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J Thorac Cardiovasc Surg 1996;112:205-206
© 1996 Mosby, Inc.

LETTERS TO THE EDITOR

Perfusion pressure and coronary bypass

Department of Cardiothoracic Surgery
The New York Hospital Cornell Medical Center
New York, NY 10021

Reply to the Editor:

The members of the Cornell Coronary Artery Bypass Outcomes Trial Group (CCABOT) thank Drs. Keats and Slogoff for their insightful comments and appreciate the opportunity to expand on the points that they have raised in their letter regarding our article. ¹ The trial was designed as a prospective randomized study at the outset. The criteria for major and minor outcomes were set a priori. The principal outcomes were as follows: all cause mortality, cardiopulmonary morbidity (myocardial infarction, pulmonary edema, adult respiratory distress syndrome, cardiogenic shock/low flow state, and cardiopulmonary arrest), neurologic morbidity (new major focal deficit), cognitive complications (defined by intrapatient deterioration on neurocognitive tests), and deterioration in functional status (decline on the SF-36 health survey). Minor outcomes were also determined a priori and were not included as principal outcomes. The minor cardiac outcomes included myocardial ischemia and congestive heart failure and the minor neurologic outcomes included focal deficit lasting less than 24 hours. All major and minor outcomes were counted up to the 6-month interval after the operation and were stipulated before the start of the trial.

When the major outcomes were analyzed at the completion of the trial, it was found that patients randomized to the low mean arterial pressure (MAP) group had a higher incidence of all cause death, major cardiac complications, and major neurologic complications. The combined incidence of total mortality and major cardiac and neurologic morbidity was 12.9% in the low MAP group versus 4.8% in the high MAP group (p = 0.026). The incidence of deterioration in neurocognitive function and deterioration in functional status did not differ between the two groups.

The mean arterial pressures between the low and high MAP groups differed by an average of 18 mm Hg. As shown in Table VI (the pragmatic analysis), which demonstrates the actual pressure achieved regardless of randomization group, the trend toward lower complications with higher pressures can clearly be seen.

Although it is tempting to ascribe differences in outcome to variables other than the therapeutic maneuver, which was assigned by randomization, it is extremely unlikely that the pattern of specific variables differed appreciably between the two MAP groups. The very raison d'etre of a randomized trial is the statistical balance of potential confounding factors, both those previously identified and those unknown at the inception of the trial. Table I of the article demonstrates this balance for a large number of such variables. Furthermore, although not incorporated into the paper, many additional factors were analyzed to ascertain whether there were any differences between the two MAP groups, either before or after bypass. All of these items, including MAPs, cardiac outputs, anesthetic agents, vasoactive medications, other medications, blood gases, activated clotting times, hematocrit values, and other hemodynamic parameters were not found to differ between the two treatment groups.

Pilot subsets of patients enrolled in the present trial also underwent preoperative transesophageal echocardiogram and intraoperative transcranial Doppler ultrasonography; because these subsets were selected after randomization and were examined in a nonrandom fashion, they cannot yield unbiased information on the importance of atheromatous disease or embolic load for the entire 248-patient cohort randomized to two treatment arms. Because atheromatous disease of the aorta is now thought to be a risk factor for perioperative complications of coronary bypass, ² the reproducible quantification of aortic atheroma by transesophageal echocardiography is under development. ³ Future clinical trials of coronary bypass will incorporate these procedures in all patients.

Animal and human data support the conclusion that autoregulation of cerebral blood flow occurs across the range of MAPs of 50 to 150 mm Hg. As observed, 54 mm Hg falls within this range. However, the data also suggest that the autoregulatory range of cerebral blood flow is shifted to the right in patients with longstanding hypertension. In addition, these conclusions are based on experiments in which global cerebral blood flow was measured during the conditions of normothermic pulsatile perfusion. Extension of these conclusions to the conditions of nonpulsatile, hypothermic bypass with attention to regional blood flow may not be valid. Patients with coronary artery disease are known to have an increased incidence of other vascular disease, including that of the cerebral circulation. Higher perfusion pressures may permit the maintenance of adequate blood flow to areas distal to stenotic vessels or facilitate recruitment of collateral blood flow, thus minimizing the affected area of ischemia.

References

1. Gold JP, Charlson ME, Williams-Russo P, Szatrowski TP, Peterson JC, Pirraglia PA, et al. Improvement of outcomes after coronary artery bypass: a randomized trial comparing intraoperative high versus low mean arterial pressure. J THORAC CARDIOVASC SURG 1995;110:1302-14.[Abstract/Free Full Text]
   
2. Katz ES, Tunick PA, Rusinek H, et al. Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992;20(1):70-7.[Abstract]
   
3. Hartman GS, Peterson JC, Konstatd SN, Hahn R, Szatrowski TP, Charlson ME, et al. High reproducibility in the interpretation of intraoperative transesophageal echocardiographic evaluation of aortic atheromatous disease. Anesth Analg. In press.
   

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This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Jeffrey P. Gold Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gold, J. P. Search for Related Content PubMed Articles by Gold, J. P.