REVIEW ARTICLE

Myocardial

Infarction

During

Coronary

Artery Bypass

Surgery

Uday Jain, PhD, MD

P

ERIOPERATIVE myocardial infarction (PMI) is one of the major problems during coronary artery bypass grafting surgery (CABG). Its incidence is reported to be between 2% and 82%.lJ This wide variation can be attributed to different tests and criteria for the detection of PMI, the patient population,3-s and the quality of care.” Some previous reviews of the literature in this area exist. l”-ih This review concentrates on significant new information. The literature on PM1 during noncardiac surgery has been extensively reviewed.r4 Literature on PM1 during cardiac surgery other than CABG is limited, and is not reviewed.

anticoagulation and its reversal will have to be studied to better understand the pathogenesis of PMI. PMIs may occur in the myocardium supplied by a considerably stenosed small-caliber coronary artery considered too smal1 for grafting,’ or in the distribution of a coronary artery with an occluded graft. However, many PMIs occur in the distribution of coronaries with patent new grafts.1,s”-52 Inferoposterior PM1 in the distribution of the RCA may be more common,22-28,3n.33,38even when the RCA is not stenosed or bypassed,‘?.2”.?S.‘7.2~,3i).~3,~X RISK FACTORS

CAUSES AND LOCATION

OF PMI

The pathogenesis of PM1 is not well understood though several correlates of PM1 have been identified. MIS are considered to be triggered by a set of stimuli that lead to ischemia in the presence of vu1nerability.17 Inadequate myocardial protection during cardiopulmonary bypass (CPB) may lead to PMI, though myocardial stunning is much more common. The stunned myocardium utilizes oxygen poorly,* and may be more susceptible to necrosis in the period after CPB.19 Angiographically proven vasospasm towards the end of surgery and early in the postoperative period has been reported to be a cause of PM1 in several case reports,*“-“’ even in the patients who were not known to have vasospasm before the perioperative period.25 The right coronary artery (RCA) is most commonly involved, 22-28,30,33,34.3Xeven when it is not stenosed or grafted.22,23,2s,27,2R,30,33,38 In patients undergoing reoperation for CABG, PM1 may occur because of atheroembolization from old grafts39-42 or thrombosis of old grafts after plaque fissure. 43 .- 46 Other etiologies of PM1 may also exist. Multiple etiologies may act in concert to cause a PMI. The prevalente of the triggers of PM1 is not known because studies for the identification of the triggers have not been performed. Continuous perioperative monitoring with modalities such as electrocardiography, echocardiography, and radionuclide ventriculography may provide further information. The response of the coronary arteries to CPB, cardioplegia,“’ reperfusion,4s,4y perioperative stress,

From the University of Califomia, San Francisco, San Francisco, CA 94143. Address correspondence to Uday Jain, PhD, MD, University of Califomia, Veterans Aflairs Medical Center, Anesthesiology Service, #129, 4150 Clement St, San Francisco, CA 94121. Copyright 0 1992 by W B. Saunders Company 1053-077019210605-0017$03.00/0 Key words: myocardial infarction, coronary anery bypass surgery 612

Because of the difficulty in studying the etiologies and pathogenesis of PMI, past studies have concentrated on studying the risk factors for PMI. Many risk factors have been identified.s2”-s2d These can be broadly divided into those related to the preoperative condition of the patient, the perioperative care, or both. Preoperative

