# Increased Left Ventricular Myocardial Extracellular Volume Assessed by Cardiac Computed Tomography as a Consequence of Aortic Stenosis and Coexisting Cardiovascular Risk Factors

## TL;DR

This study shows that certain risk factors and aortic stenosis severity are linked to increased heart tissue fibrosis in patients scheduled for a heart valve procedure.

## Contribution

The study identifies hypertension, smoking, and severe aortic stenosis as independent predictors of increased myocardial extracellular volume in TAVI candidates.

## Key findings

- Higher extracellular volume was observed in patients with hypertension, smoking history, and severe aortic stenosis.
- ECV correlated positively with cardiovascular risk factors and aortic valve calcium score, and negatively with aortic valve area.
- Regression analysis confirmed hypertension, smoking, and smaller aortic valve area as independent predictors of increased ECV.

## Abstract

Background/Objectives: Extracellular volume (ECV) expansion reflects myocardial fibrosis and may play a role in subjects with severe aortic stenosis (AS) receiving transcatheter aortic valve implantation (TAVI). This study aimed to assess the relationship between cardiovascular risk factors (CVRF), AS severity and left ventricular myocardial ECV measured by cardiac computed tomography (CCT). Methods: 61 patients qualified for TAVI underwent pre-procedural CCT. CVRFs were recorded, including advanced age, male gender, obesity, hypertension, hypercholesterolemia, hypertriglyceridemia, type 2 diabetes, and smoking. The CCT protocol included non-contrast (for aortic valve calcium score, AVCS), angiographic (for vascular access planning), and delayed phases (for left atrial appendage thrombus assessment). ECV was calculated from attenuation values of the interventricular septum and left ventricular cavity assessed in native and delayed phases. Patients were stratified based on the presence/absence of individual CVRFs, median AVCS, and aortic valve area (AVA). Results: Mean ECV was higher in patients with hypertension (28.01% vs. 26.93%, p = 0.03), smokers (28.71% vs. 26.52%, p = 0.01), AVCS ≥ 2975 (28.08% vs. 26.95%, p = 0.02), and AVA < 0.95 cm2 (28.63% vs. 26.53%, p = 0.01). Positive correlations were found between ECV and the number of CVRFs (r = 0.49, p = 0.01), BMI (r = 0.30, p = 0.01), systolic BP (r = 0.31, p = 0.02), and AVCS (r = 0.36, p = 0.01); AVA correlated negatively (r = −0.59, p = 0.01). Regression showed that hypertension, smoking, and smaller AVA were independent predictors of higher ECV. Conclusions: Among TAVI candidates, hypertension, smoking, and more advanced AS are independently associated with increased myocardial ECV on CCT. These findings may reflect subclinical myocardial remodeling and support the added diagnostic value of ECV in pre-TAVI assessment.