 |
 |
 |
 |
 |
 |
 |
|
|
|
|||||||||
|
|||||||||||
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
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
Reprints: Dr. Parish, ULM College of Pharmacy, Shreveport Campus, 1725 Claiborne Ave., Shreveport, LA 71103, fax 318/632-2007, rparis{at}lsuhsc.edu
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
Published Online, May 13, 2008. www.theannals.com, DOI 10.1345/aph.1K272
This article has been cited by other articles:
|
|
 |
|
  C. Bergamini, M. Cicoira, A. Rossi, and C. Vassanelli Oxidative stress and hyperuricaemia: pathophysiology, clinical relevance, and therapeutic implications in chronic heart failure Eur J Heart Fail, May 1, 2009; 11(5): 444 - 452. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
 |
 |
 |
 |
