Reduced relative lymphocyte count in african-americans with decompensated heart failure.

BACKGROUND: A reduction in relative lymphocyte count (%L) has been reported in whites with heart failure that inversely correlated with jugular venous pressure thereby implicating systemic venous hypertension with splanchnic congestion. OBJECTIVES: : To study whether a reduced %L (<20%) occurs in African-Americans (AA) with heart failure and to address pathophysiologic mechanisms having the potential to influence lymphocyte biology and survival, we monitored patients with or without systemic venous hypertension, hypoalbuminemia, hypovitaminosis D, and secondary hyperparathyroidism. METHODS: In 131 AA (90 men; 53 +/- 12 years): 113 were hospitalized, 50 with decompensated biventricular failure (DecompHF), 24 with acute left heart failure, and 39 with heart disease, but no heart failure (HDNHF); and 18 were outpatients with compensated heart failure. At the time of admission or outpatient visit, we monitored: white blood cell count and %L; and serum albumin, 25(OH)D, and parathyroid hormone (PTH). RESULTS: White blood cell count did not differ among the groups, whereas %L was reduced only in those with DecompHF (15 +/- 1%; P < 0.05) versus 25 +/- 2% with left heart failure, 29 +/- 1% in HDNHF, and 28 +/- 3% in compensated heart failure. Serum albumin was reduced in DecompHF (2.8 +/- 0.1; P < 0.05), but not in any of the other groups. Reduced 25(OH)D (<30 ng/mL), in keeping with hypovitaminosis D, was found in all AA, whereas elevated serum PTH (>65 pg/mL) was found only in those with DecompHF (123 +/- 22 pg/mL). CONCLUSIONS: A relative lymphocytopenia, together with hypoalbuminemia and elevated PTH, were found only in hospitalized AA with DecompHF. These findings implicate splanchnic congestion and the enteric loss of lymphocytes and albumin with an associated secondary hyperparathyroidism.

Hypovitaminosis D and valvular calcification in patients with dilated cardiomyopathy.

BACKGROUND: In patients with dilated (idiopathic) cardiomyopathy (DCM), little is known about the presence of valvular calcification and its association with hypovitaminosis D, which may predispose affected tissues to calcification. Our objectives were 2-fold: to conduct a retrospective assessment of echocardiographic evidence of valvular calcification in patients with DCM who were known to have hypovitaminosis D (25(OH)D <30 ng/mL) and to conduct a prospective assessment of serum 25(OH)D in patients with DCM, who had demonstrated echocardiographic evidence of valvular calcification. METHODS: The retrospective study consisted of 48 African American patients (34 men, 14 women; 52.3 +/- 1.5 years) having DCM and ejection fraction <35% with serum creatinine <2.0 mg/dL and 25(OH)D <30 ng/mL; and 20 white patients in the prospective study (20 men; 71.0 +/- 3.0 years) having DCM and ejection fraction <35% with serum creatinine <2.0 mg/dL and echocardiographic evidence of valvular calcification. In the retrospective study, a transthoracic echocardiogram was obtained to address mitral valvular and annular calcification, aortic valvular calcification, and sinotubular calcification; whereas in the prospective study, serum 25(OH)D level was monitored in patients with known valvular calcification. Serum parathyroid hormone (PTH) was monitored in both studies. RESULTS: In the retrospective study, hypovitaminosis D was found in 19 patients (31%) with valvular calcification and in whom serum PTH was increased (83 +/- 8 pg/mL). In the prospective study, 15 of 20 elderly patients (80%) with known DCM and valvular calcification were found to have hypovitaminosis D (25(OH)D <30 ng/mL), whereas serum PTH was normal (43 +/- 4 pg/mL). CONCLUSIONS: In patients with DCM without marked renal dysfunction, valvular calcification was seen more frequently and associated with hypovitaminosis D, whereas in elderly patients with valvular calcification, hypovitaminosis D is common, suggesting that the duration of vitamin D deficiency may determine the extent of valvular calcification. The role of hypovitaminosis D in the appearance of valvular calcification deserves further study.

