Presented at the Fourteenth Annual Meeting of The Society of Thoracic Surgeons, Jan 23-25, 1978, Orlando, FL.

Left Main Coronary Artery Stenosis: Hernodynamic Monitoring to Reduce Mortality Charles H. Moore, M.D., T. Randolph Lombardo, B.A., James A. Allums, M.D., and Fallon T. Gordon, M.D. ABSTRACT A review of 20 consecutive patients with left main coronary artery stenosis operated on in 1976 indicated a general hemodynamic pattern characterized by systolic hypertension and an increase in heart rate that occurred early during the induction phase of anesthesia. From January through August, 1977, 28 patients with this stenotic condition were operated on with hemodynamic monitoring of left ventricular pressure and cardiac output by a Swan- Ganz catheter inserted before induction of anesthesia. Pharmacological interventions to optimize preload with volume, reduce afterload with nitroprusside or nitroglycerine, control heart rate with propranolol, and improve contractility with dopamine resulted in a decrease in mortality from 20% in Group 1 (1976) to 3.5% in Group 2 (1977). We conclude that control of systemic blood pressure, heart rate, and preload has notably reduced the mortality in this group of patients and that hemodynamic monitoring provides precise guidelines for therapeutic interventions. The surgical management of left main coronary artery stenosis continues to carry a high operative mortality 13, 7, 12, 13,17, 181. Recently, use of the intraaortic balloon pump (IABP) has been advocated in an effort to reduce mortality in this high-risk group of patients [3-61. A review of 20 consecutive patients with left main coronary artery stenosis operated on in 1976 at St. Elizabeth Hospital, Beaumont, TX, indicated a general hemodynamic pattern characterized by systolic hypertension and an increase in the heart rate-pressure product that occurred early during the induction phase of anesthesia. In several patients the increased myocardial oxygen demand quickly exceeded available oxygenated blood supply across the stenotic left main coronary artery. Progressive myocardial Presented at the Fourteenth Annual Meeting of The Society of Thoracic Surgeons, Jan 23-25, 1978, Orlando, FL. Address reprint requests to Dr. Moore, 2900 North St, Suite 203, Beaumont, TX 77702. ischemia, ventricular failure, and hypotension followed, resulting in arrhythmias or death in rapid sequence. In view of these potentially preventable hemodynamic perturbations, we have chosen, as an alternative to preoperative IABP, to monitor systemic arterial pressure, left ventricular filling pressure, and cardiac output during the early preinduction and complete perioperative period in these patients. By controlling the variables of cardiac function, that is, preload, afterload, heart rate, and contractiiity, we hoped to minimize myocardial injury. Materials and Methods Twenty patients with left main coronary artery stenosis operated on in 1976 (Group 1) are compared with 28 consecutive patients with the same condition (Group 2) operated on from January through August, 1977. Left main coronary artery stenosis is defined as 70% or more cross-sectional area stenosis. Left main coronary artery equivalent was excluded from this study. Clinical factors included age, sex, findings on electrocardiogram (ECG), and clinical status. Clinical status was divided into three categories: (1) angina, stable or unstable, the latter including recent onset of pain or a change in the pattern of pain or one of the following subsets: progressive or previously stable angina on effort occurring with minimal provocation, pain at rest associated with disabling effort angina, or prolonged episodes of pain without infarction; (2) highly unstable angina (preinfarctional), as defined by 20 minutes of persistent pain and ECG changes with pain despite maximum medical treatment in the hospital with nitrates, propranolol, and narcotics; and (3) recent myocardial infarction (MI) without symptoms of angina. In Group 1, the mean age was 60 k 7.8 years (range, 41 to 70 years). Of the 20 patients, 16 (80%) were men. Eleven patients (55%) had abnormal ECGs, and 12 patients (60%) were in 445 0003-4975/78/0026-0509$01.25 @ 1978 by Charles H. Moore

