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Ann Thorac Surg 1998;66:697-698
© 1998 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts, USA
Address reprint requests to Dr Aldea, Department of Cardiothoracic Surgery, Boston University School of Medicine, Boston Medical Center, 88 E Newton St, Boston, MA 02167
In this issue of The Annals, Dr Kaukoranta and colleagues [1] compare myocardial protection during antegrade cardioplegia (AC) and retrograde cardioplegia (RC). Clinical studies attempting to evaluate the relative merit of individual modifications in cardioplegia delivery with regard to specific clinical outcomes should be interpreted with caution. Clinical studies are often limited by inadequate sample size and therefore lack the resolution to demonstrate a statistically significant impact on mortality, incidence of perioperative myocardial infarction, or inotropic requirements, which occur infrequently. These studies assess different patient populations with varied coronary arterial and venous anatomy (and pathology), different degrees of regional and global ischemia (and dysfunction), and different associated comorbid conditions. Extent and method of coronary grafting (number of arterial grafts, need for endarterectomy) differ, leading to variation in completeness of revascularization, cross-clamp times, and pump times. Myocardial protection protocols vary from patient to patient and among surgeons (frequency of administration, total cardioplegia dose per gram of myocardium per duration of cross-clamp). Finally, measurements of regional myocardial function, metabolism, and flow delivery are difficult (and expensive) to perform and interpret. Because of the limitations, cardioplegia administration practices rely on principles defined by well-executed experimental studies. The wide acceptance of such experimental results led to the development and implementation of practical administration strategies and equipment, which are largely responsible for consistently outstanding clinical outcomes in patients undergoing coronary artery bypass grafting despite the documented relentless increase in perioperative comorbid conditions.
Myocardial protection ultimately depends on an adequate distribution of cardioplegia solution to all regions of the heart distal to coronary artery occlusions [2, 3]. The ideal dose, temperature, composition, and the interval of cardioplegia delivery necessary to adequately protect the heart are still debated. Retrograde cardioplegia administration enhances delivery of cardioplegia to jeopardized myocardium beyond coronary artery obstructions. More than 60% of practicing surgeons routinely use RC as an adjunct to AC, confirming its widespread acceptance [4]. However, despite these advances, myocardial protection remains imperfect. Postoperatively, there is evidence of cellular and subcellular alterations even in apparently normal hearts with preserved function [5]. Clinicians are aware of inhomogeneous delivery of cardioplegia in the presence of coronary artery obstruction, and of physiologic differences in myocardial flow (cardioplegia delivery) between myocardial layers, leading to potential subendocardial ischemia and damage. It is generally assumed, however, that in the absence of coronary artery obstruction, flow within a myocardial layer is uniform. Patterns of myocardial flow delivery to small myocardial regions are less well recognized. An emphasis on the inherent inhomogeneous nature of regional myocardial flow both in the beating heart and during cardioplegia delivery is necessary to underscore the need for a routine use of a broad, comprehensive approach to cardioplegia delivery in all patients.
Myocardial perfusion in the normal myocardium is both temporally and spatially heterogeneous, both at rest and during pharmacologic vasodilatation. These patterns are not related to epicardial gross coronary vascular anatomy (proximity to epicardial vessels). With progressive decrease in coronary perfusion pressure, absolute flow as well as the number of regions with flow reserve diminishes most dramatically in the subendocardium [6]. Normal hearts, therefore, even in the absence of coronary artery disease, under physiologic conditions, contain small regions that are more vulnerable to ischemia.
