BACKGROUND Guidelines recommend nonstatin lipid-lowering agents in patients at very high risk for major adverse cardiovascular events (MACE) if low-density lipoprotein cholesterol (LDL-C) remains ≥70 mg/dL on maximum tolerated statin treatment. It is uncertain if this approach benefits patients with LDL-C near 70 mg/dL. Lipoprotein(a) levels may influence residual risk. OBJECTIVES In a post hoc analysis of the ODYSSEY Outcomes (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trial, the authors evaluated the benefit of adding the proprotein subtilisin/kexin type 9 inhibitor alirocumab to optimized statin treatment in patients with LDL-C levels near 70 mg/dL. Effects were evaluated according to concurrent lipoprotein(a) levels. METHODS ODYSSEY Outcomes compared alirocumab with placebo in 18,924 patients with recent acute coronary syndromes receiving optimized statin treatment. In 4,351 patients (23.0%), screening or randomization LDL-C was <70 mg/dL (median 69.4 mg/dL; interquartile range: 64.3–74.0 mg/dL); in 14,573 patients (77.0%), both determinations were ≥70 mg/dL (median 94.0 mg/dL; interquartile range: 83.2–111.0 mg/dL). RESULTS In the lower LDL-C subgroup, MACE rates were 4.2 and 3.1 per 100 patient-years among placebo-treated patients with baseline lipoprotein(a) greater than or less than or equal to the median (13.7 mg/dL). Corresponding adjusted treatment hazard ratios were 0.68 (95% confidence interval [Cl]: 0.52–0.90) and 1.11 (95% Cl: 0.83–1.49), with treatment-lipoprotein(a) interaction on MACE ( P interaction = 0.017). In the higher LDL-C subgroup, MACE rates were 4.7 and 3.8 per 100 patient-years among placebo-treated patients with lipoprotein(a) >13.7 mg/dL or ≤13.7 mg/dL; corresponding adjusted treatment hazard ratios were 0.82 (95% Cl: 0.72–0.92) and 0.89 (95% Cl: 0.75–1.06), with P interaction = 0.43. CONCLUSIONS In patients with recent acute coronary syndromes and LDL-C near 70 mg/dL on optimized statin therapy, proprotein subtilisin/kexin type 9 inhibition provides incremental clinical benefit only when lipoprotein(a) concentration is at least mildly elevated. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402 )

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Background: Obesity continues to increase exponentially across the globe. BMI has been the traditional method used to define and quantify the severity of obesity. In recent years, visceral fat has emerged as an important measure of cardiovascular risk. Although MRI and CT scan can estimate the degree of visceral fat, these methods are not feasible in the routine clinical setting. Visceral Adiposity Index (VAI) is a recently derived index to measure visceral fat based on the knowledge of Waist Circumference (WC), plasma HDL, triglycerides and BMI. The study aimed to compare VAI with other adiposity indices in Acute MI and to also assess its ability to detect metabolic syndrome. Methods: In this crosssectional study, 213 patients (Acute STEMI-106, Controls-107) were included. The lipid profile and all other routine laboratory investigations were performed. Waist and hip circumference (HC) were measured. VAI and other adiposity indices were measured such as atherogenic index (AI), Conicity index (CI), Waist Hip Ratio (WHR) and Waist Height Ratio (WHtR) using appropriate formulae. Results: Patients with metabolic syndrome had higher VAI index (p=0.0001), higher AI index (p=0.0001), higher CI (p=0.0001), higher BMI (p=0.0001), higher WC (p=0.0001) and higher HC (p=0.0001). An ROC curve plotted for each adiposity index to detect metabolic syndrome showed VAI to have the maximal AUC. A VAI of 2.69 was chosen as the cutoff value which had a sensitivity of 70.1% and specificity of 74.35 % (AUC=0.81, CI-0.74 to 0.87; P=0.0001). Conclusion: VAI is an excellent and simple tool to detect Mets as compared to other adiposity indices. It remains to be seen if VAI could accurately reflect the degree of cardiovascular risk from prospective cohort studies.