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Am J Physiol Heart Circ Physiol (January 19, 2007). doi:10.1152/ajpheart.01384.2006
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Submitted on December 20, 2006
Accepted on January 19, 2007

Determinants of Contractile Reserve in Viable, Chronically Dysfunctional Myocardium

Michael D. Banas1, Sunil Baldwa2, Gen Suzuki1, John M. Canty3, and James A Fallavollita4*

1 Center for Research in Cardiovascular Medicine, University at Buffalo, Buffalo, New York, United States
2 the VA Western New York Health Care System, Buffalo, New York, United States; Canandaigua VA Medical Center, Canandaigua, New York, United States; Center for Research in Cardiovascular Medicine, University at Buffalo, Buffalo, New York, United States
3 the VA Western New York Health Care System, Buffalo, New York, United States; Center for Research in Cardiovascular Medicine, University at Buffalo, Buffalo, New York, United States
4 the VA Western New York Health Care System, Buffalo, New York, United States; Center for Research in Cardiovascular Medicine, University at Buffalo, Buffalo, New York, United States; Department of Medicine, University at Buffalo, Buffalo, New York, United States

* To whom correspondence should be addressed. E-mail: jaf7{at}buffalo.edu.

There is considerable variability in the sensitivity of inotropic reserve to identify viability in chronically dysfunctional myocardium. This is partially related to the underlying pathophysiology, with more frequent contractile reserve in chronically stunned (with normal resting perfusion) than hibernating myocardium (with reduced flow). This study was undertaken to determine the physiological responses to transient and graded stimulation in chronically stunned and hibernating myocardium in order to define the relative roles of acute catecholamine desensitization and biphasic responses. Pigs were chronically instrumented with a fixed LAD stenosis that resulted in chronically stunned myocardium after two months. One month later hibernating myocardium was confirmed by regional dysfunction (wall-thickening, 3.2±0.3 vs. 5.5±5 mm in remote, p=0.01) with reduced resting flow (0.70±0.07 vs. 0.92±0.09 ml/min/g in remote, p=0.01) without infarction. Wall-thickening in dysfunctional regions significantly increased during both graded and transient epinephrine stimulation in chronically stunned (from 3.6±0.3 to 5.6±0.5 and 4.9±0.5 mm, respectively) and hibernating myocardium (from 3.3±0.3 to 5.4±0.6 and 5.0±0.7 mm, respectively), and returned to baseline within 15 minutes. Although a biphasic response during graded stimulation was common, the subsequent decrement in function was small and similar in both groups (Stunned 0.7±0.2 mm, Hibernating 1.1±0.3 mm, p=0.25). We conclude that: 1) the extent of contractile reserve during {beta}-adrenergic stimulation is similar in chronically stunned and hibernating myocardium, 2) there are no significant differences between the responses to transient as compared to graded catecholamine stimulation, and 3) submaximal catecholamine stimulation does not induce additional stunning in either chronically stunned or hibernating myocardium.







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