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Ann Thorac Surg 2001;71:662
© 2001 The Society of Thoracic Surgeons

Invited commentary

Robert C. Gorman, MDa, Joseph H. Gorman, III, MDa

a Department of Surgery, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104, USA

e-mail: rcgorman{at}mail.med.upenn.edu

Coronary artery disease (CAD) is now the most common cause of heart failure (HF) in the United States. The mechanism of HF due to CAD is complex and multifactorial. In addition to irreversibly damaged (infarcted) myocardium, the ischemic syndromes of myocardial stunning and hibernating myocardium contribute to the manifestations and progression of heart failure in some patients with left ventricular (LV) dysfunction secondary to CAD. However, in other patients myocardial infarction insidiously leads to HF in the absence of ongoing ischemia or recurrent infarction. Loss of contractile function in this later group is attributed to postinfarction LV remodeling. The mechanism of this remodeling process remains poorly understood. What causes progressive ventricular failure in spite of an adequate amount of normally functioning myocardium immediately after infarction? How and where is normal myocardium lost during this apparently self-perpetuating process? The answers to these important questions have profound clinical implications. Our ignorance with regard to the mechanism of this phenomenon is manifest in the inconsistent results of the operations we prescribe to control it (ie, LV aneurysmectomy, LV volume reduction procedures and cardiac myoplasty).

Doctor Guccione and his associates using finite element analysis and an ovine model of left ventricular aneurysm have provided us with new insights into this important clinical problem by focusing our attention on changes that occur in the normally perfused myocardium immediately adjacent to the infarct (the borderzone). The authors’ analysis demonstrates that borderzone contractile function is impaired beyond what would be expected due to changes in LV geometry and stress distribution. Although not explicitly stated by the authors, their results imply that the remodeling process fundamentally alters the borderzone myocardium. The implications of this finding are obvious and important for surgeons. Procedures designed to restore a more normal LV geometry late in the remodeling process may be ineffective because they are applied after the borderzone myocardium has been irreparably damaged. Surgical and medical strategies designed to prevent or control postinfarction LV remodeling could potentially preserve borderzone function and therefore be more effective.

Doctor Guccione’s elegant study suggests a new paradigm for the surgical treatment of HF due to CAD.


Related Article

Mechanism underlying mechanical dysfunction in the border zone of left ventricular aneurysm: a finite element model study
Julius M. Guccione, Scott M. Moonly, Pavlos Moustakidis, Kevin D. Costa, Michael J. Moulton, Mark B. Ratcliffe, and Michael K. Pasque
Ann. Thorac. Surg. 2001 71: 654-662. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:


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M. Morita, C. E. Eckert, K. Matsuzaki, M. Noma, L. P. Ryan, J. A. Burdick, B. M. Jackson, J. H. Gorman III, M. S. Sacks, and R. C. Gorman
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Ann. Thorac. Surg., August 1, 2011; 92(2): 617 - 624.
[Abstract] [Full Text] [PDF]

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