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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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.

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.

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

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

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:

• Aslanger E, Yıldırımtürk Ö, Şimşek B, Sungur A, Türer Cabbar A, Bozbeyoğlu E, Karabay CY, Smith SW, Değertekin M. A new electrocardiographic pattern indicating inferior myocardial infarction. J Electrocardiol. 2020 Jul-Aug;61:41-46.
• Aslanger EK, Smith SW. Response to: “A new electrocardiographic pattern indicating inferior myocardial infarction”. J Electrocardiol. 2020 Nov 18

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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.

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.

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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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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Сообщение Two masks of the same syndrome: Wellens syndrome появились сначала на ClinCaseQuest.

	PRECISE-DAPT Scale	DAPT Scale
Time of use	During coronary stenting	After 12 months DAPT in the absence of cardiovascular events
DAPT duration strategies	Short-term DAPT (3-6 months) or standard/long-term DAPT (12-24 months)	Standard DAPT (12 months) or long-term DAPT (30 months)
Scoring	PRECISE-DAPT, DAPT Scales	Age >75 years 65-75 years Smoking Diabetes mellitus MI at presentation Prior PCI or MI Paclitaxel-eluting stent Stent diameter less 3 mm CHF or LVEF 30 < 30 % Vein graft stent	-2 points -1 point 0 point +1 point +1 point +1 point +1 point +1 point +1 point +2 point +2 point
Scale values	From 0 to 100 points	From -2 to 10 points
Decision threshold	>25 points – short-term DAPT	>2 points – long-term DAPT

For PRECISE-DAPT scores, use a nomogram: note the values for each of the five clinical parameters and draw a vertical line to the Scale Score axis to determine the score for each clinical parameter. Then add the scores for each clinical measure to determine the total score.

NB! Time of use of this score – during stenting of the coronary arteries.

Depending on the obtained results, and the calculated data decision can be made on short-term DAPT (3-6 months) or standard/long-term DAPT (12-24 months), taking into account the presence of the risks of bleeding.

The range of values is from 0 to 100 points.

Сообщение PRECISE-DAPT, DAPT on-line calculator появились сначала на ClinCaseQuest.