff GR, Smith SW. Posterior reperfusion T-waves: Wellens’ syndrome of the posterior wall. Emerg Med J. 2017 Feb. 34(2):119-23. [Medline].
  10. Tatli E, Aktoz M, Buyuklu M, Altun A. Wellens’ syndrome: the electrocardiographic finding that is seen as unimportant. Cardiol J. 2009. 16(1):73-5. [Medline].
  11. Narasimhan S, Robinson GM. Wellens syndrome: a combined variant. J Postgrad Med. 2004 Jan-Mar. 50(1):73-4. [Medline].
  12. Sowers N. Harbinger of infarction: Wellens syndrome electrocardiographic abnormalities in the emergency department. Can Fam Physician. 2013 Apr. 59(4):365-6. [Medline]. [Full Text].
  13. Balasubramanian K, Balasubramanian R, Subramanian A. A dangerous twist of the ‘T’ wave: A case of Wellens’ Syndrome. Australas Med J. 2013. 6(3):122-5. [Medline]. [Full Text].
  14. Singh B, Singh Y, Singla V, Nanjappa MC. Wellens’ syndrome: a classical electrocardiographic sign of impending myocardial infarction. BMJ Case Rep. 2013 Feb 18. 2013:[Medline].
  15. Movahed MR. Wellens’ syndrome or inverted U-waves?. Clin Cardiol. 2008 Mar. 31(3):133-4. [Medline].
  16. Y-Hassan S. The pathogenesis of reversible T-wave inversions or large upright peaked T-waves: Sympathetic T-waves. Int J Cardiol. 2015 Jul 15. 191:237-43. [Medline].
  17. Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14. 2017:[Medline].
  18. Abuarqoub A, Naranjo M, Shamoon F. Myocardial bridging with left ventricular hypertrophy presenting as Wellens pattern. Ann Transl Med. 2017 Oct. 5(20):401. [Medline]. [Full Text].
  19. Hsu YC, Hsu CW, Chen TC. Type B Wellens’ syndrome: Electrocardiogram patterns that clinicians should be aware of. Ci Ji Yi Xue Za Zhi. 2017 Apr-Jun. 29(2):127-8. [Medline]. [Full Text].

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]]> SCORE2 and SCORE2-OP scales for determining cardiovascular risk https://clincasequest.hospital/score2-score2-op/ Tue, 14 Sep 2021 14:00:34 +0000 https://clincasequest.hospital/?p=30425 Apparently healthy people are those without established ASCVD, type 2 DM, or severe comorbidities. In the 2016 ESC prevention guidelines, the Systemic Coronary Risk Estimation…

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Apparently healthy people are those without established ASCVD, type 2 DM, or severe comorbidities. In the 2016 ESC prevention guidelines, the Systemic Coronary Risk Estimation (SCORE) algorithm was used to estimate 10-year risk of CVD death. However, CVD morbidity (non-fatal myocardial infarction, non-fatal stroke) combined with CVD mortality better reflects the total burden of ASCVD. The updated SCORE algorithm – SCORE2 – used in these guidelines, estimates an individual’s 10-year risk of fatal and non-fatal CVD events (myocardial infarction, stroke) in apparently healthy people aged 40–69 years with risk factors that are untreated or have been stable for several years.

NB! The SCORE2 charts do not apply to persons with documented CVD or other high-risk conditions such as DM, FH, or other genetic or rare lipid or BP disorders, CKD, and in pregnant women.

Several specific considerations apply to CVD risk estimation in older people.

First, the gradient of the relationship between classical risk factors, such as lipids and BP, with CVD risk attenuates with age.

Second, CVD-free survival dissociates from overall survival progressively with increasing age, because risk for non-CVD mortality increases (‘competing risk’). For these reasons, traditional risk models that do not take into account the competing risk of non-CVD mortality, tend to overestimate the actual 10-year risk of CVD, and hence overestimate the potential benefit of treatment. The SCORE2-OP algorithm estimates 5-year and 10-year fatal and non-fatal CVD events (myocardial infarction, stroke) adjusted for competing risks in apparently healthy people aged ≥70 years.

Algorithm of use

To estimate a person’s 10-year risk of total CVD events, one must first identify the correct cluster of countries and the accompanying risk table for their sex, smoking status, and (nearest) age. Within that table, one then finds the cell nearest to the person’s BP and non-HDL-C. Risk estimates then need to be adjusted upwards as the person approaches the next age category.

SCORE2 & SCORE2-OP in populations at low CVD risk:

SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator
SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator

SCORE2 & SCORE2-OP in populations at moderate CVD risk:

SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator
SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator

SCORE2 & SCORE2-OP in populations at high CVD risk:

SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator
SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator

SCORE2 & SCORE2-OP in populations at very high CVD risk:

SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator
SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator

ASCVD = atherosclerotic cardiovascular disease; CV = cardiovascular; CVD = cardiovascular disease; SBP = systolic blood pressure; HDL-C = high-density lipoprotein cholesterol; SCORE2 = Systematic Coronary Risk Estimation 2; SCORE2-OP = Systematic Coronary Risk Estimation 2-Older Persons.

Risk regions based on World Health Organisation cardiovascular mortality rates

SCORE2, SCORE2 scale, SCORE2-OP, SCORE2-OP scale, cardiovascular risk, cardiovascular risk assessment, CVD risk assessment, CVD risk, medical calculator, online medical calculator

Low-risk countries: Belgium, Denmark, France, Israel, Luxembourg, Norway, Spain, Switzerland, the Netherlands, and the United Kingdom.

Moderate-risk countries: Austria, Cyprus, Finland, Germany, Greece, Iceland, Ireland, Italy, Malta, Portugal, San Marino, Slovenia, and Sweden.

High-risk countries: Albania, Bosnia and Herzegovina, Croatia, Czech Republic, Estonia, Hungary, Kazakhstan, Poland, Slovakia, and Turkey.

Very-high-risk countries: Algeria, Armenia, Azerbaijan, Belarus, Bulgaria, Egypt, Georgia, Kyrgyzstan, Latvia, Lebanon, Libya, Lithuania, Montenegro, Morocco, Republic of Moldova, Romania, Russian Federation, Serbia, Syria, The Former Yugoslav Republic (Macedonia), Tunisia, Ukraine, and Uzbekistan.

A source:
Frank L J Visseren, François Mach, Yvo M Smulders, David Carballo, Konstantinos C Koskinas, Maria Bäck, Athanase Benetos, Alessandro Biffi, José-Manuel Boavida, Davide Capodanno, Bernard Cosyns, Carolyn Crawford, Constantinos H Davos, Ileana Desormais, Emanuele Di Angelantonio, Oscar H Franco, Sigrun Halvorsen, F D Richard Hobbs, Monika Hollander, Ewa A Jankowska, Matthias Michal, Simona Sacco, Naveed Sattar, Lale Tokgozoglu, Serena Tonstad, Konstantinos P Tsioufis, Ineke van Dis, Isabelle C van Gelder, Christoph Wanner, Bryan Williams, ESC Scientific Document Group, 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice: Developed by the Task Force for cardiovascular disease prevention in clinical practice with representatives of the European Society of Cardiology and 12 medical societies With the special contribution of the European Association of Preventive Cardiology (EAPC), European Heart Journal, Volume 42, Issue 34, 7 September 2021, Pages 3227–3337, https://doi.org/10.1093/eurheartj/ehab484

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Сообщение SCORE2 and SCORE2-OP scales for determining cardiovascular risk появились сначала на ClinCaseQuest.

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