Pro: Surgery is the preferred treatment for acute myocardial infarction

PRO AND CON J. Earl Wynands, MD, Editor

SURGERY FOR ACUTE MYOCARDIAL

INFARCTION

Pro: Surgery Is the Preferred Treatment for Acute Myocardial Infarction Arvind Koshal, MD, FRCSC

I

MMEDIATE ATTEMPTS at reperfusion of a myocardium within the first 4 to 6 hours of an acute evolving myocardial infarction (AEMI) have been shown to significantly reduce mortality and improve left ventricular function.’ Reperfusion can be achieved by thrombolysis, angioplasty, or coronary artery bypass grafting. Thrombolytic therapy with or without angioplasty is limited in achieving adequate revascularization compared with coronary artery bypass surgery. In high-risk patients, ie, patients in cardiogenie shock, surgical therapy seems to have taken a new approach with the advent of mechanical assist devices and their usage as bridging devices for subsequent transplantation, or allowing “stunned” myocardium to recover. There is little doubt that the optimal approach for cardiogenic shock resulting from postinfarction rupture of a papillary muscle or ventricular septum is surgical. ACUTE EVOLVING MYOCARDIAL

INFARCTION

Reperfusion of ischemic myocardium in the first few hours after coronary artery occlusion is an attempt to salvage viable ischemic myocardium by improving coronary blood flow and limiting damage to the myocardium. It is important to realize that thrombolysis, angioplasty, and coronary artery bypass surgery have been used individually or in combination with each other, but have different modes of achieving reperfusion. Thrombolysis

Thrombolytic therapy is aimed at dissolving the clot within the coronary artery that

caused the acute myocardial ischemia. There is a pharmacologic intervention plateau-at approximately 75%-in maintenance of patency of the acute infarct-related vessel.2 The recanalization is prolonged by an average of 45 to 50 minutes, even with high-dose thrombolytic therapy.3 Serious bleeding episodes and recurrent ischemic events are unpredictable. There is also an inability to accurately diagnose reperfusion at the bedside. This makes the task of deciding which patient should undergo coronary angiography difficult, especially because there is a time delay in waiting for the result of thrombolysis.4 Current criteria used for eligibility for thrombolysis in most studies allow only 14% to 35% of patients with acute myocardial infarction to be candidates for thrombolytic therapy. Patient selection is not established for thrombolytic therapy in low-risk patients with inferior myocardial infarction or myocardial infarction with ST segment depression. In highrisk patients (those in cardiogenic shock and/or pulmonary edema), the role of thrombolytic therapy is uncertain. Angioplasty

After successful thrombolysis, most patients are left with a critical obstruction of the

From the Department of Cardiothoracic Surgery, University of Ottawa Heart Institute. Ottawa Civic Hospital, Ontario, Canada. Address reprint requests to Arvind Koshal, MD, FRCSC, Department of Cardiothoracic Surgery, University of Ottawa Heart Institute, Ottawa Civic Hospital, Ottawa, ONT, Canada KI Y 4E9. o 1990 by W.B. Saunders Company. 0888~6296/90/0401-0021$03.00/0

Journal of Cardiorhoracic Anesthesia, Vol4, No 1 (February), 1990: pp 13 l-135

131

132

infarct-related coronary artery and, therefore, are at a high risk for reocclusion. It seems logical that reocclusion could be avoided if coronary angioplasty was carried out immediately after thrombolysis. However, neither of the two separate large trials, those by Mueller et al3 and Simoons et aLs could show that coronary arteriography followed by angioplasty was necessary immediately after intravenous thrombolytic therapy, but showed, in fact, that it may be undesirable. It is thought that the presence of lumen thrombus before angioplasty and the mechanical injury and distortion of the thrombus that are induced by inflating the balloon cause significant platelet and clotting activation and are the mechanisms of the increased incidence of postangioplasty occlusion in patients with acute myocardial infarction.6 Attempts are now being made to perform coronary angioplasty a few days after the acute occlusion on a nonemergent basis, but the value of this strategy has not been proven. It is being addressed by an ongoing thrombolysis in myocardial infarction (TIMI-IIB) trial.7 The need to maintain a patent coronary artery supplying an infarcted myocardium has been shown. Patients who had complete perfusion of an infarct-related artery had a mortality rate in 1 year of 5%, whereas those with partial or no reperfusion had a 35% mortality rate, even though there was no difference in the ejection fraction between these groups.* When angioplasty was performed successfully after unsuccessful streptokinase therapy, there was a striking improvement in ejection fraction, even though reperfusion was carried out too late to salvage reasonable amounts of myocardium.g Patency of the infarct-related artery is an important predictor of left ventricular improvement because it reduces infarct expansion, left ventricular remodeling, and dilation, and may also supply collaterals to areas of the myocardium by other diseased vessels, thereby preserving myocardial viability.” Schroeder” has suggested that the incidence of late ventricular fibrillation may be reduced by maintaining late myocardial reperfusion and that it is of clinical value. Surgical Reperfusion

