Hyperhomocysteinemia in patients with heart failure referred for cardiac transplantation: preliminary observations.
BACKGROUND
Hyperhomocysteinemia is becoming recognized as a risk factor for cardiovascular disease, yet there are limited data on the prevalence of hyperhomocysteinemia in patients with heart failure.


OBJECTIVE
The purpose of this study was to examine the prevalence of hyperhomocysteinemia in patients with severe heart failure and to correlate serum homocysteine levels with factors that may affect homocysteine metabolism.


METHODS
Serum homocysteine levels were measured at the time of cardiac transplant evaluation in 89 consecutive patients with severe heart failure. Homocysteine levels for patients with ischemic cardiomyopathy (ICM) were compared with levels obtained in patients with nonischemic cardiomyopathy (NICM), and homocysteine levels were correlated with demographic and hemodynamic parameters as well as functional status.


RESULTS
The mean plasma homocysteine level was increased (14.3 +/- 5.3 micromol/l, normal <9.0 micromol/l) and was equivalent between patients with ICM versus NICM (14.7 +/- 5.8 micromol/l vs. 13.8 +/- 4.5 micromol/l, p = 0.44). Elevated homocysteine levels were seen in a large proportion (89%) of patients and were equally common to patients with NICM (94%) and ICM (85%). Serum homocysteine levels correlated with serum creatinine (r = 0.51, p < 0.001), with a history of diabetes (p = 0.028), and with a history of peripheral vascular disease (p = 0.045). Only 6% of patients were receiving folic acid therapy at the time of transplant referral.


CONCLUSIONS
Hyperhomocysteinemia is common in patients with severe heart failure, and plasma homocysteine levels are uniformly elevated regardless of the etiology of heart failure. Elevated plasma homocysteine levels are likely a consequence of heart failure-related renal insufficiency.
Schofield
Richard S
RS
Division of Cardiovascular Medicine and Shands Transplant Center, University of Florida College of Medicine, Gainesville, Florida, USA. schofrs@medicine.ufl.edu
Wessel
Timothy R
TR
Walker
Tracy C
TC
Cleeton
Timothy S
TS
Hill
James A
JA
Aranda
Juan M
JM
D015415:Biomarkers / Q000097:blood; D009202:Cardiomyopathies / Q000378:metabolism / Q000628:therapy; D003324:Coronary Artery Disease / Q000378:metabolism / Q000628:therapy; D003404:Creatinine / Q000097:blood / Q000652:urine; D005260:Female; D005431:Florida; D005492:Folic Acid / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000601:surgery*; D016027:Heart Transplantation; D006397:Hematinics / Q000627:therapeutic use; D006710:Homocysteine / Q000097:blood / Q000187:drug effects; D006801:Humans; D020138:Hyperhomocysteinemia / Q000188:drug therapy / Q000378:metabolism* / Q000601:surgery*; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome
D015415:Biomarkers; D006397:Hematinics; D006710:Homocysteine; D005492:Folic Acid; D003404:Creatinine