ArticleJournal of cardiovascular echography
Discrepancy in Myocardial Responses to Pressure Overload versus Volume Load Lesions.
Article in Journal of cardiovascular echography. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pressure and volume loads are vital components of every congenital heart disease. Numerous studies have concentrated on investigating myocardial remodeling under varying loading conditions in animal models. The objective of this study was to compare myocardial responses in lesions with volume overload, specifically ventricular septal defects (VSD), and lesions with pressure overload, such as coarctation. Methodology: For this purpose, three study groups have been involved: a VSD group ( Results: The CoA groups displayed significant septal hypertrophy compared to the other two study groups: IVSd (CoA: 8 ± 1.6 vs. VSD 5.7 ± 0.9). LV dilatation was more marked in the VSD group: LV end-diastolic dimension (CoA: 30 ± 3 vs. 25 ± 1.7). Systolic septal and mitral annular velocities were reduced in the CoA group and intriguingly exaggerated in the VSD group: Septal basal systolic myocardial velocity: (VSD: 9 ± 2 vs. CoA: 5 ± 1 vs. Controls: 7 ± 0.8). Myocardial GLS was markedly reduced in the CoA group. Conclusions: Besides the well-known eccentric-concentric hypertrophy paradigm in volume-pressure loading of the myocardium, pressure load seems to reduce myocardial velocities and LV function to a greater extent than volume loading. This is putatively mediated via myosin class switching, reduced myofilament sensitivity to calcium, and disrupted mechanical-electrical synchrony.
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