Background: Atherosclerosis is a multi-factorial disease, and low-density lipoprotein cholesterol (LDL-C) is a critical risk factor in developing atherosclerotic cardiovascular disease (ASCVD). Cholesteryl-ester transfer-protein (CETP), synthesized by the liver, regulates LDL-C and high-density lipoprotein cholesterol (HDL-C) through the bidirectional transfer of lipids. The novelty of CETP inhibitors (CETPis) has granted new focus towards increasing HDL-C, besides lowering LDL-C strategies. To date, five CETPis that are projected to improve lipid profiles, torcetrapib, dalcetrapib, evacetrapib, anacetrapib, and obicetrapib, have reached late-stage clinical development for ASCVD risk reduction. Early trials failed to reduce atherosclerotic cardiovascular occurrences. Given the advent of some recent large-scale clinical trials (ACCELERATE, HPS3/TIMI55-REVEAL Collaborative Group), conducting a meta-analysis is essential to investigate CETPis’ efficacy. Methods: We conducted a thorough search of randomized controlled trials (RCTs) that commenced between 2003 and 2023; CETPi versus placebo studies with a ≥6-month follow-up and defined outcomes were eligible. Primary outcomes: major adverse cardiovascular events (MACEs), cardiovascular disease (CVD)-related mortality, all-cause mortality. Secondary outcomes: stroke, revascularization, hospitalization due to acute coronary syndrome, myocardial infarction (MI). Results: Nine RCTs revealed that the use of a CETPi significantly reduced CVD-related mortality (RR = 0.89; 95% CI: 0.81–0.98; p = 0.02; I2 = 0%); the same studies also reduced the risk of MI (RR = 0.92; 95% CI: 0.86–0.98; p = 0.01; I2 = 0%), which was primarily attributed to anacetrapib. The use of a CETPi did not reduce the likelihood any other outcomes. Conclusions: Our meta-analysis shows, for the first time, that CETPis are associated with reduced CVD-related mortality and MI.

The efficacy and safety profile of mavacamten, a cardiac myosin inhibitor for the treatment of hypertrophic cardiomyopathy (HCM) is not well-established, prompting the need for an updated meta-analysis. The authors conducted an extensive search across multiple electronic databases, including Embase, MEDLINE (via Pubmed), and CENTRAL, to identify randomized controlled trials (RCTs) assessing the efficacy and safety of mavacamten in HCM. Review Manager 5.4 (Revman) was employed to pool risk ratios (RR) and mean differences (MD). Our literature search yielded 4 RCTs with a total of 503 patients. Mavacamten was found to be associated with higher rates of greater than or equal to 1 New York Heart Association (NYHA) class improvement (RR 2.20, 95% CI: 1.48–3.28; I²=51%) and change from baseline in the Kansas City Cardiomyopathy Questionnaire- Clinical Summary Score (KCCQ-CSS) (MD 7.50, 95% CI: 3.44–11.55; I² =50%). Mavacamten was also associated with improved resting left ventricular outflow tract (LVOT) gradient (MD −38.33, 95% CI: −49.38 to −27.28; I² =75%), Valsalva LVOT gradient (MD −48.08, 95% CI: −62.21 to −33.96; I² =78%), post-exercise LVOT gradient (MD −37.1, 95% CI: −44.37 to −29.84; I² =0%), LVMI (MD −16.91, 95% CI: −28.29 to −5.54; I² =88%), and lower rates of septal reduction therapy (SRT) (RR 0.30, 95% CI: 0.22–0.40; I² =0%). There were no significant differences between mavacamten and placebo regarding the composite functional outcome, greater than or equal to 1 treatment-emergent adverse event, greater than or equal to 1 serious adverse event, and atrial fibrillation. The authors; findings suggest that mavacamten contributes to improvements in NYHA class, KCCQ-CSS scores, and LVOT gradients while reducing the incidence of SRT in patients with HCM.

This case represents the association between the presence of large fibroid tumor and pulmonary embolism in 47-year-old women. We highlight the diagnostic investigations and treatment methods for PE, followed by further evaluation of the underlying explanation of this pathology and eliminating other related risk factors.