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Ann Thorac Surg 1998;66:1093-1096
© 1998 The Society of Thoracic Surgeons
a Division of Cardiac Surgery, University of Innsbruck, Innsbruck, Austria
b Department of Anesthesiology and General Intensive Care, University of Innsbruck, Innsbruck, Austria
Address reprint requests to Dr Bonatti, Division of Cardiac Surgery, Innsbruck University Hospital, Anichstr 35, A-6020 Innsbruck, Austria
e-mail: (johannes.o.bonatti{at}uibk.ac.at)
Presented at "Facts and Myths of Minimally Invasive Cardiac Surgery: Current Trends in Thoracic Surgery IV," New Orleans, LA, Jan 24, 1998.
Abstract
Background. In conventional coronary artery bypass grafting, the rate of perioperative myocardial infarction is reported in the 2% to 6% range; however, significantly higher rates are observed if sensitive myocardial marker proteins are used to detect perioperative myocardial damage. For minimally invasive direct coronary artery bypass grafting, few data are available concerning myocardial marker protein release.
Methods. Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 ± 8.5 years) received minimally invasive direct coronary artery bypass grafting procedures via minithoracotomy on the beating heart. Electrocardiography and transesophageal and transthoracic echocardiography as well as determination of creatine kinase-MB mass concentration and cardiac troponin I level were used for ischemic monitoring.
Results. One patient had a perioperative myocardial infarction according to standard criteria and died despite mechanical circulatory support. Determination of cardiac troponin I level showed small but definitive ischemic damage in 4 of 9 patients (44%) who presented transient ischemic signs intraoperatively or postoperatively. In 2 of these 4 patients pathologic findings could be detected on angiographic restudies.
Conclusions. Subclinical myocardial injury is a common event in minimally invasive coronary artery bypass grafting on the beating heart. Cardiac troponin I could serve as an adequate diagnostic tool for diagnosis of perioperative myocardial infarction in minimally invasive direct coronary artery bypass grafting.
In conventional coronary artery bypass grafting (CABG), the incidence of perioperative myocardial infarction (PMI) is reported to be in the range of 2% to 6% [1, 2] if electrocardiographic changes and creatine kinase-MB (CK-MB) activity elevations are used to diagnose PMI [3]. Significantly higher rates of small PMI are observed, however, if more sensitive marker proteins (eg, troponins) are used to detect myocardial injury [3]. For minimally invasive direct coronary artery bypass grafting (MIDCABG) on the beating heart, limited data concerning PMI rates and myocardial marker protein release are available [4, 5]. Therefore, the aim of this study was to assess the extent of myocardial damage in MIDCABG with the sensitive and specific marker cardiac troponin I.
Patients and methods
Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 ± 8.5 years) undergoing MIDCABG procedures via minithoracotomy on the beating heart were studied. All patients gave informed consent for the additional blood samples to be drawn. Patient characteristics are shown in Table 1.
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Intraoperative and postoperative ischemic monitoring
Intraoperatively continuous ST segment monitoring was applied using leads II and V. All patients had twelve-lead electrocardiographic (ECG) recordings preoperatively, immediately postoperatively, and 20 hours thereafter. Myocardial ischemia was defined as an ST-segment elevation of more than 0.2 mV in two contiguous leads. Myocardial infarction was defined as the appearance of new Q waves of 0.04 seconds or more or a reduction in R waves of more than 25% in at least two leads.
Transesophageal echocardiography using a Hewlett Packard Sonos 1500 was performed intraoperatively with the transgastric short-axis view continuously from skin to skin. Immediately postoperatively and 20 hours thereafter a transthoracic echocardiographic control was performed. Transesophageal and transthoracic echocardiography were assumed to indicate myocardial ischemia if new reversible wall motion abnormalities appeared.
Creatine kinase-MB mass concentration and cardiac troponin I (cTnI; Sanofi Diagnostics, Marnes la Coquet, France) were measured after induction of anesthesia, before target vessel occlusion, 10 minutes after target vessel occlusion, 10 minutes after target vessel reperfusion, at the end of the operation, and 6 hours and 20 hours thereafter. CK-MB mass concentration and cTnI level exceeding 4.0 ng/mL and 0.1 ng/mL, respectively, indicated myocardial injury.
Statistical analysis
Continuous variables are depicted as means ± standard deviation. Patient subgroups were compared using Student’s t test for unrelated samples.
Results
Severe myocardial ischemia and ventricular fibrillation developed in the immediate postoperative period in 1 patient. The patient died despite mechanical cardiocirculatory support, and myocardial infarction was confirmed at autopsy.
