Svetlana Mosteoru, Giuseppe Biondi Zoccai, Luigi Spadafora
{"title":"Innovation and Challenges in Preventive Cardiology: Highlights from ESC Preventive Cardiology 2025.","authors":"Svetlana Mosteoru, Giuseppe Biondi Zoccai, Luigi Spadafora","doi":"10.1097/FJC.0000000000001741","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001741","url":null,"abstract":"","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707566","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}
Hongli Zhang, Jihong Ren, Yan He, Kexin Zhao, Yuting He, Zhaoxia Sun, Yuanxin Zhu, Hongxia Bao, Shuang Wang
{"title":"GPX4: A Key Regulator of Mitochondrial Function and Glycolysis in Pulmonary Artery Smooth Muscle Cells.","authors":"Hongli Zhang, Jihong Ren, Yan He, Kexin Zhao, Yuting He, Zhaoxia Sun, Yuanxin Zhu, Hongxia Bao, Shuang Wang","doi":"10.1097/FJC.0000000000001742","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001742","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is a progressive cardiovascular disease characterized by elevated pulmonary arterial pressure and vascular remodeling. However, the underlying mechanisms remain unclear. This study reveals a novel mechanism by which oxidative stress reduced glutathione peroxidase 4 (GPX4) expression in both rat and human pulmonary arterial smooth muscle cells (PASMCs), establishing a reciprocal regulatory relationship between GPX4 and reactive oxygen species (ROS). GPX4 deficiency in PASMCs exacerbated inflammation, evidenced by increased IL-6 and TNF-α, and promoted extracellular matrix (ECM) remodeling, indicated by elevated fibronectin and collagen II. Moreover, GPX4 inhibition disrupted mitochondrial function by downregulating key mitochondrial regulators peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α) and mitochondrial transcription factor A (TFAM). Simultaneously, it promoted glycolysis, leading to increased lactate production through the upregulation of lactate dehydrogenase A (LDHA) and hexokinase 2 (HK2). These effects were associated with the long non-coding RNA TUG1, which appeared to modulate GPX4 stability. Collectively, our findings identify GPX4 as a critical regulator of inflammation, ECM remodeling and metabolic homeostasis in PASMCs, providing new insights into the molecular mechanisms underlying PAH and identify potential therapeutic targets.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707565","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}
Giuseppe Biondi-Zoccai, Vassilios S Vassiliou, Maria Camilla Palumbo, George W Booz
{"title":"Phthalates and Cardiovascular Risk: A Call for Awareness in Clinical Practice.","authors":"Giuseppe Biondi-Zoccai, Vassilios S Vassiliou, Maria Camilla Palumbo, George W Booz","doi":"10.1097/FJC.0000000000001732","DOIUrl":"10.1097/FJC.0000000000001732","url":null,"abstract":"<p><strong>Abstract: </strong>Phthalates, widely used as plasticizers in industrial and medical products, are increasingly recognized as cardiovascular health disruptors. Their ubiquity poses a significant threat, particularly to patients with or at risk of cardiovascular disease. This review examines the multifactorial risks linked to phthalate exposure, including oxidative stress, epigenetic (re)programming, mitochondrial dysfunction, and endocrine disruption. Preclinical models-ranging from isolated cardiomyocytes to whole-animal systems demonstrate direct cardiotoxic effects, while epidemiological studies suggest a considerable global cardiovascular burden. Iatrogenic exposure through drug packaging, tubing, dialysis, and surgical equipment is especially concerning in frail patients, yet remains underrecognized in clinical guidelines. Vulnerable populations such as neonates, pregnant women, and patients undergoing cardiovascular procedures may face disproportionately high exposure levels. Despite the availability of safer alternatives, regulatory responses are inconsistent and clinical awareness is limited. Further longitudinal studies and biomarker-based surveillance are needed to quantify cumulative risk. Addressing this overlooked hazard is essential to protect patients from preventable harm and promote safer, precision cardiovascular care in the era of pervasive plastic use. We call for urgent reassessment of current practices, integration of environmental toxicology into medical training, and systematic adoption of phthalate-free materials.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659336","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}
Chiara Giuliana, Simone Filomia, Marta Ricci, Gaetano Pinnacchio, Alessia D'Aiello, Gianluigi Saponara, Daniela Pedicino, Gemma Pelargonio, Marco Giuseppe Del Buono, Tommaso Sanna
