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Ann Thorac Surg 2003;75:S678-S684
© 2003 The Society of Thoracic Surgeons

I: Pathophysiology of ischemic-reperfusion injury

Increased susceptibility of hypertrophied hearts to ischemic injury

Ingeborg Friehs, MDa, Pedro J. del Nido, MDa*

a Department of Cardiac Surgery, Children‘s Hospital and Harvard Medical School, Boston, Massachusetts, USA

* Address reprint requests to Dr del Nido, Department of Cardiac Surgery, Children’s Hospital, Harvard Medical School, 300 Longwood Ave, Boston, MA 02115, USA
e-mail: pedro.delnido{at}tch.harvard.edu

Presented at the 3rd International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, June 2–6, 2002.

Abstract

Cardiac hypertrophy is an adaptive response that compensates for increased workload by normalizing wall stress and preserving cardiac contractile function. In advanced stages, however, clinical and experimental studies have shown that when the high workload is maintained, hypertrophy progresses to ventricular dilatation, contractile dysfunction, and decreased tolerance to ischemia/reperfusion. Development of hypertrophy is accompanied by distinct qualitative and quantitative changes in contractile protein expression and isoform switching, cytosolic calcium regulation, and substrate delivery and use. We have focused our investigations on changes in substrate delivery and capillary density in pressure overload hypertrophy and on the effects that these changes have on tolerance to ischemia/reperfusion. This report summarizes our work in this area using a model of aortic banding in 10-day-old rabbits, which exhibits the same pattern of concentric hypertrophy early, followed by ventricular dilatation and contractile dysfunction that is clinically apparent.




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