Article Text

  1. M. S. Shook1,
  2. R. A. Ahokas1,
  3. S. K. Bhattacharya1,
  4. M. D. Nelson1,
  5. K. P. Newman1,
  6. K. T. Weber1
  1. 1University of Tennessee Health Science Center, Memphis, TN.


Purpose Circulating markers of oxidative stress have been reported to be increased in Caucasians with congestive heart failure (CHF), irrespective of its etiologic origins, where activation of the circulating renin-angiotensin-aldosterone system is expected. Whether this is also true in African Americans (AAs) with CHF is uncertain. In experimental studies of aldosteronism, an associated secondary hyperparathyroidism (SHPT) leads to intracellular Ca2+ overloading and the appearance of oxidative stress. Herein we hypothesized oxidative stress would be present in AAs with CHF and would be accompanied by SHPT.

Methods and Results We monitored serum parathyroid hormone (PTH) and thiobarbituric acid-reactive substances (TBARs) in 25 AAs (20 M, 5 F; 52.4 ± 2.6 years): (a) 9 (8 M, 1 F; 46.6 ± 4.4 years) were hospitalized because of their decompensated heart failure (Decomp) due to either a dilated or ischemic cardiomyopathy and reduced ejection fraction (EF), who were treated with an ACE inhibitor, furosemide, and spironolactone; (b) 4 were asymptomatic and compensated (Comp) outpatients (4 M, 0 F; 55.3 ± 7.35 years) with comparable EF, etiologic basis of their heart failure, and medical treatment; and (c) 12 were outpatients (8 M, 4 F; 55.9 ± 7.8 years) without heart failure (normal EF) who served as controls (Cont). In Cont and those with Comp failure, we found (mean ± SEM) serum PTH to fall in the normal range (12-65 pg/mL) at 29 ± 6 and 50 ± 11 pg/mL, respectively, whereas in those with decompensated failure, PTH was elevated (88 ± 8 pg/mL; p < .05). Serum TBARs in Cont and Comp were 10.3 ± 0.7 and 12.1 ± 1.8 nmol MDA/mL, respectively, and which did not differ from one another. In contrast, serum TBARs were elevated (p < .05) in those with decompensated failure (17.2 ± 2.0 nmol MDA/mL).

Conclusions Circulating evidence of oxidative stress at a systemic level was found in AAs with decompensated failure where SHPT was also present. This was not the case in AAs with compensated failure and non-heart failure controls. These findings suggest a role for PTH-mediated overloading of intracellular Ca2+ in diverse tissues may be involved in the systemic appearance of oxidative stress.

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