Key result
Thoracic aortic calcification predicted 3-year cardiovascular mortality in low-gradient aortic stenosis (HR 1.085; 95% CI 1.019-1.156; P=0.011), whereas valvular calcification was key in high-gradient.
Why the study?
High valvulo-arterial impedance despite low valvular gradient in LGAS suggests high vascular load, prompting comparison of the prognostic contributions of TAC and VAC on CV mortality after TAVI in LGAS versus HGAS.
Does the prognostic impact of thoracic aortic calcifications (TAC) and valvular aortic calcifications (VAC) on 3-year cardiovascular mortality differ between patients with low-gradient and high-gradient aortic stenosis undergoing TAVI?
Cohort (n=1,396)
Does the prognostic impact of thoracic aortic calcifications (TAC) and valvular aortic calcifications (VAC) on 3-year cardiovascular mortality differ between patients with low-gradient and high-gradient aortic stenosis undergoing TAVI?
Hazard Ratio: 1.085 (95% CI 1.019–1.156)
p-value: p=0.011
Thoracic aortic calcification is a major prognostic factor for cardiovascular mortality in low-gradient aortic stenosis, whereas valvular aortic calcification is the key prognostic factor in high-gradient aortic stenosis following TAVI.
TAC/VAC associations with post-TAVI CV mortality differ by gradient and should not yet change practice; leaves open gradient-specific prognostic validation.
AIMS: In low-gradient aortic stenosis (LGAS), the high valvulo-arterial impedance observed despite low valvular gradient suggests a high vascular load. Thoracic aortic calcifications (TACs) and valvular aortic calcifications (VACs) are, respectively, surrogates of aortic load and aortic valvular gradient. The aim of this study was to compare the respective contributions of TAC and VAC on 3-year cardiovascular (CV) mortality following TAVI in LGAS vs. high-gradient aortic stenosis (HGAS) patients. METHODS AND RESULTS: A total of 1396 consecutive patients were included. TAC and VAC were measured on the pre-TAVI CT-scan. About 435 (31.2%) patients had LGAS and 961 (68.8%) HGAS. LGAS patients were more prone to have diabetes, coronary artery disease (CAD), atrial fibrillation (AF), and lower left ventricular ejection fraction (LVEF), P<0.05 for all. During the 3 years after TAVI, 245(17.8%) patients experienced CV mortality, 92(21.6%) in LGAS and 153(16.2%) in HGAS patients, P=0.018. Multivariate analysis adjusted for age, gender, diabetes, AF, CAD, LVEF, renal function, vascular access, and aortic regurgitation showed that TAC but not VAC was associated with CV mortality in LGAS, hazard ratio (HR) 1.085 confidence interval (CI) (1.019-1.156), P=0.011, and HR 0.713 CI (0.439-1.8), P=0.235; the opposite was observed in HGAS patients with VAC but not TAC being associated with CV mortality, HR 1.342 CI (1.034-1.742), P=0.027, and HR 1.015 CI (0.955-1.079), P=0.626. CONCLUSION: TAC plays a major prognostic role in LGAS while VAC remains the key in HGAS patients. This confirms that LGAS is a complex vascular and valvular disease.
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Harbaoui et al. (2021) conducted a cohort in Low- and high-gradient aortic stenosis (n=1,396). Thoracic aortic calcifications (TAC) was evaluated on 3-year cardiovascular mortality (HR 1.085, 95% CI 1.019-1.156, p=0.011). Thoracic aortic calcification predicted 3-year cardiovascular mortality in low-gradient aortic stenosis (HR 1.085; 95% CI 1.019-1.156; P=0.011), whereas valvular calcification was key in high-gradient.
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