Risk Factors

Ischemia. It may be related to preoperative conditions as wel1 as perioperative care. Ischemia evaluated by a history of angina, or the use of anti-ischemia therapies including intravenous nitroglycerin and intra-aortic balloon counterpulsation, was found to be a risk factor for PMI.‘3.s’1J3-h3Unstable angina is reported to be associated with a higher morbidity and mortality compared to stable angina.h4-ó6 Similar results were observed in the 8991 CASS patients.h7-hy Acute MI prior to surgery was a risk factor for PMI.70-so Failed angioplasty may lead to ischemia and has been shown to be associated with increased morbidity and mortality of the subsequent CABG.*’ The duration of chronic symptomatic coronary artery disease (CAD) may also be a risk factor for PMI.8Z Perioperative ischemic episodes detected by ECG and echocardiographic monitoring are associated with a greater incidence of PMI.x3-n6 However, treatment of preoperative ischemic episodes by nitrates may not reduce the incidence of PMI.X7 Compared to ischemia in the prebypass period, ischemia in the postbypass period may have a stronger correlation with PMI.Xh.8s Coronary insufficiency determined by ECG, echocardiography, and thallium or other scintigraphy during coronary vasodilation by exercise, dipyridamole,sy or adenosine has been reported to be associated with PM1 during noncardiac surgery. Such testing is not generally done prior to CABG because of the use of coronary angiography. Excessive platelet activation. which may be present preoperatively, may lead to ischemia; and in spite of

Journal of Cardiothoracic and VascularAnesthesia,

Vol 6, NO 5 (October), 1992: pp 612-623

MI DURING CABG

613

ischemic preconditioning, yo also to PMI.yl Reduced intrinsic fibrinolytic capacity such as due to low levels of tissue plasminogen activator may lead to an increased incidence of PMI.92 Ischemia may lead to reduction in the anticoagulant and vasorelaxing properties of the coronary micocirculation, thus predisposing to MI.4y,y3,93a

difficulty in measuring ischemia during CPB, few studies have quantified it. Intramyocardial acidosis can be measured with myocardial electrodes and is indicative of ischemia.llsJ1y Low amplitude cardiac electrical activity during cardioplegic arrest is also a measure of ischemia and has been shown to correlate with PMI.izo

Extent of Coronary Stenosis

Greater numbers of coronary arteries with stenosis or greater stenosis of the coronaries were found to be risk factors for PM1 and other adverse outcomes.50,54,67,68,69,94 PM1 may primarily occur in the myocardium supplied by small-caliber coronaries and grafts with poor distal runoff.1J.51,52Microvascular disease due to diabetes mellitus may increase the risk. 95 Absente of collaterals is a risk factor for PMI.94,96Ventricular aneurysm and lack of use of internal mammary grafts may also increase the morbidity.54

Cardioplegia

Though some CABGs are performed without the use of cardioplegia, the vast majority of patients receive cardioplegia during aortic occlusion. 121Cardioplegia makes the heart flaccid, causing a substantial reduction in myocyte metabolism. Hypothermia is also commonly used, though the further reduction in metabolism due to it is modest. Hence, both cold and warm cardioplegia have been used. Potassium cardioplegia is most commonly used,122-124though other agents such as adenosine have also been evaluated. Ventricular Dysfunction Crystalloid cardioplegia is used,125J26 though blood carVentricular dysfunction and congestive heart failure dioplegia is becoming increasingly popular.123J27J28 Blood (CHF) have been identified as major risk factors for PM1 cardioplegia may cause less coronary endothelial damage and other adverse outcomes in many studies.50,54,55,67-69J2,97 and may be associated with a lower rate of PM1 than Ventricular dysfunction may be a marker for extensive crystalloid cardioplegia. Cardioplegia may be administered coronary stenosis. antegrade in the aortic root, retrograde in the coronary sinus, or in both locations.127-134Each of the methods has its Reoperation own risks and benefits. The volume of cardioplegia used Patients who present for reoperation for CABG are may also affect the outcome.82 Oxygenation of cardioplegia reported to be at greater risk for PM1 and other adverse may be beneficial.135 sequelae.82~98-i05J05bThe increased risk of PM1 in these Most of the studies of cardioplegia have evaluated the patients may be due to atheroembolization from an old protection of myocytes whereas the protection of coronary graft to the coronaries. Alternatively, PM1 may be caused endothelial cells and conduction tissue has not been adeby acute thrombosis of old grafts due to plaque fissure.43quately evaluated. This may be because of the smal1 mass of 46,106The old grafts may be more susceptible to plaque these tissues. There are indications that these tissues are fissure than the coronaries. Thrombolitic reperfusion of not optimally protected, potentially leading to cardiac chronically occluded saphenous vein grafts may also lead to conduction disorders and small-vessel closure in the postMI.‘O’ CPB period. Patients for reoperation may have smaller MIS, and in Various cardioplegia additives have been found to be the short term, may be less likely to have serious complicauseful in experimental studies. 136~137 In clinical studies, none tions or death due to their MIs.~~ However, they have more of the additives has been shown to be clearly beneficial. reinfarctions and unstable angina and their follow-up death This may be because of the difficulty in designing studies to rate is similar to that of the patients undergoing the first evaluate the multiple factors that lead to PMI. CABG who have PMI.108,*09The incidence of PM1 during Many different cardioplegia administration protocols reoperation after failed angioplasty subsequent to a previhave been described. Warm induction of cardioplegia has ous CABG is reported to be moderate.llOJ1’ recently been described. 13*Use of normothermic reperfuOther Preoperative Risk Factors sion cardioplegia has also been described.139 Continuous warm blood aerobic cardioplegia may be beneficial.140J41 The other risk factors identified include smokir@” and The studies comparing various cardioplegia administration advanced age.54~s5~67~h8~82~112-115 Female gender is a risk factor protocols with each other are few and inconclusive as only a for PMI.55,67-h9,69a Smal1 height has been described as a risk factor.69 When correction for height is made, female gender smal1 number of patients were studied. A number of studies may not be a risk factor. are currently in progress to determine the relative merits of various types of cardioplegia and administration protocols. INTRAOPERATIVE

