What is appropriate secondary prevention after acute myocardial infrartion?

Aspirin
Aspirin at low to medium doses (75–325mg daily) reduces mortality, reinfarction and particularly stroke by 10–45% after myocardial infarction. It has been estimated that there is about one serious haemorrhage, gastrointestinal or intracerebral, for every event prevented. At the moment there is no comparable evidence for dipyridamole, ticlopidine or clopidogrel.

Beta blockers
There is overwhelming evidence for the beneficial effect of beta blockers, both within the first few hours of myocardial infarction and for up to three years afterwards. Reduction in mortality ranges from 15 to 45%, almost all of it accounted for by fewer instances of sudden death. All beta blockers appear equally suitable, except those with partial agonist activity. The contraindications are controversial, but most would include asthma, severe heart block and otherwise untreated heart failure, but patients
with poor left ventricular function benefit most. In asthmatic patients, particularly, heart rate limiting calcium channel blockers (verapamil or diltiazem) may be useful alternatives to beta blockers in the absence of uncontrolled heart failure.

Lipid-lowering drugs
The large secondary prevention trials with simvastatin and pravastatin (4S, CARE, LIPID) have demonstrated unequivocally the value of cholesterol lowering even in patients with “average” total LDL cholesterol levels of about 5mmol/l. It is arguable that any patient who has had a myocardial infarct should be offered treatment with a statin on the basis that their level of LDL cholesterol is too high for them. However, this is not orthodox practice at present. The previous practice of only measuring cholesterol levels some months after an infarct should be abandoned and the levels assayed on admission at the same time as cardiac enzymes. This gives a reliable figure for usual cholesterol levels: a delay of a couple of days in sampling will not. Following the VA-HIT study treating patients with HDL cholesterol levels 1 mmol/l with a fibrate should be considered but again is not yet established practice.

ACE inhibitors
These drugs would of course be used in patients with symptomatic heart failure but should also be used in asymptomatic patients with ejection fractions <40%. This is associated with significant decreases in mortality (20–30%) and in sudden death, as well as in reinfarction. All ACE inhibitors so far tested share these effects. Treatment should be started within 1–2 days of the infarct and should be continued indefinitely. Whether all patients should be given these drugs post-infarction, in the absence of
contraindications, is a more difficult issue. In unselected populations the benefits of treatment are much less clear cut. However, data from the recent HOPE trial1 suggest substantial risk reduction for higher risk vascular patients – which may include a large proportion of patients who have suffered a myocardial infarction. Other ongoing trials (such as EUROPA, using Perindopril) may help clarify this issue.

Other action
In addition to these relatively specific measures, diabetes and hypertension must of course be treated as required, and smoking discouraged. Some have advocated the use of fish oils especially in dyslipidaemic patients, either as supplements or as fish. The use of warfarin has been controversial for many years. It is highly effective in preventing cardiovascular events, particularly stroke, but at the cost of more adverse effects than aspirin and the inconvenience of monitoring. It is therefore not recommended for first-line use by most cardiologists.

Finally, it should be remembered that all of this translates into a considerable burden for our patients. Evidence-based medicine will lead to the prescription of 4 or more drugs, usually indefinitely. We must be prepared to make a case for the patient to accept that it really is worthwhile. At the moment, for whatever reasons, most of these proven measures are underused.