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2009 Southern Regional Meeting Abstracts


Session: Case Reports in Cardiovascular Medicine

CONSEQUENCES OF SYSTEMIC VENOUS HYPERTENSION DUE TO DECOMPENSATED BIVENTRICULAR FAILURE
Zaidi SS, Shahbaz AU, Weber KT. University of Tennessee Health Science Center, Memphis, TN.

Case Report: Purpose. Irrespective of its etiologic origins, elevations in systemic venous pressure lead to an engorgement of hepatic and splanchnic venous circulations to cause hepatic and gastrointestinal dysfunction. To illustrate less-well recognized consequences of systemic venous hypertension and their reversible nature, we report on a patient having recurrent episodes of decompensated biventricular failure.
Case Report. A 55-year-old African-American male with a history of heart failure due to dilated cardiomyopathy of uncertain origin with reduced ejection fraction (<30%) was hospitalized on several occasions because of his symptoms and signs of systemic venous hypertension that included elevated jugular venous pressure and tricuspid regurgitation. His hepatic and splanchnic congestion would improve with bed rest and medical therapy. On each admission, he was found to have: elevated serum B12 (1090±240 pg/mL), without elevation of serum transaminases (AST, 25±8 U/L; and ALT, 22±6 U/L); hypoalbuminemia (2.44±0.2 gm/dL); and relative lymphocytopenia (7±0.7%) with normal white blood cell count (4.9±0.4 K/mm3). Positive technetium-dextran70 scintigraphy was consistent with a protein-losing enteropathy. Each hospitalization led to improved clinical status and decline in B12 (580±50 pg/mL) and rise in albumin (3.2±0.2 gm/dL) and lymphocytes (16±3.8%). When he had attained euvolemia as an outpatient (30±5 days), there was evidence of continued improvement: B12, 548±17 pg/mL; albumin 3.43±0.05 gm/dL); and relative lymphocytes (25±2%).
Conclusion. Our patient demonstrates less well-recognized consequences of systemic venous hypertension that can accompany decompensated biventricular failure. These include the release of stored B12 from the congested liver and the enteric loss of albumin and lymphocytes from the congested splanchnic territory. Serial monitoring of these parameters once elevations in systemic venous pressure and expanded intravascular volume have been eliminated serve to illustrate their reversibility.