Unstable Angina: Risk Stratification for Significant Coronary Artery Disease in The Era of High-Sensitivity Cardiac
Luis Paiva1,2, Maria João Vieira3,4, Rui Baptista1,5
1Faculdade de Medicina, Universidade de Coimbra, Portugal.
Introduction:
High-sensitivity troponin (hsTn) has a very high diagnostic accuracy for myocardial infarction (MI), and patients who were formerly diagnosed with unstable angina (UA) are being reclassified as having NSTEMI in the era of hsTn. This paradigm shift has changed the clinical features of UA, which remain poorly characterized, specifically the occurrence of obstructive coronary artery disease (CAD) and the need for myocardial revascularization. The main purpose of this study was to clinically characterize contemporary UA patients, assess predictors of obstructive CAD, and develop a risk model to predict significant CAD in this population.
Methods:
We conducted a retrospective cohort study of 742 patients admitted to the hospital with UA. All patients underwent coronary angiography. The endpoint of the study was the presence of obstructive CAD on angiography. The cohort was divided into two groups: patients with significant coronary artery disease (CAD+) and those without CAD (CAD-). We developed a score (UA CAD Risk) based on the multivariate model and compared it with the GRACE, ESC, and TIMI risk scores using ROC analysis.
Results:
Obstructive CAD was observed on angiography in 53% of the patients. Age, dyslipidemia, troponin level, male sex, ST-segment depression, and wall motion abnormalities on echocardiography were independent predictors of obstructive CAD. hsTn levels (undetectable vs. nonsignificant detection) had a negative predictive value of 81% to exclude obstructive CAD. We developed a prediction model with obstructive CAD as the outcome (AUC: 0.60).
Conclusions:
In a contemporary UA cohort, approximately 50% of the patients did not have obstructive CAD on angiography. Commonly available cardiac tests at hospital admission show limited discrimination power in identifying patients at risk of obstructive CAD. A revised diagnostic and etiology algorithm for patients with UA is warranted.
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