Acute effect of sildenafil on myocardial ischemic territories in patients with stable coronary artery disease
The Egyptian Heart Journal • 2013
Publication Information
Authors
Mohamed Salem *, Ahmed Bendary, Shaimaa Moustafa, Ahmed Ramzy, Osama Sanad
Keywords
Sildenafil;
Coronary artery disease; Stable angina
Journal
The Egyptian Heart Journal
Publisher
Not Available
Volume
Not Available
Issue
Not Available
Pages
Not Available
publication.type
International
Paper Link
Not Available
Supplementary Materials
Not Available
Abstract
Abstract Objectives: To test the safety of sildenafil in patients with stable coronary artery disease (CAD).
Methods: Sixty-one patients with stable CAD, documented by coronary angiography were included in this phase I study. Patients were randomized to either single dose sildenafil or matched placebo. Speckle tracking echocardiography was done at baseline and 60 min after sildenafil/pla-cebo intake to calculate peak systolic strain (PSS) of the most severely affected myocardial segments and the global longitudinal PSS.
Results: The baseline mean segmental PSS in the sildenafil group changed by 52%, 3 ± 1% at baseline versus 7 ± 2% after sildenafil intake, P = 0.01. However, no significant changes were reported in the placebo group, 7 ± 3% at baseline versus 7.25 ± 3%, P = 0.1. The baseline mean global longitudinal PSS in the sildenafil group changed by 9% (15 ± 4% at baseline versus 18 ± 3% after sildenafil, P = 0.03). In placebo patients, the change was only 3% from baseline (14.8 ± 2% at baseline compared to 15 ± 2% after placebo intake, P = 0.1). Sildenafil was well tolerated without clinical or hemodynamic deterioration after its intake.
Conclusion: Sildenafil intake is safe in patients with stable CAD, it induced marginal improvements in the peak systolic strain of different myocardial ischemic territories.
Methods: Sixty-one patients with stable CAD, documented by coronary angiography were included in this phase I study. Patients were randomized to either single dose sildenafil or matched placebo. Speckle tracking echocardiography was done at baseline and 60 min after sildenafil/pla-cebo intake to calculate peak systolic strain (PSS) of the most severely affected myocardial segments and the global longitudinal PSS.
Results: The baseline mean segmental PSS in the sildenafil group changed by 52%, 3 ± 1% at baseline versus 7 ± 2% after sildenafil intake, P = 0.01. However, no significant changes were reported in the placebo group, 7 ± 3% at baseline versus 7.25 ± 3%, P = 0.1. The baseline mean global longitudinal PSS in the sildenafil group changed by 9% (15 ± 4% at baseline versus 18 ± 3% after sildenafil, P = 0.03). In placebo patients, the change was only 3% from baseline (14.8 ± 2% at baseline compared to 15 ± 2% after placebo intake, P = 0.1). Sildenafil was well tolerated without clinical or hemodynamic deterioration after its intake.
Conclusion: Sildenafil intake is safe in patients with stable CAD, it induced marginal improvements in the peak systolic strain of different myocardial ischemic territories.
Staff Members - Benha University