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Ventricular tachycardia (VT) in the setting of previous myocardial infarction is usually related to scarring or ischaemia. When ischaemic heart disease is not the cause, the management and long-term prognosis are different.
A man of 64 was transferred to a tertiary interventional centre for coronary assessment. In the previous six weeks he had been admitted twice to his local hospital with VT. On each occasion he gave a history of sweating, nausea and palpitations; there was no associated chest pain, breathlessness or syncope. 11 years previously he had had a myocardial infarction, but the only risk factor for ischaemic heart disease was smoking in the past. On examination, the heart rate was 250/min, without haemodynamic compromise or any other abnormal findings. The electrocardiogram (Figure 1a) showed a broad complex tachycardia. Peak creatine kinase was 248 iu/L and troponin I was raised at 2.95 μg/L. Chest X-ray showed borderline cardiomegaly. On each occasion the patient was successfully cardioverted with an intravenous bolus of 100 mg lidocaine. After the second episode, oral amiodarone was prescribed.
On transfer the patient was in sinus rhythm (Figure 1b). Coronary angiography and ventriculography showed no abnormality. On echocardiography, left ventricular size and function were normal but the right atrium and right ventricle were dilated with impaired function. On MRI (Figure 2) the right ventricular free wall appeared thin, with the suggestion of small aneurysmal pockets and fatty infiltration. These findings were consistent with a diagnosis of arrhythmogenic right ventricular dysplasia (ARVD). The patient was treated with a beta-blocker and an angiotensin converting enzyme inhibitor and fitted with an implantable cardiac defibrillator. The amiodarone was discontinued because of previous thyroid dysfunction when taking this drug.
ARVD is a cardiomyopathy characterized by localized or widespread fibro-fatty infiltration of the right ventricular myocardium. The consequences include right heart failure and ventricular arrhythmias with left bundle branch block morphology, and risk of sudden death.1,2 This condition most commonly presents in the second to fourth decades of life and has a male predominance. In some 50% of cases it is hereditary,3,4 but in the present case there was no family history of heart disease or sudden death.
In this case, the history of myocardial infarction led to an erroneous preliminary diagnosis of VT related to coronary artery disease. The basis of this past diagnosis remains unknown. The patient stated, however, that he had required cardioversion on two occasions during that illness. It was also at this time that amiodarone therapy was initiated—subsequently discontinued because of thyroid dysfunction. It seems possible, then, that this episode was in fact a primary arrhythmic rather than ischaemic event.
The electrocardiographic findings shown in Figure 1b are typical, with left axis deviation, partial right bundle branch block, T wave inversion in leads V1 to V3, and post-excitation potentials called epsilon waves.5 The record made during tachycardia shows a left bundle branch block morphology and inferior QRS axis consistent with an origin near the right ventricular outflow tract. Together with the MRI evidence of right ventricular dysfunction and fatty infiltration of the myocardium6 these features are diagnostic for ARVD.4
The management of ARVD centres on prevention of arrhythmia and sudden death as well as treatment for heart failure. Implantation of a defibrillator allows immediate termination of life-threatening arrhythmia.7 For refractory heart failure, cardiac transplantation is a final option.