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

被引:0
作者
Bennett, Jonathan [1 ,2 ]
Thornton, George D. [1 ,2 ]
Nitsche, Christian [1 ,2 ,3 ]
Gama, Francisco F. [2 ]
Aziminia, Nikoo [1 ,2 ]
Gul, Uzma [2 ]
Shetye, Abhishek [2 ]
Kellman, Peter [4 ]
Davies, Rhodri H. [1 ,2 ]
Moon, James C. [1 ,2 ]
Treibel, Thomas A. [1 ,2 ]
机构
[1] UCL, Inst Cardiovasc Sci, London, England
[2] Barts Heart Ctr, Cardiovasc Imaging Dept, London, England
[3] Med Univ Vienna, Div Cardiol, Vienna, Austria
[4] NHLBI, NIH, Bethesda, MD USA
关键词
aortic valve; aortic valve stenosis; hypertrophy; left ventricular; magnetic resonance imaging; myocardium; GLOBAL LONGITUDINAL STRAIN; MYOCARDIAL FIBROSIS; IMPLANTATION; MASS; SURVIVAL;
D O I
10.1161/CIRCIMAGING.124.017425
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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% (P<0.001*), primarily driven by cellular compartment regression (18.7%, P<0.001*), with a smaller reduction in the extracellular compartment (7.2%, P<0.001*). This unbalanced regression led to an apparent increase in extracellular volume fraction (27.4 +/- 3.1% to 30.2 +/- 2.8%; P<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, P=0.01). Mode of intervention (transcatheter versus surgical) did not influence the above myocardial parameters post-AVR (all P>0.05). The asterisk in P 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.
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