This 79-year-old man with type II diabetes, hypertension, 2.5 pack per day smoking history for 46 years, and a strong family history of premature coronary disease (father died at 61 years of age of myocardial infarction) suffered a myocardial infarction in 1974 and had cardiac arrest as a result of ventricular fibrillation on the third day of that hospitalization. Coronary revascularization was undertaken with a four-vessel bypass in February, 1999. He developed symptoms of heart failure in 2006, with an echocardiogram showing akinesis of the inferior and posterobasal walls and an ejection fraction of 20% with moderate mitral regurgitation. He was treated with furosemide, carvedilol, candesartan, and statins and continued with New York Health Association (NYHA) class II to III symptoms, with an electrocardiogram demonstrating left bundle branch block (LBBB) with variable QRS durations of 120 to 130 msec. He was thought perhaps to be a candidate for cardiac resynchronization therapy. Outpatient tissue Doppler study confirmed an ejection fraction of 20% but fell short of the usual criteria for left ventricular dyssynchrony. Electrophysiologic study demonstrated easily inducible sustained monomorphic ventricular tachycardia, both at baseline and after procainamide challenge, prompting implantation of a single-chamber Medtronic defibrillator using the left cephalic vein. His ejection fraction was 25% in 2009. With progressive symptoms of heart failure in 2010 despite maximal medical therapy, and with a QRS duration of 140 msec, the decision was made to upgrade his device to a cardiac resynchronization therapy (CRT) system. The left subclavian system was still patent, allowing for passage of an active fixation atrial lead and a coronary sinus lead. Venography demonstrated that his coronary venous anatomy was limited, with few branches available and most atretic, consistent with his diabetes. One branch served as a reasonable target, with acceptable pacing thresholds without phrenic nerve stimulation. His paced QRS duration narrowed, but symptoms of heart failure have persisted. His level of depression worsened with the death of his wife, and he had occasional dietary indiscretion. Atrioventricular optimization was performed. With ongoing symptoms despite maximal medical therapy and dietary modification, and in an effort to maximize longevity of the implantable cardioverter-defibrillator (ICD), the left ventricular lead was inactivated 1 year later.

The patient was taking carvedilol 6.25 mg twice daily, furosemide 100 mg daily, potassium chloride 20 mEq daily, glyburide 2.5 mg daily, simvastatin 20 mg daily, amlodipine 5 mg daily, fish oil 1000 mg daily, and aspirin 81 mg daily.

The patient experienced dyspnea at 100 yards and one flight of stairs and had occasional orthopnea.