Myocardial preservation

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Objective assessment of preservation of myocardium has been stimulated by interest in myocardial infarction and by the hypothesis that infarct size is an important determinant of prognosis and one potentially amenable to favorable modification during the early evolution of ischemic injury. Recently, the importance of myocardial preservation in the setting of cardiac surgery has received increasing attention. In this discussion, the basis for some clinically applicable noninvasive techniques for objectively assessing the extent of myocardial injury will be presented, followed by some results from experimental studies delineating one approach to preserving ischemic myocardium in the setting of cardiac surgery.

As opposed to other criteria, such as electro-physiologic changes or alterations in left ventricular function which may be reversible manifestations of ischemia as well as infarction, biochemical indices of cell death are theoretically suitable for estimating the extent of infarction (or infarct size) in absolute terms.1

Assessment of myocardial creatine kinase (CK) depletion and subsequently plasma CK time-activity curves has proven particularly useful. After coronary occlusion in rabbits, myocardial CK depletion is proportional to infarct size estimated morphologically and to regionally decreased blood flow assessed with radioactively-labeled microspheres. In dogs S-T segment elevation, ultrastructural and microscopic evidence of necrosis, and impaired myocardial function correlate with myocardial CK depletion as well. After coronary occlusion, plasma CK curves correlate closely with myocardial CK depletion measured directly in conscious experimental animals.1–4

Since marked variation in the CK disappearance rate (kd) within an individual study could distort enzymatic estimates of infarct size, we have recently . . .



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