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Ann Thorac Surg 1999;68:1498-1501
© 1999 The Society of Thoracic Surgeons

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Supplement: Minimally Invasive Cardiac Surgery

Beating heart surgery: why expect less central nervous system morbidity?

^a Department of Anaesthesia, University Campus, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada
^b Department of Surgery, University Campus, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada

Address reprint requests to Dr Murkin, Department of Anaesthesia, London Health Sciences Centre, University Campus, 339 Windermere Rd, London, ON, Canada N6A 5A5
e-mail: jmurkin{at}julian.uwo.ca

Presented at Evolving Techniques and Technologies in Minimally Invasive Cardiac Surgery, San Antonio, TX, Jan 22–23, 1999.

Abstract

Background. The incidence and etiology of brain dysfunction after conventional coronary artery bypass surgery using cardiopulmonary bypass (CPB) are reviewed.

Methods. Stroke rates and incidences of cognitive dysfunction from various studies are considered. Mechanisms of injury including cerebral embolization as detected by transcranial Doppler and retinal angiography, and imaging-based evidence for postoperative cerebral edema, are discussed. Preliminary results from a prospective clinical trial assessing cognitive dysfunction after beating heart versus conventional coronary artery bypass with CPB are discussed.

Results. Initial evidence for lower overall postoperative morbidity, and for a lower incidence of cognitive dysfunction specifically, after nonpump coronary revascularization is presented.

Conclusions. Beating heart surgery results in less potential for generation of cerebral emboli and appears to produce a lower incidence of cognitive dysfunction in both short- and intermediate-term postoperative follow-up periods as compared with conventional coronary artery bypass surgery using CPB.

Since its successful clinical introduction by Gibbon in 1953, use of cardiopulmonary bypass (CPB) has become the mainstay of cardiac surgery, facilitating a variety of complex procedures. Until recently, use of CPB was synonymous with coronary artery bypass (CAB) surgery, a procedure of which it has been estimated over 800,000 are performed annually worldwide [1]. Independent of the cost, the complexity, and the high degree of technical support associated with CPB, there has been steadily mounting evidence of some degree of end-organ dysfunction associated with its usage. For a majority of patients, this results in clinically undetectable sequelae; for a significant minority, the results can be devastating.

In one of the most recent large-scale multiinstitutional studies, Roach and colleagues documented a 6.1% incidence of serious adverse neurological events in a survey of 2,108 patients undergoing CAB surgery at 24 US institutions [1]. Three percent of these patients suffered perioperative stroke (cerebrovascular accident [CVA]), while a further 3.1% experienced prolonged unconsciousness, seizures, or encephalopathy. Patients suffering adverse neurological sequelae underwent significantly prolonged hospitalization, and 47% were transferred to some form of chronic care facility versus 8% of those without such complications. The mortality rate of those patients with strokes, stupor, or coma was 21% versus 2% for those without. Of those factors identified as most significantly correlating with adverse neurological outcomes, advanced age and duration of CPB were among the strongest.

In a prospective study of 2,000 patients undergoing CAB surgery, Tuman and associates demonstrated an exponential increase in risk of stroke associated with advancing age [2]. While the overall rate of stroke was 2.8%, for those patients aged less than 65 years, the incidence of stroke was 0.9%, whereas 9% of those over 75 years suffered stroke. As well as age, duration of CPB and prior CVA were also significant risk factors. Interestingly, yet not necessarily surprisingly, unlike neurological complications, the risk of adverse cardiovascular events was not significantly correlated with patient’s ages (Fig 1). This implies coronary revascularization can be carried out technically successfully in older patients, but risk of collateral damage, eg, stroke, is significant. Overall, these data are not dissimilar to those reported by Gardiner and colleagues in a retrospective review of 3,279 CAB patients, of whom 14.5% were aged 70 years or older, and who were operated on between 1974 and 1983 [3]. Based on 1983 data, they reported an overall stroke rate of 2.4%, of which, the stroke rate was 6.2% for those patients older than 70 years, and 7.1% for those 76 years or older.

View larger version (25K): [in this window] [in a new window]   Fig 1. For both myocardial infarction and low cardiac output state, there is no appreciable effect of age on probability of an adverse event. For neurologic deficit, however, there is an exponential increase in risk of morbidity associated with increasing age. (Reproduced with permission from Tuman KJ, McCarthy RJ, Najafi H, Ivankovich AD. Differential effects of advanced age on neurologic and cardiac risks of coronary artery operations. J Thorac Cardiovasc Surg 1992;104:1510–7.)

