sildenafil-citrate and Coronary-Thrombosis

Sildenafil was the first oral compound to be approved for the treatment of erectile dysfunction. It is a selective inhibitor of isoform 5 of phosphodiesterase, which is the enzyme responsible for the breakdown of 3', 5'-cyclic guanosine mono-phosphate. Sildenafil-associated myocardial infarction (MI) is rarely seen in patients without previous history of coronary artery disease. A 43-year-old man presented with sudden onset of chest pain. It was determined that his chest pain started after sildenafil intake. Findings consistent with acute anterior MI were observed on electrocardiography. Coronary angiography showed total occlusion of left anterior descending artery with thrombosis. Coronary angioplasty and stenting was successfully performed.

Topics: Angioplasty, Balloon, Coronary; Coronary Angiography; Coronary Thrombosis; Erectile Dysfunction; Humans; Myocardial Infarction; Sildenafil Citrate

Acute myocardial infarction (MI) in the setting of sexual intercourse following the concomitant use of cocaine, alcohol, and sildenafil has not been previously reported. We present a case of a middle-aged patient with no previous history of angina pectoris or coronary artery disease who presents with severe ischemic chest pain and an MI induced by cocaine, alcohol, sildenafil, and sexual intercourse.

Topics: Alcohol Drinking; Angioplasty, Balloon, Coronary; Cocaine-Related Disorders; Coitus; Coronary Angiography; Coronary Thrombosis; Drug-Eluting Stents; Humans; Male; Middle Aged; Myocardial Infarction; Phosphodiesterase 5 Inhibitors; Piperazines; Purines; Sildenafil Citrate; Sulfones; Treatment Outcome

We sought to assess the effect of sildenafil, a highly-specific type 5 phosphodiesterase (PDE5) inhibitor, on platelet-mediated cyclic coronary flow reductions occurring in a canine model of coronary thrombosis despite aspirin therapy.. The PDE5 inhibitors augment the antithrombotic effects of nitric oxide in vitro and in vivo, but it has been proposed that the PDE5 inhibitor sildenafil is prothrombotic.. Cyclic coronary flow reductions were induced in the left anterior descending coronary artery by creation of a stenosis, endothelial injury, and thrombus formation followed by treatment with aspirin, heparin, and tissue plasminogen activator. After an initial observation period, dogs were treated with or without sildenafil (100 microg/kg bolus followed by 4 microg/kg/min infusion).. Cyclic coronary flow reductions ceased in five of six animals 18 +/- 5 min after initiation of sildenafil but continued in all six control animals. The portion of the observation period during which the coronary artery was patent increased from 52 +/- 9% to 83 +/- 5% after sildenafil administration (p = 0.008) but did not differ between the first and second observation periods in untreated dogs (49 +/- 11% vs. 44 +/- 11%, respectively). Among animals with plasma free sildenafil levels > or =20 nmol/l, cyclic coronary flow reductions were 73 +/- 12% less frequent and the time to cessation of cycling 72 +/- 14% shorter than in animals with levels <20 nmol/l (p < 0.05 for both). Sildenafil transiently decreased blood pressure 7 +/- 1% but did not change heart rate. Sildenafil treatment reduced ex vivo thrombin-induced platelet aggregation by 39 +/- 3% (p < 0.005).. Sildenafil improves coronary patency in a canine model of platelet-mediated coronary artery thrombosis, likely via inhibition of platelet aggregation.

Topics: Animals; Aspirin; Blood Coagulation; Blood Pressure; Coronary Circulation; Coronary Thrombosis; Coronary Vessels; Dogs; Fibrinolytic Agents; Heart Rate; Heparin; Periodicity; Phosphodiesterase Inhibitors; Piperazines; Platelet Aggregation; Purines; Sildenafil Citrate; Sulfones; Tissue Plasminogen Activator; Vascular Patency