Background: Calcific aortic stenosis (AS) is due to progressive tissue deposition of calcium, subsequent stiffening and eventually poor opening of the aortic valve. Increased mechanical stress on the valve tissue due to high heart rate (HR) or high blood pressure (BP) has been suggested to play a role in AS progression but literature is scarce. In a prospective cohort of AS patients, we assessed impact of resting HR and systolic blood pressure (SBP) on AS progression.
Purpose: To assess impact of HR and BP on AS progression in a prospective cohort of asymptomatic AS patients, COFRASA (clinicalTrial.gov_number_NCT00338676) – GENERAC (clinicalTrial.gov_number_NCT00647088).
Methods: A comprehensive clinical evaluation including HR and BP measurement was performed at baseline in an ongoing prospective cohort of pure isolated at least mild degenerative AS. AS severity was evaluated at baseline and yearly thereafter using echocardiography (mean pressure gradient (MPG, mmHg)) and computed tomography (degree of aortic valve calcification (AVC, arbitrary unit (AU)). Annual progression was calculated as [(final measurement - baseline measurement)/follow-up duration] for both MPG and AVC measurements.
Results: We enrolled 236 patients with at least 2 years of follow-up. Mean age was 72±10 years, 75% were men. Mean HR was 66±12bpm, mean SBP 126±17 mmHg. Forty-eight patients (20%) had systolic hypertension (SHTN = SBP≥140 mmHg) at inclusion. Seventy-five (32%) had a HR<70 bpm. After a mean follow-up of 4.2±1.8 years, HR and SBP as continuous variables had no impact on AS progression (HR: mean MPG progression r=0.1, p=0.95, mean AVC progression r=0.05, p=0.48; SBP: mean MPG progression r=0.1, p=0.95, mean AVC progression r=0.08, p=0.21). This was true in univariate analysis and after adjustment for age, sex, and baseline severity and valve anatomy. Same results were obtained when dividing the population in HR≥70 or HR 70 bpm, and with or without SHTN.
Conclusion: In our prospective cohort of AS patients, we did not find any impact of HR and SBP on AS progression. This was true overall and after adjustment for age, sex, valve anatomy or baseline AS severity. Our results do not suggest a role of HR and SBP in progression of AS. Although slow HR has been shown to be associated with better cardiovascular outcomes, and although SHTN should be adequately treated, no influence on AS progression should be expected.