Effect of simvastatin on coronary flow reserve in patients with atherosclerosis and hypercholesterolemia: an intracoronary Doppler study

In Brief Background Early stages of coronary atherosclerosis are accompanied by a functional impairment of coronary vasodilator capacity and endothelial dysfunction. Reduced coronary flow reserve has been reported in patients with hypercholesterolemia, despite angiographically normal coronary arteries. The aim of the study was to evaluate the effect of simvastatin on coronary flow reserve. Methods The study was an open non-placebo-controlled serial investigation in which every patient acted as his own control: 36 male patients with hypercholesterolemia and a non-significant coronary artery lesion in a not previously revascularized coronary artery. Intracoronary Doppler measurements were performed. Coronary flow reserve, relative coronary flow reserve and average peak velocity were performed at baseline, after 3 months on a lipid-lowering diet (control period), and after another 12 months of simvastatin 40 mg/day. In the same patient cohort, significant reduction in lesion plaque plus media has been demonstrated by intravascular ultrasound. Results Changes in coronary flow reserve were not influenced by either diet or simvastatin (2.5±0.6 vs. 2.6±0.5 vs. 2.6±0.6, P=ns). Maximum hyperemic flow (34.8±12.2 vs. 36.7±12.5 vs. 42.5±13.1, P<0.001) as well as resting flow (14.3±5.3 vs. 14.5±4.4 vs. 16.6±4.6, P<0.001) increased significantly after 12 months simvastatin therapy. Conclusion Despite plaque plus media, regression simvastatin therapy for 12 months does not affect coronary flow reserve obtained using serial intracoronary Doppler studies. Simvastatin, however, increases the hyperemic flow velocity. With an intracoronary Doppler wire the lipid-lowering effect of simvastatin on coronary flow reserve and the coronary microcirculation was studied in 36 male patients with hypercholesterolemia. In the same patient cohort, significant reduction in lesion plaque plus media has been demonstrated by intravascular ultrasound. Changes in coronary flow reserve were not influenced either by dietor by 12 months of simvastatin therapy (2.5±0.6 vs. 2.6±0.5 vs. 2.6±0.6, P=NS). Maximum hyperemic flow (34.8±12.2 vs. 36.7±12.5 vs. 42.5±13.1, P<0.001) as well as resting flow (14.3±5.3 vs.14.5±4.4 vs. 16.6±4.6, P<0.001) increased significantly after 12 months of simvastatin therapy. Despite plaque plus media regression, simvastatin therapy for 12 months does not affect coronary flow reserve obtained using serial intracoronary Doppler studies. Simvastatin, however, increases the hyperemic flow velocity. Simvastatin therapy does not influence coronary flow reserve (measured by intracoronary Doppler) in patients with atherosclerosis and hypercholesterolemia.