The patient was hospitalized in 2004 for unstable angina pectoris. A coronary angiogram demonstrated triple vessel disease, and he successfully underwent coronary artery bypass surgery.

In 2011 he was admitted to hospital because of a paroxysm of atrial fibrillation, which converted spontaneously to sinus rhythm during the stay.

During late winter 2012 the patient experienced increasing exercise intolerance and fatigue. He had no chest pain. He developed pitting edema of the lower extremities, which soon extended above his knees, and he had noticed intermittent palpitation. He had episodes of orthopnea, causing him to sleep sitting in a chair at night.

He was admitted to hospital on April 13, 2012 with signs of congestive heart failure. An electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular response, left bundle branch block (LBBB), and QRS width of approximately 160 ms. An echocardiogram the next day demonstrated a dilated left ventricle with an end-diastolic diameter of 66 mm and obvious dyssynchronous contractility. The left ventricular ejection fraction (LVEF) was reduced, at 20%, because of apical akinesia and inferior and lateral hypokinesia. No significant valvular disease was present. Chest radiography on admission showed cardiac enlargement and signs of pulmonary congestion.

The patient was initially treated with an intravenous diuretic, a beta blocker, an angiotensin receptor blocker, and a mineralocorticoid receptor antagonist, but the uptitration of these drugs was limited by hypotension, renal failure, and a tendency to hyperkalemia. The patient had to be periodically treated with dobutamine and dopamine, and he also received an infusion of levosimendan. Atrial fibrillation and periodic atrial flutter with insufficient rate control was initially treated with amiodarone, and direct current cardioversion was planned. Preparing for cardioversion, transesophageal echocardiography was performed, revealing a thrombus in the left atrial appendage. This finding caused cardioversion to be postponed and amiodarone to be discontinued because rhythm conversion was considered unfavorable in this situation. Instead, digoxin was added. On this treatment the patient showed some improvement clinically and the LVEF increased to approximately 30%, but he was still symptomatic even at minimal physical exertion.

The patient was monitored on telemetry, which revealed short runs of nonsustained ventricular tachycardia. On April 25, 2012, with the patient still hospitalized and on telemetry, a run of ventricular tachycardia degenerated into ventricular fibrillation. He was immediately resuscitated and defibrillated into atrial fibrillation and suffered no neurologic sequelae. Amiodarone was commenced. He had no signs of acute coronary syndrome.