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Author Notes:

Correspondence to: Arshed A. Quyyumi, MD, Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1462 Clifton Road NE, Suite 507, Atlanta, GA 30322. E‐mail: aquyyum@emory.edu

The sponsors of this study had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data or in the preparation, review, or approval of the article.

Disclosures: None

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Research Funding:

Dr Vaccarino, Dr Quyyumi, Dr Bremner, Dr Shah, Dr Samady, and Dr Sheps report research support from NIH. This work was supported by the NIH (P01 HL101398, P20HL113451‐01, P01HL086773‐06A1, R01 HL109413, R01HL109413‐02S1, UL1TR000454, KL2TR000455, K24HL077506, and K24 MH076955).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cardiac & Cardiovascular Systems
  • Cardiovascular System & Cardiology
  • endothelial function
  • epicardial
  • flow
  • mental stress
  • microvascular
  • resistance
  • INDUCED MYOCARDIAL-ISCHEMIA
  • ARTERY-DISEASE
  • ENDOTHELIAL DYSFUNCTION
  • VASODILATOR RESPONSE
  • CARDIAC EVENTS
  • BLOOD-FLOW
  • OXIDE
  • ATHEROSCLEROSIS
  • RISK
  • CIRCULATION

Coronary and Peripheral Vasomotor Responses to Mental Stress

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Journal Title:

Journal of the American Heart Association

Volume:

Volume 7, Number 10

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Type of Work:

Article | Final Publisher PDF

Abstract:

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 demandadjusted 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 endotheliumindependent, coronary microvascular function. Moreover, the coronary microvascular responses to MS are reflected in the peripheral microvascular circulation.

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© 2018 The Authors.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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