Key result
Following dipyridamole administration, patients with hypertrophic cardiomyopathy demonstrated significantly lower maximum coronary blood flow (131 vs 192 ml/100g min) compared to control subjects.
Why the study?
Does dipyridamole administration reveal impaired coronary vasodilatory capacity in patients with non-obstructive hypertrophic cardiomyopathy compared to controls?
Case-Control (n=26)
No
Does dipyridamole administration reveal impaired coronary vasodilatory capacity in patients with non-obstructive hypertrophic cardiomyopathy compared to controls?
Patients with non-obstructive hypertrophic cardiomyopathy demonstrate impaired coronary vasodilatory capacity, which correlates with left ventricular muscle mass and reduced exercise tolerance.
To investigate mechanisms for a reduced coronary vasodilatory capacity in patients with hypertrophic cardiomyopathy (HCM), maximum coronary blood flow and minimum coronary vascular resistance were measured by administering dipyridamole (0.56 mg/kg) to 19 patients with non-obstructive HCM and to 7 control subjects. The maximum coronary blood flow was significantly lower (131 +/- 46 vs 192 +/- 41 ml/100 g . min, p less than 0.01, mean +/- SD) and the minimum coronary vascular resistance was significantly higher (0.64 +/- 0.23 vs 0.44 +/- 0.13 mmHg/ml/100 g . min, p less than 0.05) in HCM patients. There were no significant correlations between maximum coronary blood flow or minimum coronary vascular resistance and the baseline left ventricular end-diastolic pressure or the severity of systolic narrowing of the left anterior descending artery of the septal perforator. In contrast, the minimum coronary vascular resistance was correlated significantly with the left ventricular muscle mass (r = 0.55, p less than 0.05), but its correlation to small coronary vessel disease could not be studied. In addition, HCM patients with a reduced exercise tolerance (less than 7 metabolic units) demonstrated a significantly lower maximum coronary blood flow and higher minimum coronary vascular resistance than control subjects. These findings suggest that: (1) there is a group of HCM patients who have a reduced coronary vasodilatory capacity, (2) abnormal coronary vasculature is a possible underlining mechanism of HCM, either due to inadequate growth unassociated with left ventricular hypertrophy or as small coronary vessel disease, and (3) a reduced coronary vasodilatory capacity.
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Shimamatsu et al. (1987) conducted a case-control in Hypertrophic cardiomyopathy (n=26). Dipyridamole vs. Control subjects was evaluated on Maximum coronary blood flow (ml/100g min) (p=<0.01). Following dipyridamole administration, patients with hypertrophic cardiomyopathy demonstrated significantly lower maximum coronary blood flow (131 vs 192 ml/100g min) compared to control subjects.
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