Coronary vasomotion in response to sympathetic stimulation in humans: importance of the functional integrity of the endothelium.

The coronary vasomotor response to the cold pressor test was studied with use of quantitative coronary angiography in 32 patients without evidence of coronary artery disease and 55 patients with such disease; in a subset of 22 patients (9 with normal coronary arteries and 13 with coronary artery disease), the effects of the cold pressor test were compared with the effects of the endothelium-dependent vasodilator acetylcholine with simultaneous intracoronary Doppler flow velocity measurements to assess the influence of endothelial dysfunction. The cold pressor test induced vasodilation of 8.9 +/- 5.7% in all 77 analyzed vessel segments of the group with normal arteries (p less than 0.01). In contrast, in patients with coronary artery disease, the 52 analyzed stenotic segments were constricted by -12.1 +/- 9.5% (p less than 0.01), the 57 analyzed vessel segments with luminal irregularities were constricted by -8.9 +/- 5.2% (p less 0.01) and 40 (85%) of 47 angiographically normal segments also were constricted by -7.0 +/- 4.9% (p less than 0.05). Preserved vasodilating capability was demonstrated by intracoronary nitroglycerin in all analyzed segments. In nine patients with normal coronary arteries, the analyzed vessel segments were dilated in response to both the cold pressor test and intracoronary acetylcholine by 10.9 +/- 5.4% and 13.4 +/- 4.7%, respectively. In contrast, in all 13 patients with coronary artery disease, vasoconstriction of identical vessel segments by -9.1 +/- 3.7% and -23 +/- 10.4%, respectively, was observed after both the cold pressor test and intracoronary acetylcholine. Intracoronary propranolol did not significantly affect either the vasodilative response in 11 normal coronary arteries (11.3 +/- 4.4% before and 8.6 +/- 4.3% after beta-blockade) or the vasoconstrictor response in 8 atherosclerotic coronary arteries (-11.4 +/- 4.6% before and -14.6 +/- 5.3% after beta-blockade). The dilation of normal and the constriction of atherosclerotic coronary arteries with cold pressor testing exactly mirror the response to the endothelium-dependent dilator acetylcholine. Endothelial dysfunction in coronary atherosclerosis resulted in a loss of normal dilator function and permitted vasoconstrictor responses to sympathetic stimulation. Thus, coronary vasomotion of large epicardial arteries in response to sympathetic stimulation by the cold pressor test in humans is intimately related to the integrity of endothelial function.

Hierarchy of levels of ischemia-induced impairment in regional left ventricular systolic function in man.

We tested the hypothesis that different subsets of ischemia-induced wall motion disorders are characterized by specific patterns of abnormal regional left ventricular systolic function. Regional contraction was quantitatively assessed from two-dimensional echocardiograms by an automated integrative analysis considering the time course of wall motion during the entire contraction sequence in 20 patients with chronic myocardial infarction, in 13 patients with impending myocardial infarction (less than 2 hr after the onset of symptoms), and in nine patients during transient myocardial ischemia. Wall motion abnormalities were detected in all patients by the integrative analysis. In contrast, the sensitivity for detecting wall motion abnormalities was 80% during chronic infarction, 77% during impending infarction, and 56% during transient ischemia if only end-diastolic and end-systolic frames were compared for assessment of overall regional systolic function. There were distinct differences in the time course of abnormal wall excursion between the three groups. Chronic infarction was characterized by a monophasic contraction pattern, with abnormal synergy in regional contractile events occurring predominantly during early systole. In contrast, transient ischemia caused predominantly mid-to-late systolic abnormal synergy followed by late systolic shortening corresponding to a polyphasic contraction pattern. During impending infarction, an intermediate temporal contraction pattern was present with both early and mesosystolic abnormal synergy.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative assessment of temporal and spatial ventricular wall motion in normal and infarcted human left ventricles.

A new integrated method for quantitating temporal and spatial systolic wall motion heterogeneity was developed and applied in 15 normal subjects and 26 patients with previous myocardial infarction (MI). After frame by frame digitizing, right anterior oblique left cineventriculograms (LV) were analyzed with 90 spaced radii. For each radius shortening fractions at sequential systolic time points relative to end diastole were correlated with corresponding normalized time points using linear regression method, yielding the radial correlation coefficient (r) and the radial regression slope (b) for temporal and spatial information. High radial r values with small standard deviations were observed in normal LV (0.972 +/- 0.016) and in non-MI regions (0.964 +/- 0.018), indicating temporally homogeneous radial shortening. A significant temporal heterogeneity in wall motion was demonstrated in MI regions (0.480 +/- 0.304) (p less than 0.001). In comparison with normal b values (0.449 +/- 0.106), there were decreased b values in MI regions (0.203 +/- 0.211) (p less than 0.001) and increased b values in non-MI regions (0.695 +/- 0.213) (p less than 0.001), suggesting hypokinetic and compensative hyperkinetic contraction in corresponding regions. Thus, temporal and spatial wall motion throughout systole could be assessed quantitatively by the present computer-assisted method with two simple integrated parameters.