A major advantage of surgical reperfusion is that coronary artery bypass grafting can be performed not only on the infarct-related vessels,

ARVIND KOSHAL

but also on any associated severely occluded coronary arteries. The problem of a high incidence of restenosis (such as with angioplasty) does not occur. General anesthesia and hypothermia, along with cardioplegia and topical myocardial cooling, tend to reduce myocardial oxygen demand. Cardiopulmonary bypass decreases preload and afterload during surgery. Surgical reperfusion of the ischemic myocardium was attempted by Keon et al.” In 1970, they performed aortocoronary bypass grafting in three patients within a few hours of the onset of chest pain and infarction. DeWood et ali3 and Philips et ali4 subsequently separately published studies of large series of patients who underwent urgent surgical reperfusion and reported mortality rates of 5.2% in transmural infarction and 3% in nontransmural infarction. Most of these surgical studies were criticized for not providing prospective randomized protocols. A randomized controlled study of urgent surgical reperfusion in AEMI was compared with conventional medical therapy-l5 Sixty-eight patients were randomized into a medical and a surgical group. There were three (8.8%) early deaths and four (11.7%) late deaths in the medical group, and one (2.9%) early death and no late deaths in the surgical group. It was concluded that urgent surgical reperfusion in AEMI was safe and seemed to reduce early and late mortality; however, there was no difference in left ventricular functional improvement among the survivors in both groups 3 months after the infarct. Long-term (10 or more years) follow-up has very recently been reported from the earlier work of DeWood et all6 A study of 387 patients followed for 10 to 13 years (mean, 11.4 years) showed that the long-term mortality rate of medical and surgical groups was 41% (82/200) versus 27% (51/187) (P = 0.0007). The recurrent myocardial infarction rate was not different between surgically reperfused or conventionally medically treated patients (23% in both groups). However, the mortality in patients with recurrent infarction was higher in the medical therapy group-36.6% (15/41) versus 17.5% (7/40) (P = 0.04). The same series confirmed that early reperfusion (within 4 to 5 hours), and not late reperfusion (beyond 6 hours), resulted in better long-term survival and better left ventricular function than conventional medical therapy.

PRO: SURGERY FOR ACUTE MYOCARDIAL

INFARCTION

These studies strongly suggest that incomplete revascularization, such as is being performed by thrombolysis, with or without angioplasty, will not show the beneficial long-term effects that have been shown by early surgical reperfusion. Emergency coronary artery bypass grafting has been performed following thrombolytic therapy, because of unsuccessful angioplasty of the infarct-related vessel, angiographic demonstration of left main coronary artery stenosis or left main coronary artery equivalent lesion, multivessel disease with complex lesions not amenable to angioplasty, or failure to restore patency of the infarct-related vessel by thrombolysis. There is, of course, an increased blood loss if surgery is performed immediately after thrombolytic therapy. If the operation can be deferred for 12 hours, postoperative bleeding and the need for reexploration for bleeding will decrease. CARDIOGENIC SHOCK AFTER ACUTE MYOCARDIAL

INFARCTION

Infarction of more than 40% of the left ventricular myocardium generally results in cardiogenic shock. This is associated with a high mortality when treated by nonsurgical endeavors. Information regarding effective thrombolytic therapy or angioplasty in this setting is limited, as most randomized studies have excluded patients in cardiogenic shock. Scattered reports are available regarding the efficacy of early aortocoronary bypass grafting in cardiogenie shock ‘*,13*however, no large randomized trials have been’reported. The wide acceptability and success of cardiac transplantation in the last few years have altered the outcome of some patients dying from end-stage heart failure. Patients in cardiogenic shock who could benefit from cardiac transplantation if a donor heart were immediately available have been supported by univentricular or biventricular assist devices as a bridge until a cardiac transplant was feasible. However, it is recommended that all patients in cardiogenic shock first be placed on maximal inotropic support and/or intra-aortic balloon pump assist. If they cannot be adequately supported in this manner, a decision regarding an appropriate assist device should be made depending on the presence of univentricular or biventricular fail-

