Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery.

Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude that intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion.     

Emergency coronary artery bypass surgery after intracoronary thrombolysis for evolving myocardial infarction

Sixteen patients underwent emergency coronary artery bypass surgery immediately after intracoronary streptokinase infusion for acute evolving myocardial infarction. Of these, 11 patients had 70% residual stenosis in the recanalised vessel, and in five thrombolysis was unsuccessful. There were no hospital deaths. All the patients sustained myocardial necrosis, the peak activity of creatine phosphokinase correlating with the time to reperfusion. Chest tube drainage (mean 960 ml) was significantly higher than for control patients but did not correlate with the total dosage of streptokinase. No patients had further myocardial infarction or developed recurrent angina. Selected patients may benefit from coronary bypass surgery after intracoronary streptokinase infusion. If necessary this may be performed immediately with low mortality and morbidity.     

Emergency coronary artery bypass surgery after intracoronary thrombolysis for evolving myocardial infarction.

Sixteen patients underwent emergency coronary artery bypass surgery immediately after intracoronary streptokinase infusion for acute evolving myocardial infarction. Of these, 11 patients had 70% residual stenosis in the recanalised vessel, and in five thrombolysis was unsuccessful. There were no hospital deaths. All the patients sustained myocardial necrosis, the peak activity of creatine phosphokinase correlating with the time to reperfusion. Chest tube drainage (mean 960 ml) was significantly higher than for control patients but did not correlate with the total dosage of streptokinase. No patients had further myocardial infarction or developed recurrent angina. Selected patients may benefit from coronary bypass surgery after intracoronary streptokinase infusion. If necessary this may be performed immediately with low mortality and morbidity.     

Early percutaneous transluminal coronary angioplasty or coronary bypass surgery following thrombolytic treatment of acute myocardial infarction

Coronary reocclusion rates following intracoronary streptokinase (IC-SK) infusion remain significantly high despite anticoagulation. Early intervention by coronary angioplasty (PTCA) or coronary bypass surgery (CABG) was advocated to minimize such risk and/or maintain coronary reperfusion. Of 71 consecutive patients (60 men, 11 women; mean age, 54.9 years) who underwent IC-SK infusion for acute myocardial infarction (MI) 50 had early CABG, 18 had PTCA, and three had both procedures. Sixty-four of the 71 had successful thrombolysis. Thirty-six patients had either CABG or PTCA within three days, 22 patients within seven days, and 13 patients within two weeks. There was no immediate or in-hospital mortality, and all patients remained alive through the follow-up period of three to 36 months. Functional class (FC) 1 was achieved in 45 patients, FC 2 in 22 patients, FC 3 in three patients, and FC 4 in one patient. Sixty-seven patients (94 percent) were free of chest pain through the follow-up period. These data suggest that early intervention by CABG and/or PTCA in suitable candidates could be achieved with reduced risk and expected to yield favorable results. This favorable trend could be related to maintenance of myocardial perfusion by these procedures, initially induced by thrombolysis. Long-term, large-scale studies are needed to confirm the role of optimal timing of such procedures, but we believe that such results indicate that early revascularization yields promising results.     

Perioperative myocardial infarction in coronary bypass surgery

Thirteen of 199 consecutive patients undergoing coronary artery bypass surgery revealed definite perioperative myocardial infarction (PMI) in electrocardiography (ECG). The occurrence of PMI was not higher in the group of 44 patients who had intermittent aortic cross-clamping than in those patients treated with cold chemical cardioplegia. In 83 patients serum MB isoenzyme of creatine kinase (CK) and LD1 isoenzyme of lactic dehydrogenase were determined. Patients with unchanged ECG had peak CK-MB levels of 0 to 49 U/l (mean 18.7 U/l +/- 2.6 SEM) at 18 hours postoperatively while patients with PMI showed CK-MB levels of 64-350 U/l (mean 207 +/- 53 U/l); the difference was significant (p less than 0.01). In patients with unchanged ECG, LD1 was 139 +/- 19 U/l and 594 +/- 95 U/l in those with PMI (p less than 0.01). Risk factors for PMI were: age greater than or equal to 60 years, coronary endarterectomies, or cardiopulmonary bypass time greater than or equal to 100 minutes. One patient died of PMI while the remaining patients had postoperative courses comparable to those patients without PMI.     

