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- W44263496 abstract "The cytoskeletal protein desmin is upregulated in ischemic heart failure (HF). To test the hypothesis that wall stress mechanisms influence desmin upregulation we examined its transmural distribution in HF. HF was induced in sheep (coronary embolization). LV EF and end-systolic and -diastolic areas (ESA, EDA) were measured at baseline and 4- or 12mos later. Desmin content was measured in myocardium via histochemistry and image analysis. Multivariate regression with beta coefficient (β) assessed which parameter exerted the greatest influence on the outcome. *p=0.05. EF decreased from 55% to 24%*. ESA and EDA increased 235%* and 123%* at 12mos. Desmin content was greatest in the LV endocardium (+30% compared to epicardium), increased with HF progression (145%* and 259%* at 4- and 12-mos), inversely correlated to EF (r=-0.61*), and better predicted EF (β=-1.18*) and ESA (β=0.89*) than meso- or epicardial. Transmural desmin better predicted cardiac dysfunction/remodeling than parallel measurements of fibrosis (r=0.32*) or myocyte hypertrophy (r=0.36*). Desmin upregulation shows a transmural endo->epicardial gradient in HF. Endocardial desmin content better correlates to worsening HF than meso- or epicardial desmin, suggesting that intra-myocyte remodeling, likely related to mechanical stretch, are useful predictors of LV function and disease progression. Funding provided by AHA, FAER, NHF, and SCA." @default.
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- W44263496 date "2009-04-01" @default.
- W44263496 modified "2023-09-24" @default.
- W44263496 title "Endocardial desmin in heart failure" @default.
- W44263496 doi "https://doi.org/10.1096/fasebj.23.1_supplement.795.6" @default.
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