Hypoalbuminemia and lymphocytopenia in patients with decompensated biventricular failure.

BACKGROUND: In patients hospitalized with decompensated biventricular failure having hypoalbuminemia and lymphocytopenia without underlying hepatic or renal disease, we addressed the presence of a protein-losing enteropathy (PLE). METHODS: We studied 78 patients having a dilated cardiomyopathy, who were hospitalized with congestive heart failure (CHF) and hypoalbuminemia of uncertain origin. In the first 19 patients, we investigated the presence of PLE using Tc-Dex scintigraphy together with serum albumin 2 to 4 weeks later when compensation had been restored. In the next 59 patients, presenting with reduced serum albumin and relative lymphocyte count at admission, these parameters were again monitored (2-4 weeks) later when symptoms and signs of CHF had resolved. RESULTS: PLE, documented by Tc-Dex(70) scintigraphy, was found in 10 of 19 patients and whose hypoalbuminemia (2.7 +/- 0.1 g/dL, mean +/- standard error of mean) were corrected (3.3 +/- 0.1 g/dL; P < 0.05) with the resolution of CHF, whereas in the 9 patients without a PLE, reduced baseline serum albumin (2.6 +/- 0.1 g/dL) failed to improve on follow-up (2.6 +/- 0.2 g/dL) in keeping with malnutrition. Relative lymphocyte count was reduced (14.6 +/- 1.5%) in patients with PLE but was normal (21.4 +/- 3.3%; P < 0.05) in those without PLE. Serum albumin and relative lymphocyte count were each reduced at admission (2.8 +/- 0.1 g/dL and 14.4 +/- 1.0%, respectively) in 59 patients and increased (P < 0.05) to normal values (3.5 +/- 0.1 g/dL and 24.9 +/- 1.0%) 2 to 4 weeks after they were compensated. CONCLUSIONS: Enteral losses of albumin and lymphocytes account for the reversible hypoalbuminemia and lymphocytopenia found in patients hospitalized with CHF having splanchnic congestion.

Elevated serum cobalamin in patients with decompensated biventricular failure.

BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 +/- 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 +/- 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.

Hypovitaminosis D in African Americans residing in Memphis, Tennessee with and without heart failure.

BACKGROUND: Factors contributing to heart failure (HF) in African Americans (AA) are under investigation. Reduced 25(OH)D confers increased cardiovascular risk, including HF. METHODS: We monitored serum 25(OH)D, 1,25(OH)2D3, parathyroid hormone (PTH), and creatinine clearance in 102 AA residing in Memphis: 58 hospitalized with decompensated HF of >or=4 weeks in 34 (21 men; 53.3 +/- 1.8 years) or of 1 to 2 weeks in 24 (17 men; 49.6 +/- 2.4 years) and associated with a dilated cardiomyopathy and reduced ejection fraction (<35%); 19 outpatients with compensated HF (14 men; 52.6 +/- 2.7 years) with comparable ejection fraction; 16 outpatients (9 men; 55.4 +/- 2.9 years) with heart disease, but without HF; and 9 healthy volunteers (3 men; 35.8 +/- 3.5 years). RESULTS: Serum 25(OH)D 65 pg/mL was found in all AA with decompensated HF of >or=4 weeks (132.4 +/- 12.0 pg/mL) and 67% with 1 to 2 weeks duration (82.3 +/- 7.9 pg/mL), but only 11% with compensated HF (45.8 +/- 6.1 pg/mL), 12% without HF (29.6 +/- 5.4 pg/mL), and none of the volunteers (31.1 +/- 3.9 pg/mL). Creatinine clearance did not differ between patient groups. CONCLUSIONS: Hypovitaminosis D is prevalent amongst AA residing in Memphis, with or without HF. Elevations in serum PTH in keeping with secondary hyperparathyroidism are only found in AA with decompensated HF, where hypovitaminosis D and other factors are contributory.