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Everolimus-eluting stent implantation for unprotected left main coronary artery stenosis. The PRECOMBAT-2 (Premier of Randomized Comparison of Bypass Surgery versus Angioplasty Using Sirolimus-Eluting Stent in Patients with Left Main Coronary Artery Disease) study Contemporary prevalence of pulmonary arterial hypertension in adult congenital heart disease following the updated clinical classification Pulmonary Artery Denervation for Patients With Residual Pulmonary Hypertension After Pulmonary Endarterectomy Evaluation and Management of Aortic Stenosis in Chronic Kidney Disease: A Scientific Statement From the American Heart Association Low shear stress induces vascular eNOS uncoupling via autophagy-mediated eNOS phosphorylation Pulmonary Hypertension Caused by a Coconut Left Atrium Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease Incidence and Management of Restenosis After Treatment of Unprotected Left Main Disease With Second-Generation Drug-Eluting Stents (from Failure in Left Main Study With 2nd Generation Stents-Cardiogroup III Study) Radial versus femoral artery access in patients undergoing PCI for left main coronary artery disease: analysis from the EXCEL trial Definition and Management of Segmental Pulmonary Hypertension

Clinical Trial2021 Aug 1;152:34-42.

JOURNAL:Am J Cardiol. Article Link

Effect of Lipoprotein (a) Levels on Long-term Cardiovascular Outcomes in Patients with Myocardial Infarction with Nonobstructive Coronary Arteries

SD Gao, WJ Ma, MY Yu Keywords: Lp(a); MINOCA; STEMI; prognostic value; MACE

ABSTRACT

The association between elevated lipoprotein(a) [Lp(a)] and poor outcomes in coronary artery disease (CAD) has been addressed for decades. However, little is known about the prognostic value of Lp(a) in patients with myocardial infarction with nonobstructive coronary arteries (MINOCA). A total of 1179 patients with MINOCA were enrolled and divided into low, medium, and high Lp(a) groups based on the cut-off value of 10 and 30mg/dL. The primary endpoint was major adverse cardiovascular events (MACE), a composite of all-cause death, nonfatal MI, nonfatal stroke, revascularization, and hospitalization for unstable angina or heart failure. Kaplan-Meier and Cox regression analyses were performed. Accuracy was defined as area under the curve (AUC) using a receiver-operating characteristic analysis. Patients with higher Lp(a) levels had a significantly higher incidence of MACE (9.5%, 14.6%, 18.5%; p = 0.002) during the median follow-up of 41.7 months. The risk of MACE also increased with the rising Lp(a) levels even after multivariate adjustment [low Lp(a) group as reference, medium group: hazard ratio (HR) 1.55, 95% confidence interval (CI): 1.02-2.40, p = 0.047; high group: HR 2.07, 95% CI: 1.32-3.25, p = 0.001]. Further, clinically elevated Lp(a) defined as Lp(a) ≥30 mg/dL was closely associated with an increased risk of MACE in overall and in subgroups (all p <0.05). When adding Lp(a) (AUC 0.61) into the Thrombolysis in Myocardial Infarction (TIMI) score (AUC 0.68), the combined model (AUC 0.73) yielded a significant improvement in discrimination for MACE (ΔAUC 0.05, p = 0.032). In conclusion, elevated Lp(a) was strongly associated with a poor prognosis in patients with MINOCA. Adding Lp(a) to traditional risk score further improved risk prediction. Our data, for the first time, confirmed the Lp(a) as a residual risk factor for MINOCA.