RISK FACTORS

Cardiopulmonaty Bypass

Increased duration of CPB and aortic occlusion are associated with PMI.54,82,94J16.117 However, the duration and extent of ischemia during CPB may be a greater risk factor than the total duration of CPB. Ischemia is likely to be greater in patients with longer CPB. Because of the

Other Intraoperative Risk Factors

Coronary endarterectomy,55~82J4z reperfusion143 and ventricular fibrillation during it,‘@ ventricular tachycardia,54 ischemic period during CPB,lua and intraoperative hemodynamic instability54 have been recognized as risk factors.

614

DIAGNOSIS

OF PMI

Because the patients are sedated for several days after surgery, they seldom complain of angina or other symptoms indicative of PMI. Though postoperative ventricular dysfunction may be caused by PMI, it is much more likely to be caused by reversible myocardial stunning during aortic occlusion,‘X,‘4sJ46 rcperfusion injury,‘“‘-“’ and protamine administration.15Z The occurrence of arrhythmias, cardiac conduction changes, and new-onset pacemaker dependence has low sensitivity and specificity for the detection of PMI. Thus, smal1 PMIs are usually not diagnosed clinically and tests for PM1 are needed. The commonly performed tests for PM1 include serum enzymes, electrocardiography (ECG), echocardiography, and radionuclide techniques including infarct avid scintigraphy, myocardial perfusion scintigraphy, and radionuclide ventriculography. There is no generally accepted standardization of any of these tests for the detection of PMI. The results of different tests are often not in concordante. To detect a PMI, the postoperative result of a test has to be compared with the preoperative result. Some of the tests, such as serum enzymes, myocardial perfusion scintigraphy, and infarct avid scintigraphy do not become positive for several hours after the onset of a PMI. Hence, they are not wel1 suited for detecting the onset and trigger of a PMI. The above two scintigraphic tests cannot be repeated at brief intervals, thus making them unsuitable for following the perioperative course of a patient. ECG, echocardiography and radionuclide ventriculography have been used for continuous perioperative monitoring and may show changes at the onset of an MI. However, the specificity of these tests for the detection of the onset of MI is low. The vast majority of PMIs may be of the subendocardial variety.‘~? However, most of the tests, such as ECG and planar scintigraphy, are much more sensitive in detecting transmural MIS compared to subendocardial MIS. Thus, the diagnosis of smal1 PMIs, especially in real time, remains an unsolved problem. Many studies have evaluated the various methods for the detection of PMI.1’7.1s3-lh2