Very similar results were reported by Murkin and associates [5]. In a prospective study of 316 CAB patients, while the overall stroke rate was 2.5%, 85% of patients demonstrated either new neurological signs or cognitive dysfunction at 7 days postoperatively. At 2 months postoperatively, 45% manifested signs of neurobehavioral dysfunction. Also of concern are the results from late postoperative follow-up from this same group, in which 97 patients were reassessed an average of 3 years postoperatively and manifested a 35% incidence of neurobehavioral dysfunction [6].

These results are not dissimilar to those of Sotaniemi and associates [7]. They reported that patients experiencing intellectual decline 1 month after aortic valve surgery, while cognitively indistinguishable at 1 year from those not experiencing such early postoperative dysfunction, had a much higher rate of cognitive decline 5 years postoperatively when compared with those patients not experiencing early postoperative sequelae. In sum, these studies imply that for those patients in whom cognitive decline is apparent in the month or so after CAB surgery (with CPB), this is likely a permanent injury.

Mechanisms of CNS injury

In the context of cardiac surgery, it is apparent that cerebral embolization and/or ischemic hypoperfusion are the mechanisms most likely etiologic in the genesis of neurocognitive injury. Gold and associates have reported on the lower incidence of morbidity including CVA in CAB patients in whom mean arterial pressure (MAP) was maintained at greater than 80 mm Hg. While this may imply a requirement for higher MAP to better optimize cerebral well-being during CPB, it is also apparent that during CPB, cerebral venous hypertension may be another unrecognized, yet equally significant contributor by decreasing cerebral perfusion pressure through restriction of cerebral venous outflow.

It has been observed that extradural pressure, measured via an intracranial catheter, is independent of central venous pressure, and frequently exceeds it. This has also been observed by recording proximal superior vena cava (SVC) pressure as measured using the introducer port of a pulmonary artery access cannula. As described, it is apparent that dislocation of the heart in the presence of a single, two-stage venous return cannula during CPB may occlude the SVC, giving rise to inadequate cerebral perfusion pressure (CPP) despite apparently adequate MAP, due to jugular venous hypertension. This results in both cerebral venous hypertension, and a decrease in cerebral blood flow as measured using transcranial Doppler (TCD) [8]. Repositioning the heart, or resiting the venous cannula, readily rectifies the problem, once it has been recognized.

That this type of injury may give rise to cerebral dysfunction can be inferred from the small series of Harris and associates [9]. They described cerebral edema in the immediate postoperative period in 6 of 6 adult patients undergoing uncomplicated CAB surgery using CPB. How much this can be ascribed to cerebral venous hypertension, how much to what has been described as the ‘whole-body inflammatory response’ associated with CPB, and how much to other as yet unknown mechanisms is still not clear. It is apparent, however, that CPB induces myriad changes that are to the detriment of the systemic as well as the cerebral milieu.

Cerebral embolization

The evidence for cerebral embolization as a mechanism of injury during CPB is even more compelling. Using TCD, emboli have been detected during instrumentation of the aorta and heart as has been described by Stump and Newman [16]. (Fig 2). Stump, Hammond and associates have reported lower mean numbers of cerebral emboli and a decreased rate of postoperative cognitive dysfunction since instituting modifications of surgical technique geared towards reducing the amount of extraneous handling and instrumentation of the aorta, as a consequence of the causality between aortic instrumentation and cerebral emboli demonstrated by TCD [10]. The use of membrane oxygenators and employment of arterial line microfiltration has also been demonstrated to decrease cerebral embolic load, but it was only with the clinical outcome study by Pugsley and associates that this technical intervention has been definitively associated with a lower incidence of postoperative cognitive dysfunction [11].

View larger version (17K): [in this window] [in a new window]   Fig 2. Fifty-eight percent of the embolic signals detected during cardiopulmonary bypass were associated with specific surgical manipulations or time intervals. Forty-two percent of the embolic signals were not associated with one of the 13 categories listed in the figure. The miscellaneous events were often spontaneous and few in number. Embolic signals associated with surgical maneuvers were often detected in greater numbers (n = 196). (Reproduced with permission (for print media only) from Stump DA, Newman SP. Emboli detection during cardiopulmonary bypass. In: Tegler CH, Babikian VL, Gomez CR, eds. Neurosonology. St. Louis: Mosby, 1996;252–5.)

Some of the most important work in the area of intraoperative assessment of ascending aortic atherosclerotic load has been done by the group from St. Louis, including Kouchoukis, Davila-Roman, Barzilai, and colleagues. They have used epiaortic scanning in several thousand CAB patients to identify atherosclerotic plaque in the ascending aorta in order to optimize aortic cannulation and clamp sites. In their studies, an exponential increase in the prevalence of ascending aortic atherosclerosis with increasing age was clearly shown [12], virtually mirroring the exponential increase in stroke risk with age shown by Tuman and associates [2]. This correlation, along with the results of a 200-plus patient postmortem study by Blauth and colleagues, in which an association between increasing age, diabetes mellitus, aortic atherosclerosis, and cerebral atheroemboli was clearly established, has underscored the relationship between aortic atherosclerotic load and risk of perioperative stroke. It can thus be estimated that if used as the standard of care, the relatively simple expedient of epiaortic scanning could potentially decrease the perioperative stroke rate by up to 50%.

