The success of thrombolytic therapy has increased the need for a management plan to be prepared for each postinfarct patient. The risks of reinfarction and sudden death should be assessed in every patient so that the most appropriate treatment can be selected. Unless contraindicated, all patients should be given aspirin and a beta blocker. An ACE inhibitor is added if there is significant left ventricular dysfunction. Warfarin should be used, instead of aspirin, if the patient is at risk of thromboembolism. Postinfarct patients should also be advised on how to control the risk factors for atherosclerosis.


The early management of patients with acute myocardial infarction has been clarified by several international multi centre trials. Protocols for giving thrombolytic therapy to patients who present within 12 hours of the onset of symptoms of acute myocardial infarction are now universal. However, there is less agreement about the management of patients in the post-infarct phase. The likelihood of death is highest during the acute phase of an infarct, and remains higher than for the general population. In this article, post-infarct management is considered to be from around the time of hospital discharge. This may be as early as 5 or 6 days after the infarction.


A number of factors contribute to the difficulty of deciding on appropriate post-infarct management.

First, post-infarct patients are at risk of a variety of events including unstable angina, reinfarction, heart failure, arrhythmias, systemic thromboembolism and sudden death.

Second, the risk of these events varies markedly from patient to patient so that each patient requires an individual assessment of risk. Thrombolytic therapy has actually accentuated this issue by increasing the heterogeneity of risk among post-infarct patients. The average mortality in the year after infarction has been reduced from approximately 10% in patients who do not receive thrombolytic therapy to 4% in those who do. However, only one third to one half of patients actually receive thrombolytic therapy after their infarct.

Third, many drugs have been recommended for the treatment of post-infarct patients. Most of the information about their efficacy was obtained in the prethrombolytic era and not all have been tested in randomised trials. Even for those drugs which are individually effective, there is limited information about their combination, particularly whether or not their effects are additive.

Natural history of the infarct

Coronary artery disease may result in further ischaemia including reinfarction. The presence of a substantial segment of infarcted myocardium may cause early heart failure. Late heart failure and death may result from progressive left ventricular dilatation and deterioration of left ventricular function. This process, known as remodelling, is initiated by expansion of the infarcted myocardium. It is more likely in large anterior infarcts, particularly if the blocked artery remains occluded. The infarcted myocardium may also be a focus for ventricular arrhythmias and for mural thrombosis and subsequent thromboembolism.

Assessment of prognosis

The extent of left ventricular damage is the major determinant of risk in post-infarct patients. There is a strong argument that left ventricular function should be measured in all post-infarct patients. Echocardiography is the easiest way of assessing the size and function of the infarcted myocardium as well as global left ventricular function. Radionuclide ventriculography, when available, also provides satisfactory information about left ventricular function.

In addition, all patients ought to go through a process of post-infarct risk stratification. There is good evidence that this stratification can be based on symptoms.

  • Patients with angina at rest or on mild exertion, and who are potential candidates for re-vascularisation, should undergo coronary angiography and appropriate intervention before discharge.
  • Mildly symptomatic patients should also be considered for angiography.
  • Asymptomatic patients should generally undergo exercise testing before or shortly after discharge and, if there is evidence of ischaemia, should also be referred for coronary angiography.
  • Patients with severe heart failure following acute myocardial infarction are at extreme risk of death and should be considered for investigation e.g. angiography with a view to urgent re-vascularisation.
  • Patients who experience serious ventricular arrhythmias beyond the first 48 hours should undergo electrophysiological testing to help in the selection of appropriate therapy.

Ischaemic events

Recurrent ischaemia may be a life threatening event for a post-infarct patient. It may occur as a result of reocclusion of the coronary artery which caused the infarct. Alternatively, in patients with multi vessel disease, it may originate from established stenoses in other arteries.

