PDE5抑制剂西地那非抑制早衰心室复合物:首次临床经验。

IF 2.8 4区 医学 Q2 PHYSIOLOGY
David C Hutchings, Christopher P Denton, Luigi Venetucci, Andrew W Trafford
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引用次数: 0

摘要

磷酸二酯酶-5抑制剂西地那非在药物性长QT羊模型中抑制室性心律失常。在该研究中,室性心律失常通过减少室性早搏复合物(PVC)和延迟PVC发作而消除,从而防止“r - t”室性心动过速。对心律失常患者的影响尚缺乏证据。在本病例研究中,一名50岁女性,有室性早搏和系统性硬化症病史,根据目前的治疗建议,开始使用西地那非治疗雷诺现象。开始时,患者佩戴7天心脏监护仪。观察到两种类型的室性早搏:一种明显的形态出现在前一次窦性搏动(“晚”)400 ms后。西地那非消除晚期室性早搏,并显著降低早期室性早搏的频率。在西地那非治疗期间保留的早期室性早搏中,室性早搏出现在心脏周期较晚的时间,距离前T波顶点21 ms。在冲洗期间,室性早搏在频率和时间上向基线值恢复。我们报告了第一例提示西地那非在人类中的抗心律失常特性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Suppression of premature ventricular complexes with the PDE5 inhibitor sildenafil: First clinical experience.

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.

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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
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.
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