Рациональная фармакотерапия в кардиологии (Oct 2023)
Wellens’ syndrome in clinical practice
Abstract
Despite the declining cardiovascular mortality, the incidence of myocardial infarction (MI) is still high, and therefore the issues of its timely diagnosis remain extremely relevant. In addition to the main diagnostic criteria and typical electrocardiographic (ECG) signs, there are many secondary patterns that suggest MI. Wellens’ syndrome (WS) is one of these ECG patterns, which indicates that the patient is at high risk of left ventricular anterior wall MI, caused by occlusion of the anterior interventricular artery (AIA) or its critical stenosis. Despite the relatively low incidence of WS, it is necessary to increase physicians’ awareness in order to prevent MI and reduce its possible negative consequences.This article presents clinical cases of WS, which show the importance of its diagnosis in the management of patients with anginal pain. The first patient is 43-year-old with a diagnosis of class III exertional angina, a history of anginal pain, and the presence of inverted T waves in V2-V3 leads. AIA stenting was performed on the 7th day of hospitalization. The second patient is 67-year-old with a similar diagnosis and history, biphasic T waves in I, aVL, V1-V3 and V5-V6 leads, deeply inverted T waves in V4. Stenting of the AIA and right coronary artery (RCA) was performed on days 5-6 after the most severe episode of anginal pain and after the anginal pain became recurrent. In both cases, WS was not diagnosed. The third patient, 57-year-old, with T wave inversion in II, III, aVF, leads ST segment elevation of less than 1 mm in lead III, minimal ST segment depression in aVL and V2-V3 leads, followed in less than 2 hours by ST segment elevation in II, III, aVF leads. In this patient, WS was diagnosed in a timely manner, urgent coronary angiography was performed, 99% RCA stenosis was detected, and RCA stenting was performed. The outcome is left ventricular inferior wall non-Q wave MI. The last cited case of WS indicates that this syndrome develops not only with AIA damage, but also with damage to other coronary arteries.
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