Syndromes in internal medicine & critical care

[drfaten]

Wellens syndrome was first described by de Zwaan, Wellens, and colleagues in the early 1980s when they recognized a subset of patients with unstable angina who had specific precordial T-wave changes and subsequently developed a large anterior wall myocardial infarction.1 Wellens syndrome refers to these specific electrocardiographic 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.2  Syndrome criteria include characteristic T-wave changes; a history of anginal chest pain; normal or minimally elevated cardiac enzyme levels; and finally an ECG without Q waves, without significant ST elevation, and normal precordial R-wave progression. Recognition of this ECG abnormality is of paramount importance because this syndrome represents a preinfarction stage of coronary artery disease that often progresses to a devastating anterior wall infarction.   

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

The more common form, which occurs 76% of the time, is deep inversion of the T-wave segment in the precordial leads.3 The ST segment will be straight or concave, and pass into a deep negative T wave at an angle of 60-90 degrees. The T wave is symmetric. In Wellens syndrome, these changes generally occur in leads V1 -V4 but may also occasionally involve V5 and V6. V1 is involved in approximately 66% of patients and lead V4 nearly 75% of the time


Wellens syndrome represents critical stenosis of the left anterior descending coronary artery (LAD). The LAD arises from the left coronary artery and travels in 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.6  A lesion in the LAD can have severe consequences, as evidenced by the LAD’s nickname “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 of congestive heart failure and death

treatment

1-Salicylates
These agents have antiplatelet properties

Antihypertensive Agents
These agents reduce high blood pressure
Metoprolol

Antianginal Agents
These agents can reduce blood pressure

Antiplatelet Agents
These agents inhibit platelet aggregation

Low Molecular Weight Heparins
These agents inhibit thrombogenesis

[EdibK]

 I just saw an interesting case presentation of ECG changes related to cerebrovascular disease, including strokes and subdural, subarachnoid and epidural hematomas. These changes may include QT prolongation and symmetric deep T wave inversions, widespread and pronounced in precordial leads V2-V6. Therefore these become an option in the differential diagnosis of the Wellens syndrome.
Thank you for your great presentation.