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ARTICLES |
1 Scott Professor of Clinical Pharmacy Research, Department of Clinical and Administrative
Sciences, College of Pharmacy, The University of Louisiana, Monroe, LA; Adjunct Professor, Department of
Internal Medicine, School of Medicine Louisiana State University Health Sciences Center, Shreveport, LA
2 Assistant Professor, Department of Clinical and Administrative Sciences, College of Pharmacy,
The University of Louisiana; Adjunct Assistant Professor, Department of Family Medicine, School of
Medicine, Louisiana State University Health Sciences Center
* To whom correspondence should be addressed. E-mail: rparis{at}lsuhsc.edu.
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Abstract |
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OBJECTIVE: To summarize findings regarding the association of inflammatory processes with chronic heart failure (HF).
DATA SOURCES: We conducted PubMed/MEDLINE searches (1966-January 2008) of primary literature using the following key words: ACE inhibitors, allopurinol, angiotensin-receptor antagonists, cardiomyopathy, chemokines, cytokines, diuretics, heart failure, inflammation, interleukins, HMG-CoA reductase inhibitors, immunotherapy, medications used in heart failure, thalidomide, tumor necrosis factor, and uric acid.
STUDY SELECTION AND DATA EXTRACTION: All articles that appeared to be relevant were read; of 305 articles examined, 87 were selected for discussion. Articles were selected if they were written in English and focused on any of the key words or appeared to have substantial content addressing inflammation in HF.
DATA SYNTHESIS: Cytokines, uric acid, and other inflammatory mediators are associated with
physiologic effects that are also prominent features of HF (eg, reduced contractility and cardiac output,
endothelial dysfunction, hypercoagulability, autonomic dysfunction as evidenced by reduced resting heart
rate variability, insulin resistance). With the exception of elevated tumor necrosis factor-
as a
cause of insulin resistance, it is not clear whether elevated inflammatory mediators directly cause HF
signs and symptoms or whether they are incidental markers. Awareness of these associations has occurred
relatively recently; there have been few clinical studies of efforts to directly modify inflammatory
mediators. Most currently accepted drug therapies of HF reduce concentrations of circulating cytokines,
but the significance of these findings awaits directed study.
CONCLUSIONS: Loss of myocardial function, autonomic dysfunction, and glucose intolerance are interrelated and linked by underlying chronic low-grade inflammation. Drug therapy with statins, pentoxifylline, and perhaps urate-lowering agents, in addition to current therapies, holds promise for treatment of HF.
Key Words: angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists, cardiomyopathy, diuretics, heart failure, HMG-CoA reductase inhibitors, interleukins.
Reprints: Dr. Parish, ULM College of Pharmacy, Shreveport Campus, 1725 Claiborne Ave., Shreveport, LA 71103, fax 318/632-2007, rparis@lsuhsc.edu
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