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Original Investigation
February 3, 2021

Association of Global Longitudinal Strain With Clinical Status and Mortality in Patients With Chronic Heart Failure

Author Affiliations
  • 1Department of Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
  • 2German Center for Cardiovascular Research (DZHK), partner site Rhine-Main, Mainz, Germany
  • 3Preventive Cardiology and Preventive Medicine, Department of Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
  • 4Center for Thrombosis and Haemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
  • 5Institute for Clinical Chemistry and Laboratory Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
JAMA Cardiol. 2021;6(4):448-456. doi:10.1001/jamacardio.2020.7184
Key Points

Question  Can global longitudinal strain, an echocardiographic biomarker of cardiac function, be used in evaluation of patients with heart failure?

Findings  In this cohort study of 2186 patients, global longitudinal strain reflected the severity of chronic heart failure. In addition, global longitudinal strain was associated with cardiac and all-cause mortality independent of clinical profile, heart failure symptoms, cardiac structure, and systolic and diastolic function.

Meaning  Global longitudinal strain may be a helpful clinical tool to improve risk stratification in individuals with chronic heart failure.

Abstract

Importance  Global longitudinal strain (GLS) is an emerging echocardiographic biomarker of cardiac function in heart failure (HF). Evidence from large-scale studies comprehensively investigating GLS for its association with clinical phenotypes and mortality in asymptomatic and symptomatic chronic HF is limited.

Objective  To assess the factors associated with GLS and its prognostic value in patients with chronic HF.

Design, Setting, and Participants  The observational, prospective MyoVasc cohort study enrolled 3289 individuals with asymptomatic to symptomatic HF between January 17, 2013, and April 27, 2018. The median follow-up was 3.2 years (interquartile range, 2.0-4.0 years). Participants with stages A to D HF according to American Heart Association (AHA) criteria were examined at a dedicated study center. Echocardiography was performed with GLS measurement by independent reviewers. Data were analyzed from September 2, 2019, to January 15, 2020.

Main Outcomes and Measures  All-cause and cardiac mortality were recorded by structured follow-up and validated via death certificates.

Results  In the study sample, data on GLS were available on 2440 individuals, of whom 2186 (mean [SD] age, 65.0 [10.5] years; 1418 [64.9%] men) were classified as having AHA HF stages A to D. Mean (SD) GLS worsened across AHA stages from stage A (n = 434; −19.44 [3.15%]) to stage B (n = 629; −18.01 [3.46%]) to stages C/D (n = 1123; −15.52 [4.64%]). Age (β = −0.27; 95% CI, −0.47 to −0.067; per decade, P = .009), female sex (β = −1.2; 95% CI, −1.6 to −0.77; per decade, P < .001), obesity (β = 0.64; 95% CI, 0.25-1.0; P = .001), atrial fibrillation (β = 1.2; 95% CI, 0.69-1.6; P < .001), myocardial infarction (β = 1.5; 95% CI, 1.00-2.1; P < .001), and estimated glomerular filtration rate (β = −0.53; 95% CI, −0.73 to −0.32; per SD, P < .001) were independently associated with GLS in multivariable regression analysis. Global longitudinal strain was associated with the severity of HF as reflected by N-terminal prohormone B-type natriuretic protein (NT-proBNP) levels after additionally adjusting for cardiac structure and function (P < .001). During follow-up, GLS was associated with all-cause mortality (hazard ratio [HR] per SD, 1.55; 95% CI, 1.19-2.01; P < .001) and cardiac death (HR per SD, 2.32; 95% CI, 1.57-3.42; P < .001) independent of image quality, observer variability, clinical profile, HF medications, NYHA class, and cardiac structure and function. After further adjustment for the NT-proBNP level, GLS remained associated with cardiac death (HR per SD, 1.60; 95% CI, 1.07-2.41; P = .02) but not all-cause mortality (HR per SD, 1.26; 95% CI, 0.95-1.66; P = .11).

Conclusions and Relevance  In patients with chronic HF, GLS was associated with clinical and cardiac status, reflected neurohormonal activation, and was associated with cardiac mortality independent of clinical and cardiac status. These findings suggest that GLS may serve as a useful tool to improve risk stratification in patients with HF.

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