Why the study?
Women with INOCA are at increased risk of developing HFpEF, but the mechanisms linking these conditions remain poorly understood.
Is ultra-high sensitivity cardiac troponin I associated with abnormalities in myocardial perfusion and left ventricular structure and function in women with INOCA?
Is ultra-high sensitivity cardiac troponin I associated with abnormalities in myocardial perfusion and left ventricular structure and function in women with INOCA?
In women with INOCA, ultra-high sensitivity cardiac troponin I is associated with increased LV mass and altered diastolic strain, supporting cardiomyocyte injury as a potential pathway to adverse remodeling and HFpEF.
Answers are grounded in this paper and cite their sources.
u-hscTnI associates with LV mass and diastolic strain abnormalities in INOCA women; leaves open whether injury mediates HFpEF progression.
Women are disproportionally impacted by ischemia and no obstructive coronary artery disease (INOCA), and such women are at increased risk of developing heart failure with preserved ejection fraction (HFpEF), however the mechanisms linking these conditions remain poorly understood. The aim of this study was to determine whether ultra-high sensitivity cardiac troponin I (u-hscTnI), an indicator of cardiomyocyte injury, is associated with abnormalities in myocardial perfusion and left ventricular (LV) structure and function in women with INOCA. 327 women with INOCA enrolled in the Women's Ischemia Syndrome Evaluation-Coronary Vascular Dysfunction (WISE-CVD) study underwent vasodilator stress cardiac magnetic resonance imaging (CMRI) and u-hscTnI measurements (Simoa HD-1 Analyzer, Quanterix Corporation). Multivariable linear regression was used to evaluate associations between u-hscTnI concentrations and myocardial perfusion (MPRI), LV mass index and feature-tracking derived strain measures of LV function. u-hscTnI concentrations were quantifiable in 100% of the cohort and ranged from 0.004 to 79.6 pg/mL. In adjusted models, u-hscTnI was associated with LV mass index (+2.03; 95% CI 1.17, 2.89; p < 0.01) and early diastolic radial strain rate (SR) (+0.13; 95% CI 0.01, 0.25; p = 0.03), early diastolic circumferential SR (−0.04; 95% CI −0.08, 0.002; p = 0.06) and early diastolic longitudinal SR (−0.03; 95% CI −0.07, 0.002; p = 0.06). u-hscTnI was not associated with MPRI (p = 0.39) in adjusted models. Together, these findings support cardiomyocyte injury as a putative pathway towards adverse LV remodeling and dysfunction; however, further research is needed to define the specific mechanism(s) driving myocellular injury in INOCA.
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Quesada et al. (2022) studied this question.
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