Unstable angina and non-ST elevation myocardial infarction

Non-ST elevation acute coronary syndromes are responsible for approximately 1 million admissions to U.S. hospitals and twice as many to European hospitals each year. Thus, they are among the most common serious illnesses in adults, and are associated with an in-hospital mortality of approximately 5%. The most common cause is rupture of an atherosclerotic coronary plaque, resulting in subtotal coronary occlusion. Diagnosis is based on the clinical picture of retrosternal chest pain, aided by electrocardiographic findings of ST segment deviations and biomarker abnormalities (elevation of troponin and natriuretic peptides) and cardiac imaging (myocardial scans showing perfusion defects). Treatment involves antiischemic agents (nitrates and β blockers), antiplatelet drugs (aspirin, P2Y(12), and glycoprotein IIb/IIIa receptor blockers), and anticoagulants (unfractionated and low-molecular-weight heparins). Patients should undergo risk stratification, and those with high-risk factors should undergo coronary arteriography promptly with the intent to carry out coronary revascularization. Those at low risk should continue to receive intensive antiischemic and antithrombotic therapy. At discharge, patients should receive intensive lipid-lowering therapy with high doses of a statin, as tolerated.     

Unstable angina and non-ST-segment elevation myocardial infarction

Opinion statement In the last 20 years there have been enormous advances in our understanding of the acute coronary syndromes and how to manage patients presenting with them. In the 1980s, we began to understand the importance of thrombus formation was in the pathophysiology of acute coronary syndromes. Randomized studies also showed that appropriate antithrombotic therapy reduced the subsequent occurrence of myocardial infarction and death. In the 1990s, other therapeutic modalities and particularly percutaneous coronary intervention have come to the forefront as effective therapy in these syndromes. The glycoprotein IIb/IIIa receptor antagonists along with coronary stent implantation have proved extremely beneficial in short- and long-term management. We also have learned the importance of risk-factor modification in preventing subsequent events. In the future, greater efforts will focus on primary prevention.     

Unstable angina pectoris and non-Q-wave myocardial infarction

Unstable angina pectoris and non-Q-wave myocardial infarction are clinical syndromes that share many pathophysiologic and clinical features. In the spectrum of coronary artery disease, these syndromes lie between chronic stable angina and Q-wave myocardial infarction. Although both conditions are associated with significant morbidity and mortality, patients presenting with these syndromes can be further risk stratified into higher and lower risk based on a number of readily available clinical features and biochemical parameters. Such risk stratification can allow for more tailored treatment and better resource allocation. Although routine early coronary angiography and revascularization has not been shown to be superior to conservative management, certain high-risk patients may benefit from a more aggressive strategy. Medical therapy with the use of antiplatelet, anticoagulant, and antiischemic agents remains the cornerstone of emergent treatment for patients presenting with these syndromes. The recent demonstration of a reduction in both morbidity and mortality with the glycoprotein IIb/IIIa antagonists has further expanded the armamentarium of available agents. Following initial stabilization, risk stratification with stress testing can help identify patients with a large residual ischemic burden who may benefit from coronary angiography with revascularization if feasible.     