133

ure, as well as suitability for a subsequent cardiac transplant. The major categories of available support devices include centrifugal pumps, orthotopic prosthetic ventricles (total artificial heart), and heterotopic prosthetic ventricles (ventricular assist devices). Figure 1 shows the overall survival with some of the currently available systems. The Novacor device (Baxter Health Care Corp, Oakland, CA) is an implantable left ventricular assist system. The Thoratec heterotopic ventricles (Thoratec Laboratories Corp, Berkeley, CA) in this series were used as a left ventricular assist in 21% and biventricular assist in 79%.17 Initial management of cardiogenic shock after unsuccessful angioplasty with or without thrombolytic therapy has included the intraaortic balloon pump. Recently, extracorporeal membrane oxygenation by a percutaneous femorofemoral cannulation technique in the cardiac catheterization laboratory has been tried. Experience with this is limited. These patients should undergo immediate aortocoronary bypass grafting to provide any significant benefit. ACUTE ISCHEMIC VENTRICULAR SEPTAL DEFECT

Medical treatment of a postinfarction ventricular septal defect carries an extremely high mortality-25% die within 24 hours, 50% within a week, and about 85% within two months.” In patients who are hemodynamically unstable, immediate surgical repair of the ventricular septal defect with or without coronary artery bypass grafting remains the only viable option. In other instances, if a delay up to 6 weeks can be undertaken without hemodynamic instability, the results of surgical closure are even better. Hill and Stiles,” using data from various centers, reported a survival of 57% in patients who were operated upon within 30 days, and 67% in those operated upon after 30 days. PAPILLARY MUSCLE RUPTURE

Acute mitral regurgitation and cardiogenic shock after papillary muscle rupture is associated with a 70% mortality within 24 hours and 90% within 2 weeks. 2o Initial support with the intraaortic balloon pump to decrease the regurgitant fraction of left ventricular ejection followed by

ARVIND KOSHAL

134

100 90

80

CENTRIFUGAL n=25 m

TRANSPLANTED Fig 1.

SYMBION

TAH

NOVACOR

w57

n=17

n=51 B

THORATEC

DISCHARGED

-

OVERALL

SURVIVAL

Survival with various mechanial assist devices. TAH, total artificial heart.

combined coronary artery bypass grafting and mitral valve replacement are still the preferred treatment in this setting. Vlahakes and Daggett” have shown a 75% survival in patients undergoing mitral valve replacement for regurgitation caused by coronary artery disease. Eighty-eight percent of their patients were in cardiogenic shock and required the intra-aortic balloon pump. There are other scenarios in acute myocardial infarction of patients that preferentially need surgical management. These include significant left main coronary artery or triple-vessel disease and some cases of angina after a recent infarction not responsive to medical treatment. Surgery in these situations may have to be performed on a semiurgent basis. CONCLUSION

There is little doubt that surgical reperfusion in the AEMI stage is the most effective way

of maintaining patency of an infarct-related artery and reducing myocardial oxygen demand. The logistics involved in operating within a few hours of AEMI preclude a large number of centers from using this route. However, it should be clearly understood that where feasible, surgery is the best approach. Certainly, angiographic documentation of significant left main coronary artery disease or severe triple-vessel disease is a surgical indication. Management of cardiogenic shock after AEMI has now seen the use of mechanical assist devices and subsequent cardiac transplantation. This has reduced the previous high mortality associated with medical management. Postangioplasty failures in cardiogenie shock as well as rupture of ventricular septum or papillary muscle are still treated surgically because no good medical alternatives are available. Surgery continues to be an active therapeutic option in the treatment of AEMI.

