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Am Heart J. 2014 May;167(5):707-14. doi: 10.1016/j.ahj.2014.01.008. Epub 2014 Feb 22.

Inflammation and future risk of symptomatic heart failure in patients with stable coronary artery disease.

Author information

1
Cardiology Department, Rabin Medical Center, Petah-Tikva, Israel. Electronic address: a_alon1@netvision.net.il.
2
Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Gertner Institute for Epidemiology and Health Research Policy, Sheba Medical Center, Tel-Hashomer, Israel.
3
The Israel Society for the Prevention of Heart Attacks, Neufeld Cardiac Research Institute, Sheba Medical Center, Tel-Hashomer, Israel.
4
Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; The Israel Society for the Prevention of Heart Attacks, Neufeld Cardiac Research Institute, Sheba Medical Center, Tel-Hashomer, Israel.
5
Cardiology Department, Rabin Medical Center, Petah-Tikva, Israel.

Abstract

BACKGROUND:

Heart failure (HF) carries poor prognosis in coronary artery disease (CAD) patients despite advances in therapy. Inflammation predicts recurrent cardiovascular events in CAD patients. It is unknown whether increased levels of inflammatory markers are associated with incident HF in these patients.

AIM:

The aims of this study were to evaluate the association between inflammatory markers and future HF risk in patients with stable CAD and to explore possible mediation by myocardial infarction (MI).

METHODS:

The study comprised 2,945 patients with stable CAD without HF at baseline during a median follow-up of 7.9 years. Inflammatory baseline markers were the basis of this study.

RESULTS:

Heart failure was diagnosed in 508 patients (17.2%). Patients who developed HF were older and had more often previous MI, diabetes, hypertension, and peripheral vascular disease. Baseline levels of C-reactive protein (CRP), fibrinogen, and white blood cells (WBCs) were significantly higher in patients who developed HF compared with those who did not. Age-adjusted incident HF rates were related to elevated baseline inflammatory markers in a dose-response manner. Adjusting for multiple confounders, the HF hazard ratios were 1.38 (95% CI 1.11-1.72), 1.33 (95% CI 1.07-1.66), and 1.36 (95% CI 1.10-1.68) for the third tertiles of CRP, fibrinogen, and WBC levels, respectively. Hazard ratio for the fifth quintile of a combined "inflammation score" was 1.83 (95% CI 1.40-2.39). Mediation by MI preceding the HF onset during follow-up accounted for 10.4%, 10.8%, and 8.6% of the association of subsequent HF with CRP, fibrinogen, and WBC, respectively.

CONCLUSIONS:

Increased levels of CRP, fibrinogen, and WBC are independently related to the incidence of HF in patients with stable CAD.

PMID:
24766981
DOI:
10.1016/j.ahj.2014.01.008
[Indexed for MEDLINE]

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