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Invited Commentary
December 26, 2019

Correlating Cardiac Origin Neurohormonal Stress Levels With Heart Failure Outcomes

Author Affiliations
  • 1Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California
  • 2Now with Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City
JAMA Cardiol. Published online December 26, 2019. doi:10.1001/jamacardio.2019.4766

An irony exists in the clinical assessment of ambulatory patients with advanced heart failure. It is self-evident that the primary cause of advanced heart failure is failing heart muscle. However, common biomarkers used to assess patients with advanced heart failure do not directly quantify either the health of heart muscle or the signaling that causes muscle health to deteriorate. Natriuretic peptide levels permit the assessment of intracardiac volume loading (preload) and are linearly associated with pulmonary capillary wedge pressure.1 The ST2 biomarker and galectin-3 levels quantify myocardial fibrosis rather than cardiomyocyte remodeling.2 Cardiac magnetic resonance imaging techniques detect scar tissue and other types of nonmyocyte infiltration.3 In sum, the common imaging and blood-based biomarkers assess hemodynamics, inflammatory response to stress, and globally damaged myocardium but not actual cellular myocardial health.

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