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Editorial
. 2021 Jun;16(2):216-222.
doi: 10.26574/maedica.2021.16.2.216.

Wellens Sign: Monography and Single Center Experience

Affiliations
Editorial

Wellens Sign: Monography and Single Center Experience

Anamaria Avram et al. Maedica (Bucur). 2021 Jun.

Abstract

Objective:Wellens syndrome has been described as a clinical and electrocardiographic complex that identifies a subset of patients with unstable angina (UA) at an impending risk of myocardial infarction (MI) and death in studies published almost four decades ago, before the wide use of cardiac biomarkers such as troponins. The clinical implications of Wellens sign in a contemporary cohort of patients with non-ST elevation acute coronary syndromes (NSTEACS) is yet to be defined. Material and methods:We performed a prospective analysis of patients with acute coronary syndrome (ACS) and Wellens sign who underwent coronary angiography between January 2018 and December 2019. Patients follow-up visits were at one month and at six months. Clinical, electrocardiographic, biological and echocardiographic data were recorded at both follow-up visits. Results: A total of 79 patients were included in the statistical analysis, of whom 16 (20.25%) had pure Wellens syndrome (normal myocardial necrosis biomarkers). The prevalence of type A Wellens sign was higher than previously reported (45.6%). The culprit coronary artery was most frequently LAD (49 pts, 62.03%), followed by LM (10 patients, 12.66%), right coronary artery (RCA) (eight pts, 10.13%), instent restenosis (three pts, 3.8%), left circumflex artery (LCX) (two pts, 2.53%) and bypass graft (one pt, 1.27%). Ischaemic reccurence rate within six months was 18,99%. The rate of reccurent percutaneous revascularization procedures was 11.54% and the rate of repeat target vessel revascularization (TVR) was 5.77% at six months. All-cause mortality rate at six months was 7.59%, with 5.06% cardiovascular deaths. Conclusion: Early recognition of subtle ECG changes resembling Wellens sign in patients with chest pain is crucial as it reflects a large area of myocardium at risk. In our study, the culprit coronary artery was most frequently LAD (62.03%), with 36.7% proximal LAD culprit lesion, followed by LM (12.66%). Wellens syndrome should be considered a high risk condition that makes the conventional methods for risk assesment using risk scores unnecessary, useless and potentially deleterious. In our study, according to GRACE 1.0 risk score, 70.89% of patients were in the low risk group (1-108 points, estimated in-hospital death risk < 1%). No patient died during the initial hospitalization. All-cause mortality rate at six months was 7.59%, with 5.06% cardiovascular deaths.

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Figures

TABLE 1.
TABLE 1.
Wellens syndrome etiology
FIGURE 1.
FIGURE 1.
Type A Wellens electrocardiographic pattern (see text for further explanations).
FIGURE 2.
FIGURE 2.
Type B Wellens electrocardiographic pattern (see text for further explanations).
TABLE 2.
TABLE 2.
Differential diagnosis of Wellens sign – adapted from (10)
TABLE 3.
TABLE 3.
Baseline demographic and clinical characteristics

References

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