446 The Annals of Thoracic Surgery Vol 26 No 5 November 1978 category 1 in terms of clinical status, 6 (30%) were in category 2, and 2 (10%) were in category 3. In Group 2 the mean age was 56 f 9.6 years (range, 41 to 75 years). Of the 28 patients, 26 (93%) were men. Fourteen patients (50%) had an abnormal ECG, and 18 (64%) were in clinical category 1, 7 (25%) were in category 2, and 3 (11%) were in category 3. Statistical analysis of each clinical factor in the two groups by Student t test showed no significant difference (p < 0.05) between the two groups. Coronary arteriography revealed that in Group 1, 2.9 coronary arteries were diseased per patient and in Group 2,2.96, as judged on a maximum of 3 coronary arteries. Ventricular function was assessed by left ventriculography, and the ejection fraction (EF) was measured by the method of Dodge-Kennedy using the ellipsoid calculation on a three-dimensional scale. The mean EF of Group 1 was 44 f 14, and that of Group 2 was 48 f 10. The mean left ventricular end-diastolic pressure (LVEDP) in Group 1 was 11 f 6 mm Hg and in Group 2,12 f 9 mm Hg. There was no statistically significant difference between the two groups. Premedication for both groups consisted of morphine, diazepam, and scopolamine. In Group 1, however, propranolol was discontinued twenty-four hours before operation, whereas in Group 2, it was continued to the time of operation. In addition in Group 2, Nitrol Ointment (nitroglycerin) was applied to the skin before the procedure. lnstrumentation and Monitoring In the operating room, all patients had ECG monitoring of standard limb leads (I, 11, 111), percutaneous radial artery cannulation for arterial pressure monitoring, and percutaneous subclavian vein cannulation for fluid administration and central venous pressure monitoring. In Group 2 patients, a Swan-Ganz catheter with a thermistor tip was inserted percutaneously under local anesthesia into the subclavian vein. A pressure monitor was used to float the balloon tip into the pulmonary artery and fluoroscopic control with the Phillips C-arm image amplified portable fluoroscope was employed in the operating room to confirm the position in the pulmonary artery. Left ventricular filling pressure was continuously monitored using the pulmonary artery end-diastolic pressure. Serial cardiac outputs were determined by thermodilution with the Edwards Laboratories Model 9520 cardiac output computer. The following hemodynamic variables were calculated using standard formulas: cardiac index, stroke volume, stroke work, and systemic vascular resistance [15]. In Group 2, ventricular function curves were constructed by plotting either stroke work or cardiac index against left ventricular filling pressure and then by rapid infusion of dextran solution to raise this pressure 4 mm Hg or more and repeating the measurements of cardiac output and arterial pressure. The ventricular function curves offer a quantitative assessment of ventricular performance [15] since the filling pressure was controlled and there were minimal changes in heart rate or systemic arterial pressure resulting from the dextran infusion in the time required for duplicate measurements of cardiac output. An indirect index of myocardial oxygen demand was calculated for all patients by multiplying heart rate by systolic blood pressure to obtain the rate-pressure product. Baseline values were obtained at the time of premedication, a second determination was made 15 minutes after arrival in the operating room, and a third determination was made at 30 minutes. Anesthesia was standardized in both groups; induction consisted of thiopental, morphine, diazepam, and curare. Anesthesia was maintained with 50% nitrous oxide and oxygen in all patients. In Group 1, there were no treatment interventions before induction of anesthesia. In Group 2, however, optimal hemodynamic values were established as follows: mean blood pressure, 80 to 90 mm Hg (as a measure of afterload); left ventricular filling pressure, 5 to 15 mm Hg (as a measure of preload); heart rate, 70 to 90 contractions per minute; cardiac index, 3.5 f 1 liters per minute; and systemic vascular resistance, less than 35 Wood units. The upper limits for rate-pressure product were arbitrarily set at 12,000. Treatment interventions in Group 2 (Table) were as follows: afterload reduction with nitroprusside, 5 to 10 pg per kilogram per minute; heart rate reduction with reduction of rate-pressure product by intravenous adminis-

447 Moore et al: Left Main Coronary Artery Stenosis Treatment Interventions in Group 2 Patients Optimal Hemodynamic Values Preload Afterload HR CI Treatment (LVFP 5-15 (MBP, 80-90 (70-90 (3.5* 1 RPP Intervention mm Hg) mm Hg) contractionslmin) Llmin) (12,000) Nitroprusside r t Propranolol t t Volume 1 1 Dopamine t 1 1 LVFI' = left ventricular filling pressure; MBP = mean blood pressure; HR = heart rate; CI = cardiac index; RPP = rate-pressure product. r t tration of propranolol in increments of 0.5 to 1.0 mg; and alterations of preload by infusion of low molecular weight dextran or by intravenous administration of furosemide. If an increase in myocardial contractility was desired, dopamine, 5 to 30 pg per kilogram per minute, was used. More recently, nitroglycerin, 1 to 2 pg per kilogram per minute administered intravenousiy, has been used instead of nitroprusside for afterload reduction. The nitroglycerin solution is prepared by dissolving twenty tablets of 0.4 mg nitroglycerin in 20 ml saline solution and then passing it through a