Three days following his myocardial infarction, the patient is doing well. He has had no heart failure, no recurrent angina and no evidence of heart block or ventricular arrhythmias. He is receiving aspirin 81 mg daily, clopidogrel 75 mg daily, metoprolol 50 mg bid, ramipril 5 mg daily and pravastatin 40 mg daily.
The patient was discharged home on the fourth day following myocardial infarction. In addition to the usual secondary prophylactic agents, he was also instructed to take 1 g/day of omega-3 fatty acid supplements (EPA/DHA), as this intervention has been shown in the GISSI-Prevenzione trial to lower the risk of arrhythmic death.12 An ICD was not implanted; however, a follow-up radionuclide angiogram was scheduled in three months’ time, to re-evaluate the patient ’s left ventricular ejection fraction.
Guidelines typically suggest waiting at least 40 days following myocardial infarction and 90 days following revascularization, to allow time for ventricular remodeling (positive or negative) and to ensure that the patient survives the early postmyocardial infarction period.2,13
Three months later, the patient was asymptomatic and still taking his medications. The follow-up ejection fraction was 38%. A Holter monitor was also completed and did not show any evidence of ventricular arrhythmias. The patient was seen in consultation by an electrophysiologist who discussed the potential role of an ICD (and its potential complications). A determination was made that an ICD was not indicated at the present time.
The patient was lost to follow-up for two years, but then returned to his primary care physician, having stopped his ramipril and beta-blocker due to side effects. His clopidogrel had already been stopped one year following his myocardial infarction. He remained asymptomatic with no shortness of breath on exertion, angina, syncope or palpitation. His blood pressure was now 175/100 and his ECG showed sinus rhythm at 80 beats per minute and an incomplete left bundle branch block (QRS width of 130 msec) and left axis deviation.
He was eventually restarted on a different beta-blocker and full doses of an angiotensin receptor-blocking agent. A follow-up radionuclide angiogram was done three months later and revealed a left ventricular ejection fraction of 29%. A repeat coronary angiogram showed a patent circumflex stent and no new coronary lesions. An echocardiogram showed a large posterolateral wall motion abnormality, an estimated left ventricular ejection fraction of 30-35%, moderate left ventricular hypertrophy and moderate mitral regurgitation. The primary care physician was reluctant to consider an ICD because the patient “was doing well” (i.e. no clinical symptoms). However, the patient had been doing some reading on the internet and wished to see his electrophysiologist to discuss his options.
The patient undergoes an uneventful placement of a single-chamber implantable defibrillator. Two years later, he has been compliant with medications and has not received any therapy from the ICD, nor suffered any adverse consequence.
What else can be done to reduce the chance of this patient dying suddenly?
This patient has suffered an acute ST elevation myocardial infarction that was complicated (<48 hours) by the development of ventricular fibrillation. In this context, the arrhythmia is often referred to as “primary ventricular fibrillation”1 although this term is often a source of confusion, as the arrhythmia is actually secondary to the acute myocardial infarction. Given the potential for confusion with “idiopathic ventricular fibrillation”, this term should probably be abandoned.
It is traditionally felt that ventricular fibrillation (VF) occurring within 48 hours of a myocardial infarction does not confer an increased risk of arrhythmic death and thus does not warrant specific therapy, such as an implantable defibrillator (ICD) or antiarrhythmic drugs.2 This is based on data from the GISSI-1 trial, which suggests that patients with this type of arrhythmia in the acute phase of an acute (AMI) have a similar prognosis to patients with comparable myocardial infarctions without VF.3 Accordingly, current guidelines suggest that an implantable defibrillator is not indicated in this setting (Class III).2
However, this decision is contingent on two key facts. First, the arrhythmia in question must be polymorphic ventricular tachycardia or ventricular fibrillation, as the occurrence of monomorphic ventricular tachycardia generally implies the existence of an arrhythmogenic substrate4 and an unfavorable prognosis,5 warranting specific therapy. Secondly, it should be clear that the arrhythmia in question occurred in the context of a definite myocardial infarction. As sustained ventricular arrhythmias may increase serum troponin (even in the absence of coronary artery disease), clinicians should have other corroborating evidence of myocardial infarction (history of chest pain, ECG changes, wall motion abnormality, occluded artery) before attributing a potentially lethal ventricular arrhythmia to an acute myocardial infarction.6
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