American Journal of Cardiovascular Drugs最新文献

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.

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.

Background: 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.

Methods: This is a retrospective cohort study of atorvastatin and rosuvastatin users from 1 January 2018 to 31 December 2021. Inverse probability of treatment weighting was used to mitigate confounding. Poisson regression models were used to estimate adjusted relative risks.

Results: Of 136,680 patients (median age 61 years, 42.6% female), 46,292 were treated with atorvastatin and 90,388 rosuvastatin. During follow-up, there were 619 cases of proteinuria, 1843 cases of hematuria, and 19 cases of end-stage renal disease. Compared with atorvastatin, rosuvastatin was associated with a nonsignificant increase in the risk of hematuria (adjusted risk ratio [aRR] 1.1, 95% confidence interval [CI] 0.98-1.24) and proteinuria (aRR 1.02, 95% CI 0.83-1.25). Risk of cardiovascular events was significantly lower with rosuvastatin (aRR 0.77, 95% CI 0.70-0.83). Rosuvastatin was associated with a lower risk of myocardial infarction (aRR 0.75, 95% CI 0.63-0.91) and stroke (aRR 0.76, 95% CI 0.62-0.94) but not heart failure (aRR 0.82, 95% CI 0.63-1.06). Significant cardiovascular risk reduction was observed with rosuvastatin in the first 6 months.

Conclusions and relevance: Compared with atorvastatin, rosuvastatin was associated with a significantly lower risk of cardiovascular events and a nonsignificant increase in hematuria and proteinuria. Overall, the cardiovascular benefits of rosuvastatin appear to outweigh the minor renal risks.

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.

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.

Purpose: 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.

Methods: In this prospective, observational, single-centre study, consecutive patients with HFrEF were enrolled and divided into two groups on the basis of the timing of SGLT2i initiation: Group 1 (in-hospital) and Group 2 (post-discharge). The differences in terms of ARNI introduction within hospitalization were evaluated in the two groups. Changes in echocardiographic parameters (left ventricular ejection fraction [LVEF], left ventricular end-diastolic volume [LVEDV], left ventricular end-systolic volume [LVESV], E/e' ratio) at 6-month follow up have been compared among patients treated with ARNI+SGLT2i and SGLT2i alone.

Results: A total of 285 patients were enrolled, 151 for G1 and 134 for G2. Early in-hospital use of SGLT2i was an independent predictor of ARNI initiation before discharge (odds ratio, OR: 3.31; 95% confidence intervals, CI 1.87-5.84; p < 0.001). Among the 89 patients of G1 who completed 6 months of follow-up, early in-hospital therapy with SGLT2i and ARNI represents an independent significant predictor of LVEF > 10% improvement, compared with those treated with SGLT2i alone (OR: 5.353; 95% CI 1.504-12.070; p < 0.003).

Conclusions: Early in-hospital initiation of SGLT2i in patients with HFrEF is associated with a higher likelihood of in-hospital ARNI introduction and with significant improvements in left ventricular systolic function at 6-month follow-up.