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The relationship between either heart rate or diastolic time and ST segment depression has been evaluated during supine and upright exercise in 16 coronary artery disease patients. Diastolic perfusion time and ST segment depression were related by a linear regression, which was independent of exercise posture. The entity of ST segment depression was greater during supine than in upright exercise for the same heart rate. The assessment of the relationship between heart rate and diastolic perfusion time during two exercises showed that at the same heart rate, diastolic perfusion time was shorter in supine posture. In conclusion, the greater entity of ST segment depression induced by supine rather than upright exercise might be explained by the effect of supine posture on diastolic perfusion time.

The present study has been performed to assess the effects of alinidine on diastolic duration during exercise in chronic coronary artery disease. Twelve male patients with stable effort angina and without previous myocardial infarction were studied. They received alinidine or placebo in a double-blind randomized crossover trial for 3 days after a wash-out period of 4 days. Alinidine was administered at a dosage of 30 mg 3 times a day. At the end of each treatment the patients underwent upright bicycle exercise. Left ventricular time intervals were obtained by means of carotid thermistor plethysmography. Diastolic duration was calculated by subtracting the electromechanical systole from the R-R interval and expressed as a percentage of the cardiac cycle (%D). Alinidine increased both total exercise duration from 246.7 +/- 120.7 to 346.6 +/- 114.1 s (p less than 0.05) and time to 0.1-mV ST segment depression from 98.3 +/- 53 to 187.2 +/- 105 s (p less than 0.05). Similarly the drug induced a reduction of the rate-pressure product and of the extent of ischemic ST segment depression during exercise. %D was increased by alinidine both at rest and during exercise. A direct linear regression between R-R and %D was found after both alinidine and placebo treatments either at rest or during exercise. Nevertheless, no difference was observed between both slopes and intercepts. Therefore, since the relationship between R-R interval and %D was unaffected by alinidine, it was possible to hypothesize that the changes in diastolic duration were due only to the bradycardic action of the drug.

The electromechanical events occurring during acute myocardial ischemia were assessed in 10 patients who developed spontaneous angina during cardiac catheterization. Aortic pressure and electrocardiogram were recorded, and heart rate and systolic and diastolic time intervals were measured under control conditions, at the onset of angina and during the relief of chest pain. In 5 patients spontaneous angina was accompanied by an increase in heart rate and systemic arterial pressure and by ST segment changes in anterior or anterolateral precordial leads. Diastolic time, expressed as percent of cardiac cycle, shortened from 48.8 +/- 3.6% at rest to 33.6 +/- 4.8% (p less than 0.01) at the onset of angina, as a consequence of a significant increase in both electromechanical systole and heart rate, and returned to control values within 10 min after sublingual nitroglycerin. In the remaining 5 patients, spontaneous angina was accompanied by a decrease in heart rate and systemic arterial pressure and by ST segment changes in the inferior or inferolateral leads. The diastolic time increased significantly (p less than 0.05) from 39.4 +/- 6.1% at rest to 47.8 +/- 9% at the onset of angina, as a consequence of a significant decrease in heart rate and a slight decrease in electromechanical systole. Since coronary perfusion takes place mainly during diastole, our results suggest that the reflex increase in adrenergic tone may worsen myocardial ischemia by affecting diastolic perfusion time. In contrast, the increase in vagal tone may contribute to spontaneous relief of angina by prolonging diastolic perfusion time.