Skeletal Muscle Compensation for Cardiac Muscle Insufficiency in Heart Failure and Reduced Ejection Fraction
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Patients with heart failure (HF) and reduced ejection fraction (HFrEF) display exercise intolerance measured objectively as decreased peak oxygen uptake (VO2).1 In accordance with Fick’s principal and law of diffusion, reduced peak VO2 is the result of impaired convective and diffusive O2 transport.2,3 Endurance training improves peak VO2 in clinically stable HFrEF patients secondary to central and peripheral adaptations that result in increased cardiac output and O2 distribution and extraction in skeletal muscle.1 We report, using invasive hemodynamic and pulmonary gas exchange measures, exercise changes in VO2 and its determinants in an avid cyclist with severe cardiac limitation because of advanced HFrEF.
A 55-year-old male patient who had been a lifelong marathon runner was diagnosed with idiopathic nonischemic dilated cardiomyopathy 5 years before evaluation. He had a history of atrial fibrillation and was on optimal doses of carvedilol, lisinopril, and spironolactone. His ejection fraction was 20% to 25%, but he had remained in New York Heart Association class I and was able to continue cycling and intense daily exercise. In the past year, he was hospitalized twice for acutely decompensated HF, with gradually worsening effort intolerance. Given the increasing need for hospitalization, he was referred for invasive exercise testing as part of a transplant evaluation workup.
Laboratories revealed hemoglobin 13.3 g/dL, creatinine 1.5 mg/dL, sodium 132 mmol/L, troponin 0.06 ng/mL, and NT-proBNP (N-terminal pro-B-type natriuretic peptide) 14 080 pg/mL. Echocardiography showed ejection …