Pub Date : 2025-10-01DOI: 10.1007/s40256-025-00767-4
Jessica Huston, Dontia Orey, Andrew Ashchi, Andrea Ashchi Lachapelle, Ariana Genovese, Jenna Jackson, Ramsey Ashchi, Towfeeq Ashchi, Majdi Ashchi, David Sutton, Wasim Deeb, Rebecca F Goldfaden
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.
{"title":"Effect of Tirzepatide on Cardiovascular Outcomes.","authors":"Jessica Huston, Dontia Orey, Andrew Ashchi, Andrea Ashchi Lachapelle, Ariana Genovese, Jenna Jackson, Ramsey Ashchi, Towfeeq Ashchi, Majdi Ashchi, David Sutton, Wasim Deeb, Rebecca F Goldfaden","doi":"10.1007/s40256-025-00767-4","DOIUrl":"https://doi.org/10.1007/s40256-025-00767-4","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-25DOI: 10.1007/s40256-025-00766-5
Sagar Patel, Vishal Patel, Mohammed Ayyad, Arthi Palani, Joseph Allencherril
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.
{"title":"Contemporary Antianginal Therapy.","authors":"Sagar Patel, Vishal Patel, Mohammed Ayyad, Arthi Palani, Joseph Allencherril","doi":"10.1007/s40256-025-00766-5","DOIUrl":"https://doi.org/10.1007/s40256-025-00766-5","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-15DOI: 10.1007/s40256-025-00764-7
Xiaofan Yu, Jie Xu, Jiaoyu Cao, Qizhi Xu, Hongwu Chen, Dongbiao Yu, Xunxia Yao, Kaibing Chen, Likun Ma
<div><h3>Background</h3><p>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).</p><h3>Methods</h3><p>This single-center, prospective, randomized, placebo-controlled trial enrolled 180 adults diagnosed with ICM whose left ventricular ejection fraction (LVEF) was ≤ 45% and whose New York Heart Association (NYHA) grade was II–III. Participants were randomly assigned to receive either intravenous NAD⁺ (10 mg/day) or an equivalent placebo (5% glucose/normal saline) for a duration of 7 days, alongside guideline-directed medical therapy. The primary endpoint was the Change in LVEF at 1 month. Secondary endpoints included changes in N-terminal pro B-type natriuretic peptide (NT-proBNP) at 7 and 30 days; a composite of major adverse cardiac and cerebrovascular events (MACCE), which encompassed cardiac death, non-fatal myocardial infarction, stroke, and the first unplanned HF hospitalization within 6 months; and improvements in NYHA functional class.</p><h3>Results</h3><p>At 1 month, the NAD+ group demonstrated a significantly greater improvement in LVEF compared to the placebo group (45.44 ± 8.55% vs. 42.44 ± 9.09%, <i>p =</i> 0.024). A trend towards decreased NT-proBNP levels was observed in the NAD+ group at day 7 (1471.00 [828.00–2950.00]pg/mL vs. 2317.50 [1155.00–4752.50]pg/mL, <i>p</i> = 0.102). The 6-month composite MACCE rate appeared lower among those receiving NAD+ treatment compared to the placebo group (14.6% vs. 24.7%, <i>p =</i> 0.089), primarily driven by a trend toward fewer first unplanned HF hospitalizations (13.5% vs. 23.6%, <i>p =</i> 0.078). Additionally, a greater proportion of patients in the NAD+ group demonstrated improvement in NYHA functional class at both 1 month (73.0% vs. 57.3%, <i>p =</i> 0.088) and 6 months (53.9% vs. 39.3%, <i>p =</i> 0.115). No significant differences were observed in structural parameters (left ventricular end-diastolic diameter, left ventricular end-diastolic volume, left atrial diameter).</p><h3>Conclusions</h3><p>This study has confirmed that supplementation with NAD+ can enhance cardiac function in patients with from HF due to ICM, thereby affirming its beneficial impact on cardiac performance. Trends indicating reductions in NT-proBNP levels and composite clinical events (particularly HF hospitalization) and improvements in NYHA functional class were noted, suggesting potential broader clinical benefits. These f