ECG DIAGNOSIS New postoperative Q waves of at least 0.03-second duration or broadening of preexisting Q waves, or new QS deflections are generally considered to be indicative of PMI.16’ This criterion excludes the vast majority of PMIs, which are non-Q wave MIs.‘,~ The Q waves recorded on the body surface are much fewer than those recorded on the epicardium, lh4 thus reducing the sensitivity of this criterion. The Q wave criterion is not highly specific, partly because new Q waves may not be due to a new MI, but to the unmasking of an old MI.lhs The new Q waves, especially in the inferior leads, may be labile.1hh~167The QRS changes may resolve over a period of time.16x During the first two months, the QRS changes resolve more rapidly after PM1 than after an MI in the nonsurgical setting. lhXAfter that, the rates of resolution are similar in the two groups.

Thc non4 wavc MIS arc usually associated with neu Y 1 segment elevation”‘“~‘” or depression. which may reach ;I steady state within hours, unlike Q waves, which may persist indefinitely. Howcver, ST segment clevation has much lower specificity for the occurrcncc of MI. comparcd to rhc Q wave. bccause pcrioperatively. the former can be caused by changcs in body position, hypothcrmia, defìbrillation. transient cardiac conduction abnormalities after CPR and pericarditis. “’ ST dcviation mav also be caused by electrolyte imbalances. hypoglyccmia. and pancreatitis. Additionally, for the detection of the relatively transient ST clev:ltion, frequent perioperative monitoring with multilead ECGs is rcquired. Many ether ECG features have low sensitivity and specificity for the detection of MI. These include ncu peaked, flattened, biphasic. or inverted T waves, loss of R wave amplitude, cardiac conduction abnormalities, shift in QRS axis, and ventricular arrhythmias. In spite of al1 the abovc limitations. ECG and cardiac enzymes are thc two most commonly used mcthods for the diagnosis of MI. ENZYMATIC

DETECTION OF PMI

Irreversible myocyte injury Icads to the breakdown of myocyte membrancs. Intracellular substances are released and are transported to blood by cardiac lymphatics. The speed of transport depends on molecular size and solubility. Smaller molecules such as myoglobin are detected in the serum within hours. Larger molecules such as lactatc dehydrogenase (LDH) diffuse more slowly. ‘F The myocardial fraction of creatine kinasc (CK-MB) ia the most commonly used enzyme for the detection of acute MI.173-175.175a~‘75f CK-MB is detected in the serum 4 to 6 hours after the onset of MI. The peak value may occur 15 hours after the onset of MI in non-Q wavc approximately MI, and approximately 30 hours after the onset of MI in Q wavc MI. CK-MB values can hc determined at frequent intervals and activity-timc curves constructed. Such curves may provide information about the extent of infarction and reperfusion.“’ CK-MB can bc measured by immunoinhibition, immunoinhibition-immunoprecipitation, column chromatography, and electrophoresis.‘77-‘7X CK-MB values as high as 80 IU/L have been used for the diagnosis of MI.*” However. a CK-MB of 19 IUldL is reported to have a high specificity for the diagnosis of PMI.’ Ventricular infarction is not the only cause of serum CK-MB elevation. CK-MB is found in ventricular as wel1 as atria1 myocardium. In the atria1 myocardium, LDH, is less than LDH2, while in the ventricular myocardium, LDH, is greater than LDH2. Atriotomy for cannulation for CPB can lead to an increase in the serum CK-MB. Even with double atriotomies, thc peak CK-MB is usually wel1 below 50 IU/L.17” Direct current defìbrillation can causc a falscpositive CK-MB. lx0 Renal failure may lead to false-positive electrophoretic determination of CK-MB. Hypothyroidism may impair the clearance of CK-MB from bloed. Elevated levels of CK-MB may also be observed in mesenteric infarction during acute bowel necrosis.‘s’ Skeletal muscle trauma during CABG releases large amounts of CK contain-

