Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

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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 )

Drug-eluting stents (DESs) have minimized the limitations of bare-metal stents (BMSs) after percutaneous coronary interventions. Nevertheless, serious concerns remain about possible late complications of stenting, such as stent thrombosis (ST) and in-stent restenosis (ISR), although the introduction of second-generation DESs seems to have softened the phenomenon, compared to the first-generation ones. ST is a potentially catastrophic event, which has been markedly reduced by optimization of stent implantation, novel stent designs, and dual antiplatelet therapy. The exact mechanism to explain its occurrence is under investigation, and, realistically, multiple factors are responsible. ISR of BMSs has been previously considered as a stable condition with an early peak (at 6 months) of intimal hyperplasia, followed by a regression period beyond 1 year. On the contrary, both clinical and histologic studies of DESs have demonstrated evidence of continuous neointimal growth during long-term follow-up, named “late catch-up” phenomenon. The acknowledgment that ISR is a relatively benign clinical condition has been recently challenged by evidences which reported that patients with ISR can experience acute coronary syndromes. Intracoronary imaging is an invasive technology that allows identifying features of atherosclerotic plaque of stent implanted and of vascular healing after stenting; it is often used to complete diagnostic coronary angiography and to drive interventional procedures. Intracoronary optical coherence tomography is currently considered a state-of-the-art imaging technique; it provides, compared to intravascular ultrasound, better resolution (at least >10 times), allowing the detailed characterization of the superficial structure of the vessel wall. Imaging studies “in vivo,” in agreement with histological findings, suggest that chronic inflammation and/or endothelial dysfunction may induce late de novo “neoatherosclerosis” inside both BMSs and DESs. So, neoatherosclerosis has become the prime suspect in the pathogenesis of late stent failure.

The present study shows that the largest proportion of cardiogenic shock complicating ST-segment elevation myocardial infarction is observed after initial hospitalization, particularly in patients with Killip class more than 1, low systolic blood pressure at presentation and advanced age. The identification of these patients may help in preventing this complication by more aggressive pharmacological therapies, mechanical haemodynamic support, as well as coronary revascularization.