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1 Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA
2 Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
3 Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
4 Department of Surgery, University of Arkansas for Medical Sciences, Little Rock, AR, USA
5 Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA
6 Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Department of Surgery, University of Arkansas for Medical Sciences, Little Rock, AR, USA
7 Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
* To whom correspondence should be addressed. E-mail: josephjacob{at}uams.edu.
A recent report indicated that hyperhomocysteinemia (Hhe), in addition to its atherothrombotic effects, exacerbates the adverse cardiac remodeling seen in response to hypertension, a powerful stimulus for pathologic ventricular hypertrophy. The present study was undertaken to determine if Hhe has a direct effect on ventricular remodeling and function in the absence of other hypertrophic stimuli. Male Wistar-Kyoto (WKY) rats were fed one of two diets, an amino-acid defined control diet or an intermediate Hhe-inducing diet (IH). After 10 weeks of dietary treatment, rats were subjected to echocardiographic assessment of left ventricular (LV) dimensions and systolic function. Subsequently, blood was collected for plasma homocysteine measurements, and the rats were sacrificed for histomorphometric and biochemical assessment of cardiac remodeling, and for in vitro cardiac function studies. Significant LV hypertrophy (LVH) was detected by echocardiographic measurements, and in vitro results showed hypertrophy with significantly increased myocyte size in the left and right ventricles (RV). The LV and RV remodeling was characterized by a disproportionate increase in perivascular and interstitial collagen, coronary arteriolar wall thickening, and myocardial mast cell infiltration. In vitro study of LV function demonstrated abnormal diastolic function secondary to decreased compliance since the rate of relaxation did not differ between groups. LV systolic function did not vary between groups in vitro. In summary, in the absence of other hypertrophic stimuli short term intermediate Hhe caused pathologic hypertrophy and remodeling of both ventricles with diastolic dysfunction of the LV. These results demonstrate that Hhe has direct adverse effects on cardiac structure and function, which may represent a novel direct link between Hhe and cardiovascular morbidity and mortality, independent of other risk factors.
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