Beating heart surgery

With the introduction of techniques facilitating coronary artery bypass without use of CPB, beating heart surgery, there exists the potential to reduce the incidence of neurocognitive changes, and to decrease the perioperative stroke rate after coronary artery bypass grafting.

With beating heart surgery, avoidance of the embolic potential associated with aortic cannulation and decannulation, and of the generation of microgaseous and microparticulate emboli from the pump circuitry, would be expected to significantly decrease cerebral embolic load and improve outcomes. Further, because it has been shown that there is also a significant correlation between aortic atherosclerotic load and amount of cerebral embolization (Fig 3) [13], likely as a result of the ‘jet’ of perfusate through the aortic cannula scouring the atherosclerotic aortic lumen, maintenance of more normal aortic flow patterns during beating heart surgery would be expected to further decrease the incidence of cerebral and systemic atheroemboli. Avoidance of proximal aortic anastamoses and consequent elimination of use of an aortic side clamp, whether through use of all arterial grafts, or use of sequential distal (‘skip grafts’) anastamoses, will also decrease the potential for aortic atheroembolization.

View larger version (15K): [in this window] [in a new window]   Fig 3. Mean emboli counts in patients randomized to aortic palpation (Palpation Only Group) or epiaortic scanning (Scanning Group) without evidence of atherosclerotic change (Normal Aorta), contrasted with emboli counts in those evidencing atherosclerotic changes (Abnormal Aorta). In both groups, significantly more cerebral emboli were detected in patients with atherosclerotic aorta, implying shearing of atherosclerotic plaque by ‘jet’ perfusion from the aortic cannula. (Data redrawn with permission from St Amand MA, Murkin JM, Menkis AH, Downey DB. Aortic atherosclerotic plaque identified by epiaortic scanning predicts cerebral embolic load in cardiac surgery. Can J Anaesth 1997;44(Suppl):A7.)

As part of an ongoing study, we have employed a standardized battery of nine neuropsychological tests preoperatively and 5 days and 3 months postoperatively, in a series of 35 patients undergoing off-pump coronary artery bypass surgery, and a demographically similar group of 33 patients undergoing conventional CABG. Cognitive tests included measures of verbal learning and memory, Rey Auditory Verbal Learning Test; visual memory, Benton Visual Retention Test; psychomotor speed and visual concept tracking, Trail Making Tests A and B; manual motor dexterity, Grooved Pegboard; executive functioning, Cowat Word Generation Test; as well as two measures of emotional functioning, State Trait Anxiety Inventory and Geriatric Depression Scale. A 20% decrease in change score, defined as the difference between preoperative and postoperative test scores, on 20% or more of tests was defined as ‘cognitive dysfunction,’ and group results were compared using Fischer’s exact test.

While there were significant differences in number of coronary anastamoses, (3.2 vs 1.1), total operating room time (3.98 vs 4.4 h), extubation times (20 vs 5.9 h), and numbers of patients in whom sternotomy as opposed to thoracotomy incision were used (33 vs 7), between CABG and beating heart surgery patients, respectively, there were no significant differences in age (61.8 vs 57.7 years), weight (84 vs 82 kg), or male/female ratios (25/8 vs 30/5) between the two groups. There were no clinically apparent strokes in either group. Beating heart surgery patients demonstrated a significantly lower incidence of cognitive dysfunction at 5 days (66% vs 90% respectively, p = 0.025) and 3 months postoperatively (5% vs 50% respectively, p = 0.0011) compared with conventional CAB surgery patients [14].

This finding is entirely consistent with the shorter duration of stay in the intensive care unit, and shorter length of overall hospitalization, despite higher preoperative risk acuity, seen in beating heart versus conventional CAB patients, as previously reported by our group [15]. We conclude that for those patients in whom beating heart surgery is an appropriate approach to myocardial revascularization, the expectation of improved outcomes, including a lower incidence of postoperative neurocognitive dysfunction as compared with conventional CAB surgery, may be realized. Further studies are required to confirm these initial findings.

References

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8. Aavramides E.J., Murkin J.M. The effect of surgical dislocation of the heart on cerebral blood flow in the presence of a single, two-stage venous cannula during cardiopulmonary bypass. Can J Anaesth 1996;43(Suppl):A36.
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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): John M. Murkin Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Murkin, J. M. Articles by Peterson, R. C. Search for Related Content PubMed PubMed Citation Articles by Murkin, J. M. Articles by Peterson, R. C.