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A 46-year-old man with a dilated cardiomyopathy and known chronic HFrEF for the last two years now presents with a recent history of worsening shortness of breath and fatigue with physical activity. His LVEF is 25% and he has enlargement of all four chambers of his heart on echocardiography. He was last hospitalized two months ago with fluid retention that responded to high dose intravenous diuretic therapy. He did not need an intravenous inotropic or vasodilator drug. He is taking maximally tolerated doses of carvedilol, sacubitril/valsartan, spironolactone, and bumetanide. He remains in sinus rhythm and has an ICD for primary prevention of sudden cardiac death. His QRS duration on his ECG is only 100 msec; therefore, he is not a candidate for chronic resynchronization therapy. Because of his worsening exercise tolerance, he is referred for a cardiopulmonary exercise test to evaluate his functional limitation and to assess his prognosis and candidacy for advanced heart failure therapies. He walked for 4 minutes on a treadmill following a modified Naughton protocol and stopped due to dyspnea and fatigue. He only attained 70% of his predicted maximal heart rate as he was taking a beta-blocker. There were occasional premature ventricular beats during exercise but no sustained arrhythmia. His oxygen saturation by pulse oximetry remained greater than 90% throughout exercise. He had a 10 mmHg decrease in systolic blood pressure at peak exercise. His heart rate recovery was abnormal with only a 5 bpm decrease at one minute of recovery during a slow walking cool-down period. His peak VO2 was 10.5 mL/kg/min which is 29% predicted for his age and gender. His peak respiratory exchange ratio (RER) was 1.20, indicating a near maximal effort. His VE/VCO2 slope was 48 and his oxygen uptake efficiency slope (OUES) was 1.1. He had evidence of oscillatory ventilation during exercise. His end-tidal CO2 (PETCO2) at rest was 28 mmHg and it decreased during exercise to 22 mmHg. The results of this test confirmed his severe exercise limitation and were consistent with diminished cardiac output and the development of pulmonary hypertension during exercise. In addition, the low peak VO2 , elevated VE/VCO2 slope, decreased OUES, abnormal PETCO2 response, oscillatory ventilation, exertional hypotension, and abnormal heart rate recovery all indicated that this patient had a poor prognosis with his HFrEF over the next year. A subsequent right heart catheterization confirmed the presence of a low resting cardiac index and pulmonary hypertension due to an elevated pulmonary capillary wedge pressure of 34 mmHg. His transpulmonary gradient was elevated at 15 mmHg but he had a favorable response to intravenous nitroprusside with a resulting pulmonary vascular resistance (PVR) of 2.1 Wood units. Based on these studies he was listed for cardiac transplantation. He subsequently required several hospitalizations for volume overload in the next few months and required inotropic therapy. He was unable to be weaned from milrinone and a left ventricular assist device was implanted ...

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