Key result
Upstream atherosclerosis was associated with reduced vasodilator responses to substance P (42.0% vs 84.1%, p<0.05) but increased relaxation to bradykinin (100.6% vs 70.2%, p<0.05).
Why the study?
Does upstream epicardial atherosclerosis alter the vascular reactivity of small intramyocardial arteries in human hearts?
Observational
Does upstream epicardial atherosclerosis alter the vascular reactivity of small intramyocardial arteries in human hearts?
Absolute Event Rate: 42% vs 84.1%
p-value: p=<0.05
Upstream epicardial atherosclerosis does not cause global impairment of endothelium-dependent vasorelaxation or smooth muscle hyperreactivity in downstream intramyocardial arteries.
Supports selective microvascular endothelial changes without global impairment; leaves open translation to human coronary disease.
Little is known about how the vascular reactivity of the coronary microcirculation is affected by upstream atherosclerotic disease. We have examined, with a wire myograph, the responses of intramyocardial arteries from hearts in which the epicardial vessels were either free of atherosclerotic lesions (non-diseased group) or were affected by atherosclerosis (diseased group). Vasodilator responses of preconstricted vessels to substance P (84.1 +/- 12.6 compared to 42.0 +/- 19.7%) were less in vessels from the diseased group (p < 0.05). In contrast, the relaxation to bradykinin (70.2 +/- 21.2 compared to 100.6 +/- 7.9%) was increased in vessels from the diseased group (p < 0.05). The dilator responses to acetylcholine, adenosine diphosphate, histamine and sodium nitroprusside showed no significant differences between arteries from each group. 5-Hydroxytryptamine was without any significant vasodilator effect in arteries from either group. Assessment of contractile function revealed that the responses to 5-hydroxytryptamine, acetylcholine, U46619, endothelin-1 and L-N(G)-monomethylarginine in each group were not significantly different. Histamine, noradrenaline and dopamine were without any significant contractile response. These results demonstrate that upstream atherosclerosis does not confer any global impairment of endothelium-dependent vasorelaxant responses or smooth muscle hyperreactivity to vasoconstrictors in the arteries that penetrate the myocardium.
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Chester et al. (1998) conducted an observational in Atherosclerosis. Upstream atherosclerosis vs. Non-atherosclerotic epicardial vessels was evaluated on Vasodilator responses of preconstricted vessels to substance P (p=<0.05). Upstream atherosclerosis was associated with reduced vasodilator responses to substance P (42.0% vs 84.1%, p<0.05) but increased relaxation to bradykinin (100.6% vs 70.2%, p<0.05).
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