millipore filter into 250 ml dextrose in water. Pharmacological interventions to achieve optimal hemodynamic values were used in Group 2 patients before induction of anesthesia, during induction, and throughout the perioperative period. Operative Technique The operative technique was standardized in all Group 1 and Group 2 patients using moderate systemic hypothermia, 30 C, with intermittent aortic cross-clamping and the heart fibrillating. Distal anastomoses were placed using intermittent ischemia with a short period of reperfusion between each graft. Proximal anastomoses were placed during the period of rewarming, with the heart beating and utilizing partial aortic occlusion. The membrane oxygenator was used and a left ventricular vent was avoided unless left ventricular filling pressure exceeded 20 mm Hg. In 3 patients in Group 2 potassium cardioplegia was used as a method of myocardial protection rather than intermittent ischemic arrest. The criteria for assessing perioperative MI have been described previously [141. They include serial ECGs with development of new Q waves or loss of R waves, and elevation of the creatine phosphokinase (CPK)-myocardial band (MB) isoenzymes as determined by multiplying total CPK by percentage of MB; a value exceeding 100 is indicative of infarction. The third criterion is a positive postoperative myocardial scan using technetium pyrophosphate in the presence of a negative scan preoperatively. Results In Group 1, the mean number of grafts per patient was 3 & 0.6 (range, 2 to 5), mean ischemia time was 36 f 14 minutes (12 minutes per graft), and total bypass time was 104 k 32 minutes. In Group 2, the mean number of grafts was 3.5 f 0.8 per patient (range, 2 to 5), mean ischemia time was 43 f 15 minutes (11.8 minutes per graft), and mean bypass time was 108 k 25 minutes. There was no statistically significant difference in the two groups with respect to any variable (p < 0.05). Three patients in Group 2 had potassium cardioplegia with a mean ischemia time of 78 minutes and a mean bypass time of 118 minutes. Perioperative MI occurred in 2 patients (10%) in Group 1 and 1 (3.6%) in Group 2. Operative mortality was 4 (20%) in Group 1 and 1 (3.6%) in Group 2. Ventricular fibrillation occurred in 5 patients in Group 1 before cardiopulmonary bypass and in no patients in Group 2. The mean rate-pressure product preoperatively was 10,656 f 2,231 in Group 1 and 9,591 k 1,078 in Group 2. There was an increase in rate-pressure

448 The Annals of Thoracic Surgery Vol 26 No 5 November 1978 product in both groups within 15 minutes in the operating room, the respective values being 15,486 k 3,341 and 16,571 k 4,927, not a statistically significant difference. At 30 minutes Group 1 maintained a mean value of 15,031 k 3,673 and had received no specific treatment intervention. Group 2 had treatment interventions in 57% of the patients and the mean value of rate-pressure product was reduced to 10,779? 2,472. This was significantly different from Group 1 ( p < 0.01). The results of perioperative MI in Group 1 were 2 positive ECGs, an elevated CPK-MB level with a mean value of 100 IU (range, 20 to 250 IU), and in 8 patients (40%) positive scans. In Group 2, 1 ECG was positive for infarction, the mean CPK-MB value was 37 (range, 17 to 150), and 9 patients (33%) had positive scans. Of Group 2 patients, 18 (64%) had a rate-pressure product greater than 12,000 requiring treatment intervention, and 16 (57%) had increased systemic vascular resistance of more than 35 Wood units. Data were not available from Group 1 to make comparative analyses of the following hemodynamic derivatives: cardiac output, cardiac index, stroke work index, systemic vascular resistance, and ventricular function curves. Comment A review of our 1976 series of 20 patients with left main coronary artery stenosis indicated an unacceptable high mortality of 4 patients or 20%. Although the anesthetic record indicated a significant increase in the rate-pressure product in the operating room over preoperative values, it was even more striking that 5 patients subsequently had hypotension unresponsive to vasopressor intervention, serious arrhythmias, and ventricular fibrillation and that 3 of these patients died. From our clinical experience, supported by an early rise in CPK-MB determinations, it became clear to us that myocardial injury was occurring early as the patients arrived in the operating room. Rather than aggravate the situation by insertion of the IABP under local anesthesia with its attendant complications [21, we adopted the following approach: adequate premedication and continuation of propranolo1 up to the time of operation [lo] and the supplemental use of Nitro1 Ointment. This approach has been satisfactory in 40% of our patients. Adrenergic hyperactivity preceding cardiac operation reaches a peak during the first few minutes in the