REFERENCES 1. Braunwald E: Thrombolytic perfusion of acute myocardial infarction: Resolved and unresolved issues. J Am Co11Cardiol 12:85A-92A, 1988 2. Topol EJ, Califf RM, George BS, et al: A randomized trial of immediate versus delayed elective angioplasty

after intravenous tissue plasminogen activator in acute myocardial infarction. N Engl J Med 317:581-588, 1987 3. Mueller HS, Rao AK, Forman SA, and the TIMI Investigators: Thrombolysis in Myocardial Infarction (TIMI): Comparative studies of coronary reperfusion and systemic

PRO: SURGERY FOR ACUTE MYOCARDIAL INFARCTION

fibrinogenolysis with two forms of recombinant tissue-type plasminogen activator. J Am Co11 Cardiol l&479-490, 1987 4. Califf RM, Q’Neill WW, Stack RS, et al: Failure of simple clinical measurements to predict perfusion status after intravenous thrombolysis. Ann Intern Med 108:658682,1988 5. Simoons ML, Arnold AE, Betriu A, et al: The European Cooperative Study Group for Recombinant TissueType Plasminogen Activator ((u-TPA). Thrombolysis with tissue plasminogen activator in acute myocardial infarction: No additional benefit from immediate percutaneous coronary angioplasty. Lancet 1: 197-202, 1988 6. Nobuyoski M, Kimura T, Nosaka H, et al: Restenosis after successful percutaneous transluminal angioplasty. Serial angiographic follow-up of 229 patients. J Am Co11 Cardiol 12:616-623, 1988 7. Passamani E, Hodges M, Herman M, and the TIM1 Investigators: The Thrombolysis in Myocardial Infarction (TIMI)-phase II pilot study: Tissue plasminogen activator followed by percutaneous transluminal coronary angioplasty. J Am Co11 Cardiol lO:Sl-64B, 1987 (suppl B) 8. Kennedy JW, Ritchie JL, Davis KB, Fritz JK: Western Washington trial of intracoronary streptokinase in acute myocardial infarction. N Engl J Med 309:1477-1482, 1983 9. Fung AY, Lai P, Topol EJ, et al: Value of percutaneous transluminal coronary angioplasty after acute myocardial infarction. Am J Cardiol58:686-691, 1986 10. Feyter PJ, Van Eenige MJ, Vander Wall EE: Effects of spontaneous and streptokinase-induced recanalization on left ventricular function in acute myocardial infarction. Circulation 67:1039-1044, 1983 11. Schroeder

R: Ventricular

fibrillation

complicat-

135

ing myocardial infarction. N Engl J Med 318:381-382, 1988 (letter) 12. Keon WJ, Abbas SZ, Shankar KR, et al: Emergency aortocoronary bypass grafting: Cardiogenic shock. Can Med Assoc J 1051291-1296, 1971 13. DeWood MA, Spores J, Berg R: Acute myocardial infarction: A decade of experience with surgical reperfusion in 701 patients. Circ 68:11-l l-11-18, 1983 (suppl II) 14. Phillips SJ, Kongtahworn C, Skinner D: Emergency coronary artery reperfusion: A choice of therapy for evolving myocardial infarction. J Thorac Cardiovasc Surg 86:679-688, 1983 15. Koshal A, Beanlands DS, Davies RA, et al: Urgent surgical reperfusion in acute evolving myocardial infarction-A randomized controlled study. Circ 78:1-17 I-I178, 1988 (suppl I) 16. DeWood MA, Notske RN, Berg R Jr, et al: Medical and surgical management of early Q wave myocardial infarction. J Am Co11 Cardio 1401:65-89, 1989 17. Hill JD: Bridging to Cardiac Transplantation. AnnThoracSurg 47:167-171,1989 18. Kirklin J, Barrett Boyce B: Post-infarction ventricular septal defect, in Kirklin JW, Barrett Boyce B (eds): Cardiac Surgery. New York, NY, Wiley, 1986, pp 301-310 19. Hill JD, Stiles QR: Acute ischemic ventricular septal defect. Circ 79:1-l 12-1-l 15, 1989 (suppl I) 20. Austen WG, Sokol DM, DeSauchs RW, et al: Surgical treatment of papillary muscle rupture complicating acute myocardial infarction. N Engl J Med 278:1137-1141, 1968 21. Vlahakes GJ, Daggett WM: The surgical treatment of cardiogenic shock, in Roberts W (ed): Difficult problems in adult cardiac surgery. Chicago, IL, Year Book Medical, 1985, pp 54-61