The respective contribution of systemic vascular resistance (R) and total arterial compliance (C) to the arterial load remains to be established in humans. Effective arterial elastance (Ea), i.e., the left ventricular end-systolic pressure (LVESP)-over-stroke volume ratio, is a reliable estimate of arterial load. It is widely accepted that Ea mainly relates to mean aortic pressure (MAP) and thus to the R-to-T ratio (R/T ratio), where T is cycle length. We tested the contribution of R/T and 1/C to Ea in 20 normotensive and 46 hypertensive subjects (MAP range: 84-160 mmHg). The multilinear model applied (Ea = 1.00R/T + 0.42/C - 0.04; r2 = 0.97). The sensitivity of Ea to a change in R/T was 2.5 times higher than to a similar change in 1/C in both normotensive and hypertensive adults. The LVESP was more strongly related to systolic aortic pressure (SAP; r2 = 0.94) than to MAP (r2 = 0.83), and LVESP matched 90% SAP (bias = 0 +/- 5mmHg). An alternative model of Ea is proposed, in which Ea is proportional to the heart rate x SAP product-over-cardiac index ratio whatever the MAP.

ACE inhibition restored CPT-induced and flow-mediated coronary artery dilations in patients with essential hypertension. These results indicate that impaired coronary vasomotor responses may be reversible in recently diagnosed hypertension.

The reduction in coronary reserve observed in untreated hypertensive patients with normal myocardial mass suggests that structural abnormalities of the coronary microvasculature may occur before left ventricular hypertrophy. Treated patients with normal mass before treatment had a coronary reserve comparable to that of normotensive control subjects, whereas normalization of arterial pressure with persistent left ventricular hypertrophy was associated with a marked impairment of coronary reserve.

Coronary microcirculation dysfunction may be associated with myocardial perfusion defects on thallium imaging in diabetic patients without coronary artery stenosis. Microvascular coronary adaptation to increased myocardial oxygen demand in response to sympathetic stimulation evoked by the cold pressor test was examined in 22 type 2 diabetic patients with thallium imaging defects and in 15 control subjects. Both the diabetic patients and control subjects had angiographically normal coronary arteries and no other risk factors. Despite a similar increase in the rate-pressure product in the two groups (22.6 ؎ 12.4% in diabetic patients and 31.8 ؎ 8.2% in control subjects, NS), coronary blood flow increase in the left anterior descending artery (mean flow velocity measured by intracoronary Doppler multiplied by the cross-sectional area measured by digital angiography) was significantly lower in diabetic patients than in control subjects (14.7 ؎ 19.8 vs. 75.5 ؎ 13.5%, respectively; P ‫؍‬ 0.0001). In addition, when there was a positive correlation between the two parameters in control subjects (r ‫؍‬ 0.651, P < 0.01), there was no relationship in diabetic patients (r ‫؍‬ 0.054). In conclusion, vasodilation of the coronary microcirculation in response to sympathetic stimulation evoked by the cold pressor test is impaired in type 2 diabetic patients without epicardial artery lesions. This microvascular impairment during sympathetic stimulation may explain exercise-induced myocardial perfusion abnormalities observed in these patients and may impair microcirculatory coronary vasodilation during current life stress episodes such as exercise, mental stress, or cold exposition. Diabetes 50:1180 -1185, 2001 I t has been shown that endothelium-dependent epicardial coronary artery vasodilation in response to acetylcholine (1) or physiological stimuli (2) is impaired in diabetic patients with angiographically normal coronary arteries. Microvascular functional abnormalities have also been reported by Nasher et al. (3), who have shown that metabolic vasodilation of coronary microcirculation evoked by atrial pacing is reduced in diabetic patients. Similar impairment has also been reported in hypertensive patients with angiographically normal coronary arteries (4) and by Zeiher et al., who showed that coronary blood flow failed to increase during exercise (5) or during the cold pressor test (CPT) in patients with early atherosclerosis (6) and without significant coronary artery stenosis, suggesting that the endothelial function is impaired at the microvascular level. Such coronary microcirculation dysfunction may be associated with myocardial perfusion defects on 99m Tc sestamibi single photon emission computed tomography (SPECT) imaging in humans with angina and minimally obstructive coronary artery disease (7) and might contribute to myocardial ischemia when myocardial oxygen demand is increased, even in the absence of coronary artery stenosis.In diabetes, it has been suggested that coronary functional abnormalities and microvas...