Key result
Mental stress-induced coronary blood flow response correlates positively with endothelium-dependent microvascular function in CAD.
Why the study?
Does mental stress induce coronary microvascular changes that correlate with endothelial function in patients with stable coronary artery disease?
Cohort (n=38)
Yes
Does mental stress induce coronary microvascular changes that correlate with endothelial function in patients with stable coronary artery disease?
This physiological study demonstrates that coronary microvascular endothelial dysfunction impairs vasodilatory responses during mental stress, offering a mechanistic link to mental stress-induced ischemia in stable coronary artery disease.
Answers are grounded in this paper and cite their sources.
May link endothelial dysfunction to mental stress responses in stable CAD; hypothesis-generating and requires prospective trials before practice change.
Background Coronary microvascular dysfunction may contribute to myocardial ischemia during mental stress ( MS ). However, the role of coronary epicardial and microvascular function in regulating coronary blood flow ( CBF ) responses during MS remains understudied. We hypothesized that coronary vasomotion during MS is dependent on the coronary microvascular endothelial function and will be reflected in the peripheral microvascular circulation. Methods and Results In 38 patients aged 59±8 years undergoing coronary angiography, endothelium‐dependent and endothelium‐independent coronary epicardial and microvascular responses were measured using intracoronary acetylcholine and nitroprusside, respectively, and after MS induced by mental arithmetic testing. Peripheral microvascular tone during MS was measured using peripheral arterial tonometry (Itamar Inc, Caesarea, Israel) as the ratio of digital pulse wave amplitude compared to rest (peripheral arterial tonometry ratio). MS increased the rate‐pressure product by 22% (±23%) and constricted epicardial coronary arteries by −5.9% (−10.5%, −2.6%) (median [interquartile range]), P =0.001, without changing CBF . Acetylcholine increased CBF by 38.5% (8.1%, 91.3%), P =0.001, without epicardial coronary diameter change (0.1% [−10.9%, 8.2%], P =not significant). The MS ‐induced CBF response correlated with endothelium‐dependent CBF changes with acetylcholine ( r =0.38, P =0.03) but not with the response to nitroprusside. The peripheral arterial tonometry ratio also correlated with the demand‐adjusted change in CBF during MS ( r =−0.60, P =0.004), indicating similarity between the microcirculatory responses to MS in the coronary and peripheral microcirculation. Conclusions The coronary microvascular response to MS is determined by endothelium‐dependent, but not endothelium‐independent, coronary microvascular function. Moreover, the coronary microvascular responses to MS are reflected in the peripheral microvascular circulation.
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Hammadah et al. (2018) conducted a cohort in Stable coronary artery disease (n=38). Mental stress (mental arithmetic testing) vs. Resting baseline was evaluated on Correlation between mental stress-induced coronary blood flow (CBF) response and endothelium-dependent CBF changes with acetylcholine (r=0.38, p=0.03). In patients with stable coronary artery disease, the mental stress-induced coronary blood flow response correlated significantly with endothelium-dependent coronary blood flow changes (r=0.38, p=0.03).
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