Plasma MicroRNA Clusters in Human Left Ventricular Remodeling

Plasma MicroRNA Clusters in Human Left Ventricular Remodeling EDITORIAL Plasma MicroRNA Clusters in Human Left Ventricular Remodeling A Biomarker and Discovery Platform See Article by Shah et al Arun Padmanabhan, MD, PhD Saptarsi M. Haldar, MD mpaired cardiac function results in increased neurohormonal activity, a stress response initially mounted to augment cardiac output. However, chronic or ex- Icessive activity of the neurohormonal response contributes to progressive myo- cardial damage and the clinical manifestations of the heart failure (HF) syndrome. This myocardial injury leads to a vicious cycle of organ remodeling, wherein the shape, thickness, volume of the ventricular cavity, and the functional state of the cells populating the stressed heart are adversely altered in a manner that further 1,2 compromises cardiac performance. Early work in animal models of myocardial infarction demonstrated the pathophysiologic significance of cardiac remodeling and a role for neurohormonal blockade in its prevention and reversal. These find- ings were subsequently extended to humans with myocardial infarction–associated HF and cardiac dilation in the absence of HF, with the severity of remodeling serv- 3,4 ing as a poor prognostic indicator. Current guideline-directed medical therapy for HF is associated with regression of ventricular dilation and improvement of ejection fraction in a subset of patients, a process called left ventricular http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation: Heart Failure Wolters Kluwer Health

Plasma MicroRNA Clusters in Human Left Ventricular Remodeling

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Publisher
Wolters Kluwer
Copyright
© 2018 American Heart Association, Inc.
ISSN
1941-3289
eISSN
1941-3297
D.O.I.
10.1161/CIRCHEARTFAILURE.117.004793
Publisher site
See Article on Publisher Site

Abstract

EDITORIAL Plasma MicroRNA Clusters in Human Left Ventricular Remodeling A Biomarker and Discovery Platform See Article by Shah et al Arun Padmanabhan, MD, PhD Saptarsi M. Haldar, MD mpaired cardiac function results in increased neurohormonal activity, a stress response initially mounted to augment cardiac output. However, chronic or ex- Icessive activity of the neurohormonal response contributes to progressive myo- cardial damage and the clinical manifestations of the heart failure (HF) syndrome. This myocardial injury leads to a vicious cycle of organ remodeling, wherein the shape, thickness, volume of the ventricular cavity, and the functional state of the cells populating the stressed heart are adversely altered in a manner that further 1,2 compromises cardiac performance. Early work in animal models of myocardial infarction demonstrated the pathophysiologic significance of cardiac remodeling and a role for neurohormonal blockade in its prevention and reversal. These find- ings were subsequently extended to humans with myocardial infarction–associated HF and cardiac dilation in the absence of HF, with the severity of remodeling serv- 3,4 ing as a poor prognostic indicator. Current guideline-directed medical therapy for HF is associated with regression of ventricular dilation and improvement of ejection fraction in a subset of patients, a process called left ventricular

Journal

Circulation: Heart FailureWolters Kluwer Health

Published: Feb 1, 2018

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