Patients who do not develop Q waves on their electrocardiogram and are assumed to have had a small transmural or subendocardial infarct require particular attention in relation to ischaemic events. Included among these are patients with aborted infarcts as a result of thrombolytic therapy. The amount of myocardium at risk may have been large or even life threatening as judged by the initial ST elevation on the ECG. However, recanalisation of the occluded artery aborts the large infarct and leaves the patient with a small infarct in relation to the territory at risk. Unfortunately, the coronary lesion may remain unstable with the potential for further occlusion and completion of the infarct. Many cardiologists regard the aborted infarct as an indication for angiography and revascularisation. If this has not been done, the recurrence of ischaemic symptoms in a patient who is left with a small infarct after thrombolysis should be treated with significant concern and urgency.

Post-infarct mortality is reduced by 20-25% with a beta blocker and by approximately 15% with aspirin. Both drugs significantly reduce the incidence of nonfatal ischaemic events. The mechanism of action of beta blockers is unknown, but the benefits have only been shown in beta blockers without intrinsic sympathomimetic activity. Aspirin has an antiplatelet effect decreasing the tendency for reocclusion of the original coronary lesion. The benefits of aspirin have been tested in a large number of trials using a range of doses. However, it is common practice to use 100 mg or 150 mg per day in post-infarct patients. Unless there are specific contraindications or the post-infarct risk is very low, all post-infarct patients should be treated with a beta blocker and aspirin. The duration of treatment has not been well defined. Maximum benefit occurs in the first 12 months. Beta blockers have been shown to have a prognostic benefit for up to 3 years. Both medications can be continued long term.

Left ventricular dysfunction

Left ventricular remodelling can continue for up to a year or more after infarction. In clinical trials, ACE inhibitors given to patients with post-infarction heart failure or with ejection fractions of <40% significantly reduced mortality, probably partly by attenuating left ventricular dilatation. There is ongoing debate as to whether ACE inhibitors benefit all post-infarct patients or just those at risk as a result of left ventricular dysfunction.

At present, common clinical practice is to give ACE inhibitors to all patients with significant left ventricular dysfunction or left ventricular failure, but not to give them routinely. This practice may be modified as more information becomes available. In the SAVE study1, captopril reduced mortality in patients on aspirin and beta blockers, indicating an independent beneficial effect of ACE inhibitors.

The reduction in post-infarct mortality by ACE inhibitors is probably a class effect since it also occurred in the SOLVD study using enalapril2 and in the AIRE study using ramipril.3 The doses of captopril (50 mg 3 times daily), enalapril (10 mg twice daily) and ramipril (5 mg twice daily) used in the SAVE, SOLVD and AIRE studies were quite high compared with those commonly used in clinical practice. It is not known if the lower, more commonly used, doses have a beneficial prognostic effect. In the light of current knowledge, it is appropriate that the doses used in the trials should be the target doses, unless adverse effects occur.

How long patients should be treated for is uncertain. In patients with symptoms of left ventricular dysfunction, the treatment will probably need to be lifelong. Since remodelling can occur for 12 months in asymptomatic patients, ACE inhibitor treatment should be for at least this long in this subgroup and there is a strong argument that it should be even longer.


Prevention of ventricular arrhythmias is one of the most challenging aspects of post-infarct management. All patients who have ventricular arrhythmias which require antiarrhythmic treatment should probably have the treatment selected by electrophysiological testing, although there is some recent evidence that empirical treatment with sotalol may be as effective. There is no place for empirical treatment with other antiarrhythmics because of the risk of proarrhythmic effects.

The role of electrophysiological testing in post-infarct patients who do not have overt ventricular arrhythmias is controversial. There is a consensus that it is not necessary in patients who have normal left ventricular function. Some cardiologists argue that testing should be performed routinely in patients who have impaired left ventricular function, particularly if complex ectopics are seen on the ECG or a Holter monitor. They argue that electrophysiology testing identifies patients at risk of sudden death and helps in the selection of appropriate treatment. This is not routine practice as it has not yet been tested in randomised clinical trials, so the best way of treating 'positive' patients is unknown.

Beta blockers are the only antiarrhythmic drugs which reduce sudden death after infarction, although some trials with amiodarone have shown promising results. There is a strong argument for the routine use of beta blockers post-infarction. There is no role for the empirical use of other antiarrhythmic drugs in post-infarct patients. All antiarrhythmics have the potential to provoke arrhythmias as well as decrease them and, in clinical trials, several Type 1 antiarrhythmics have been associated with an increase in mortality rather than a decrease.