Nine of the 14 surviving patients (64%) showed signs of transient myocardial ischemia on ECG, echocardiography, or both (Table 2), which appeared only intraoperatively during target vessel occlusion in 3 patients (21%) and solely postoperatively in another 3 (21%). Three further patients (21%) exhibited reversible signs of myocardial ischemia both intraoperatively and postoperatively. The CTnI level was elevated in 4 of the 9 patients (44%) showing ischemia, and the CK-MB mass concentration was increased in 5 of them (56%). The CK-MB mass concentration was additionally above normal values in 3 further patients without any ECG or echocardiographic signs of ischemia. In 2 of the patients who showed elevated cTnI levels, pathologic findings in the bypass graft or target vessel could be detected on angiographic restudies (Fig 1). Myocardial ischemic time was 25.5 ± 4.9 minutes in patients without cTnI level elevation and 30.2 ± 11.1 minutes in patients with cTnI level elevation (not significant).
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Data on myocardial infarction rates after MIDCABG are sparse in the current literature; according to the reports available, the rates lie in the 0% to 5% range [6–8].
Electrocardiographic and echocardiographic signs of myocardial ischemia are frequently observed during target vessel occlusion. They are usually regarded as reversible and described as well tolerable in several reports concerning minimally invasive CABG on the beating heart [9, 10]. Transient signs of myocardial ischemia during coronary vessel occlusion were detected intraoperatively in 3 of our patients (21%), a rate that is in accordance with data in the literature [6]. Reversible postoperative ischemic signs were noted in 42% of surviving patients and might be explained by internal mammary artery or target coronary artery spasm, a phenomenon that is also frequently encountered after conventional arterial coronary artery bypass procedures.
The results in our present study have shown that intraoperative or postoperative transient signs of myocardial ischemia in ECG or echocardiography in approximately 50% lead to significant elevation of the cTnI level. This can be regarded as a small but irreversible damage to the myocardium. Previous studies have shown that CABG performed under cardioplegic arrest also leads to significantly higher rates of myocardial injury if the markers CK-MB mass, cardiac troponin T level, and cTnI level were used to assess myocardial necrosis [3, 11–13]. Ischemic damage, however, might not be detectable clinically in the majority of these cases.
Concerning release of cTnI in MIDCABG, Birdi and coworkers [4] recently found that release of this marker is significantly higher in CABG performed via sternotomy under cardioplegic arrest than in CABG performed via minithoracotomy on the beating heart. Myocardial ischemic times given by this group were comparable with our results, and the degree of cTnI release was in accordance with our observations. Similar results were obtained by Hadjinikolaou and associates [5], who compared cardiac troponin T levels in patients undergoing CABG performed minimally invasively on the beating heart or conventionally on the arrested heart. They found no rise in cardiac troponin T level in the minimally invasive group, whereas a significant rise was detected in patients having conventional operations. However, the extent of coronary artery disease, the number of bypass grafts, and the myocardial ischemic times were much more pronounced in the latter group and therefore this control group does not seem ideal.
Two patients with elevated cTnI levels and transient ECG or echocardiographic signs of myocardial ischemia in our series showed clinical correlates detected by angiography. Patients with significant cTnI level elevation lacking conventional signs of PMI after MIDCABG, in our opinion, should undergo further diagnostic workup because inadequate surgical results might be the underlying cause. Cardiac troponin I in this way could serve as a guiding tool to indicate angiographic restudy after MIDCABG, which is at present used routinely after these procedures at several centers.
The CK-MB mass concentration was elevated in 56% of our patients with transient ischemic signs. Its lower cardiac specificity compared with cTnI [13] might be underlined by the fact that it also showed abnormal values in 3 of our patients who clinically did not present any myocardial ischemic signs at all.
From our data we conclude that subclinical myocardial injury is a common event in minimally invasive CABG on the beating heart. Myocardial ischemia detected by ECG and echocardiography is commonly regarded as reversible and negligible. Whether myocardial ischemia leads to necrosis can be detected if the sensitive myocardial marker protein cTnI is measured in serial blood samples. This myocardial marker could serve as the gold standard for adequate diagnosis of PMI in clinical studies and quality control of MIDCABG. According to our results, an elevated cTnI level justifies angiographic restudy.
References
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S. Muraki, C. D. Morris, J. M. Budde, D. A. Velez, Z.-Q. Zhao, R. A. Guyton, and J. Vinten-Johansen Experimental off-pump coronary artery revascularization with adenosine-enhanced reperfusion J. Thorac. Cardiovasc. Surg., March 1, 2001; 121(3): 570 - 579. [Abstract] [Full Text] [PDF]
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