MI WRING

CAEG

615

ing approximately 1% CK-MB.182 This may substantially dilute the total CK-MB% and may artificially elevate the total CK-MB value. CK-MB% greater than 1%iB3 and 2%i*4 is reported to be associated with a poor prognosis. In this population, CK and CK-MB may be more suitable discriminators than CK-MB%. Analysis of the isoforms (subgroups) of CK-MB and CK-MM may allow early diagnosis of MI, detection of reperfusion,185 and estimation of the size of an MI. A study of autopsy-proven MI found that CK-MB had the best association with MI, whereas LDH, greater than LDH2 was the next best indicator.ls6 Other enzymes, which are useful for the diagnosis of PMI, include aspartate aminotransferase (AST). Myoglobin is released in the serum 90 minutes after the onset of MI. The serum leve1 returns to normal within about 36 hours after the onset of MI. Myoglobin has limited sensitivity and specificity for the diagnosis of PMI. 177Patients with a delayed peak of serum myoglobin leve1 had postoperative cardiac failure,ls7 indicative of PMI. Serum levels of ventricular myosin fragments increase from postoperative day 3, reach a peak on postoperative day 7, and can be used for the diagnosis of PMI.lss SCINTIGRAPHIC

DETECTION OF PMI

The commonly used scintigraphic methods for the detection of PM1 are infarct-avid scintigraphy, perfusion scintigraphy, and radionuclide ventriculography.is9 Infarct-Avid Scintigraphy

Technetium-99m stannous pyrophosphate (99mTcPPi) complexes with calcium in the mitochondria of injured myocytes, in addition to the blood pool and bones. The accumulation is greatest in the myocardium when the coronary blood llow (CBF) is reduced to 20% to 40% of normal. The 99mTcPPi scintigrams may become positive 12 hours after MI and are most likely to be positive 72 hours after the MI. Most scintigrams become negative after 1 week. Increased 99mTcPPi uptake may also be observed in remote MI, ventricular aneurysm, and cardioversion. Planar or single photon emission computed tomographic (SPECT) scintigrams may be obtained. At least 3 grams of myocardial necrosis must be present to be detected by planar scintigraphy. With SPECT imaging, smaller areas of necrosis may be detected. Planar imaging has a high sensitivity for the detection of transmural MI, but is insensitive for the detection of subendocardial MI. Virtually al1 the studies on PM1 have used planar imaging. The sensitivity and specificity of planar scintigraphy for the diagnosis of PM1 is higher than that of new Q waves on the ECG.153~‘59SPECT imaging offers improved sensitivity for the detection of subendocardial MI. The incidence of PM1 with SPECT imaging was reported to be 21%, the vast majority of them being non-Q wave MI.’ Indium-1 11 or technetium-99m labelled antimyocin murine monoclonal antibody binds to intracellular myosin in injured cells.190~191 The antibody accumulation is inversely related to myocardial perfusion. The antibody can be injected soon after the onset of chest pain and scintigraphy can be performed 18 to 48 hours later. The scintigrams may

show diffuse uptake or localized uptake. Antimyosin scintigrams in many cases of unstable angina are similar to those for non-Q wave MIS. Patients with severe ischemia or stunned myocardium usually do not have any myocardial uptake. In a study of 23 patients with stable angina undergoing CABG, 82% had postoperative uptake of antimyosin antibody with 12 patients having localized uptake and 7 patients having diffuse uptake. The localized uptake was consistently situated in the grafted areas. Perfusion knaging With Single Photon-Emitting Radionuclides

Thallium-201 accumulates in the myocytes in proportion to the perfusion. Virtually al1 patients with acute MI have thallium scintigraphic defects within 6 hours. At 24 hours, half of the non-Q wave MIS may no longer be detected. This may be because of a reduction in the peri-infarction ischemic zone or spontaneous recanalization of the infarctrelated artery. Reinjection may allow the detection of redistribution in what may otherwise be considered to be a fixed defect. Perfusion imaging cannot distinguish a new MI from an old MI or star. Perfusion imaging can also be performed with 99mTc isonitrile.r9* Compared to thallium-201, the clearance of these agents from the myocardium is slower and the redistribution is less. These agents are more suitable for SPECT imaging than thallium-201. Radionuclide Ventkulography

