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Author Notes:

C. Noel Bairey Merz, MD, FAHA, FACC, FESC, 127 S. San Vicente Blvd, Suite A3600, Los Angeles, CA 90048, Phone: 310-423-9680, Fax: 310-423-9681, c.noel.baireymerz@cshs.org

All authors report no conflict of interest related to the contents of this manuscript.

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Research Funding:

Sources of Funding: Ahmed AlBadri is supported by American Heart Association Postdoctoral Fellowship Award Grant (18POST34080330). This work was also supported by contracts from the National Heart, Lung, and Blood Institutes nos. N01-HV-68161, N01-HV-68162, N01-HV-68163, N01-HV-68164, grants U0164829, U01 HL649141, U01 HL649241, K23HL105787, T32HL69751, R01 HL090957, 1R03AG032631 from the National Institute on Aging, GCRC grant M01-RR00425 from the National Center for Research Resources, the National Center for Advancing Translational Sciences Grant UL1TR000124 and UL1TR001427, and the Edythe L. Broad and the Constance Austin Women’s Heart Research Fellowships, Cedars-Sinai Medical Center, Los Angeles, California, the Barbra Streisand Women’s Cardiovascular Research and Education Program, Cedars-Sinai Medical Center, Los Angeles, The Linda Joy Pollin Women’s Heart Health Program, and the Erika Glazer Women’s Heart Health Project, Cedars-Sinai Medical Center, Los Angeles, California. This work is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or National Institutes of Health.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Hematology
  • Peripheral Vascular Disease
  • Cardiovascular System & Cardiology
  • acetylcholine
  • cardiomyocyte injury
  • coronary artery disease
  • INOCA
  • myocardial ischemia
  • risk
  • troponin I
  • vascular function
  • ENDOTHELIUM-DEPENDENT VASODILATION
  • ARTERY-DISEASE
  • MICROVASCULAR DYSFUNCTION
  • NATIONAL-HEART
  • CHEST-PAIN
  • TROPONIN-I
  • CARDIOVASCULAR EVENTS
  • MYOCARDIAL-INFARCTION
  • SENSITIVE ASSAY
  • ISCHEMIA

Coronary Vascular Function and Cardiomyocyte Injury A Report From the WISE-CVD

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Journal Title:

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY

Volume:

Volume 40, Number 12

Publisher:

, Pages 3015-3021

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Objective: Women with symptoms or signs of myocardial ischemia but no obstructive coronary artery disease (INOCA) often have coronary vascular dysfunction and elevated risk for adverse cardiovascular events. We hypothesized that u-hscTnI (ultra-high-sensitivity cardiac troponin I), a sensitive indicator of ischemic cardiomyocyte injury, is associated with coronary vascular dysfunction in women with INOCA. Approach and Results: Women (N=263) with INOCA enrolled in the WISE-CVD study (Women's Ischemic Syndrome Evaluation-Coronary Vascular Dysfunction) underwent invasive coronary vascular function testing and u-hscTnI measurements (Simoa HD-1 Analyzer; Quanterix Corporation, Lexington, MA). Logistic regression models, adjusted for traditional cardiovascular risk factors were used to evaluate associations between u-hscTnI and coronary vascular function. Women with coronary vascular dysfunction (microvascular constriction and limited coronary epicardial dilation) had higher plasma u-hscTnI levels (both P=0.001). u-hscTnI levels were associated with microvascular constriction (odds ratio, 1.38 per doubling of u-hscTnI [95% CI, 1.03-1.84]; P=0.033) and limited coronary epicardial dilation (odds ratio, 1.37 per doubling of u-hscTnI [95% CI, 1.04-1.81]; P=0.026). u-hscTnI levels were not associated with microvascular dilation or coronary epicardial constriction. Conclusions: Our findings indicate that higher u-hscTnI is associated with coronary vascular dysfunction in women with INOCA. This suggests that ischemic cardiomyocyte injury in the setting of coronary vascular dysfunction has the potential to contribute to adverse cardiovascular outcomes observed in these women. Additional studies are needed to confirm and investigate mechanisms underlying these findings in INOCA. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT00832702.
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