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Ultra-high sensitivity cardiac troponin-I concentration and left ventricular structure and function in women with

Odayme Quesada1,2, Omeed Elboudwarej1, Michael D Nelson3

  • 1Barbra Streisand Women's Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States of America.

American Heart Journal Plus : Cardiology Research and Practice
|July 5, 2022
PubMed

Insights

Cardiomyocyte injury, indicated by ultra-high sensitivity cardiac troponin I (u-hscTnI), is linked to left ventricular (LV) remodeling and dysfunction in women with ischemia and no obstructive coronary artery disease (INOCA). Further research is needed to clarify the exact mechanisms.

Area of Science:

  • Cardiology
  • Cardiovascular Imaging
  • Biomarker Research

Background:

  • Women with ischemia and no obstructive coronary artery disease (INOCA) face a higher risk of heart failure with preserved ejection fraction (HFpEF).
  • The underlying mechanisms connecting INOCA to HFpEF remain poorly understood, particularly regarding cardiomyocyte injury.

Purpose of the Study:

  • To investigate the association between ultra-high sensitivity cardiac troponin I (u-hscTnI), a marker of cardiomyocyte injury, and myocardial perfusion, left ventricular (LV) structure, and function in women with INOCA.

Main Methods:

  • Analysis of 327 women with INOCA from the WISE-CVD study.
  • Utilized vasodilator stress cardiac magnetic resonance imaging (CMRI) and u-hscTnI measurements.
  • Employed multivariable linear regression to assess relationships between u-hscTnI and LV mass index, and feature-tracking derived strain measures.

Main Results:

  • Quantifiable u-hscTnI levels were found in 100% of participants.
  • Elevated u-hscTnI concentrations were significantly associated with increased LV mass index and altered early diastolic strain rates (radial, circumferential, and longitudinal).
  • No significant association was observed between u-hscTnI and myocardial perfusion reserve index (MPRI).

Conclusions:

  • Cardiomyocyte injury, as indicated by u-hscTnI, may contribute to adverse LV remodeling and dysfunction in women with INOCA.
  • These findings suggest a potential pathway linking INOCA to HFpEF through myocellular injury.
  • Further research is required to elucidate the specific mechanisms driving cardiomyocyte injury in INOCA.
Abstract

Keywords:
Cardiomyocyte injuryDiastolic strainIschemia and no obstructive coronary artery disease (INOCA)Left ventricular dysfunctionLeft ventricular massUltra-high sensitivity cardiac troponin

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