operating room with the start of intravenous and arterial lines. It is at this time that treatment interventions should begin, and precise hemodynamic monitoring is required for optimal therapy. The Swan-Ganz catheter with thermistor tip is easy to insert percutaneously into the subclavian vein in less than 5 minutes, and we have had no serious complications in more than 100 consecutive patients using pressure monitoring and fluoroscopic control for positioning of the catheter. The hemodynamic data available by monitoring heart rate, arterial pressure, left ventricular filling pressure, and cardiac output and the derived data including cardiac index, stroke work index, and systemic vascular resistance offer precise information on the determinants of ventricular function. The fiber stretch is known from the preload (left ventricular filling pressure), and the load resisting ejection (afterload) is derived from the mean arterial pressure. Although myocardial contractility is difficult to measure, construction of ventricular function curves [151 by rapid volume loading is a precise estimation of EF. Our results in Group 2 confirm our hypothesis that myocardial injury can be prevented in left main coronary artery stenosis by maintaining optimal and physiological hemodynamics. The cardiovascular reflexes in the presence of adrenergic hyperactivity, ischemia, hypertension, and increased heart rate, combined with a fixed coronary obstruction, create an increase in myocardial oxygen consumption that exceeds supply in many patients undergoing coronary operation [8, 10, 111. Propranolol administered intravenously is most valuable in reducing the high rate-pressure product values to less than 12,000. Nitroprusside and intravenous administration of nitroglycerin appear to be beneficial in reducing afterload and improving myocardial ischemia during acute intraoperative hypertension [9, 161. In Group 2, using precise hemodynamic monitoring and pharmacological interventions as outlined, myocardial injury and mortality were markedly reduced. There

449 Moore et al: Left Main Coronary Artery Stenosis were no periods of serious hypotension or ventricular fibrillation before bypass, myocardial injury was minimized, and the only perioperative MI was not clinically notable. It was manifested only by ECG changes and mild elevation to 150 of CPK-MB isoenzymes. The sole death in Group 2 occurred 3 weeks after operation and was caused by stress ulceration and bleeding complicating a cerebral injury at the time of ventricular aneurysm resection. The death was not specifically related to the left main coronary artery stenosis. We presently reserve the use of the IABP for those patients who remain hemodynamically unstable in the presence of maximum pharmacological interventions. It could be implied that the improved surgical mortality was due to experience gained by the operating team. We perform approximately 200 cardiac bypass procedures each year, and in both Groups 1 and 2 the anesthesia, method of myocardial protection, and operative techniques were basically the same. Retrospective analysis of Group 1 clearly identified the problems of systemic hypertension, cardiac failure, arrhythmias, and fatal myocardial injury occurring during the early phase of anesthesia, before bypass, in all patients. Treatment interventions during this high-risk period in Group 2 completely eliminated the problem. We, therefore, conclude that treatment interventions to control hypertension and tachycardia, minimize oxygen utilization, and provide optimal myocardial function have been the major factor in reducing the mortality in this high-risk group of patients, and we strongly recommend that these principles of management be used in all patients undergoing myocardial revascularization. Hemodynamic monitoring has provided precise guidelines for therapeutic interventions and a level of safety and confidence to optimize myocardial performance not only in patients with left main coronary artery stenosis, but in all high-risk cardiovascular patients. References 1. Alford WC Jr, Shaker IJ, Thomas CS Jr, et al: Aortocoronary bypass in the treatment of left main coronary artery stenosis. Ann Thorac Surg 17:247, 1974 2. Beckman CB, Geha AS, Hammond GL, et al: Results and complications of intraaortic balloon counterpulsation. Ann Thorac Surg 24;550, 1977 3. Bolooki H, Williams W, Thurer RJ, et al: Clinical and hemodynamic criteria for use of the intraaortic balloon pump in patients requiring cardiac surgery. J Thorac Cardiovasc Surg 72:756, 1976 4. Cooper GN, Singh AK, Vargas LL, et al: Preoperative intraaortic balloon assist in high risk revascularization patients. Am J Surg 133:463, 1977 5. Garcia JM, Mispireta LA, Smyth NPD, et al: Surgical management of life-threatening coronary artery disease. J Thorac Cardiovasc Surg 72:593, 1976 6. Gunstensen J, Goldman BS, Scully