Abnormal coronary flow velocity pattern in patients with left ventricular hypertrophy, angina pectoris, and normal coronary arteries: a transesophageal Doppler echocardiographic study.

Previous invasive studies have suggested that coronary flow reserve is impaired in patients with left ventricular hypertrophy (LVH) and symptoms of ischemia. We tested whether transesophageal Doppler, a semiinvasive technique, can detect altered characteristics of baseline coronary blood flow velocity in such patients. Thirty patients with LVH (hypertrophic cardiomyopathy in 4, aortic stenosis in 17, hypertension in 9) were studied. Fourteen patients had asymptomatic LVH. Sixteen patients had clinical symptoms of ischemia with angiographically normal epicardial coronary arteries. Ten subjects with no cardiovascular disease were studied as a control group. Peak diastolic and systolic coronary flow velocities were recorded in the proximal part of the left anterior descending artery (LAD) with the use of pulsed Doppler guided by color flow imaging. Patients with symptomatic LVH had higher diastolic peak coronary flow velocity (81 +/- 10 cm/sec, p = 0.0001) compared with normal subjects (41 +/- 8 cm/sec) and patients with asymptomatic LVH (44 +/- 8 cm/sec). In patients with asymptomatic LVH the diastolic coronary flow velocity/indexed ventricular mass ratio was lower (0.28 +/- 0.09 cm/gm/m2, p = 0.0001) compared with symptomatic patients (0.52 +/- 0.12 cm/gm/m2) and compared with controls (0.47 +/- 0.16 cm/gm/m2). Patients with symptomatic LVH but no aortic stenosis also had higher peak systolic coronary flow velocity (38 +/- 9 cm/sec) compared with the other groups (p = 0.0001). In the group of patients with aortic stenosis a significant inverse linear relation was found between peak systolic coronary flow velocity and peak pressure gradient (r = -0.60, p 0.01). In conclusion, patients with symptomatic LVH have abnormally high baseline coronary flow velocities resulting in magnified intimal shear stress. Because flow velocity equals flow/vessel cross-sectional area, it is suggested that high coronary flow velocities in patients with symptomatic LVH result from both augmented coronary flow and failure of the vessel to enlarge commensurately with the increase in LV mass (relative functional stenosis). In patients with aortic stenosis, peak systolic coronary flow velocity appears to be influenced by transvalvular pressure drop.