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Updated: May 5, 2026

Ultrasound Based Assessment of Coronary Artery Flow and Coronary Flow Reserve Using the Pressure Overload Model in Mice
Published on: April 13, 2015
Coronary microangiopathy and cardiac hypertrophy
M Vogt1, W Motz, B Schwartzkopff
1Medizinische Klinik and Poliklinik B, University of Düsseldorf, F.R.G.
Insights
Hypertensive patients often have impaired coronary vasodilator reserve, not linked to left ventricular hypertrophy. This reduced coronary reserve in hypertension stems from primary microvascular damage, independent of heart muscle thickening.
Area of Science:
- Cardiology
- Vascular Biology
- Hypertension Research
Background:
- Coronary vasodilator reserve is frequently impaired in hypertensive patients, even without coronary heart disease.
- The cause of reduced coronary reserve in hypertension—whether left ventricular hypertrophy or primary vascular changes—remains unclear.
Purpose of the Study:
- To investigate whether impaired coronary reserve in hypertensive patients is due to left ventricular hypertrophy or primary vascular alterations.
- To quantify coronary reserve and its relationship with left ventricular muscle mass and diastolic wall stress in hypertension.
Main Methods:
- Coronary reserve was assessed in 54 hypertensive patients with angina and normal coronary arteries, and 12 normotensive controls.
- Coronary blood flow was measured using the argon gas chromatographic method.
- Coronary resistance was determined before and after dipyridamole administration; left ventricular muscle mass was assessed via ventriculography.
Main Results:
- Hypertensive patients exhibited a 124% increase in minimal coronary resistance and a 38% reduction in coronary reserve compared to controls.
- No significant correlation was found between coronary reserve, minimal coronary resistance, and left ventricular muscle mass or diastolic wall stress.
- Myocardial oxygen consumption and resting coronary flow did not differ between hypertensive and normotensive groups.
Conclusions:
- Reduced coronary vasodilator reserve in hypertensive patients is not directly related to the degree of left ventricular hypertrophy.
- The findings suggest that primary microvascular lesions, independent of left ventricular hypertrophy, are responsible for impaired coronary reserve in hypertension.
Abstract:
Even in the absence of coronary heart disease, coronary vasodilator reserve is frequently impaired in hypertensive patients. To study, whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy or is a consequence of primary vascular alterations, coronary reserve was determined in 54 hypertensive patients with angina pectoris and angiographically normal coronary arteries. Twelve normotensive persons were studied for control purposes. Coronary blood flow was measured quantitatively by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg (kg body weight)-1 i.v.). Left ventricular muscle mass was determined by ventriculography. In hypertensive patients, minimal coronary resistance was markedly increased by 124% and coronary reserve significantly reduced by about 38% compared with healthy normotensives. Hypertensives and normotensives did not differ with respect to myocardial oxygen consumption per unit weight myocardium (11.9 +/- 2.3 vs 11.4 +/- 2.4 ml O2 100g-1 min, n.s.) and resting coronary flow (92.1 +/- 20.8 vs 91.4 +/- 18.9 ml min-1. 100 g, n.s.). No significant correlation was found between minimal coronary resistance and coronary reserve and left ventricular muscle mass and between coronary reserve and diastolic wall stress. Accordingly, the reduced coronary regulation capacity in hypertensives does not parallel the degree of left ventricular hypertrophy and is not due to an increased myocardial oxygen consumption under resting conditions. Consequently, the impaired coronary reserve in hypertensive patients seems to be the consequence of primary microvascular lesions, which are independent of the process of left ventricular hypertrophy.
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