STUDY DESIGN Lerodalcibep is a third-generation proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitor that prevents PCSK9 from binding to low-density lipoprotein receptors (LDLRs).1 Low-density lipoprotein-cholesterol (LDL-C) clearance from the bloodstream is enhanced as a result of LDLR

A reduction in LDL-C is associated with improvements in CV outcomes in patients with ASCVD.¹ As such, multiple guidelines recommend LDL-C targets of <55mg/dL and <70mg/dL based on baseline risks.¹ However, many patients fail their LDL-C goals due to clinical inertia, medication nonadherence, side effects, and/or poor healthcare access.¹ Inclisiran is a first-in-class siRNA that inhibits hepatic PCSK9 production and increases LDL receptor expression and LDL-C clearance.¹ In clinical studies, twice-yearly administration of inclisiran has been shown to achieve a 50% reduction in LDL-C.¹

STUDY DESIGN Dual antiplatelet therapy (DAPT) with aspirin + a potent P2Y12 receptor inhibitor for 12 months is the mainstay for patients presenting with acute coronary syndrome (ACS) who have been treated with percutaneous coronary intervention (PCI) to prevent myocardial infarction (MI) and stent

Acute coronary syndromes (ACS) encompass a spectrum of conditions including unstable angina, non-ST-elevation myocardial  infarction (NSTEMI), or ST-elevation myocardial infarction (STEMI).¹ Although patients may present differently with ACS, they face many similar diagnostic tests, invasive management

Mixed data have been observed on the role of statins in the preventative setting of cardiovascular disease (CVD).¹ However, Dr. Raffaele Bugiardini, Department of Experimental, Diagnostic, and Specialty Medicine, University of Bologna, Italy and his colleagues conducted a recent study published in the Journal of the American College of Cardiology, which demonstrated evidence that receiving statin therapy before initial acute coronary syndrome (ACS) could reduce acute heart failure (AHF) and improve patient survival rates.²

Ticagrelor continues to be one of the often-used antiplatelet drugs in the management of acute coronary syndrome (ACS), however only 10% of the ACS patients treated with ticagrelor require coronary artery bypass surgery (CABG) due to perioperative bleeding.¹ The current North American guidelines (Including ACC/AHA) advocate a waiting period of at least 5 days after ticagrelor cessation prior to non-urgent CABG, and the 2017 European Society of Cardiology (ESC) guidelines also recommend a waiting period of at least 3 days after ticagrelor cessation for non-urgent CABG. However, from the real-life clinical point of view, it is hypothesized that early surgery is noninferior to delayed surgery for severe or massive perioperative bleeding. Therefore, the RAPID CABG trial, a physician initiated multi-centre randomized study, was conducted to evaluate the safety of early CABG surgery after a shorter ticagrelor cessation of 2 to 3 days as compared to 5 to 7 days prior CABG, among 143 patients presenting with ACS who require non emergent CABG.¹ Primary endpoint was severe/ massive bleeding by the Universal Definition of Perioperative Bleeding (UDPB): Class 3 or 4.

The results from a 6-month follow-up of RAPID CABG trial indicated patients could discontinue ticagrelor 2 to 3 days prior to CABG without increasing the risk of early post-surgical bleeding and could also reduce the average length of hospital stay.

Dyslipidemias, particularly that of an increased low-density lipoprotein cholesterol (LDL-C) and/or triglycerides (TGs), are often known to significantly elevate the risk of atherosclerotic cardiovascular disease (ASCVD).^₁ The 2019 European Society of Cardiology/European Atherosclerosis Society (ESC

Lipoprotein(a) (Lp(a)) is a unique lipoprotein that has emerged as an independent risk factor for vascular diseases.¹ In the general population, the plasma levels of Lp(a) are similar in men and women and are skewed with a tail towards the highest levels (Figure 1).²

The recent 2019 European Society of Cardiology/European Atherosclerosis Society Guidelines for the Management of Dyslipidemias have set a target low-density lipoprotein (LDL)-C goal of <55mg/dL for very high-risk patients requiring secondary prevention.¹