Rosuvastatin and atorvastatin are the two primary high-intensity statins used for cardiovascular risk reduction. However, concerns have been raised regarding the renal safety profile of rosuvastatin. This study compared risks of hematuria, proteinuria, and cardiovascular events between rosuvastatin- and atorvastatin-treated patients.

Branched-chain amino acids (BCAAs), comprising leucine, isoleucine, and valine, are essential nutrients whose metabolic homeostasis is critical to cardiovascular health. This review synthesizes the dietary sources, physiological roles, and metabolic pathways of BCAAs, explores mechanisms driving their accumulation, and evaluates current detection techniques. We highlight the regulatory impact of BCAAs and their metabolites on cardiovascular disease (CVD) through multiple pathways. We propose a combinatorial strategy integrating dietary modulation, administration of BCAA-catabolizing enzymes (e.g., BT2, JK-1), mammalian target of rapamycin (mTOR) pathway modulation, and utilization of natural compounds (e.g., Salvia miltiorrhiza, Panax notoginseng) to counteract BCAA metabolic dysregulation-induced cardiovascular pathologies. This review provides a theoretical framework for understanding BCAA metabolism in CVD, emphasizes the importance of combined monitoring of BCAAs and their metabolites (branched-chain α-keto acids [BCKAs], 3-hydroxyisobutyrate [3-HIB]), and advances precision cardiology strategies targeting metabolic pathways.

Emerging evidence suggests that sodium-glucose co-transporter-2 (SGLT2) inhibitors reduce cardiovascular events in patients with diabetes mellitus (DM) after acute myocardial infarction (AMI), but evidence in Asian populations remains limited.

Cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) are two prevalent and interrelated conditions that share common pathophysiological mechanisms, including insulin resistance and chronic inflammation. While newer glucose-lowering agents such as sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promise in improving insulin sensitivity and cardiovascular outcomes, a number of commonly used cardiovascular pharmacologic agents such as thiazide diuretics, beta-blockers, and statins have been associated with adverse effects on glucose metabolism, including increased insulin resistance and elevated risk of T2DM. This narrative review examines both the detrimental and beneficial metabolic effects of various cardiovascular drugs, explores their underlying mechanisms, and discusses the implications for the prevention and management of metabolic dysfunction in patients at high cardiometabolic risk. A clearer understanding of these effects is crucial for optimizing therapeutic strategies in individuals with or at risk for both CVD and T2DM.

Familial chylomicronemia syndrome (FCS) is a rare autosomal recessive disorder resulting in hypertriglyceridemia. Historically, treatment options for this patient population have been limited as available triglyceride-lowering medications are often ineffective. Recently, new pharmacological agents targeting apolipoprotein C-III (apoC-III) production have been found to effectively and substantially lower triglyceride levels. A literature search in PubMed and EMBASE was conducted from January 2013 to July 2025 using keywords "familial chylomicronemia syndrome", "olezarsen", "volanesorsen", and "plozasiran". Phase III trials evaluating safety and efficacy of volanesorsen, olezarsen, and plozasiran were included. From 1376 articles, 4 phase III trials fulfilled the inclusion criteria. Triglyceride (TG) levels were reduced by 73-77% with volanesorsen, a least-square means reduction in TGs between 22.4 and 43.5 percentage points with olezarsen, and a 78-80% reduction in TGs with plozasiran when compared with placebo. The number of acute pancreatitis events was also lower with the study medications versus placebo. These new apoC-III lowering medications provide a novel treatment approach for patients with FCS, a population long without effective pharmacological treatment options. Provider familiarity with the availability and purpose of these medications will allow patients to receive the best therapy available to manage FCS.

Patients with type 2 diabetes mellitus and obesity have a higher risk of cardiovascular disease and major adverse cardiovascular events. It is important that medication options for these disease states are either cardioprotective or cardioneutral so that the health of the patient is not worsened. Medications in the glucagon-like peptide-1 receptor agonists class decrease cardiovascular risk in those at high or increased risk of cardiovascular events. This review presents and discusses the current clinical and scientific evidence pertaining to tirzepatide, a glucagon-like peptide-1 receptor/glucose-dependent insulinotropic polypeptide receptor co-agonist.