First-pass or multigated equilibrium (MUGA) radionuclide ventriculography can provide an assessment of the left and right heart ejection fractions, regional wal1 motion, and the overall functional status of the heart.193-*9aThis technique cannot distinguish MI from reversible ischemia and myocardial stunning. Several studies of PM1 have used this technique.l’j2 Multigated ventriculography is suitable for continuous perioperative monitoring using a nuclear probe, which may be held in a vest. Thus, this technique may be used for detecting the onset of MI. The first-pass technique is suitable for evaluating the right as wel1 as the left ventricle, whereas the multigated technique is primarily suitable for evaluating the left ventricle. Intraoperatively, this technique has been largely supplanted by echocardiography, which may provide more detailed information with less expensive and smaller equipment while avoiding the radiation exposure. Radionuclide ventriculography may be able to provide a more accurate estimation of left ventricular ejection fraction compared to echocardiography. Positron Emission Tomography

Positron emission tomography can noninvasively provide extensive information about regional myocardial metabolism. Regional myocardial glucose uptake can be measured using i8F 2-fluoro-2-deoxyglucose (FDG). This can be used to predict the viability of ischemic myocardium. Abnormal wal1 motion in regions with adequate glucose uptake on FDG imaging is predictive of ischemic but viable myocardium.199 This tissue is most likely to benefit from coronary

616

revascularization. lf both thc wal1 motion and glucose uptake are depressed, the injury is irreversible. Though this technique can be used to diagnose PMI, it is generally not used for this purpose because of the expcnse and thc limited availability of the equipment. which is not portable. ECHOCARDIOGRAPHY

Echocardiography has been used for the detection of PMI.zn0,201Reduced wal1 motion and loss of wall thickening are indicative of PMI.202 The sensitivity and specificity of these changes for the detection of PM1 may be higher than that of some other tests such as the ECG. One advantage of echocardiography is that it can provide substantial amounts of information about the anatomy and function of the heart. The technique is suitable for real-time monitoring. Contrast echocardiography20” provides information about regional myocardial perfusion and can detect PMI. Air bubbles provide good contrast, but have to be injected into the left circulation for the best results. Sonicated albumin microspheres, which may be injected intravenously, are now being used to obtain contrast echocardiograms of the ventricular myocardium. Tissue characterization by integrated backscatter is useful for differentiating among normal, ischemic, and infarcted myocardium. These techniques require special hardware and software, which are generally not available in commercial echocardiographic systems. With the development of these modalities, echocardiography is likely to become a preferred technique for the detection of PMI. At the present time, echocardiography is not widely used for the detection of PMI, primarily because of the expense, lack of widespread familiarity with the technique, and the difficulty in performing a transthoracic examination in the immediate postoperative period. Cardiac function may be evaluated by stress echocardiography. Stress may be elicited by exercise or pharmacologic agents such as dobutamine and adenosine. These techniques may be useful for evaluating perioperative changes in cardiac function. However, they are not currently in widespread use for the detection of PMI. DRUG THERAPY TO REDUCE PMI

As discussed in the section on cardioplegia, many drugs have been evaluated for myocardial protection during CPB. As discussed in the section on ischemia, treatment of preoperative ischemic episodes by nitrates may not reduce the incidence of PMLx7 Nicardipine administered just prior to CPB may provide myocardial protection during CPB.204 Propranolol administered just before aortic occlusion may also be associated with modest reduction in the size of MI.2”5 Post-CPB infusion of nifedipine in the minimum dose of 10 p,g/kglh was found to reduce the incidence of MI and post-CPB ischemia, compared to the infusion of nitroglycerin in the minimum dose of 1 p,g/kg/min.169~206,206a~206~ After CABG, the distal anastomoses are reported to occlude at an approximate rate of 10% to 15% during the first month, 16% to 26% during the first year, 2% per year during the next 5 years, and 5% per year for the next 5

