Surgical versus non-surgical management of patients soon after acute myocardial infarction

Of 510 patients admitted to hospital with acute myocardial infarction, 34 had coronary artery bypass grafting before discharge (6-43 days (median 20) after infarction). The patients who were given grafts generally had a smaller infarction with less functional impairment than the 476 patients who were not. The outcome of coronary artery bypass grafting was investigated in a retrospective matched pair study. Patients were matched on the basis of the presence of postinfarction angina, left ventricular ejection fraction, location of the infarction, peak creatine kinase activity, Killip clinical class, and severity of coronary disease with 34 patients who were given medical treatment only. At one year follow up fewer of the operated patients had symptoms than did the matched non-operated patients. Survival at one year in the operated and non-operated groups respectively was 94% vs 91%; angina within one year occurred in 3% vs 68%; congestive heart failure in 3% vs 6%; and 0% vs 32% were referred for later bypass grafting or coronary angioplasty. It is concluded that coronary artery bypass grafting can be performed safely soon after myocardial infarction provided that left ventricular function is not seriously compromised. Such treatment is more effective than medical treatment for relief of angina during the first year after infarction.     

Stepwise risk stratification soon after acute myocardial infarction

A stepwise rise stratification procedure sequentially combining historical and clinical characteristics and treadmill exercise test results was applied to 702 consecutive men aged ≤70 years who were alive 21 days after acute myocardial infarction (Ml). Historical characteristics alone (prior Ml and prior angina or recurrence of pain in the coronary care unit) identified 10% of patients with the highest rate of reinfarction and death within 6 months (18%). Clinical contraindications to exercise testing identified another 40% of patients with an intermediate rate of cardiac events (6.4%). In the 50% of patients who underwent treadmill testing 3 weeks after Ml, the rate of cardiac events within 6 months was 4.4%: 3.9% in patients with a negative test and 9.7% in patients with a positive test (ischemic ST-segment depression ≥0.2 mV and a peak heart rate ≤135 beats/min). Patients with negative treadmill tests, who comprised 46% of patients ≤70 years and 53% of patients ≤60 years, had a cardiac death rate of <2% in the 6 months after Ml. The stepwise classification procedure correctly classified 72% of patients with hard medical events within 6 months. Thus, most patients who experience subsequent cardiac events are correctly classified on the basis of historical and clinical risk characteristics. In patients without these risk characteristics, early treadmill testing is useful for further discriminating high-risk from very low risk patients.     

Exercise testing soon after myocardial infarction.

Forty-six men under age 70, without clinical congestive heart failure or unstable angina pectoris, performed treadmill tests 3, 5, 7, 9 and 11 weeks after myocardial infarction. Patients were more frequently able to perform moderate exertion (2 mph, 14% grade) at 7 and 11 weeks than at 3 weeks following infarction. Ischemic ST-segment depression, usually unaccompained by angina pectoris, occurred in 45% of patients and was associated with a significantly increased incidence of subsequent coronary events. The presence of exercise-induced ventricular ectopic activity provided little independent prognostic information. No serious complications occurred in 210 tests. Exercise testing soon after myocardial infarction provides objective information concerning the capacity to resume physical activity, including return to work. Two tests, at 3-5 weeks and at 7-11 weeks, appear to provide most of the information contined in five tests performed during this time.     

ST-segment re-elevation and left ventricular expansion soon after acute anterior myocardial infarction.

The sum of ST-segment elevation (sigma ST on V2-4) was measured to evaluate ST-segment re-elevation during early convalescence in 57 patients with acute myocardial infarction. Following rapid ST-segment elevation resolution during the first 12 h, sigma ST again increased in many patients without signs of reinfarction or pericarditis, reaching a maximum approximately 5 days after onset. The magnitude of this re-elevation (delta sigma ST) was less than 0.3 mV in 30 patients (group A), and 0.3 mV or more in another 27 (group B). Based upon left ventriculography, the global ejection fraction in group B decreased significantly from 51 +/- 10% at the acute phase to 46 +/- 10% at the chronic phase. No such decreases were seen for group A. Regional ejection fraction in the infarcted portion improved significantly from 28 +/- 13% at the acute phase to 35 +/- 14% at the chronic phase in group A, but did not improve in group B. In addition, the non-infarcted portion in group B showed a significantly reduced regional ejection fraction. These results suggest that myocardial expansion of the infarcted portion may contribute to ST-segment re-elevation, an ominous sign of left ventricular dysfunction soon after acute myocardial infarction.     

