David C Hutchings, Christopher P Denton, Luigi Venetucci, Andrew W Trafford
{"title":"Suppression of premature ventricular complexes with the PDE5 inhibitor sildenafil: First clinical experience.","authors":"David C Hutchings, Christopher P Denton, Luigi Venetucci, Andrew W Trafford","doi":"10.1113/EP092932","DOIUrl":null,"url":null,"abstract":"<p><p>The phosphodiesterase-5 inhibitor sildenafil suppresses ventricular arrhythmias in a sheep model of drug-induced long QT. In that study, ventricular arrhythmias were abolished by reducing premature ventricular complexes (PVCs) and delaying PVC onset, thus preventing 'R-on-T' ventricular tachycardia. Evidence for effects in humans with arrhythmias is lacking. In this case study, a 50-year-old female with a history of PVCs and systemic sclerosis was started on sildenafil for Raynaud's phenomenon in line with current treatment recommendations. During initiation, the patient wore a 7-day cardiac monitor. Two subtypes of PVCs were observed: one distinct morphology arising <400 ms from the preceding sinus beat ('early') and a separate morphology >400 ms from the preceding sinus beat ('late'). Sildenafil abolished late PVCs and substantially reduced the frequency of early PVCs. Of those early PVCs remaining during sildenafil treatment, PVCs arose later in the cardiac cycle, 21 ms further from the preceding T wave apex. During washout, PVCs returned in frequency and timing towards baseline values. We report the first case suggesting an anti-arrhythmic property of sildenafil in a human.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1113/EP092932","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The phosphodiesterase-5 inhibitor sildenafil suppresses ventricular arrhythmias in a sheep model of drug-induced long QT. In that study, ventricular arrhythmias were abolished by reducing premature ventricular complexes (PVCs) and delaying PVC onset, thus preventing 'R-on-T' ventricular tachycardia. Evidence for effects in humans with arrhythmias is lacking. In this case study, a 50-year-old female with a history of PVCs and systemic sclerosis was started on sildenafil for Raynaud's phenomenon in line with current treatment recommendations. During initiation, the patient wore a 7-day cardiac monitor. Two subtypes of PVCs were observed: one distinct morphology arising <400 ms from the preceding sinus beat ('early') and a separate morphology >400 ms from the preceding sinus beat ('late'). Sildenafil abolished late PVCs and substantially reduced the frequency of early PVCs. Of those early PVCs remaining during sildenafil treatment, PVCs arose later in the cardiac cycle, 21 ms further from the preceding T wave apex. During washout, PVCs returned in frequency and timing towards baseline values. We report the first case suggesting an anti-arrhythmic property of sildenafil in a human.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.