Augmentation of Myocardial blood flow in hypertensive heart disease by angiotensin antagonists: A comparison of lisinopril and losartan

• Published in: Journal of the American College of Cardiology 2002-08, Vol.40 (4), p.703-709
• Main Authors: AKINBOBOYE, Olakunle O, CHOU, Ru-Ling, BERGMANN, Steven R
• Format: Article
• Language: English
• Subjects: Adult; Angiotensin II - antagonists & inhibitors; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors - pharmacology; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Biological and medical sciences; Blood pressure; Cardiology; Cardiovascular disease; Cardiovascular system; Coronary Circulation - drug effects; Diabetes; Drug therapy; Female; Heart; Heart Ventricles - diagnostic imaging; Heart Ventricles - drug effects; Heart Ventricles - physiopathology; Humans; Hypertension; Hypertension - complications; Hypertension - drug therapy; Hypertension - physiopathology; Hypertrophy, Left Ventricular - drug therapy; Hypertrophy, Left Ventricular - etiology; Hypertrophy, Left Ventricular - physiopathology; Lisinopril - pharmacology; Lisinopril - therapeutic use; Losartan - pharmacology; Losartan - therapeutic use; Male; Medical sciences; Middle Aged; Miscellaneous; Mortality; Patients; Personal computers; Pharmacology. Drug treatments; Scanners; Studies; Tomography, Emission-Computed
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(02)02033-8

The goal of this study was to compare myocardial perfusion reserve (MPR) before and after long-term treatment with lisinopril and losartan in patients with hypertension and left ventricular hypertrophy (LVH). Studies have suggested that treatment with angiotensin-converting enzyme inhibitors (ACEIs) improves MPR in patients with hypertension by potentiating endogenous bradykinins. Because angiotensin receptor blockers (ARBs) lack a direct effect on bradykinins, we hypothesized that they may not improve MPR. We measured pre- and post-treatment myocardial blood flow (MBF) by positron emission tomography in 17 patients (lisinopril: 9 patients, losartan: 8 patients) with hypertension and LVH at baseline and after coronary vasodilation with intravenous dipyridamole. In addition, we measured rest and hyperemic blood flow in eight normotensive controls. Post-treatment maximal coronary blood flow and MPR in the lisinopril group increased significantly compared with pretreatment values (3.5 +/- 1.2 vs. 2.6 +/- 1.1 ml/min/g, p = 0.02; 3.7 +/- 1.1 vs. 2.4 +/- 1 ml/min/g, respectively, p = 0.002, respectively). Post-treatment hyperemic flow in the patients treated with lisinopril was not significantly different from corresponding measurements in controls (3.5 +/- 1.2 vs. 3.9 +/- 1 ml/min/g, respectively, p = NS). In the patients treated with losartan, there was no difference between pre- and post-treatment MBF values and MPR. Myocardial perfusion reserve and maximal coronary flow improved in asymptomatic patients with hypertension-induced LVH after long-term treatment with lisinopril but not with losartan. Thus, ACEIs, but not ARBs, might be effective in repairing the coronary microangiopathy associated with hypertension-induced LVH.