Thromboembolic events

Systemic embolism occurs in approximately 3% of post-infarct patients, usually within 6 months of the infarct. The majority occurs in patients who have had anterior infarcts with the necessary condition for the formation of left ventricular thrombus appearing to be the presence of apical hypokinesis. Left ventricular thrombus can be identified by echocardiography. Echocardiographic features which make a thrombus more likely to embolise have been identified and a patient with a thrombus showing these features should be anticoagulated with heparin followed by warfarin. However, the absence of a thrombus on echocardiography does not exclude the possibility of a later systemic embolism.

Heparin in full anticoagulant doses decreases the incidence of ventricular thrombus formation in hospital patients with anterior myocardial infarction. In randomised trials of warfarin in myocardial infarction, the incidence of stroke has been decreased, presumably due to reduced thromboembolism. It is common clinical practice to anticoagulate patients who have had a large anterior infarct and who can take warfarin with an acceptably low risk for 6 months. These patients should not take aspirin as well.


Participation in a formal rehabilitation program can speed psychological and physical recovery and facilitate the return to work. When there is doubt about the propensity to myocardial ischaemia or left ventricular dysfunction, a rehabilitation program also provides a secure, professionally monitored environment for a gradual increase in activity. The effect of rehabilitation programs on the patient's quality of life after an infarction is difficult to measure. However, the benefits for individual patients can be quite dramatic. There is also some evidence that the exercise component of a formal rehabilitation program may reduce the risk of death. Formal rehabilitation programs should be available, and should be used, particularly if physical or psychological recovery is likely to be slow.

Secondary prevention of atherosclerosis

There is good evidence that controlling risk factors can slow the progression of atherosclerosis and reduce the incidence of ischaemic events. The recently published SSSS study4 demonstrated a significant reduction in total mortality in selected patients who had experienced a myocardial infarction or angina when their cholesterol was lowered with simvastatin.

Patients who have suffered a myocardial infarction are usually prepared to make lifestyle changes and advantage should be taken of this opportunity. Comprehensive risk factor modification, including control of hypertension and diabetes, must continue after infarction. Cessation of smoking is critical.

Patients with elevated cholesterol levels should have appropriate dietary therapy and, if necessary, drug treatment. Several studies are examining the question of whether or not patients with relatively normal cholesterol levels should have them lowered. However, it should be kept in mind that the serum cholesterol concentration is decreased for up to 3 months after an infarct, so that even when the concentration is normal immediately after the infarct, repeat measurements should be made several months later.


Patients who have suffered a myocardial infarction have an increased risk of death and reinfarction for up to one year afterwards, with the majority of events occurring a few weeks after discharge. Post-infarct patients with angina on no or minimal provocation, heart failure or ventricular arrhythmias are at extremely high risk. If any of these events occurs for the first time after discharge, the patient should be referred urgently for consideration of revascularisation, appropriate antiarrhythmic therapy or possibly implantation of a defibrillator.

All post-infarct patients should be treated with a beta blocker and aspirin unless there is a specific contraindication. Patients with significant left ventricular dysfunction should, in addition, be treated with an ACE inhibitor, particularly if they have had an anterior infarct. Patients who have had a large anterior infarct are at risk of thromboembolic events and should be considered for treatment with warfarin instead of aspirin for 6 months. Enrolment in a formal rehabilitation program will facilitate physical and psychological recovery and should be offered to patients whenever practical. Finally, those who survive the damage to their myocardium will eventually succumb to their coronary atherosclerosis and every effort should be made to reduce risk factors with a view to preventing further progression of the disease.

(See also Dental implications)

Self-test questions

The following statements are either true or false.

1. In addition to aspirin and a beta blocker, patients with large anterior infarcts should also be anticoagulated.

2. Cholesterol concentrations may be decreased for several months after an infarct

Answers to self-test questions

1. False

2. True


  1. The SAVE Investigators. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. N Engl J Med 1992;327:669-77.
  2. The SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992;327:685-91.
  3. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet 1993;342:821-8.
  4. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994;344:1383-9.