Heart failure with reduced ejection fraction (HFrEF) represents a complex clinical syndrome requiring the timely initiation of disease-modifying therapies. However, the optimal timing for introducing these therapies in the hospital setting remains an area of investigation. This study aims to evaluate whether the early in-hospital initiation of sodium-glucose co-transporter 2 inhibitors (SGLT2i) facilitates the introduction of angiotensin receptor-neprilysin inhibitors (ARNI) during hospitalization and whether this strategy is associated with improved left ventricular systolic function at 6-month follow-up.

Guideline-directed medical therapy (GDMT) is the foundation of managing heart failure with reduced ejection fraction (HFrEF). However, hypotension often limits its implementation, preventing optimal medication titration. Midodrine, an alpha-1 adrenergic agonist, has been explored as a potential option to facilitate the initiation and continuation of GDMT. Our review assesses the role of midodrine in the management of HFrEF, evaluating its benefits, risks, and clinical applicability. While emerging evidence suggests midodrine may help stabilize blood pressure and enable the optimization of GDMT in select patients with refractory hypotension, concerns remain regarding its long-term safety, potential for increased afterload, and associated mortality risks. Some observational studies indicate improved adherence to GDMT, but conflicting findings on patient outcomes, including increased mortality, highlight concerns. Still, the therapeutic promise of midodrine in HFrEF is undeniably compelling, offering the exciting possibility of transforming HFrEF management. The current evidence is low due to reliance on observational studies. Robust, large-scale randomized controlled trials are urgently needed to confirm its safety, efficacy, and precise patient selection criteria. The ongoing MIDOH-HF-P trial, results of which are anticipated in 2026, could provide vital insights into short-term benefits with GDMT. However, until robust evidence emerges and additional data are available, clinicians must exercise extreme caution when considering its off-label use.

Heart failure (HF) is a chronic and progressive condition associated with significant morbidity and mortality and reduced quality of life. Among the various comorbidities that exacerbate HF outcomes, iron deficiency (ID) is increasingly recognized as a modifiable risk factor that contributes to decreased exercise capacity, fatigue, and hospitalizations, even in the absence of anemia. Approximately 30-50% of patients with HF present with ID, highlighting the need for routine screening and targeted management. The objective of this review was to summarize the pathophysiological basis, diagnostic criteria, and clinical implications of ID in HF and to provide evidence-based recommendations for its treatment based on current guidelines and clinical trials. Key clinical trials such as FAIR-HF, CONFIRM-HF, and AFFIRM-AHF have demonstrated that intravenous iron supplementation, particularly with ferric carboxymaltose, improves functional status, symptoms, and quality of life in patients with HF and ID. These benefits are observed irrespective of the presence of anemia, and treatment is associated with a favorable safety profile. Current guidelines recommend routine screening for ID in patients with chronic HF and consideration of intravenous iron supplementation in symptomatic patients with confirmed deficiency. Oral iron has shown limited efficacy in this population. In conclusion, ID is a treatable and impactful comorbidity in HF. Early detection and appropriate intravenous iron therapy can significantly improve patient-centered outcomes and should be incorporated into standard HF management strategies.

Stable angina management and pharmacotherapy varies widely despite the longstanding availability of several drug classes. We herein review current angina management strategies through the lens of optimal medical therapy (OMT), while highlighting emerging therapies and the growing clinical significance of coronary microvascular dysfunction (CMD). This narrative review synthesizes findings from existing research and key clinical trials to outline both established and evolving treatment approaches for chronic stable angina. Beta-blockers and calcium channel blockers remain the foundation of symptom management, while nitrates, ranolazine, ivabradine, and trimetazidine may be considered for refractory symptoms. Few novel pharmacologic therapies have emerged in recent decades, underscoring a critical need for innovation-particularly in the treatment of CMD, which is increasingly recognized as a distinct pathophysiologic entity requiring targeted therapy. Advances in invasive coronary function testing have improved diagnostic accuracy for CMD, yet consensus on optimal treatment remains elusive. Emerging interventional strategies and stem cell-based interventions show promise for patients with refractory angina who lack further revascularization options. The limited progress in novel pharmacologic development reinforces the need for ongoing research to refine therapeutic strategies for CMD and expand treatment options for patients with treatment-resistant angina.

