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J Thorac Cardiovasc Surg 2002;123:617-620
© 2002 The American Association for Thoracic Surgery

Editorials

Mathematic modeling and cardiac surgery

From the Division of Cardiothoracic Surgery, Washington University School of Medicine, St Louis, Mo.

Received for publication Aug 31, 2001. Accepted for publication Sept 13, 2001. Address for reprints: Michael K. Pasque, MD, Division of Cardiothoracic Surgery, Washington University School of Medicine, Suite 3103 Queeny Tower, One Barnes-Jewish Hospital Plaza, St Louis, MO 63110 (E-mail: pasquem@msnotes.wustl.edu).

	Introduction

 
See related article on page 700.

The article by Kramer and colleagues ¹ in this month's issue of the Journal represents yet another effort by an established clinical investigative unit to extend sophisticated mathematic modeling methodology to the clinical setting of cardiac surgery. That these methods can be readily applied in this setting is well demonstrated by this investigation, as well as by others. ^2-7 What may be less apparent is the potential full impact of this technology on the day-to-day clinical practice of cardiac surgery.

By way of illustration, it was not readily accepted, until the application of mathematic modeling theory, that systolic function in patients with dilated left ventricles could be improved by means of surgical or medical interventions to effect isolated left ventricular (LV) volume reduction. The degree to which preload and afterload are inherently, unquestionably, and irrevocably tied together and, indeed, overlap has only been brought to the forefront by the application of these principles that examine ventricular systolic performance at the level of its very basic building blocks: stress and strain. The fact that a markedly dilated end-diastolic ventricular dimension results in elevated end-diastolic, and therefore elevated early systolic, ventricular wall stress was tacitly understood by mechanics investigators. That this increase in early systolic stress, however, was the equivalent of what we clinically refer to as increased afterload was not readily apparent until its clarification by means of mathematic modeling. In other words, the ventricular volume reduction that one might obtain, for instance, by eliminating severe mitral regurgitation has the ability to reduce early systolic wall stress and therefore to reduce afterload during systolic ejection.

Unfortunately, old paradigms fall hard. The appreciation that an improvement in LV ejection fraction can be expected after mitral valve repair for severe mitral regurgitation because of a reduction in . . . [Full Text of this Article]

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