Key result
AVR is linked to a ~19% reduction in LV mass regardless of myocardial fibrosis severity.
Why the study?
The relationship between the severity of myocardial fibrosis and left ventricular mass reduction following aortic valve replacement remained to be elucidated.
Does the severity of myocardial fibrosis correlate with left ventricular mass reduction after aortic valve replacement?
Cohort (n=130)
No
Does the severity of myocardial fibrosis correlate with left ventricular mass reduction after aortic valve replacement?
Myocardial fibrosis severity does not appear to affect the degree of left ventricular mass regression following aortic valve replacement for aortic stenosis or regurgitation.
Answers are grounded in this paper and cite their sources.
Mass regression after AVR occurs independently of fibrosis severity; leaves open its prognostic role in other post-AVR outcomes.
Aim. Aortic valve diseases are associated with myocardial fibrosis. The relationship between severity of myocardial fibrosis and left ventricular mass reduction (LVMR) after aortic valve replacement (AVR) still needs to be elucidated. Methods. In a single-center, retrospective trial, 130 patients underwent AVR with/without concomitant surgery. The study population was divided by etiology into aortic stenosis (AS) and aortic regurgitation (AR) groups. LV end-diastolic diameter, LV septal and posterior thicknesses, LV mass, and aortic annulus were obtained in all study patients. Left ventricular mass regression index (iLVMR) was found by the difference between preoperative iLVM and follow-up iLVM. iLVMR in months was calculated by divided iLVMR on the number of months before follow-up visit. Myocardial tissue was embedded in paraffin, and sectioned into 4 µm slices for histological staining (picrosirius red) and scanning. The fraction of myocardial volume occupied by collagen tissue was determined. Results. The left ventricular remodeling of AS and AR patients is presented in Table 3. There was significant LV mass reduction in both aortic valve disease groups in the follow-up period (AS group, p < 0.001; AR group, p < 0.05). The number of LVH cases decreased in both groups in the follow-up period (AS group, p < 0.001; AR group, p < 0.05). In Post-AVR period the ejection fraction of LV did not improve in the AS group, compare to AR group (p<0.05). In both groups number of patients with impaired LV EF was increased in Post-AVR period, but not significantly. Moreover, the LV septal thickness, and iLVEDD significantly decreased in the AS group (p<0.001 and p<0.001), compared to the AR group (p=NS, p<0.05). We did not found correlations between MF and LVM in preoperative, and follow-up periods for AS and AR groups. Moreover, MF did not correlate significantly to iLVMR and iLVMR in months. A significant correlation exists in AS patients between MF and preoperative iLVEDD (r = 0.21, p = 0.04). Conclusion. The LVM reduction was observed in both AS and AR groups. LVM of AS group recovered more quickly than that of AR group. In our study MF does not affect LVM regression. Large cohort of patients with myocardial biopsies and long-term follow-up are needed to access the impact of the MF on the LVMR.
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Aitaliyev et al. (2021) conducted a cohort in Aortic valve disease (aortic stenosis and aortic regurgitation) (n=130). Aortic valve replacement vs. Pre-operative baseline was evaluated on Indexed left ventricular mass (iLV mass) in aortic stenosis patients (p=0.001). Aortic valve replacement significantly reduced left ventricular mass in patients with aortic stenosis and regurgitation, though the severity of myocardial fibrosis did not correlate with mass regression.
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