Colchicine has been incorporated into major clinical guidelines for the secondary prevention of cardiovascular disease (CVD). However, recent randomized trials have presented contradictory results.

Nicotinamide adenine dinucleotide (NAD+) is a fundamental coenzyme that plays a crucial role in cellular energy metabolism and redox homeostasis. A deficiency in NAD+ has been associated with heart failure (HF), which often occurs in the advanced stages of cardiovascular diseases. While numerous studies have indicated that NAD+ supplementation may enhance cardiac bioenergetics and function in animal models, there is limited research investigating this potential effect in human patients. Therefore, this study aims to evaluate whether NAD+ treatment can lead to improved clinical outcomes for patients with HF due to ischemic cardiomyopathy (ICM).

Our aim was to evaluate the safety of empagliflozin in escalating doses among patients with end-stage renal disease (ESRD) undergoing maintenance hemodialysis who also have heart failure.

Cardio-renal-metabolic (CRM) syndrome is an emerging nosological entity that reflects the interaction between metabolic risk factors, chronic kidney disease, and cardiovascular disorders. In recent years, it has attracted particular interest, as it appears to be associated with a growing incidence of cardiovascular events, progression of kidney disease, and mortality. The fact that the syndrome has a complex pathophysiology, multiple risk factors, and deleterious effects on different organs and systems necessitates an interdisciplinary approach to its management. Pharmacological agents with positive effects on different components of CRM syndrome, such as sodium-glucose co-transporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, have recently been added to our pharmacological arsenal. However, these treatments are underprescribed and used at disproportionately low rates given the significant benefits they offer and the strong level of evidence supporting them, highlighting the need for greater vigilance among physicians regarding the recognition and treatment of the syndrome. This article provides recent data on the definition, pathophysiology, staging, and diagnosis of CRM syndrome and the holistic management of affected patients.

Bruton tyrosine kinase (BTK) plays a pivotal role in B-cell receptor signaling, making it a key therapeutic target in hematologic malignancies. Bruton tyrosine kinase inhibitors (BTKIs) have revolutionized the treatment landscape, improving survival outcomes in conditions such as chronic lymphocytic leukemia and mantle cell lymphoma. However, despite their clinical efficacy, BTKIs-particularly first-generation agents such as ibrutinib-are associated with significant cardiovascular toxicity, including atrial fibrillation, hypertension, bleeding, and, in rare cases, ventricular arrhythmias and heart failure. This narrative review explores the evolving landscape of BTKI-related cardiovascular toxicity, from first-generation drugs to next-generation agents that have improved safety profiles. We summarize current evidence on the incidence, mechanisms, and risk factors of BTKI-induced cardiovascular events and highlight potential predictive tools and mitigation strategies. Given the increasing use of these agents, a comprehensive understanding of their cardiovascular impact is essential for optimizing treatment selection and patient outcomes. Future research should focus on refining risk stratification models and developing cardioprotective strategies to ensure the long-term safety of BTKI therapy.

Despite the well-established benefits of statin therapy in reducing atherosclerotic cardiovascular disease (ASCVD) risk, many patients fail to achieve recommended low-density lipoprotein cholesterol (LDL-C) targets or experience statin intolerance, necessitating alternative approaches. This review examines advances in non-statin lipid-lowering therapies, focusing on proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (monoclonal antibodies and inclisiran), bempedoic acid, and other non-statin lipid medications. We evaluate their mechanisms of action, clinical efficacy, and safety profiles on the basis of landmark trials. A conceptual framework for personalized lipid management is proposed, addressing residual cardiovascular risk, statin intolerance, and complex patient profiles. Clinical decision pathways are presented for high-risk patients, statin-intolerant individuals, and those with adherence challenges. We explore emerging therapies targeting novel pathways, including lipoprotein(a), apolipoprotein C-III inhibitors, angiopoietin-like protein 3 (ANGPTL3) inhibitors, cholesteryl ester transfer protein (CETP) inhibitors, and gene-editing technologies. Implementation barriers, including cost considerations, insurance challenges, and global access disparities, are discussed alongside solutions.