Document Detail


Impaired intravascular triglyceride lipolysis constitutes a marker of clinical outcome in patients with stable angina undergoing secondary prevention treatment: a long-term follow-up study.
MedLine Citation:
PMID:  15193684     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: We sought to verify whether the intravascular metabolism of chylomicron-like emulsion may predict the clinical evolution of patients with coronary artery disease (CAD) undergoing secondary prevention therapy of CAD. BACKGROUND: Case-control studies have suggested an association between impaired intravascular catabolism of triglyceride (TG)-rich lipoproteins and CAD. However, evidence is lacking with respect to the potential clinical relevance of this metabolic disorder in CAD patients. METHODS: During a period of 4.5 +/- 0.9 years, we followed up 63 stable CAD patients (mean age 60 +/- 10 years) undergoing secondary prevention therapy (low-density lipoprotein cholesterol <100 mg/dl) in whom kinetic studies of the in vivo catabolism of chylomicron-like emulsions were performed. At enrollment into the study, fasting patients were injected intravenously with a chylomicron-like emulsion labeled with radioactive triglyceride (3H-TG) and cholesteryl esters (14C-CE) to evaluate the efficacy of intravascular TG lipolysis. RESULTS: At baseline, CAD patients displayed a diminished fractional clearance rate (FCR) for 3H-TG (-26%; p = 0.027), for 14C-CE (-37%; p = 0.015), and for delipidation index (DI) (-26%; p = 0.02) as compared with 35 control subjects. During follow-up of secondary prevention therapy, 33% of CAD patients (n = 21) presented with clinically refractory angina and aggravated coronary angiographic severity. The FCR for 3H-TG (-44%; p = 0.005) and DI (-41%; p = 0.006) in those patients with refractory angina was significantly lower than that observed in those with stable evolution. Moreover, in a Cox multivariate regression analysis, the presence of a DI less than the median value was an independent predictor of an unfavorable clinical evolution (adjusted hazard ratio 3.32; 95% confidence interval 1.21 to 9.14; p = 0.020). CONCLUSIONS: The current study establishes that delayed intravascular TG lipolysis is a strong and independent predictor of evolution to severe angina among patients undergoing secondary prevention therapy of CAD.
Authors:
Andrei C Sposito; Pedro A Lemos; Raul D Santos; Whady Hueb; Carmen G C Vinagre; Edgard Quintella; Otavio Carneiro; M John Chapman; Jose A F Ramires; Raul C Maranhão
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  43     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-06-14     Completed Date:  2004-07-23     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2225-32     Citation Subset:  AIM; IM    
Affiliation:
Heart Institute (InCor), Zerbini Foundation, Brasilia, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Angina Pectoris / metabolism*,  physiopathology,  prevention & control*
Antilipemic Agents / therapeutic use*
Biological Markers / blood
Brazil
Cholesterol, HDL / blood,  drug effects
Cholesterol, LDL / blood,  drug effects
Cholesterol, VLDL / blood,  drug effects
Coronary Angiography
Coronary Artery Disease / metabolism,  physiopathology,  prevention & control*
Emulsions
Female
Follow-Up Studies
Humans
Lipolysis / drug effects*,  physiology*
Male
Middle Aged
Severity of Illness Index
Stroke Volume / physiology
Time
Treatment Outcome
Triglycerides / metabolism*
Chemical
Reg. No./Substance:
0/Antilipemic Agents; 0/Biological Markers; 0/Cholesterol, HDL; 0/Cholesterol, LDL; 0/Cholesterol, VLDL; 0/Emulsions; 0/Triglycerides
Comments/Corrections
Comment In:
J Am Coll Cardiol. 2004 Jun 16;43(12):2233-5   [PMID:  15193685 ]

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