Clinical study
Relation among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease

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Abstract

Invasive Doppler catheter-derived coronary flow reserve, echocardiographic measurements of left ventricular hypertrophy and intravenous dipyridamole-limited stress thallum-201 scintigraphy were compared in 48 patients (40 were hypertensive or diabetic) with clinical ischemic heart disease and no or coronary artery disease. Abnormal vasodilator reserve (ratio <3:1) occured in 50% of the study group and markedly abnormal reserve (≤2:1) occurred In 27%, Coronary vasodilator reserve was significantly lower (2.2 ± 0.8 versus 3.5 ± 1.3, p = 0.0.3) and indexed left ventricular mass significantly higher (152.6 ± 42.2 versus 113.6 ± 24.0 g, p = 0.0007) in patients with a positive (n = 11) versus a negative (n = 32) thallium perfusion scan. Coronary flow reserve was linearly related to coronary flow velocity as follows: y = −0.17 × + 459; r = −0.57; p = 0.00002.

The decrement in flow reserve was not linearly related to the of left ventricular hypertrophy. Abnormal vasodilator reserve subsets found in hypertensive patients were defined on the basis of basal flow velocity, indexed left ventricular mass and clinical factors. In this series, diabetes did not cause a detetable additional decrement in flow reserve above that found with hypertension alone.

These findings demonstrate that thallium perfusion defects are associated with depressed coronary vasodilator reserve in hypertensive patients without obstructive coronary artery disease, Left ventricular hypertrophy by indexed mass criteria is predictive of which hypertensive patients are likely to have thallium defects. Depressed coronary reserve is typically found in hypestensive patients with hypertrophy and increased basal coronary flow velocity, but less typical presentations including hypertrophy and normal or low coronary low velocity are found in advanced hypertensive disease.

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This study was supported in part by the Medical College of Georgia Research Institute, Augusta. It was presented in part at the 38th Annual Meeting of the American College of Cardiology, Anaheim, California, March 1989.