LV Remodeling After Valve Replacement for Aortic Stenosis

Feb 21, 2018
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Authors:
Treibel TA, Kozor R, Schofield R, et al.
Citation:
Reverse Myocardial Remodeling Following Valve Replacement in Patients With Aortic Stenosis. J Am Coll Cardiol 2018;71:860-871.
Summary By:
David S. Bach, MD, FACC

Study Questions:

Does myocardial interstitial fibrosis that occurs in response to aortic stenosis (AS) regress following aortic valve replacement (AVR)?

Methods:

Patients with symptomatic, severe AS (n = 181, aortic valve area index [AVAi] 0.4 ± 0.1 cm2/m2) were assessed prior to AVR by echocardiography (for AS severity and diastology), cardiac magnetic resonance (CMR; for volumes, function, and focal/diffuse fibrosis), biomarkers (N-terminal pro–B-type natriuretic peptide [NT-proBNP] and high-sensitivity troponin T), and 6-minute-walk test (6MWT). CMR was used to measure the extracellular volume fraction (ECV), deriving matrix volume (left ventricular [LV] mass × ECV) and cell volume (LV mass × [1–ECV]). Assessment was repeated 1 year after AVR.

Results:

One year after AVR, there were 116 pacemaker-free survivors (age 70 ± 10 years; 54% male). Among this cohort, mean valve gradient had improved (48 ± 16 to 12 ± 6 mm Hg, p < 0.001) and indexed LV mass had decreased by 19% (88 ± 26 to 71 ± 19 g/m2, p < 0.001). Focal fibrosis by CMR late gadolinium enhancement did not change, but ECV increased (28.2 ± 2.9% to 29.9 ± 4.0%, p < 0.001); this was the result of a 16% reduction in matrix volume (25 ± 9 to 21 ± 7 ml/m2, p < 0.001) but a proportionally greater 22% reduction in cell volume (64 ± 18 to 50 ± 13 ml/m2, p < 0.001). These changes were accompanied by improvement in diastolic function, NT-proBNP, 6MWT, and New York Heart Association functional class.

Conclusions:

The authors concluded that focal fibrosis does not resolve following AVR for AS, but diffuse fibrosis and myocardial cellular hypertrophy regress; and that regression is accompanied by structural and functional improvements suggesting that diffuse fibrosis is plastic in humans, measurable by CMR, and a potential therapeutic target.

Perspective:

The myocardium consists of cells and surrounding extracellular matrix; the regression of LV mass observed following AVR for AS could be due to matrix regression alone (with reduced ECV), cellular regression alone, or proportional regression of cellular and matrix compartments. This elegant study suggests that myocardial cellular hypertrophy and extracellular matrix expansion (diffuse fibrosis, assessed with CMR T1 mapping) both regress following AVR, accompanied by structural, functional, and biomarker improvements; and that cardiac myocyte loss (associated with focal replacement fibrosis, assessed with CMR late gadolinium enhancement) is irreversible. With additional research and clinical validation, it is possible that CMR findings in the asymptomatic patient with severe AS could help guide the timing of intervention, with a goal of minimizing irreversible myocardial changes.

Keywords: Aortic Valve Stenosis, Biomarkers, Cardiac Surgical Procedures, Diagnostic Imaging, Echocardiography, Extracellular Matrix, Fibrosis, Gadolinium, Heart Failure, Heart Valve Diseases, Hypertrophy, Magnetic Resonance Imaging, Myocardium, Myocytes, Cardiac, Natriuretic Peptide, Brain, Pacemaker, Artificial, Peptide Fragments, Troponin T, Transcatheter Aortic Valve Replacement


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