Tachycardia-induced cardiomyopathy caused by atrial flutter responding to DC cardioversion

A58-year-old man presented in February 1996 to his local hospital with a true posterior myocardial infarction for which he received thrombolysis. He subsequently underwent exercise testing which was terminated because of chest pain and anterior ST depression of >2 mm after 6 minutes of a Naughton Balke protocol. He proceeded to coronary angiography which demonstrated severe triple vessel coronary artery disease. The left ventriculogram demonstrated posterior hypokinesis but overall left ventricular (LV) contractile function was well preserved with an ejection fraction (EF) calculated at 49%. He was in sinus rhythm and had chronic stable angina. In September 1996 he underwent revascularization on prognostic grounds. Five days postoperatively he developed atrial flutter for which he was started on amiodarone 200 mg once daily and subsequently discharged. Two weeks later he was readmitted with progressive dyspnoea and peripheral oedema. He was found to be in clinical heart failure and atrial flutter with a ventricular rate of 150. He subsequently underwent a successful DC cardioversion reverting to sinus rhythm following a single 200J DC shock. He was discharged on amiodarone 200 mg once daily, frusemide 80 mg once daily, enalapril 10 mg once daily and aspirin 75 mg once daily. In November 1996 he presented in atrial flutter with heart failure. An echocardiogram was performed showing a dilated hypokinetic left ventricle with an EF of approximately 20% (Table 1). He was anticoagulated and underwent a further DC cardioversion in February 1997 which successfully reverted him to sinus rhythm. Echocardiography was performed following reversion to sinus rhythm (Table 1) which revealed a dilated LV with global systolic dysfunction and functional mitral regurgitation (EF=30%). In April 1997 he reverted to atrial flutter and had significant effort dyspnoea with an exercise tolerance of 50 yards. He was again successfully cardioverted and commenced on sotalol 80 mg twice daily in an attempt to maintain sinus rhythm. He subsequently remained in sinus rhythm with a marked symptomatic improvement (New York Heart Association Grade 1 dyspnoea and no clinical evidence of cardiac failure). Echocardiography in July 1997 demonstrated a significant improvement in LV dimensions and systolic contractile function (EF=50%) with values equivalent to pre-surgery.