Discrepancy in Myocardial Responses to Pressure Overload versus Volume Load Lesions.

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 ( = 19), a coarctation (CoA) group ( = 20), and healthy age- and sex-matched controls ( = 21). The severity of VSD has been measured by its size. In contrast, the severity of discrete CoA was quantified by the pressure gradient across the coarcted segment. The parasternal long axis assessed septal hypertrophy and left ventricular (LV) dilatation-systolic myocardial LV velocities using tissue Doppler imaging. The global longitudinal strain was performed to assess LV function accurately.

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.