HE, et al: Evolving indications for preoperative intraaortic balloon pump assistance. Ann Thorac Surg 22:535, 1976 7. Iskandrian AS, Segal BL, Mundth ED: Appraisal of treatment for left main coronary artery disease. Am J Cardiol40:291, 1977 8. James TN, Isoke JH, Urthaler F: Analysis of components in a cardiogenic hypertensive chemoreflex. Circulation 52:179, 1975 9. Kaplan JA, Dunbar RW, Jones EL: Nitroglycerin infusion during coronary artery surgery. Anesthesiology 45:14, 1976 10. Kent KM, Cooper T: Cardiovascular reflexes (editorial). Circulation 52:177, 1975 11. Loeb HS, Saudye A, Croke RP, et al: Effects of pharmacologically induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction. Circulation 57:41, 1977 12. McConahay DR, Killen DA, McCallister BD, et al: Coronary artery bypass surgery for left main coronary artery disease. Am J Cardiol 37:885, 1976 13. Mehta J, Hamby RI, Hoffman I, et al: Medicalsurgical aspects of left main coronary artery disease. J Thorac Cardiovasc Surg 71:137, 1976 14. Moore CH, Gordon FT, Allums JA, et al: Diagnosis of perioperative myocardial infarction after coronary artery bypass. Ann Thorac Surg 24:323, 1977 15. Raphael LD, Mantle JA, Moraski RE, et al: Quantitative assessment of ventricular performance in unstable ischemic heart disease by dextran function curves. Circulation 55:858, 1977 16. Stinson EB, Holloway EL, Derby GC, et al: Control of myocardial performance early after openheart operations by vasodilator treatment. J Thorac Cardiovasc Surg 73:523, 1977 17. Urschel HC, Razzuk MA: Revascularization of the stenotic left main coronary artery and impaired left ventricle. J Thorac Cardiovasc Surg 69:369, 1975 18. Zeft HJ, Manley JC, Huston JH, et al: Left main coronary artery stenosis. Circulation 49:68, 1974

450 The Annals of Thoracic Surgery Vol 26 No 5 November 1978 Discussion DR. ELLIS L. JONES (Atlanta, GA): One hundred and thirty-five patients with left main coronary artery stenosis have been operated on at Emory University Hospital over the past three years. In dealing with such patients, we have evolved certain principles of prebypass management to effect a reduction in operative morbidity and mortality. In the operating room, anything that increases myocardial oxygen demand or decreases oxygen supply must be avoided. Specifically, factors that increase heart rate or left ventricular contractility or wall tension must be prevented or recognized early and treated promptly. To prevent tachycardia or hypertension during this period, we have insisted that in patients on a regimen of propranolol the drug be continued but tapered, and the last dose administered twelve hours before anesthesia induction. If tachycardia occurs anyway, small repeated doses of propranolol may be given with good results. Episodes of hypertension or increases in pulmonary capillary wedge pressure (both of which increase oxygen demand) are promptly treated with nitroglycerin administered intravenously. We have found excellent correlation between rate-pressure product, as Dr. Moore stated, and ischemic V:, precordial ECG changes before bypass. Of all conditions producing rapid irreversible deterioration in patients with left main coronary artery stenosis, hypotension is the most feared. If it occurs, it is treated with Neo-Synephrine (phenylephrine hydrochloride) to increase peripheral resistance and elevate coronary perfusion pressure. Inotropic agents have not been given. Measurement of pulmonary capillary wedge pressure with the Swan-Ganz catheter has been performed only in patients with poor left ventricular function. We have thought that routine use of this catheter in patients with left main coronary artery disease too hazardous with regard to production of ventricular arrhythmias. Inotropic agents were required at some time in the postoperative period in 17% of our patients. Intraaortic balloon pumping was needed in 4% of patients but was not used in any patient before cardiac catheterization or bypass. With precise prebypass monitoring and good anesthetic technique, stabilization with intraaortic balloon pumping prior to cardiopulmonary bypass is not necessary and may even be hazardous in patients with left main coronary artery, aortoiliac, and peripheral vascular disease. We consider routine use of preoperative intraaortic balloon pumping a less than ideal substitute for poor cardiac anesthesia. Hospital mortality for our patients with left main coronary artery disease was 4%, a figure similar to that presented today. DR. PETER v. MOULDER (Gainesville, FL): Our studies support Dr. Moore s contention that effective monitoring is important in the surgical management of left main coronary artery disease. With these circumstances controlled, surgical risk is now well below its former level and is continuing to improve. Our efforts at further improvement have been to develop a monitoring