Exercise training soon after myocardial infarction

To assess the cardiovascular effects of exercise training soon after clinically uncomplicated myocardial infarction, 70 men (mean age 54 years) underwent gymnasium training (no. = 28), home training (no. = 12) or no training (no. = 30) 3 to 11 weeks after the acute event. During this 8 week interval functional capacity increased significantly (P < 0.001) in all three groups: gymnasium training, 66 percent; home training, 41 percent; and no training, 34 percent. Peak functional capacity at 11 weeks was 11.0 ± 1.6, 10.3 ± 1.4 and 9.4 ± 1.8 (mean ± standard deviation) multiples of resting energy expenditure (METs) in the three groups—values approximating those of sedentary men of similar age without coronary heart disease. Functional capacity increased more in the gymnasium training group than in the no training group, but this difference was statistically significant only in patients without exercise-induced ischemie S-T segment depression or angina pectoris (P < 0.01). Another “training effect”—diminished heart rate response to submaximal work—was also observed in all three groups. It is concluded that (1) symptom-limited treadmill exercise testing performed soon after clinically uncomplicated myocardial infarction is feasible and safe and provides useful guidelines for physical reconditioning. (2) Patients who demonstrate nonischemic responses to treadmill exercise testing soon after infarction may safely undergo unsupervised exercise training at home. (3) Formal exercise training may not be required to restore functional capacity to nearly normal values soon after clinically uncomplicated myocardial infarction.     

Clinical implications of coronary arteriographic findings soon after non-Q-wave acute myocardial infarction

A significant incidence of death and myocardial infarction after non-Q-wave infarction belies the earlier impression that it is less serious than Q-wave infarction. Coronary angiography in the early stages after non-Q-wave infarction shows a progressive increase in the number of totally occluded vessels. This is paralleled by an increase in number of collateral vessels. Thrombus also becomes increasingly prevalent over the week after non-Q-wave infarction, and plays a role in 30 to 40% of infarctions.     

Bivalirudin versus unfractionated heparin in patients undergoing percutaneous coronary intervention after acute myocardial infarction.

BACKGROUND: Bivalirudin is replacing heparin as the anticoagulant agent of choice for elective percutaneous coronary intervention (PCI). This study aimed to assess the safety and clinical outcomes of bivalirudin versus unfractionated heparin (UFH) in patients undergoing PCI for acute myocardial infarction (AMI). METHODS: A cohort of 672 consecutive patients presenting with AMI without prior thrombolytic therapy were treated with either bivalirudin (216 patients) or UFH (456 patients). Platelet glycoprotein IIb/IIIa inhibitors were administered at the operator's discretion. The in-hospital, 30-day, and 6-month outcomes of the two groups were compared. RESULTS: Baseline clinical and angiographic characteristics were similar between the groups. In-hospital complications were similar, although there was a trend of a less major hematocrit drop in the bivalirudin group (0.9% vs. 3.1%, P=.09). All clinical outcomes were similar between the groups at 30-day and 6-month follow-ups. There was no statistical significance for acute thrombosis and subacute thrombosis between the groups, and there was no late thrombosis from either group. The event-free survival rate was similar between the groups (P=.41). CONCLUSION: The use of bivalirudin in patients undergoing PCI after AMI is safe and feasible. Bivalirudin should be considered as an alternative anticoagulant agent during PCI to treat patients presenting with AMI.     