背景:烟酰胺腺嘌呤二核苷酸(Nicotinamide adenine dinucleotide, NAD+)是一种重要的辅酶,在细胞能量代谢和氧化还原稳态中起重要作用。NAD+缺乏与心力衰竭(HF)有关,心力衰竭通常发生在心血管疾病的晚期。虽然大量研究表明,在动物模型中,补充NAD+可以增强心脏生物能量学和功能,但对人类患者的潜在影响的研究有限。因此,本研究旨在评估NAD+治疗是否可以改善缺血性心肌病(ICM)心力衰竭患者的临床结果。方法:这项单中心、前瞻性、随机、安慰剂对照试验纳入了180名诊断为ICM、左室射血分数(LVEF)≤45%、纽约心脏协会(NYHA)分级为II-III级的成年人。参与者被随机分配接受静脉注射NAD⁺(10mg /天)或等效安慰剂(5%葡萄糖/生理盐水),持续7天,同时接受指南指导的药物治疗。主要终点是1个月时LVEF的变化。次要终点包括在第7天和第30天n端前b型利钠肽(NT-proBNP)的变化;主要心脑血管不良事件(MACCE)的组合,包括心源性死亡、非致死性心肌梗死、卒中和6个月内首次计划外HF住院;以及NYHA功能类的改进。结果:1个月时,与安慰剂组相比,NAD+组LVEF改善显著(45.44±8.55%比42.44±9.09%,p = 0.024)。NAD+组在第7天观察到NT-proBNP水平下降的趋势(1471.00 [828.00-2950.00]pg/mL vs. 2317.50 [1155.00-4752.50]pg/mL, p = 0.102)。与安慰剂组相比,接受NAD+治疗组的6个月综合MACCE率较低(14.6%对24.7%,p = 0.089),主要是由于首次计划外HF住院的趋势减少(13.5%对23.6%,p = 0.078)。此外,NAD+组中更大比例的患者在1个月(73.0% vs. 57.3%, p = 0.088)和6个月(53.9% vs. 39.3%, p = 0.115)时表现出NYHA功能等级的改善。两组结构参数(左室舒张末期内径、左室舒张末期容积、左房内径)无显著差异。结论:本研究证实补充NAD+可增强ICM所致HF患者的心功能,从而肯定了其对心脏功能的有益影响。注意到NT-proBNP水平和复合临床事件(特别是心衰住院)降低的趋势以及NYHA功能分级的改善,这表明潜在的更广泛的临床益处。这些研究结果表明,NAD+补充是一种有前景的治疗策略,值得通过更广泛的多中心临床试验进一步验证。注册:中国临床试验注册中心标识号ChiCTR2200059169。
{"title":"Effect of Nicotinamide Adenine Dinucleotide on Heart Failure Caused by Ischemic Cardiomyopathy: A Randomized, Placebo-Controlled Trial","authors":"Xiaofan Yu, Jie Xu, Jiaoyu Cao, Qizhi Xu, Hongwu Chen, Dongbiao Yu, Xunxia Yao, Kaibing Chen, Likun Ma","doi":"10.1007/s40256-025-00764-7","DOIUrl":"10.1007/s40256-025-00764-7","url":null,"abstract":"<div><h3>Background</h3><p>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).</p><h3>Methods</h3><p>This single-center, prospective, randomized, placebo-controlled trial enrolled 180 adults diagnosed with ICM whose left ventricular ejection fraction (LVEF) was ≤ 45% and whose New York Heart Association (NYHA) grade was II–III. Participants were randomly assigned to receive either intravenous NAD⁺ (10 mg/day) or an equivalent placebo (5% glucose/normal saline) for a duration of 7 days, alongside guideline-directed medical therapy. The primary endpoint was the Change in LVEF at 1 month. Secondary endpoints included changes in N-terminal pro B-type natriuretic peptide (NT-proBNP) at 7 and 30 days; a composite of major adverse cardiac and cerebrovascular events (MACCE), which encompassed cardiac death, non-fatal myocardial infarction, stroke, and the first unplanned HF hospitalization within 6 months; and improvements in NYHA functional class.</p><h3>Results</h3><p>At 1 month, the NAD+ group demonstrated a significantly greater improvement in LVEF compared to the placebo group (45.44 ± 8.55% vs. 42.44 ± 9.09%, <i>p =</i> 0.024). A trend towards decreased NT-proBNP levels was observed in the NAD+ group at day 7 (1471.00 [828.00–2950.00]pg/mL vs. 2317.50 [1155.00–4752.50]pg/mL, <i>p</i> = 0.102). The 6-month composite MACCE rate appeared lower among those receiving NAD+ treatment compared to the placebo group (14.6% vs. 24.7%, <i>p =</i> 0.089), primarily driven by a trend toward fewer first unplanned HF hospitalizations (13.5% vs. 23.6%, <i>p =</i> 0.078). Additionally, a greater proportion of patients in the NAD+ group demonstrated improvement in NYHA functional class at both 1 month (73.0% vs. 57.3%, <i>p =</i> 0.088) and 6 months (53.9% vs. 39.3%, <i>p =</i> 0.115). No significant differences were observed in structural parameters (left ventricular end-diastolic diameter, left ventricular end-diastolic volume, left atrial diameter).