The myocardial matrix and the development and progression of ventricular remodeling.
Our conceptual framework of chronic heart failure is based upon the neurohormonal model. In this construct, neurohormonal systems that provide short-term homeostasis remain activated after a myocardial injury, producing progressive ventricular dysfunction and worsening heart failure. However, this model fails to explain several important clinical phenomena, that can be explained by an expanded model of heart failure that focuses on myocardial matrix events as the triggers for disease progression. This model embraces the neurohormonal model and integrates the roles of the immune system and the myocardial fibroblast within the matrix to more fully describe the initiation and progression of the disease.
Sackner-Bernstein
J D
JD
Division of Cardiology, St. Luke's-Roosevelt Hospital Center, 1111 Amsterdam Avenue, New York, NY 10025, USA. JSackner-Bernstein@slrhc. org.
D000818:Animals; D006333:Heart Failure / Q000276:immunology / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008955:Models, Cardiovascular; D009206:Myocardium / Q000166:cytology; D018377:Neurotransmitter Agents / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
D018377:Neurotransmitter Agents