The safety of static-dynamic effort soon after myocardial infarction

Many activities of daily living require static-dynamic effort. To evaluate the safety of such effort 3 weeks after myocardial infarction, 27 male patients underwent a weight-carrying test requiring 5 minutes of treadmill ambulation with graded weight loads of 10 to 30 pounds. The hemodynamic responses with weight carrying were compared to that of a predischarge graded dynamic exercise test. The peak heart rate was significantly lower (p less than 0.01) with weight carrying, the peak systolic blood pressure did not differ, and the diastolic pressure was significantly higher (P less than 0.01). ST segment depression and angina pectoris occurred less frequently with weight carrying. The type and frequency of ventricular arrhythmias were similar between the two tests. We conclude that many men are capable of performing static-dynamic activity equivalent to carrying up to 30 pounds by 3 weeks after myocardial infarction.     

Surgical treatment of acute myocardial infarction

In 1989 the following indications for surgical treatment of acute myocardial infarction are: (1) acute evolving myocardial infarction less than 6 h from onset, in patients in whom percutaneous transluminal coronary angioplasty (PTCA) or streptokinase (SK), depending on the coronary anatomy, has been unsuccessful; if single vessel disease, coronary artery bypass grafting (CABG) is unlikely; if multiple vessel disease, CABG is preferable to SK/PTCA unless a very major 'culprit' lesion can be identified with certainty; (2) postinfarction angina hours to days after a transmural myocardial infarction unyielding to maximal medical therapy and in patients with a coronary artery obstruction not amenable to PTCA; (3) occlusion of a coronary artery during cardiac catheterization that cannot be fixed by PTCA and/or SK; (4) occlusion of a coronary artery during PTCA causing hemodynamic obstruction and a threatened myocardium subtended by the obstructed coronary artery; (5) balloon-dependent patients in cardiogenic shock without mechanical defects who have adequate residual left ventricular function as determined by regional wall motion studies; (6) ventricular septal defect secondary to myocardial infarction unless there is terminal organ damage; (7) mitral valve replacement with coronary bypass for acute papillary muscle rupture; (8) semi-emergency cardiac transplantation, either with or without a mechanical bridge to transplant in young individuals (less than 50 years) who have suffered massive destruction of left ventricular myocardium by an acute coronary occlusion with or without recurring ventricular tachyarrhythmias. Ejection fraction in this clinical category is always under 0.20 and usually under 0.15.     

Surgical therapy of acute myocardial infarction

All over the world the therapy of acute myocardial infarction has concentrated upon saving the ischaemically injured, but still viable cells of the myocardium. Also the acute coronary surgery, which among our groups of coronary-surgical patients has a proportion of 3.5% with 41 patients, answers this purpose. The preferred indication groups for acute coronary-surgical operations are the occlusion of the vessel after coronary dilation and the condition after intracoronary fibrinolysis. In these 22 patients the hospital lethality was only 4.5%. The reasonable active approach in acute myocardial infarction, particularly the combination fibrinolysis - acute coronary surgery, is a hopeful enlargement of the previous therapy for the highly imperilled patients with myocardial infarction.     

Transient myocardial ischaemia after acute myocardial infarction.

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Silent myocardial ischemia after acute myocardial infarction.

Silent ischemia after myocardial infarction has definite prognostic significance but should be interpreted within the context of other prognostic indicators. The rationale for therapeutic intervention is based on the prognostic implications of silent ischemia and the potentially deleterious effect of repeated episodes of ischemia on the integrity of the left ventricle. We measured parameters of ischemia in 20 patients who showed asymptomatic ischemic ST-T changes on exercise testing in the early phase after myocardial infarction. After diltiazem administration, a reduction of exercise-induced ST-T depression from 2.3 +/- 0.8 to 0.7 +/- 0.6 mm (p less than 0.01) occurred, and regional wall-motion score at exercise, determined by radionuclide angiography, improved significantly (p less than 0.02). These and other observations warrant further studies in which the duration, severity and frequency of the ischemic episodes should be quantified and correlated with prognosis after myocardial infarction.