</p><h3>Conclusions</h3><p>This study has confirmed that supplementation with NAD+ can enhance cardiac function in patients with from HF due to ICM, thereby affirming its beneficial impact on cardiac performance. Trends indicating reductions in NT-proBNP levels and composite clinical events (particularly HF hospitalization) and improvements in NYHA functional class were noted, suggesting potential broader clinical benefits. These f","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"26 1","pages":"97 - 106"},"PeriodicalIF":3.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s40256-025-00764-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-10DOI: 10.1007/s40256-025-00763-8
Caique M. P. Ternes
{"title":"Rhythm, Risk, and Responsibility: Assessing the Safety of Testosterone Replacement in Aging Men with Androgen Deficiency","authors":"Caique M. P. Ternes","doi":"10.1007/s40256-025-00763-8","DOIUrl":"10.1007/s40256-025-00763-8","url":null,"abstract":"","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"25 6","pages":"739 - 740"},"PeriodicalIF":3.0,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-06DOI: 10.1007/s40256-025-00765-6
Kálmán Tóth
{"title":"Correction: Antihypertensive Efficacy of Triple Combination Perindopril/Indapamide Plus Amlodipine in High-Risk Hypertensives: Results of the PIANIST Study (Perindopril-Indapamide plus AmlodipiNe in high rISk hyperTensive patients)","authors":"Kálmán Tóth","doi":"10.1007/s40256-025-00765-6","DOIUrl":"10.1007/s40256-025-00765-6","url":null,"abstract":"","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"25 6","pages":"851 - 851"},"PeriodicalIF":3.0,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1007/s40256-025-00743-y
Hoi-Ying Li, Joseph Cheriyan, Tsz-Kwan Chan, Kai-Hang Yiu, Hung-Fat Tse, Ian B. Wilkinson, Yap-Hang Chan
Background
Colchicine has been incorporated into major clinical guidelines for the secondary prevention of cardiovascular disease (CVD). However, recent randomized trials have presented contradictory results.
Objective
We aimed to synthesize the current evidence on colchicine in secondary CVD protection, using a cumulative-dose approach.
Methods
We conducted a meta-analysis incorporating all randomized controlled trials (RCTs) globally. RCTs directly comparing colchicine versus placebo/standard care for the secondary prevention of cerebrovascular or coronary vascular disease were included. Odds ratios (OR) were derived for the primary outcome, defined as the prospective occurrence of major adverse cardiovascular events (MACE). Secondary outcomes included mortality, individual components of MACE, C-reactive protein, and adverse effects.
Results
In total, 14 RCTs including 31,397 participants were included. Colchicine significantly reduced MACE (OR 0.80; 95% confidence interval [CI] 0.68–0.94) in both acute atherothrombotic CVD and all CVD (OR 0.72; 95% CI 0.60–0.86) and resulted in significant prospective reductions in C-reactive protein. The threshold effect was apparent, with a protective benefit of colchicine against MACE at higher cumulative exposure ≥ 90 mg-days (OR 0.66; 95% CI 0.52–0.84). Colchicine resulted in no differences in cardiovascular or non-cardiovascular mortality.