technique that would blend the effects of preload, afterload, and contractility of the heart in a manner that could be observed continuously. One method has been to use the left ventricular pressure-derivative loop (we have used it for more than ten years); the technique is somewhat similar to the one Dr. Behrendt presented yesterday. Pattern variations in the loop occur with myocardial ischemia: the ordinarily smooth change on the ascending limb produced by the linear variation in time of the two signals comprising the pressure derivative loop becomes erratic due to hyper- and hypocontractility of various segments of the myocardium. This has been striking and the phenomenon is even more impressive with elevated afterload, although one cannot measure more than pressure load. Recently, we have applied frequency-domain transfer-function analysis using a number of paraventricular signals. A limited number of broad poles and zeros or humps and valleys represent the empirical indicator for useful measurement of the system under investigation. This looks promising: elevation of major poles occurs with increased afterload, and variation of the same pole and others occurs secondary to coronary artery occlusion. Ordinarily, one relies on a variety of measurements with limits set for each, and it is an art as well as a science to keep the mixture correct. Some unitary, graphic, or numerical indicator for the interrelated phenomena seems the next step. We hope changes in the loops, humps, bumps, and zeros will do the trick. DR. DAVID BREGMAN (New York, NY): Dr. Moore and his associates have presented an admirable clinical series of patients with critical left main coronary artery stenosis who have had careful hemodynamic monitoring without intraaortic balloon pump support. At the Presbyterian Hospital our approach is to employ the same adjunctive procedures described by Dr. Moore, including the Swan-Ganz thermodilution catheter. In addition, a pulsatile assist device is also used to maximize myocardial protection until complete revascularization is achieved. One hundred consecutive patients (82 men and 18 women) with angiographically documented critical left main coronary artery stenosis or equivalent left main coronary artery stenosis underwent a revascularization procedure. Intraoperatively, a pulsatile assist device was used as a counterpulsator. It was also used to produce pulsatile bypass synchronized in diastole. Previous studies have shown that this technique reduces the incidence of myocardial infarction during operation.

451 Moore et al: Left Main Coronary Artery Stenosis Seventy-seven patients (77%) were in either New York Heart Association Functional Class I11 or IV and had an ejection fraction of 0.4 or less and a left ventricular end-diastolic pressure of 18 mm Hg or higher preoperatively. Intraaortic balloon pumping was not employed in this series either before or after operation. All patients were weaned from cardiopulmonary bypass with the pulsatile assist device alone. One patient (1%) died in the recovery room from an anaphylactic drug reaction, and only 2 (2%) had a perioperative myocardial infarction, which was clinically insignificant. Intraoperative use of the pulsatile assist device during cardiopulmonary bypass in conjunction with careful hemodynamic monitoring successfully reduces morbidity and mortality during revascularization procedures for critical left main coronary artery stenosis, even in the presence of impaired left ventricular function. We consider it a reasonable altemative to the elective use of intraaortic balloon pumping. DR. MOORE: I thank the discussants for their kind comments. I am pleased that Dr. Jones and his group agree with our management and they certainly have had outstanding results. Dr. Moulder, high fidelity monitoring is required for measuring the pressure-derivative loops, and we consider the ventricular function curves to be a similar, easier, and more reliable method of measuring myocardial contractility. Certainly, both are a new and improved adjunct for measuring contractility in the operating room. Dr. Bregman, we were pleased to see that you also do not advocate use of the preoperative intraaortic balloon pump, but rather pulsatile bypass for protection during cardiopulmonary bypass. Certainly, other techniques such as potassium cardioplegia may be useful in this group of patients. More recently, we have been using cardioplegia for protection during operation. Finally, I do not want anyone to think that subclavian vein catheterization is an innocuous procedure. We have discovered through long and hard experience that there are many, many complications and that it is a dangerous procedure. However, after inserting central venous pressure lines in several hundred patients, we have learned to avoid these complications but still take every degree of caution in doing so.