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Ann Thorac Surg 2007;84:2010. doi:10.1016/j.athoracsur.2007.07.097
© 2007 The Society of Thoracic Surgeons
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Original Articles: Cardiovascular

Invited commentary

John V. Conte, MD

Division of Cardiac Surgery, Johns Hopkins Medical Institutions, Blalock 618, 600 N Wolfe St, Baltimore, MD 21287

(Email: jconte{at}csurg.jhmi.jhu.edu).

Myocardial infarction leads to both immediate and delayed morbidity and mortality. The process of infarct expansion, progressive border zone dysfunction, and ventricular enlargement in a process known as postinfarction remodeling is a key component of late morbidity and mortality.

In this issue of The Annals of Thoracic Surgery, Blom and colleagues [1] demonstrate in an ovine model of myocardial infarction that early ventricular restraint limits ventricular remodeling. They used a well-described infarct model, elegant magnetic resonance imaging technology, and sophisticated analytic methods to measure infarct expansion and border zone radial strain as a measure of systolic function. They demonstrated that the application of a ventricular restraint device on postinfarct day 3 resulted in significantly less infarct expansion and improved radial strain when studied at 12 weeks compared with controls without the restraint device.

Ischemic cardiomyopathy is the leading cause of congestive heart failure in the United States, and any intervention to limit its impact by curtailing the development of postinfarction remodeling will gain an eager audience. Although these investigators and others [2, 3] have demonstrated the effectiveness of passive restraint in animal models, how applicable will passive restraint be in the real world remains to be seen.

The questions are limitless: What device? When should restraint be applied? These authors used 3 days, but why not 2 days or even a golden window of several hours like that applied for catheterization lab interventions? Will the use of any device preclude later surgical revascularization because of pericardial adhesions? Is there a critical time period that the restraint is required, after which it can be removed? Could cellular or pharmacologic therapy provide additional benefits? The list goes on and on.

This treatment is clearly in its infancy. Time will tell, but if the technology develops so that ventricular restraint is easy to use and widely applicable, there could be a public health impact not seen since the development of the polio vaccine.


   References
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 References
 

  1. Blom AS, Pilla JJ, Arkles J, et al. Ventricular restraint prevents infarct expansion and improves borderzone function after myocardial infarction: a study using magnetic resonance imaging, three-dimensional surface modeling, and myocardial tagging Ann Thorac Surg 2007;84:2004-2010.[Abstract/Free Full Text]
  2. Ghanta RK, Rangaraj A, Umakanthan R, et al. Adjustable, physiological ventricular restraint improves left ventricular mechanics and reduces dilatation in an ovine model of chronic heart failure Circulation 2007;115:1201-1210.[Abstract/Free Full Text]
  3. Magovern JA, Teekell-Taylor L, Mankad S, et al. Effect of a flexible ventricular restraint device on cardiac remodeling after acute myocardial infarction ASAIO J 2006;52:196-200.[Medline]

Related Article

Ventricular Restraint Prevents Infarct Expansion and Improves Borderzone Function After Myocardial Infarction: A Study Using Magnetic Resonance Imaging, Three-Dimensional Surface Modeling, and Myocardial Tagging
Aaron S. Blom, James J. Pilla, Jeffrey Arkles, Larry Dougherty, Liam P. Ryan, Joseph H. Gorman, III, Michael A. Acker, and Robert C. Gorman
Ann. Thorac. Surg. 2007 84: 2004-2010. [Abstract] [Full Text] [PDF]




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