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.

Effect of timed semirecumbency and furosemide dosing on urinary sodium excretion in patients with compensated heart failure.

PURPOSE: The management of chronic cardiac failure, a salt-sensitive state, frequently includes administration of a loop diuretic to enhance urinary Na excretion. We hypothesized that a period of timed semirecumbency (vis-à-vis upright posture) would enhance the natriuresis that accompanies oral furosemide dosing in patients with compensated cardiac failure. METHODS: Four ambulatory patients with compensated chronic cardiac failure (NYHA Class III) of ischemic and nonischemic origin and systolic dysfunction (ejection fraction <35%), who were receiving a stable regimen of oral furosemide and angiotensin-converting enzyme inhibitor, were enrolled into the study. In the institution's Clinical Research Center, we monitored and compared urine flow rate (mL/min) and Na excretion rate (mEq/hr) in each patient in response to two different protocols. Protocol 1 consisted of an initial 90-minute period of bedrest followed by the patient's oral furosemide dose and 180 minutes of upright activity and a subsequent 90-minute period of bedrest. Protocol 2 was similar, with the exception that furosemide dosing was given after upright activity and immediately prior to the second period of bedrest. RESULTS: With each patient serving as his or her own control, both urine flow rate and urinary Na excretion rate were markedly increased when furosemide was given prior to bedrest as compared to its dosing prior to upright activity. CONCLUSIONS: In patients with compensated chronic cardiac failure, the natriuresis that accompanies oral furosemide dosing is enhanced when given just prior to a period of timed semirecumbency. This approach represents a more optimal use of this loop diuretic in patients with compensated heart failure.

Secondary hyperparathyroidism and hypovitaminosis D in African-Americans with decompensated heart failure.

OBJECTIVE: We previously noted secondary hyperparathyroidism (SHPT) in African-American patients hospitalized during February, 2005 with either untreated or treated congestive heart failure (CHF) due to ischemic or idiopathic cardiomyopathy. Herein, we hypothesized that housebound African-American patients hospitalized during the period of June 1 through August 31, 2005, with CHF would have SHPT and hypovitaminosis D. METHODS: Twenty-five African-American patients with an ejection fraction (EF) less than 35% due to ischemic or dilated (idiopathic) cardiomyopathy were monitored: 20 were hospitalized with CHF, stratified on historical grounds as of 4 weeks' or longer duration or of 1 to 2 weeks' duration in 11 and 9 patients, respectively, despite medical care that included furosemide; serum parathyroid hormone (PTH) and 25(OH)D at the time of admission in these patients were compared to five asymptomatic outpatients seen during the summer with stable, compensated failure. RESULTS: Serum PTH was elevated (127 +/- 13; 82-243 pg/mL) in all patients with CHF of 4 weeks' or longer duration (normal, 12-65 pg/mL) and was elevated in three of nine patients (59 +/- 8; 18-99 pg/mL) with CHF of 1 to 2 weeks' duration. Ionized hypocalcemia (1.09 +/- 0.03 and 1.08 +/- 0.02 mmol/L; normal, 1.12-1.30) and hypomagnesemia (0.47 +/- 0.02 and 0.46 +/- 0.03 mmol/L; normal, 0.53-0.67) were respectively found in long- or short-duration CHF. No compensated patient had elevated PTH (42 +/- 5; 17-53). Hypovitaminosis D (< or =30 ng/mL) was universally present in patients with CHF of 4 weeks' or longer duration (15.1 +/- 1.4; 7.0-23.8 ng/mL) and was also prevalent in the other groups (20.3 +/- 5.1, 7.0-54.1 ng/mL in CHF of 1 to 2 weeks' duration and 23.1 +/- 4.9; 17.2-42.7 ng/mL in compensated failure). CONCLUSIONS: In African-American patients with CHF, hypovitaminosis D, aldosteronism, and loop diuretic treatment each exaggerate Ca and Mg losses to stress a fragile Ca balance leading to ionized hypocalcemia and hypomagnesemia with SHPT.

