(Circulation. 2001;104:1214.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
From the Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Md, and GE Medical Systems (S.N.G.), Milwaukee, Wis.
Correspondence to Garth M. Beache, MD, Cardiovascular Imaging and Physiology Center, Department of Diagnostic Radiology, University of Maryland Medical Center, 22 South Greene St, Baltimore, MD 21201-1595. E-mail gbeache{at}umm.edu
Background Oxygen (O2) homeostasis is central to myocardial tissue functioning, and increased O2 demand is thought to be satisfied by a vasodilatory mechanism that results in increased blood and O2 delivery. We applied blood oxygenation leveldependent (BOLD) MRI in conjunction with vasodilatory stress to index the ability to augment intramyocardial oxygenation in hypertensive hypertrophy, the primary cause of heart failure.
Methods and Results Nine healthy controls and 10 hypertensive subjects with moderate-to-severe hypertrophy underwent imaging on a 1.5 T clinical scanner. The dipyridamole-induced change in the apparent transverse relaxation rate, R2*, which correlates with hemoglobin oxygenation, was -5.4±2.2 s-1 (95% CI, -4.0 to -6.8 s-1) in controls compared with -1.7±1.4 s-1 (95% CI, -0.8 to -2.6 s-1) in hypertensive patients (P=0.0003).
Conclusions Patients with hypertensive hypertrophy demonstrate an impaired ability to increase intramyocardial oxygenation during vasodilatory stress, as indexed by BOLD MRI. The capacity to image vascular function with BOLD MRI may advance the understanding of the development of ventricular dysfunction in hypertension.
Key Words: magnetic resonance imaging hypertension hypertrophy angiotensin-converting enzyme inhibitors endothelium, vascular
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