Kontaras Konstantinos, Varnavas Varnavas, Kyriakides Zenon S
2nd Department of Cardiology, Hellenic Red Cross General Hospital, Athens, Greece.
Am J Cardiovasc Drugs. 2008;8(1):1-7. doi: 10.2165/00129784-200808010-00001.
Sildenafil was the first oral compound to be approved for the treatment of erectile dysfunction. In this paper, we review the current knowledge of the effects of sildenafil on myocardial infarction and sudden cardiac death. The first factor we examine is the sexual activity itself. As several studies have shown, the relative risk for an acute coronary syndrome during intercourse is not very high. Several studies examining the effects of sildenafil on mortality have been published during recent years. The great majority of these studies found that sildenafil is not an extra risk factor for an acute coronary syndrome or sudden cardiac death. In 1997, the rate of myocardial infarction in men 55-64 years of age was 1542 per 1,000000 in the US. According to this, the expected number of deaths as a result of myocardial infarction in patients 55-64 years of age receiving sildenafil, in the 24-hour period after use, from late March 1997 to mid November 1998, should have been 52. Instead, the number of reported deaths were only 15. One very optimistic finding was that sildenafil not only does not increase mortality, but in fact 'preconditions' the heart and has a cardioprotective effect. Besides, many studies have shown that sildenafil does not reduce the exercise tolerance in men with known coronary artery disease. As far as BP is concerned, the differences before and after the use of sildenafil are not clinically significant. The only contraindications for sildenafil are co-administration with alpha-adrenoceptor antagonists or with nitric oxide donors. According to the most recent studies, isoform 5 of phosphodiesterase has also been detected in the myocardium and controls the soluble pool of 3', 5'-cyclic guanosine monophosphate (cGMP). Sildenafil is very specific for cGMP but it may increase cyclic adenosine monophosphate in the myocardium indirectly. This does not occur with small therapeutic doses of the drug. There is some dispute regarding the association of sildenafil with arrhythmias, where the available evidence is not clear. However, there are suspicions that sildenafil may cause sympathetic activation. The overall conclusion is that sildenafil is a safe drug and that its appropriate use does not seem to increase the risk for myocardial infarction or sudden cardiac death.
西地那非是首个被批准用于治疗勃起功能障碍的口服化合物。在本文中,我们综述了目前关于西地那非对心肌梗死和心源性猝死影响的知识。我们研究的第一个因素是性活动本身。正如几项研究所表明的,性交期间发生急性冠状动脉综合征的相对风险并不很高。近年来发表了几项研究西地那非对死亡率影响的研究。这些研究中的绝大多数发现,西地那非不是急性冠状动脉综合征或心源性猝死的额外风险因素。1997年,美国55至64岁男性的心肌梗死发病率为每100万人中有1542例。据此,在1997年3月下旬至1998年11月中旬使用西地那非的55至64岁患者中,预计在用药后24小时内死于心肌梗死的人数应为52人。相反,报告的死亡人数仅为15人。一个非常乐观的发现是,西地那非不仅不会增加死亡率,实际上还能“预处理”心脏并具有心脏保护作用。此外,许多研究表明,西地那非不会降低已知患有冠状动脉疾病男性的运动耐量。就血压而言,使用西地那非前后的差异在临床上并不显著。西地那非的唯一禁忌是与α-肾上腺素能拮抗剂或一氧化氮供体合用。根据最新研究,磷酸二酯酶同工型5也已在心肌中被检测到,并控制着环磷酸鸟苷(cGMP)的可溶性池。西地那非对cGMP具有高度特异性,但它可能间接增加心肌中的环磷酸腺苷。小治疗剂量的该药物不会出现这种情况。关于西地那非与心律失常的关联存在一些争议,现有证据并不明确。然而,有人怀疑西地那非可能会引起交感神经激活。总体结论是,西地那非是一种安全的药物,其合理使用似乎不会增加心肌梗死或心源性猝死的风险。