ST segment depression elicited by dipyridamole infusion in asymptomatic hypertensive patients.

In asymptomatic patients with essential hypertension, electrocardiographic changes suggestive of myocardial ischemia can be elicited by rapid pressure lowering or by pronounced coronary arteriolar dilation. The aim of this study was to assess whether dipyridamole infusion might induce ischemiclike electrocardiographic changes in asymptomatic essential hypertensive patients and to describe the clinical and echocardiographic correlates possibly associated with this response. We therefore studied a control group of 20 normotensive individuals and a group of 28 asymptomatic patients with mild-to-moderate essential hypertension. All underwent dipyridamole-echocardiography testing (12-lead electrocardiogram and two-dimensional echocardiographic monitoring with dipyridamole infusion, 0.84 mg/kg over 10'). No patient showed transient regional dyssynergy during dipyridamole infusion. None of the normotensive and 10 of 28 of the hypertensive participants had horizontal or downsloping ST segment depression more than 0.1 mV during dipyridamole (0% versus 36%, p<0.0l). Hypertensive patients with ("responders") (n=10) and without ("nonresponders") (n=18) ST segment depression showed similar values of percent fractional shortening in baseline conditions (32 ±5 versus 33 ±6, p=NS) and at peak dipyridamole infusion (45 ±8 versus 43±5,p=NS). The peak early to peak late velocity ratio values (evaluated from transmitral flow tracings by Doppler technique) were also similar in baseline conditions (0.86±0.14 versus 0.94±0JO, /?=NS) and at peak dipyridamole (0.72±0.15 versus 0.78 ± 0.32, p=NS). Responders had higher values of left ventricular mass index (149±35 versus 124±28 g/nv2, p<0.05) and duration of hypertension (11.0±6J versus 5.5 ±4.7 years, p<0.05) than nonresponders. All responders showed angiographically normal coronary arteries. Thus, a significant number of asymptomatic essential hypertensive patients showed dipyridamole-induced ischemiclike ST segment depression, in spite of angiographically normal coronary arteries, in the absence of any detectable regional or global, systolic or diastolic, left ventricular dysfunction. (Hypertension 1990;16:19-25)