Early impairment of myocardial blood flow reserve in men with essential hypertension: A quantitative myocardial contrast echocardiography study

Objective. Aims of this study were to: (1) demonstrate whether quantitative myocardial contrast echocardiography could detect an index of myocardial blood How reserve through the analysis of refilling curves generated by microbubble transit into myocardium both at rest and after vasodilatation induced by dipyridamole; and (2) explore with this method myocardial microcirculatory function in two different models (ie, patients with essential hypertension and control subjects). Methods: Two groups of strictly age-matched men were studied (case-control study): 12 patients who were adults (28.2 +/- 0.2 years) and asymptomatic with never-treated essential hypertension, a mild degree of left ventricular hypertrophy, and normal left ventricular function; and 12 control subjects. Quantitative myocardial contrast echocardiography was performed in all study participants. We used second-generation ultrasound microbubbles as echocardiography contrast agent. Real-time color-coded power modulation was performed with a phased-array system interfaced to a S3 transducer (1.3-3.6 MHz). Results: In control subjects there was little increase in myocardial blood volume (30%) between basal and hyperemic status (P < .05); in patients with hypertension this parameter increased by 22% (P < .05). Myocardial blood velocity increased after dipyridamole by 270% in control subjects (P < .01), whereas for patients with hypertension this parameter increased only by 150% (P < .02). The index of myocardial blood flow reserve was significantly lower for patients with hypertension than in control subjects (3.3 +/- 0.3 vs 4.4 +/- 0.3, respectively, P < .01). Conclusion: Results of our study documented that myocardial microcirculation in young adult patients with hypertension showed an early impairment in the vasodilatation capacity of the resistance arterioles under dipyridamole-induced hyperemia, as demonstrated by a reduction of myocardial blood flow reserve. Myocardial blood velocity increased after dipyridamole induction in control subjects, whereas patients with hypertension showed a significantly lesser increase. Myocardial blood flow reserve was significantly lower for patients with hypertension because of an early impairment in vasodilatation capacity of resistance arterioles under dipyridamole-induced hyperemia.