Is Viagra Safe?
June 30, 2002 4 minutes read
Is Viagra Safe?
Abstract & Commentary
Synopsis: Cardiovascular effects of sildenafil are of relatively minimal degree even in patients with known CAD.
Source: Arruda-Olson AM, et al. JAMA. 2002;287:719-725.
Erectile dysfunction (ED) affects 30 million men in the United States and, since it usually occurs with increasing age, significant coronary artery disease (CAD) frequently coexists with this condition.1 Millions of prescriptions have been written for sildenafil citrate (ie, Viagra) over the past 3 years for patients with and without CAD despite the fact that adverse cardiac events including acute myocardial infarctions, ventricular tachycardia, hypotension, and even death have been associated with its use.2-7 Although multiple questions have been raised regarding the accuracy of these reports and the potential for reporting bias, the important central issue has always been whether the adverse cardiovascular events associated with sildenafil’s use reflect a risk from the drug itself or if these events occurred simply because of the inherent risk of physical activity in patients with CAD.
Arruda-Olson and colleagues recently reported in JAMA the results of a randomized, double-blind, placebo-controlled, crossover trial conducted on 105 men with an average age of 66 years who were afflicted with ED and known or highly suspected CAD. These patients were carefully studied with respect to their resting heart rate, diastolic blood pressure, wall motion score index (ie, a measure of the extent and severity of wall motion abnormalities), and exercise capacity. Arruda-Olson et al concluded that in men with stable CAD, sildenafil had no effect on symptoms, exercise duration, or presence or extent of exercise-induced ischemia as assessed by exercise echocardiography.
Comment by Harold L. Karpman, MD, FACC, FACP
The study by Arruda-Olson et al suggests that the cardiovascular effects of sildenafil are of relatively minimal degree even in patients with known CAD in that the presence and degree of ischemia and the heart rate at which ischemia occurred were no different in the control group or the group of patients who took sildenafil. These findings confirm previously reported noninvasive and invasive studies that have demonstrated how sildenafil influences coronary flow reserve but apparently does not significantly influence ischemia per se in a clinically important way. The available evidence also suggests that even though sildenafil does not provoke myocardial ischemia and is not associated with measurable adverse hemodynamic abnormalities, its use may be associated with dramatic decreases in blood pressure if nitrates are used within 24 hours of taking sildenafil and, therefore, the combination of these 2 agents is contraindicated.8
Since sildenafil itself does not appear to potentiate myocardial ischemia in patients with known CAD who are not taking nitrates, the important clinical issue appears to be how to assess risk when patients with established CAD request treatment for ED. Recognizing that the workloads of sexual activity are generally analogous to walking a mile in 20 minutes or climbing 2 flights of stairs in 10 seconds, the patient’s description of his functional capacity and/or limitations will be helpful in assessing whether sexual activity is likely to precipitate clinically important ischemia with secondary symptoms. Also, a provocative stress test (ie, treadmill, stress echocardiogram, Cardiolite nuclear study, etc) should be considered if the patient has significant functional abnormalities or symptom production or if he/she is at high risk for CAD because of associated diabetes, hypertension, is a cigarette smoker, etc. If any of the functional tests are significantly abnormal, limitation of sexual activities may be advised in these patients simply because of the severity of their CAD and not because of alleged untoward hemodynamic effects of sildenafil.
In summary, it seems more likely that the cardiac events reported with sildenafil in patients with known CAD are related more to the physical demands of sexual activity in a patient with CAD than to the drug itself. Although the relative risk of myocardial infarction may be increased 2-2½ times in the 2 hours after sexual activity in men with or without angina, the absolute risk remains small.9 However, in all patients with known CAD, a thorough discussion should be conducted with them about the risk of sexual activities if sildenafil is being prescribed and, if functional capacity is limited or significant symptoms are part of the picture, a provocative stress test is indicated. Sildenafil use should not be denied in patients solely because they possess the diagnosis of CAD.
Dr. Karpman, Clinical Professor of Medicine, UCLA School of Medicine, is Associate Editor of Internal Medicine Alert.
References
1. National Institutes of Health Consensus Development Panel on Impotence. Impotence. JAMA. 1993;270: 83-90.
2. Feenstra J, et al. Lancet. 1998;352:957-958.
3. Porter A, et al. Clin Cardiol. 1999;22:762-763.
4. Shah PK. N Engl J Med. 1998;339:699.
5. Hayashi K, et al. Jpn Heart J. 1999;40:827-830.
6. Cheitlin MD, et al. Circulation. 1999;99:168-177.
7. Harrold LR, et al. Arch Intern Med. 2000;160: 3401-3405.
8. Webb DJ, et al. Am J Cardiol. 1999;83:21C-28C.
9. Muller JE, et al. JAMA. 1996;275:1405-1409.
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