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Left Ventricular Hypertrophy in Aortic Stenosis: Early Cell and Matrix Regression 2 Months Post-Aortic Valve Replacement. | LitMetric

AI Article Synopsis

  • In aortic stenosis, the heart's left ventricle thickens, but after aortic valve replacement (AVR), it begins to reverse this hypertrophy, though the details of this process are not fully understood.
  • A study involving 39 patients assessed changes in the heart's structure and function before and about 8 weeks after AVR, revealing a significant reduction in left ventricular mass primarily due to a decrease in the cellular component.
  • After AVR, while the cellular area shrank more than the extracellular space, an increased extracellular volume fraction was linked to a decline in heart function, even though the method of surgery (surgical or transcatheter) didn't affect outcomes.

Article Abstract

Background: In aortic stenosis, the myocardium responds with left ventricular hypertrophy, which is characterized by increased left ventricular mass due to cellular hypertrophy and extracellular matrix expansion. Following aortic valve replacement (AVR), left ventricular hypertrophy regression occurs, but early cellular and extracellular dynamics are unknown.

Methods: Patients with severe symptomatic aortic stenosis undergoing surgical or transcatheter AVR were prospectively recruited. Pre- and early post-AVR cardiac magnetic resonance imaging assessed left ventricular remodeling, global longitudinal strain, and T1 mapping to determine extracellular volume fraction and volume of cellular and extracellular compartments.

Results: In all, 39 patients (aged 71.4±9.8 years, male 79%, aortic valve peak velocity 4.4±0.5 m/s) underwent cardiac magnetic resonance before and at median 7.7 weeks post-AVR. Left ventricular mass index reduced significantly by 15.4% (<0.001*), primarily driven by cellular compartment regression (18.7%, <0.001*), with a smaller reduction in the extracellular compartment (7.2%, <0.001*). This unbalanced regression led to an apparent increase in extracellular volume fraction (27.4±3.1% to 30.2±2.8%; <0.001*). Although there was no significant change in global longitudinal strain post-AVR, an increase in extracellular volume fraction was associated with worsening of global longitudinal strain (Pearson r=0.41, =0.01). Mode of intervention (transcatheter versus surgical) did not influence the above myocardial parameters post-AVR (all >0.05). The asterisk in values indicates a statistical significance of <0.05.

Conclusions: Within 8 weeks of AVR for aortic stenosis, substantial left ventricular hypertrophy regression occurs involving both cellular and extracellular compartments, demonstrating the early myocardial adaptability to afterload relief. Cellular compartment regression is greater than extracellular regression, leading to an apparent increase in extracellular volume fraction. Mode of intervention did not affect degree of reverse remodeling, indicating that both are effective at resulting beneficial changes post-AVR.

Registration: URL: https://www.isrctn.com; Unique identifier: NCT04627987.

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Source
http://dx.doi.org/10.1161/CIRCIMAGING.124.017425DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11649182PMC

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