Conclusions
Colchicine significantly reduces MACE in both acute atherothrombotic and all CVD across multiple ethnicities, with a threshold protective effect that clinically corresponds to treatment with 0.5 mg daily for at least 6 months. Importantly, there was no signal of increased all-cause mortality.
Registration
PROSPERO identifier no. CRD420251003142.
背景:秋水仙碱已被纳入心血管疾病(CVD)二级预防的主要临床指南。然而,最近的随机试验给出了相互矛盾的结果。目的:采用累积剂量法,综合目前秋水仙碱对继发性心血管疾病保护作用的证据。方法:我们对全球所有随机对照试验(rct)进行了荟萃分析。包括直接比较秋水仙碱与安慰剂/标准护理对脑血管或冠状动脉疾病二级预防的随机对照试验。得出主要结局的优势比(OR),定义为主要不良心血管事件(MACE)的预期发生。次要结局包括死亡率、MACE的个体成分、c反应蛋白和不良反应。结果:共纳入14项rct,共31,397名受试者。秋水仙碱显著降低急性动脉粥样硬化性血栓性CVD和所有CVD的MACE (OR 0.80; 95%可信区间[CI] 0.68-0.94) (OR 0.72; 95% CI 0.60-0.86),并导致c反应蛋白的显著预期降低。阈值效应很明显,当累计暴露≥90 mg-days时,秋水仙碱对MACE具有保护作用(OR 0.66; 95% CI 0.52-0.84)。秋水仙碱对心血管和非心血管死亡率没有影响。结论:秋水仙碱可显著降低多种族急性动脉粥样硬化血栓形成和所有CVD患者的MACE,具有阈值保护作用,临床相当于每天0.5 mg治疗至少6个月。重要的是,没有迹象表明全因死亡率增加。注册:普洛斯彼罗标识号CRD420251003142。
{"title":"Colchicine for the Secondary Prevention of Cardiovascular Diseases: A Cumulative-Dose Meta-analysis of Randomized Controlled Trials including 31,397 Subjects Worldwide","authors":"Hoi-Ying Li, Joseph Cheriyan, Tsz-Kwan Chan, Kai-Hang Yiu, Hung-Fat Tse, Ian B. Wilkinson, Yap-Hang Chan","doi":"10.1007/s40256-025-00743-y","DOIUrl":"10.1007/s40256-025-00743-y","url":null,"abstract":"<div><h3>Background</h3><p>Colchicine has been incorporated into major clinical guidelines for the secondary prevention of cardiovascular disease (CVD). However, recent randomized trials have presented contradictory results.</p><h3>Objective</h3><p>We aimed to synthesize the current evidence on colchicine in secondary CVD protection, using a cumulative-dose approach.</p><h3>Methods</h3><p>We conducted a meta-analysis incorporating all randomized controlled trials (RCTs) globally. RCTs directly comparing colchicine versus placebo/standard care for the secondary prevention of cerebrovascular or coronary vascular disease were included. Odds ratios (OR) were derived for the primary outcome, defined as the prospective occurrence of major adverse cardiovascular events (MACE). Secondary outcomes included mortality, individual components of MACE, C-reactive protein, and adverse effects.</p><h3>Results</h3><p>In total, 14 RCTs including 31,397 participants were included. Colchicine significantly reduced MACE (OR 0.80; 95% confidence interval [CI] 0.68–0.94) in both acute atherothrombotic CVD and all CVD (OR 0.72; 95% CI 0.60–0.86) and resulted in significant prospective reductions in C-reactive protein. The threshold effect was apparent, with a protective benefit of colchicine against MACE at higher cumulative exposure ≥ 90 mg-days (OR 0.66; 95% CI 0.52–0.84). Colchicine resulted in no differences in cardiovascular or non-cardiovascular mortality.</p><h3>Conclusions</h3><p>Colchicine significantly reduces MACE in both acute atherothrombotic and all CVD across multiple ethnicities, with a threshold protective effect that clinically corresponds to treatment with 0.5 mg daily for at least 6 months. Importantly, there was no signal of increased all-cause mortality.</p><h3>Registration</h3><p>PROSPERO identifier no. CRD420251003142.</p></div>","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"26 1","pages":"107 - 120"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s40256-025-00743-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-30DOI: 10.1007/s40256-025-00762-9
Kayode Ogunniyi, Chukwuemeka Christian Aghasili, Olumide Akinmoju, Victor Olamiposi Olaiya, Oluwamisimi Abib, Adetayo Y. Odueke, Hakeem Adegboyega Popoola, Victor Onyenokwe, David Onaolapo, Abdul-Azeez Muhammed Usman, Adam Friedman, Toluwalase Awoyemi, Jay Nfonoyim, Francesco Rotatori
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.