{"title":"Treating the Broken Heart: Role of Stellate Ganglion Block in Takotsubo Syndrome.","authors":"Chiara Giuliana, Simone Filomia, Marta Ricci, Gaetano Pinnacchio, Alessia D'Aiello, Gianluigi Saponara, Daniela Pedicino, Gemma Pelargonio, Marco Giuseppe Del Buono, Tommaso Sanna","doi":"10.1097/FJC.0000000000001734","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001734","url":null,"abstract":"<p><p>Takotsubo syndrome (TTS) is an acute stress-induced cardiomyopathy characterized by transient left ventricular dysfunction, often mimicking acute myocardial infarction but without obstructive coronary artery disease. While typically reversible, TTS can be complicated by serious adverse events, including life-threatening ventricular arrhythmias (VAs). The pathophysiology is complex but strongly linked to sympathetic nervous system hyperactivity and a surge in catecholamines, often termed \"neurogenic stunned myocardium\". This review discusses the role of arrhythmias in TTS, the influence of the autonomic nervous system, and explores the rationale, mechanisms, and potential applications of stellate ganglion block (SGB), particularly left SGB, in the management of TTS-related arrhythmias, illustrated by a clinical case.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626411","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}
{"title":"Heart failure with preserved ejection fraction: how far we've come - a brief report from two outstanding educational events.","authors":"Antonio Abbate","doi":"10.1097/FJC.0000000000001733","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001733","url":null,"abstract":"","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512021","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}
Gaetano Santulli, Urna Kansakar, Stanislovas S Jankauskas, Fahimeh Varzideh
{"title":"Comparative LDL-C Lowering Efficacy of Non-Statin Therapies: Inclisiran is Better than Ezetimibe, PCSK9 inhibitors, and Bempedoic Acid.","authors":"Gaetano Santulli, Urna Kansakar, Stanislovas S Jankauskas, Fahimeh Varzideh","doi":"10.1097/FJC.0000000000001731","DOIUrl":"10.1097/FJC.0000000000001731","url":null,"abstract":"","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12424469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484513","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}
{"title":"Aerobic exercise rehabilitation training alleviates skeletal muscle atrophy caused by heart failure in mice through the SIRT1/PGC-1α pathway.","authors":"Jiawei Zhang, Xiao Chen, Chunxiao Wan","doi":"10.1097/FJC.0000000000001722","DOIUrl":"10.1097/FJC.0000000000001722","url":null,"abstract":"<p><p>To investigate the potential effects of aerobic exercise rehabilitation training (AET) on the progression of myocardial infarction (MI) in a left anterior descending (LAD) coronary artery ligation model in mice, and to explore the underlying mechanisms.MI was induced in male C57BL/6 mice by ligating the LAD coronary artery. After one week rest, the mice underwent either adaptive ladder training or treadmill training for five consecutive days. The H9C2 cell model was used to simulate AngII-induced myocardial injury, cardiac function was assessed via echocardiography, and gastrocnemius muscle laminin expression was analyzed by immunofluorescence. Skeletal muscle-related gene expression was evaluated by immunoblotting, and the effects of AET on mitochondrial function were assessed using immunoblotting and commercial kits. Additionally, JC-1 staining was employed to examine mitochondrial dysfunction and further confirm the underlying mechanisms.AET significantly improves cardiac function in MI mice and could mitigate skeletal muscle atrophy in these mice. Further analysis revealed that activation of the SIRT1/ PGC-1α pathway by AET enhances mitochondrial function in MI mice. Additionally, SIRT1 activation was shown to alleviate skeletal muscle mitochondrial dysfunction induced by heart failure in vitro.AET can alleviate skeletal muscle atrophy induced by heart failure in mice through the SIRT1/PGC-1α pathway.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173666","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}
Michele Marchetta, Rocio I Lopez, Austin C Hogwood, Georgia Thomas, Gerardina Abbate, Roshanak Markley, Justin M Canada, Antonio Abbate
{"title":"Heart Rate Lowering With Ivabradine and Burden of Symptoms in Patients With Postural Orthostatic Tachycardia Syndrome.","authors":"Michele Marchetta, Rocio I Lopez, Austin C Hogwood, Georgia Thomas, Gerardina Abbate, Roshanak Markley, Justin M Canada, Antonio Abbate","doi":"10.1097/FJC.0000000000001705","DOIUrl":"10.1097/FJC.0000000000001705","url":null,"abstract":"<p><strong>Abstract: </strong>Postural orthostatic tachycardia syndrome (POTS) is a clinical syndrome of tachycardia on standing leading to palpitations, dizziness, chest pain, and/or fatigue. An exaggerated norepinephrine response with standing is often present in POTS, but it remains unclear whether the tachycardia is compensatory for a reduced stroke volume or whether the tachycardia is itself causing the symptoms of POTS. We herein report the effects