Unstable angina pectoris evolving to acute myocardial infarction: significance of ECG changes during chest pain

We retrospectively evaluated 32 patients with unstable angina (UA) and no evidence of increased oxygen demand during episodes of chest pain (no significant changes in heart rate and blood pressure), who developed an acute myocardial infarction (AMI) during the same hospitalization. Based on the type of ST changes during anginal pain, two groups were defined: Group A included 19 patients who developed ST elevation during AMI; 15 of these 19 patients (79%) were in Killip class I, two were in class II, and there was one patient each in classes III and IV, respectively. Only one of the 19 patients died. Group B included 13 patients who developed ST depression during AMI; nine of these 13 patients were in Killip class IV and the remaining four patients died before they could be evaluated. Ten patients died (77%) (p less than 0.01), seven in electromechanical dissociation and three in cardiogenic shock. Postmortem examination, performed in four patients, revealed total obstruction of the left main coronary artery. It is concluded that patients with UA who, during attacks of chest pain, develop ST depression and no evidence of increased oxygen demand may have a poor prognosis when they develop an AMI. This selected group of high-risk patients appears to need immediate intensive medical care and most probably early surgical treatment.     

Long-term results of coronary artery bypass surgery for unstable angina: incidence of mortality,myocardial infarction,and angina resumption

To determine if routine treadmill testing would be helpful in identifying patients at high risk for subsequent events, the first 81 patients to undergo coronary artery bypass0 surgery for unstable angina pectoris at Stanford University Medical Center were reevaluated at four intervals after surgery. Evaluations, including assessment of angina pectoris and a treadmill test, were done at mean times of 18,40, and 72 months after surgery. At a mean time of 90 months postoperatively, angina status was determined in survivors. The prevalence of angina rose from 19% during the first year to 53% during the fourth and fifth postoperative years. Cardiac deaths and myocardial infarctions were frequent during the first postoperative year, and were more frequent in patients with three-vessel disease and those with one or more severely narrowed coronary arteries which were not bypassed. Cardiac events were rare between 12 and 36 months after operation; clinical and treadmill variables did not predict these events. During the fourth and subsequent postoperative years, the incidence of cardiac events increased. While the presence of stable angina pectoris was the clinical variable most useful prognostically, treadmill testing added additional independent prognostic information (p<0.0001). During the intervals between visits 1 and 2, and visits 2 and 3, cardiac events were ten times more frequent in persons with a maximal heart rate of 130 beats/min or less on the treadmill at 18 and 40 months. We conclude that the prevalence of angina increased steadily during the first 5 postoperative years. Myocardial infarction and cardiac death rates were high during the first postoperative year, low during the second and third postoperative years, and then began to rise thereafter. The early events were more frequent in persons with three-vessel disease and one or more severely narrowed coronary arteries which were unbypassed. The late events were more frequent in persons with a maximal heart rate of 130 beats/min or less on treadmill exercise testing. No other clinical or treadmill variables added additional independent prognostic information.     

Unstable angina: current concepts of pathogenesis and treatment

During the past 15 years, we have learned an enormous amount about the pathogenesis and treatment of unstable angina. In most cases of unstable rest angina, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. However, any process that acutely changes the supply-demand ratio (decreased supply or increased demand in the presence of a decrease in supply) can precipitate the clinical presentation of unstable angina. Standard acute antithrombotic drug therapy is effective in decreasing progression to infarction. Newer agents (low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibitors) are more effective, and their use is evolving. Percutaneous intervention and bypass surgery can reduce symptoms and multiple hospitalizations, in most cases without a decrease in the long-term mortality rate. Because the cost of hospitalization is extremely high and the clinical presentation and outcome are heterogeneous, better triage methods are required.     

Congenital coronary aneurysms with angina pectoris and myocardial infarction treated with saphenous vein bypass graft

A young woman with bilateral congenital coronary arterial aneurysms associated with myocardial infarction and angina pectoris was successfully treated with a saphenous vein bypass graft. Possible clinical and laboratory manifestations of such aneurysms are discussed, and possible complications of saphenous vein graft surgery in treatment of this lesion are noted. The finding of coronary arterial aneurysms during coronary arteriography warrants close follow-up study since in many patients the lesion appears to progress to myocardial infarction.     

Perioperative myocardial infarction related to coronary bypass surgery.