years.“” Long-term trcatment wjith antiplatelet and antico agulant drugs can rcduce the occlusion rate.“‘,L”T-“? Thc antiplatelet drugs that have been uscd are aspirin. dipyridamole, sulfnpyrazone, triflusal, and ticlopidine.l’? Heparin and coumadin have been used for anticoagulation. In somc of thc clinical trials that did not fìnd aspirin to hc eficacious, the treatmcnt was started more than 72 hours postoperatively. Trials that initiated therapy within 24 hours found a beneficial effect of aspirin. Compared to t hc aspirin treatment group, the control group was reported to have a 16% grcater incidencc of graft occlusion.?ld Aspirin therapy may be cspecially beneficial for vessels with diameters up to 2.5 mm.?” Different dose levels and combinations with other drugs did not change the cfficacy of aspirin.- IC1In various types of vascular diseases. no additional benefìt was found when dipyridamole was added to aspirin. Continued treatment beyond 3 months after surgery may not significantly improve thc results. Choice of anesthetic agent has not been shown to affect the incidence of large MIs.?‘~ Howevcr, on the basis of thc present data, it cannot be stated that anesthetics have no influence on the occurrence of PMI. PROGNOSIS AFTER PMI

Some studies found that PM1 did not adversely affect the prognosis, whereas others found an adverse effect.ZJx,21y The studies that did not find an adverse effect include those that found that PM1 may not reduce surviva1116,22’Jor the resting left ventricular (LV) performance.221 For patients who survived PMI. the long-term functional status was found to be no different from that of the patients who did not have PMI.li4 Patients with PM1 were found to have a benign clinical course.153 Thc reduction in LV ejection fraction after PM1 was detected early postoperatively and did not change signifìcantly during prolonged follow-up.‘” Postoperative clinical course and mortality were not found to be affected by the occurrence of new Q waves.i63 In a study of 328 patients, it was found that silent ischemia detected by ambulatory ECG monitoring during the first year after CABG in patients with predominantly good LV function was not associated with new cardiac events.22X The studies that found an adverse effect of PM1 include those that found that PM1 decreases surviva19h,2Z4-22hand exercise ability.220 The risk was higher in the presencc of poor LV function and inadequate revascularization.?” In a study of 1,340 CASS patients,Z24 the hospita1 mortality was found to be 10% in patients with new Q waves and 1% in patients without new Q waves. In both groups, the 3-year mortality after hospita1 discharge was 5%. Patients with PM1 had a 51% probability of remaining free of new cardiac complications at 2 years, whereas patients without PM1 had a 96% probability. ‘17The 5-year survival was 76% in patients with PM1 and 90% in patients without PMLy6 PM1 was found to be an important predictor of late survival, surpassed only by LV function, age, and the number of associated illnesses.2Z” PM1 was found to be associated with higher operative mortality, but cardiac status and late survival were not affected by it in S-year follow-up.l’h In

617

MI DURING CABG

patients with PMI, increased incidence of late MIsz and CHF2z9 have been reported. The prognosis is worse in patients who have postoperative ischemia detected by ECG dysfunction in the immediate monitoring. 230 Ventricular postoperative period is common even in the absente of PMI 231,232 Because of PMI, the overall rate of MI in patients having CABG may be higher than that in medically treated patients for a period of 10 years.233,234 However, the incidence of death after MI is lower in patients who had CABG.234 Better results are associated with a more complete revascularization. 235 Because of the occurrence of PM1 and other adverse sequelae in the perioperative period, the overall outcome with CABG may not be superior to that with medical therapy.236~2iy The saphenous

vein grafts become atherosclerosed coronary arteries.237-244

at a higher rate than the

FUTURE RESEARCH

The interplay of various factors that lead to PM1 needs to be elucidated.245 Sensitive, specific, and convenient tests for the identification of PM1 need to be developed. Once this is done, prevention and management of PM1 may be optimized. Perioperative drug therapy for this purpose needs to be developed. The effect of various types of PM1 on prognosis needs to be studied in much greater detail. ACKNOWLEDGMENT

The author thanks Mary-Louise Ganley

for expert

editorial

assistance.

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Myocardial infarction during coronary artery bypass surgery.

REVIEW ARTICLE Myocardial Infarction During Coronary Artery Bypass Surgery Uday Jain, PhD, MD P ERIOPERATIVE myocardial infarction (PMI) is o...
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