Cigarette Smoke Exacerbates Ventricular Remodeling and Dysfunction in the Volume Overloaded Heart

Cigarette smoking is an independent risk factor for heart disease and is linked to sudden cardiac death. In this study, we examined the effects of cigarette smoke (CS) on the volume overload stressed heart. Our hypothesis was that CS exacerbates volume overload (VO)–induced cardiac dysfunction by ac...

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Bibliographic Details
Published in:Microscopy and microanalysis 2012-02, Vol.18 (1), p.91-98
Main Authors: Bradley, Jessica M., Nguyen, Jonathan B., Fournett, Alyssa C., Gardner, Jason D.
Format: Article
Language:English
Subjects:
Abdomen
Animals
Cardiovascular disease
Cardiovascular diseases
Cigarettes
Collagen
Coronary vessels
Extracellular matrix
Fistula
Gene Expression Profiling
Heart - physiopathology
Heart attacks
Laparotomy
Models, Animal
Myocardium - pathology
Proteins
Rats
Rats, Sprague-Dawley
Risk factors
Smoking - adverse effects
Software
Special Section: Keystone Meeting on Extracellular Matrix
Surgery
Vascular endothelial growth factor
Ventricular Remodeling
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Summary:Cigarette smoking is an independent risk factor for heart disease and is linked to sudden cardiac death. In this study, we examined the effects of cigarette smoke (CS) on the volume overload stressed heart. Our hypothesis was that CS exacerbates volume overload (VO)–induced cardiac dysfunction by accelerating ventricular remodeling. VO stress was surgically induced in male Sprague-Dawley rats by abdominal aortocaval fistula (ACF). Rats, with and without ACF, were exposed to either room air or CS (6 cigarettes/day) for 6 weeks. Temporal echocardiogram measurements indicated that CS significantly increased VO-induced left ventricular dilatation, prevented compensatory wall thickening, and depressed fractional shortening. Morphological analysis of ventricular collagen revealed that CS blunted compensatory collagen expression (45% decrease versus ACF alone). CS exacerbated the VO-induced increase of MMP-9 and TIMP-1 expression in the heart. CS also blocked the compensatory increases of HIF-1α, VEGF, and TGF-β in the VO-stressed heart. These data indicate that CS worsens VO remodeling by disrupting compensatory mechanisms, thereby promoting eccentric dilation and dysfunction.
ISSN:1431-9276
1435-8115
DOI:10.1017/S1431927611012207