Frank lead electrocardiograms were recorded from 149 normal and abnormal adult males using four different electrode placements. All chest electrodes were placed at: (1) the fourth intercostal space level, (2) the fifth intercostal space level, (3) the fourth intercostal space level with V₄ substituted for C, and (4) the fifth intercostal space level with V₄ substituted for C.Differences in mean values of many commonly used amplitudes and orientations were not statistically significant among the four recording methods, but amplitude differences for individual subjects were often large and difficult to predict. When V₄ is substituted for C, as commonly done in some laboratories, R_x decreased and R_z increased by more than 10 per cent in about 40 per cent of the cases. In about 70 per cent of the cases, R_x and R_z changed significantly when electrode level was shifted from the fifth to the fourth intercostal space. For these 70 per cent, it does not appear possible to accurately predict increase or decrease of R_x, R_z, or QRS_m.Analysis programs which depend on individual amplitude measurements are likely to be significantly affected by electrode placement. It is suggested that criteria for analysis programs developed using a specified version of the Frank system should ideally be applied only to electrocardiograms recorded in the same manner.     

Early ambulation physical activity: myocardial infarction and coronary artery bypass surgery

The accepted pattern of care for the patient recovering from myocardial infarction or coronary bypass surgery in the 1980s is characterized by an earlier resumption of physical activity, a consequent decrease in imposed invalidism, and earlier discharge from the hospital for appropriately selected patients. Early ambulation has been demonstrated to be desirable, feasible, cost-effective, and safe.     

Timing of coronary artery bypass graft surgery following acute myocardial infarction: a critical literature review

Despite more than 30 years' experience with coronary artery bypass surgery, controversy still exists about the optimal timing of surgical revascularization following acute myocardial infarction. To review the published information on this topic, a Medline search of the literature published between 1984 and October 2000 was performed. After reviews and individual case reports we re excluded, 11 retrospective and prospective studies remained for analysis. Pervasive heterogeneity with respect to inclusion criteria, outcome measurement, definitions, variance among studies of measured time between myocardial infarction (MI) and coronary artery bypass graft (CABG), differences in study endpoints, and evolution of surgical techniques and medical regimens over this time precluded formal meta-analysis. Although prospective randomized trials are lacking, the preponderance of data from the 11 retrospective and prospective observational studies suggests that timing of bypass surgery after infarction is not an independent predictor of outcome and that delaying coronary bypass surgery for an arbitrary period of time following acute MI is unwarranted. Rather, ventricular function, post-infarction ischemia, noncardiac comorbid conditions, and the urgency of the surgery itself constitute the important predictors of perioperative mortality, and these clinical factors should be used to estimate perioperative risk and decide upon the risk:benefit relationship for CABG in this patient population.     

Unstable angina before and after infarction: thoughts on pathogenesis and therapeutic strategies

The pathophysiology of unstable angina both before and after infarction is incompletely understood, because the patient population with the diagnosis of unstable angina is not uniform and the definition of this condition is not precise. The question must be asked, "Why does a patient suddenly become unstable?" Several conditions can be responsible alone or in combination with each other. These conditions include extracardiac (aggravating) factors, rapid progression of coronary atherosclerosis, rapid decrease in coronary lumen size as a result of hemorrhage into an atherosclerotic plaque, transient platelet aggregation in severely diseased vessels, transient coronary artery thrombosis, and abnormal coronary artery vasoconstriction (spasm) in normal or diseased vessels. Fig. 1 summarizes a hypothetical scheme relating the above conditions to the degree of coronary artery stenosis. In patients with unstable angina before infarction, most investigators believe that severe coronary atherosclerosis and its consequences are the major pathogenic mechanisms when ischemic heart disease is present. If spasm is the mechanism, then the use of vasodilators is warranted. However, if thrombosis is clearly defined, then thrombolytic therapy in the early stages seems reasonable. If severe coronary artery disease is found (with or without thrombosis), therapy with anticoagulants such as intravenous heparin during the acute phase of the illness can be argued strongly. A similar argument could be made for the use of antiplatelet agents during the convalescent phase. If extracardiac (aggravating) factors are present, they must be corrected appropriately.(ABSTRACT TRUNCATED AT 250 WORDS)