{"title":"Advances in Non-statin Lipid Therapies: A Narrative Review of Evolving Strategies for Cardiovascular Risk Reduction","authors":"Kayode Ogunniyi, Chukwuemeka Christian Aghasili, Olumide Akinmoju, Victor Olamiposi Olaiya, Oluwamisimi Abib, Adetayo Y. Odueke, Hakeem Adegboyega Popoola, Victor Onyenokwe, David Onaolapo, Abdul-Azeez Muhammed Usman, Adam Friedman, Toluwalase Awoyemi, Jay Nfonoyim, Francesco Rotatori","doi":"10.1007/s40256-025-00762-9","DOIUrl":"10.1007/s40256-025-00762-9","url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"26 1","pages":"35 - 57"},"PeriodicalIF":3.0,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-28DOI: 10.1007/s40256-025-00757-6
Luigi Spadafora, Federico Russo, Ewelina Bukowska-Olech, Giorgia Panichella, Manuel Garofalo, Stefano Cacciatore, Pierre Sabouret, Gianmarco Sarto, Beatrice Simeone, Erica Rocco, Attilio Lauretti, Francesco Versaci, Giuseppe Biondi Zoccai, Iginio Colaiori, Valentina Valenti, Sebastiano Sciarretta, Marco Bernardi
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.
{"title":"Cardiovascular Safety of Bruton Tyrosine Kinase Inhibitors: From Ibrutinib to Next-Generation Agents","authors":"Luigi Spadafora, Federico Russo, Ewelina Bukowska-Olech, Giorgia Panichella, Manuel Garofalo, Stefano Cacciatore, Pierre Sabouret, Gianmarco Sarto, Beatrice Simeone, Erica Rocco, Attilio Lauretti, Francesco Versaci, Giuseppe Biondi Zoccai, Iginio Colaiori, Valentina Valenti, Sebastiano Sciarretta, Marco Bernardi","doi":"10.1007/s40256-025-00757-6","DOIUrl":"10.1007/s40256-025-00757-6","url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"26 1","pages":"21 - 34"},"PeriodicalIF":3.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s40256-025-00757-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-26DOI: 10.1007/s40256-025-00761-w
Theocharis Koufakis, Demetrios Vlahakos, Charalambos Vlachopoulos, Emmanouil Kallistratos, Kalliopi Kotsa, Evangelos N. Liberopoulos, Ioannis Stefanidis, Erifili Hatziagelaki
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.
{"title":"Definition, Classification, Diagnosis, and Management of an Emerging Threat: Cardio-Renal-Metabolic Syndrome","authors":"Theocharis Koufakis, Demetrios Vlahakos, Charalambos Vlachopoulos, Emmanouil Kallistratos, Kalliopi Kotsa, Evangelos N. Liberopoulos, Ioannis Stefanidis, Erifili Hatziagelaki","doi":"10.1007/s40256-025-00761-w","DOIUrl":"10.1007/s40256-025-00761-w","url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":7652,"journal":{"name":"American Journal of Cardiovascular Drugs","volume":"26 1","pages":"11 - 19"},"PeriodicalIF":3.0,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}