of heart rate (HR) lowering with ivabradine, a selective I f channel blocker, on symptom burden in patients with POTS. After ivabradine treatment, there was a significant reduction in the change in HR with standing in all patients from 40 (30-70) to 15 (8-19) bpm ( P = 0.011), without significant changes in blood pressure. The Malmö score was significantly reduced in all patients from 86 (74-92) to 39 (32-66) ( P = 0.005). A correlation between change in HR with standing and the change in Malmö score (R = +0.828; R 2 quadratic = 0.635; P < 0.001) was present. The parallel improvement in HR response and symptoms with ivabradine suggests that the tachycardia response in POTS may not be considered compensatory but rather central to the pathophysiology of POTS symptoms.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"28-32"},"PeriodicalIF":2.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010102","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}
{"title":"Flavin Adenine Dinucleotide Ameliorates Pressure Overload-Induced Heart Failure by Activating the Short-Chain Acyl-CoA Dehydrogenase.","authors":"Chunyu Chen, Xue Qin, Yuhong Cao, Liyuan Qing, Zhichao Ma, Qingping Xu, Huan Peng, Guifang Jin, Zhicheng Yang, Jieyu Xing, Sigui Zhou","doi":"10.1097/FJC.0000000000001698","DOIUrl":"10.1097/FJC.0000000000001698","url":null,"abstract":"<p><strong>Abstract: </strong>Flavin adenine dinucleotide (FAD), a cofactor that catalyzes the reaction of flavin protein, participates in fatty acid β-oxidation, which has been shown to inhibit pathological cardiac hypertrophy and fibrosis in spontaneously hypertensive rats. However, the therapeutic advantage of FAD for heart failure (HF) treatment has not been investigated. This study aimed to explore the effects and underlying mechanisms of FAD in a transverse aortic constriction-induced HF mouse model and in vitro tert-butyl hydroperoxide (tBHP)-induced cardiomyocyte apoptosis model experiments. FAD considerably inhibited tBHP-induced cardiomyocyte apoptosis. In addition, FAD significantly increased the activity and expression of the short-chain acyl-CoA dehydrogenase enzyme and adenosine triphosphate (ATP) content while reducing the content of free fatty acids and reactive oxygen species both in vitro and in vivo. Meanwhile, FAD increased the mitochondrial membrane potential, suppressed mitochondrial membrane swelling, and decreased myocardial fibrosis and TUNEL-positive apoptosis cells in the TAC-induced HF mice. In conclusion, our results indicate that FAD plays a positive role in preventing and treating HF, which can be attributed in part to the activation of short-chain acyl-CoA dehydrogenase.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"84-96"},"PeriodicalIF":2.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811523","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}
{"title":"Role of Muscarinic Acetylcholine Receptors in Oxytocin-Induced Cardioprotection Against Ischemia-Reperfusion Injury in Rats.","authors":"Mahdieh Faghihi, Mohammadreza Ahmadi-Beni, Fariba Houshmand","doi":"10.1097/FJC.0000000000001701","DOIUrl":"10.1097/FJC.0000000000001701","url":null,"abstract":"<p><strong>Abstract: </strong>Oxytocin (OT) has been shown to provide myocardial protection against ischemia-reperfusion (I/R) injury. This study investigates the involvement of muscarinic receptors in the OT-induced cardioprotection, focusing on its potential mechanisms and effects on myocardial infarction (MI) and ischemic arrhythmias. Male rats anesthetized with pentobarbital sodium were subjected to 25-minute ischemia followed by 120-minute reperfusion after intraperitoneal administration of OT (0.01 μg), atropine (1.5 µg/kg), or saline. Cardioprotection was evaluated by monitoring lactate dehydrogenase, malondialdehyde, and cardiac creatine kinase isoenzyme levels, infarct size, arrhythmia severity, ventricular fibrillation (VF), and mortality. OT markedly reduced infarct size, oxidative stress, and the severity of ischemic arrhythmias, including ventricular tachycardia and VF, compared with saline-treated I/R animals. OT also significantly improved survival rates. Pretreatment with atropine abolished most protective effects of OT but did not significantly alter its suppression of VF, suggesting the involvement of muscarinic receptor-independent mechanisms. These findings highlight that the OT-induced cardioprotection, mediated in part by acetylcholine locally released in the left ventricle, extends beyond infarct limitation to include potent antiarrhythmic effects. The dual impact of OT on MI and arrhythmias provides insights into the mechanisms underlying its preconditioning effect and its potential application in MI management.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"109-117"},"PeriodicalIF":2.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025552","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}