Heart Failure PDF Print E-mail

Heart disease and heart failure (congestive heart failure- CHF) is the leading cause of death in the western world.

A myocardial infarction (heart attack) causes a portion of the heart muscle to die. Due to improved treatment of patients in the early period after a heart attack, over 90 % of these patients will now survive. Over time however, about 50% of these survivors develop CHF-congestive heart failure even though they rarely suffer another heart attack.

Unfortunately over half of all these patients with CHF will die within five years. These CHF patients’ hearts become progressively dilated (enlarged) as a result of a pathological process called ventricular remodeling. We have previously shown that regional wall stress and three-dimensional geographic strain occurs in the healthy tissue surrounding an infarction.

We believe this ongoing stress and strain results in ventricular dilatation (remodeling) with resultant congestive heart failure. (Akinetic Myocardial Infarcts Contains Contracting Myocytes – A Finite Element Model Study.) Using several large animal models of ischemica cardiomyopathy, we are investigating the pathogenesis of this important disease on a mechanical, cellular, biochemical and molecular/genetic level.

A: model configuration obtained for an end-diastolic LV chamber pressure of 2.67 kPa (20 mmHg) and diastolic stiffness of 0.876 kPa. Normal endocardium is shaded in red; akinetic endocardium is shaded in blue. B: model configuration obtained for an end-systolic LV chamber pressure of 13.33 kPa (100 mmHg), diastolic stiffness of 0.876 kPa, and akinetic segments. Normal endocardium is shaded in red; akinetic endocardium is shaded in blue. C: comparison on endocardial surface between end diastole (red) and end systole (blue) when viewed from the anterior direction.

Dang, et al. Am J Phys (2003)

finite element 

Using this new understanding, our goal is to develop novel surgical and medical strategies to prevent (not reverse) the development of heart failure, regardless of its etiology (ischemic or non-ischemic).

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Perelman School of Medicine at the University of Pennsylvania.