Elsevier

American Heart Journal

Volume 141, Issue 2, February 2001, Pages 247-253
American Heart Journal

Congestive Heart Failure
Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain*,**

https://doi.org/10.1067/mhj.2001.111767Get rights and content

Abstract

Background Myocyte death could play a role in heart failure (HF) irrespective of the presence of coronary artery disease. The study aimed to assess this hypothesis by use of the cardiac troponin I (cTnI) assay. Methods and Results Seventy-one patients with nonischemic HF, New York Heart Association (NYHA) class II-IV, with a normal coronary angiogram and after exclusion of myocardiopathies were evaluated in the study. The control group included 9 healthy subjects and 15 patients hospitalized for severe noncardiac dyspnea. Cardiac TnI concentrations were determined at admission with a research reagent (cTnIus) characterized by a detection limit of 0.026 ng/mL and a high analytic sensitivity of 0.002 ng/mL. cTnIus levels were more than 0.026 ng/mL in 19 HF patients, ranging between 0.027 and 0.463 ng/mL, whereas no cTnIus level was detectable in the control group. With use of a reference assay, only 2 HF patients had abnormal cTnI values. Severe HF was observed in 17 of these 19 patients, assessed by NYHA class IV or by the presence of pulmonary edema. Patients with an increased cTnIus level had a more restrictive mitral Doppler pattern (P <.001) and a more distinctive left ventricular (LV) concentric remodeling (P <.0001), whereas LV ejection fraction was similar in both HF groups. The increased cTnIus level was also associated with a LV wall strain biologic marker (ie, an increased brain natriuretic peptide plasma level) (P <.001). Conclusions cTnI assay is a promising biochemical method for detecting cardiac myolysis in HF, independent of the presence of coronary artery disease. This subtle myolysis could be in part related to the severely increased LV wall strain. (Am Heart J 2001;141:247-53.)

Section snippets

Patients

We included patients with acute or stable chronic congestive HF at admission to our cardiology intensive care unit or during programed 1-day hospitalization. Patients with angina pectoris; recent or acute Q- or non-Q-wave myocardial infarction; severe pulmonary, renal, or hepatic disease; or a history of surgery within 30 days of inclusion were not eligible. To exclude all cases of coronary artery disease, patients were enrolled only when a coronary angiogram showed no atherosclerotic

Patients

Among the 71 patients, 35 patients with stable congestive HF were studied while ambulatory during programmed 1-day hospitalization, whereas the other 36 patients were studied at admission for acute congestive HF. Among the 35 patients with stable HF, 3 were in NYHA class IV, 6 in class III, and 24 in class II. Among the 36 patients with acute HF, 28 were admitted because of pulmonary edema, 2 died, 4 required mechanical ventilation, and 9 required inotropic drugs during their in-hospital stay

Discussion

This study shows (1) evidence of cardiac myolysis during severe HF in patients without coronary artery disease and (2) a correlation between cardiac myolysis, LV concentric remodeling, and a marker of LV chamber strain (BNP).

The transition from compensated to decompensated LV dysfunction is a major pathogenic and clinical event during the course of HF. Progressive cardiac myocyte loss seems to be associated with LV chamber dysfunction. The mechanisms of myocyte loss include necrosis and

Acknowledgements

We thank David Young for his help in the preparation of this manuscript.

References (22)

  • E Missov et al.

    Circulating cardiac troponin I in severe congestive heart failure

    Circulation

    (1997)
  • Cited by (130)

    • Cardiac troponins and adverse outcomes in European patients with atrial fibrillation: A report from the ESC-EHRA EORP atrial fibrillation general long-term registry

      2022, European Journal of Internal Medicine
      Citation Excerpt :

      In support of these results, the Rate Control in Atrial Fibrillation (RATAF) trial found that cTn was detectable even in stable patients with permanent AF, preserved left ventricular ejection fraction and without ischemic heart disease or HF and a moderate reduction of heart rate by beta-blockers and calcium channel blockers, was significantly associated with lower cTn levels [45]. Other known mechanisms of cTn release in AF patients, include high atrial rates, reduced ventricular perfusion during AF, cell injury, apoptosis, myocardial strain, inflammation, and acute or chronic renal impairment [4,46–49]. In our cohort, AF patients with elevated cTn levels had a significant independent higher risk of all cause-death and MACE.

    • Physiology and pathophysiology of cardiovascular senescence in elderly

      2018, Archives des Maladies du Coeur et des Vaisseaux - Pratique
    View all citing articles on Scopus
    *

    Supported by a grant from the French Federation of Cardiology. Cardiac Tnlus and BNP assays were gifts from Sanofi-Diagnostics-Pasteur, Marne-la-Coquette, France, and Cisbio International, Gif-Sur-Yvette, France.

    **

    Reprint requests: Damien Logeart, MD, Service de Cardiologie, Hôpital Beaujon, 100 Bd Gal Leclerc, 92110 Clichy, France. E-mail: [email protected]

    View full text