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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 )

HSP72 is implicated in cardioprotection in combination with some other factors, and its pre-operational level, among other parameters, might be of prognostic value.

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The 2019 coronavirus pandemic (COVID-19), due to the new SARS-CoV-2 virus, represents the greatest global public health crisis and an unprecedented challenge to find effective ways to prevent and treat. In the active phase of a pandemic, early results allow these preventive measures to be implemented on a scale compatible with the pandemic. If the results are convincing, their value will be difficult to overestimate, since additional one or two outbreaks of this infection are expected. Clinical data is emerging rapidly from a large number of people afflicted with SARS-CoV-2, which should provide clinicians with accurate evidence of the effectiveness of different preventive and treatment methods. In particular, an active search is underway for cellular mechanisms that SARS-CoV-2 uses to penetrate tissues. These include information about the receptor of the angiotensin-converting enzyme receptor (ACE 2). SARS-CoV-2, a single-stranded envelope RNA virus, attaches to cells via a viral spike (S) protein that binds to the ACE 2. After binding to the receptor, the viral particle uses the receptors of the host cell and endosomes to enter the cells. Human type transmembrane serine protease 2 (TMPRSS 2) facilitates penetration into the cell via protein S. Once inside the cell, viral polyproteins are synthesized that encode the replicate transcriptase complex. The virus then synthesizes RNA through its RNA-dependent RNA polymerase. Structural proteins are synthesized leading to the completion of the assembly and release of viral particles. These stages of the virus life cycle provide potential targets for drug therapy. Current clinical and scientific data do not support discontinuation of ACE inhibitors or angiotensin receptor blockers in patients with COVID-19, and an ongoing discussion is addressed in this review.