Patterns of regional crystalloid and blood cardioplegia delivery to small myocardial segments (less than 0.5 g) were demonstrated to be equally inhomogeneous. As with the beating heart model, as coronary perfusion pressure decreases, cardioplegia delivery to the subendocardium falls disproportionally [7, 8]. Patterns and characteristics of regional cardioplegia flow delivery vary not only with coronary perfusion pressure but with the route of cardioplegia delivery as well. Although RC is able to deliver regional cardioplegia to areas beyond coronary artery obstruction not properly protected by AC alone, results in better cooling, and is more effective at evacuating air trapped in the coronary arteries, it provides significantly less "nutritive" cardioplegic flow as compared with AC (more shunting) [2, 3, 8]. At standard clinical cardioplegia perfusion pressures, nutritive flow was more than three times greater with AC than with RC (1.37 ± 0.31 versus 0.39 ± 0.09 mL/g-min; p < 0.001) [8]. Cardioplegia flow for both routes of delivery was uneven (inhomogeneous), with some regions receiving sixfold to tenfold higher flows than others. Retrograde cardioplegia regional flow delivery was more than twice as heterogeneous as AC [8]. Inhomogeneous delivery of cardioplegia is further accentuated by the presence of coronary artery obstruction (drop in perfusion pressure), left ventricular distention, or hypertrophy. This inhomogeneity may explain the patchy nature of subendocardial infarction noted with hypoxia or with reduced perfusion pressures.
The specific patterns of regional cardioplegia flow delivery differ with the route of administration and are complementary [8]. Other studies using microspheres confirmed the inhomogeneity of cardioplegia delivery even in the absence of coronary artery obstruction. Gates and colleagues [9] have demonstrated that in both explanted human and animal hearts as many as 12.5% to 32% of all capillary beds perfused by RC are not perfused by AC, suggesting that combined AC and RC use enhances regional myocardial cardioplegia distribution. Isolated RC may result not only in a focal uneven distribution to left ventricle but an even greater maldistribution to the right ventricular septum and free wall. This uneven distribution is not affected by temperature, coronary sinus perfusion pressure, or aortic root venting and can be further accentuated by variation in coronary venous anatomy and coronary sinus catheter malposition beyond the posterior interventricular vein.
Variation in myocardial flow is an inherent elemental property of the heart. This uneven distribution of cardioplegia highlights the limitations of using global measurements to infer regional "well being" or adequate protection. Inhomogeneous delivery of cardioplegia may be sufficient to result in asynchronous electrical activity and a "flat" electrocardiogram, while individual small regions may have ongoing metabolic activity that may result in postischemic injury. Furthermore, the patchy nature of such damage may go undetected by global measurements of ventricular function, because hypercontractile areas can compensate for small areas of regional dysfunction. Thus, preserved ventricular function, a normal electrocardiogram, or even focal metabolic measurements (such as pH, lactate, or adenosine triphosphate) do not exclude the presence of other small undetected regions of myocardial damage. The clinical significance of such incomplete or inadequate protection will only be apparent in patients with limited cardiac reserve such as those with acute ischemia or depressed ventricular function.
The importance of adjunctive use of AC and RC is further reinforced by studies of cardiac energetics. In studies using phosphorus-31 magnetic resonance spectroscopy, the efficacy of the RC route alone with respect to both distribution and rate of energy recovery was lower than AC and RC. When RC was administered under normothermic conditions, even in the absence of interrupted flow, ischemic metabolism ensued [10]. The clinical significance of adequate regional cardioplegic flow delivery and preservation of cardiac energetics is demonstrated by the ability to attenuate the extent of damage after an acute ischemic injury (long term) as well as to preserve regional and global myocardial function (short term). Again, RC has been demonstrated to decrease edema, myocardial water content, and diastolic dysfunction in isolated hearts, but the best preservation of left and right ventricular function is noted when AC and RC are used in a complementary fashion [2, 3, 8].
The continued debate over the superiority of one element of cardioplegia delivery over another (intermittent versus continuous, antegrade versus retrograde, warm versus tepid or cold, substrate-enhanced versus plain) is misplaced. It ignores a large body of experimental studies documenting the need for a flexible, but broad approach to myocardial protection to overcome the limitations of each individual element, focusing on their complementary or adjunctive use and, most importantly, on addressing the individual needs of the patient. The complexity, cost, and clinical benefits of such broader approaches are often misrepresented by alternative overly simplistic challenges. Such utilitarian, cost-minded alternatives ignore limitations of individual approaches and are not only short-sighted but potentially dangerous. Because our clinical abilities to reliably identify patients at high risk for postbypass dysfunction and accurately measure adequacy of regional cardioplegia delivery and myocardial protection are, at best, limited, I believe that we should try err to on the side of more complete and comprehensive myocardial protection.
References
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