Normoglycemia in nondiabetic African Americans hospitalized with heart failure.

BACKGROUND: In nondiabetic patients hospitalized with multiorgan failure, neurohormonal activation can lead to stress-induced hyperglycemia (>140 mg/dL), as could Mg(2+) and Zn(2+) deficiencies. However, it is currently uncertain whether nondiabetic African Americans (AA) hospitalized with either chronic, decompensated biventricular failure (DecompHF) having hepatic and splanchnic congestion, ionized hypomagnesemia and hypozincemia, or acute left heart failure (LHF) would exhibit hyperglycemia at admission. METHODS: We retrospectively examined admission serum glucose in 77 AA patients without a history of diabetes, who were hospitalized with heart failure. This examination included 41 patients admitted during a 4-month period with chronic DecompHF and whose clinical presentation included findings of expanded intra- and extravascular volumes, together with echocardiographic evidence of marked tricuspid regurgitation and distended inferior vena cava, without respiratory variation. These patients were compared with 14 nondiabetic patients hospitalized during the same time period with acute LHF. We also studied admission serum glucose in 22 patients who were admitted with DecompHF having documented hypomagnesemia and hypozincemia. RESULTS: Admission serum glucose (mean +/- standard error of mean) in patients with chronic DecompHF was 105.41 +/- 4.08 mg/dL and was modestly elevated (140-160 mg/dL) in 3 patients. In those with acute LHF, glucose was 94.86 +/- 3.96 mg/dL and did not exceed 140 mg/dL in any patient. Glucose (103.2 +/- 4.3 mg/dL) was not elevated in patients having chronic DecompHF and reduced ionized Mg(2+) and serum Zn(2+) (0.44 +/- 0.01 mmol/L and 69.6 +/- 3.2 mug/dL, respectively). CONCLUSIONS: Hyperglycemia at admission was infrequent in nondiabetic AA patients hospitalized with either acute LHF or chronic DecompHF, which may have also included hypomagnesemia and hypozincemia. This calls into question the need for intensive insulin therapy in these patients.

Micronutrients in African-Americans with decompensated and compensated heart failure.

Heart failure is thought to be more common and of greater severity in African-Americans (AAs). Potential mechanisms remain uncertain. The importance of micronutrient deficiencies in the pathophysiologic expression of congestive heart failure (CHF) in AAs remains to be explored, including hypovitaminosis D, which can promote secondary hyperparathyroidism (SHPT), together with hypozincemia and hyposelenemia, the 2 most crucial trace minerals integral to diverse biologic functions. Serum parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), Zn, and Se were monitored in 30 AAs hospitalized during June through December 2005, with decompensated failure and reduced ejection fraction (EF) (<35%) of predominantly nonischemic origin treated with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB), furosemide, and spironolactone. Based on their symptomatic status before hospitalization, 15 patients were stratified as having protracted (>or=4 weeks) CHF, whereas 15 patients had short-term (1-2 weeks) CHF. These hospitalized patients were compared with 10 AA outpatients with stable, similarly treated compensated failure and comparable EF, and 9 AA normal volunteers without cardiovascular disease. Serum PTH was elevated in all patients with protracted CHF and in 60% of patients with short-term CHF, but not in compensated patients or normal volunteers. However, serum 25(OH)D was reduced in all patients with >or=4 weeks and 80% with either 1-2 weeks CHF or compensated failure compared with volunteers. Serum Zn was below normal in 11 of 15 patients with protracted CHF, in 8 of 15 patients with shorter duration CHF, and in 5 of 10 patients with compensated failure. Serum Se was reduced in all patients with >or=4 weeks, 60% with short-term CHF, and 90% of compensated patients. Concomitant to hypovitaminosis D, hypozincemia, and hyposelenemia, SHPT is a covariant of CHF in housebound AAs.