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Ann Thorac Surg 1999;68:130
© 1999 The Society of Thoracic Surgeons
a Cullen Cardiovascular Research Laboratories, Department of Cardiovascular Surgery, Texas Heart Institute, MC1-268, Box 20345, Houston, TX 77225-0345, USA
e-mail: kkadison{at}biost.1.thi.tmc.edu.
Invited commentary
Mueller and colleagues propose that angiogenesis is the sole mechanism responsible for the success of transmyocardial laser revascularization (TMLR). They believe that the channels created by the laser are replaced by scar tissue that acts as a substrate for angiogenesis. The authors suggest that this substrate is more efficient than that produced by infarcted myocardium. In principle, their hypothesis leaves two important questions unanswered. First, if additional blood is indeed reaching the myocardium, as nuclear scans of randomized clinical trials in the United States have indicated, what is the source of that blood if not patent endocardial connections? And second, if angiogenesis (which needs at least 6 weeks to reach its full potential) is the sole mechanism of action, how can one explain the immediate benefits of TMLR?
Joseph T. Wearn [1], who was the first to coin the terms "myocardial sinusoids" and "endosinusoidal connections," was inspired by the earlier work of Thebesius and also by his own observation of long-term survival in patients with chronic occlusions of the coronary ostia secondary to syphilitic aortitis. He argued that for these patients to lead relatively active lives despite complete obliteration of the coronary blood supply, an endocardial source of blood, such as the Thebesian system, had to be necessary. The same principle applies to patients who undergo TMLR as sole therapy, in whom epicardial arteries continue to be affected by progressive occlusive disease and cannot account for the increase in myocardial perfusion detected in nuclear scans. To support this point, Berwing and colleagues [2] have presented real-time contrast echocardiographic evidence that, in humans, left ventricular blood perfuses approximately 1.5 cm3 of the myocardium around laser channels during each systole. Transmyocardial laser revascularization is also known to produce impressive subacute effects, especially when used as an adjunct to coronary artery bypass grafting (CABG) in technically difficult cases involving compromised systolic function and complex, diffuse, distal occlusive disease. At our institution, we prospectively randomized 21 high-risk patients (mean left ventricular ejection fraction <45%), half of whom had undergone previous CABG, for CABG alone (n = 10) or CABG + TMLR with a CO2 laser (n = 11). When adjunctive TMLR was used, the perioperative morbidity and mortality were significantly reduced. The need for a postoperative intraaortic balloon pump or left ventricular assist device decreased from 70% and 30%, respectively, in the CABG group to 20% and 0%, respectively, in the CABG + TMLR group (p < 0.01). The perioperative mortality was 40% in the CABG group versus 0% in the CABG + TMLR group (p < 0.001). A randomized, multicenter series of 221 patients conducted by Allen and other Ho:YAG users [3] also showed statistically significant improvement in CABG mortality from 7% to 0.9% with the use of adjunctive TMLR. Clearly, a mechanism other than angiogenesis alone was responsible for this dramatic improvement during weaning from cardiopulmonary bypass in these series of patients, each treated with different laser modalities.
The choice of the acutely ischemic pig model also raises concerns regarding the clinical relevance of the present study. It can only be speculated how the response in this model can be applied to chronically ischemic but viable myocardium in humans. We applaud the authors for their meticulous histologic work; however, drawing any clinical conclusions from an experimental pig study is hazardous at best.
References
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