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Department of Anesthesia and Perioperative Care, University of California, San Francisco, leungj{at}anesthesia.ucsf.edu (Leung) Department of Cardiovascular Anesthesiology, Kaiser Permanente Medical Center, San Francisco, CA (Bellows)
In Response:
We thank Bilotta et al. for their interest in our article (1). Classically, contractile reserve is defined as an improvement in regional wall motion abnormalities during infusion of small-dose dobutamine. In contrast, development of new regional wall motion abnormalities or worsening of baseline systolic function with escalating doses of dobutamine is indicative of ischemic myocardium, and myocardial segments that remain akinetic or dyskinetic during dobutamine infusion are considered nonviable (2). Myocardial segments that did not improve with dobutamine infusions were considered nonviable in our study. Because our study goal was to determine if contractile reserve of left ventricular regional function in the reperfusion period after cardiopulmonary bypass predicts subsequent myocardial viability, we employed the standard definitions of normal and positive responses to dobutamine infusion to measure the left ventricular contractile response. We agree that myocardial segments with worsening regional function during large-dose dobutamine infusion should be considered ischemic, but few patients in our study had such a biphasic response. The separation of these into a third category (ischemic, viable, but clearly lacking contractile response) in the analysis did not substantially improve the sensitivity of dobutamine infusion in predicting subsequent viability.
The study cited by Bilotta et al. regarding restoration of coronary blood flow consisted of a different patient population than ours (3). These were patients who had suffered an acute myocardial infarction and were studied within 2 wk of hospital admission before myocardial revascularization using dobutamine stress echocardiography. In this small study of 24 patients, 75% of patients developed worsening or new regional wall motion abnormalities with dobutamine infusion and the remainder developed severe chest pain. The high incidence of ischemic changes is likely attributable to the fact that ß blockade was withdrawn for 48 h in the vulnerable period immediately after acute myocardial infarction (3). In contrast, few myocardial segments had such response in our study, suggesting the adequacy of coronary vascular reserve after revascularization. In fact, after myocardial revascularization, despite restoration of coronary blood flow, persistent mechanical dysfunction may occur; this is classically known as stunned myocardium (4). In our study, strict hemodynamic protocol was in place for stopping dobutamine infusion in addition to monitoring for electrocardiographic and echocardiographic abnormalities. The safety of our protocol is further supported by the fact that the response to dobutamine infusion was not related to the occurrence of postoperative myocardial infarction.
All results in our study relating to the sensitivity and specificity of dobutamine infusions were obtained from the 72 patients who received both the dobutamine infusion and completed the postoperative thallium studies.
References
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