Abstract 3714: Dual Blockade of Renin-Angiotensin System Promotes Left Ventricular Hypertrophy Regression in Patients With Patient-Prosthesis Mismatch Following Aortic Valve Replacement
Background: Left ventricular (LV) hypertrophy regression is generally seen following aortic valve replacement (AVR) for aortic stenosis but patients with patient-prosthesis mismatch (PPM) continue to show some degrees of LV hypertrophy after surgery. The renin-angiotensin system (RAS) plays a major role in promoting and sustaining LV hypertrophy. In a controlled, randomized study, we tested the hypothesis that dual RAS blockade with angiotensin-converting enzyme inhibitor (ACEi) + angiotensin II receptor blocker (ARB) can be more effective in decreasing LV hypertrophy than a largely employed association such as ACEi + β-blockers in PPM patients.
Methods and Results: Among 251 patients undergoing isolated AVR for aortic stenosis, we enrolled a total of 136 patients having evidence of PPM (effective orifice area <0.85 cm2/m2) at postoperative echo (within 7 days from surgery). At discharge, they were randomized to ramipril + candesartan (n=68) or ramipril + methoprolol (n=68). After the 18-month treatment, they underwent a 24-h blood pressure (BP) monitoring and echocardiographic examination. At baseline, age, 24-h blood pressure, LV morpho-functional parameters and transprosthetic gradients were similar between the two groups. All 136 patients completed 18-months follow-up. LV mass index significantly decreased in both groups (ACEi + ARB: 165±19 to 122±17 g/m2, p<0.0001; ACEi ± β-blockers: 161±18 to 137±20 g/m2, p<0.0001). Systolic function remained unchanged; LV diastolic parameters increased significantly in both groups. The extent of 24-h BP decrease was similar between the two groups (−13.3/16.3% vs. −12.3/15.8%, p=0.63/p=0.71), whereas the decrease of LV mass (−27% vs. −14.8%, p<0.005) and the improvement of diastolic function were greater in ACEi + ARB group.
Conclusions: In comparison with ACEi + β-blockers, ACEi + ARB treatment showed a greater antiremodelling effect, that can be reasonably ascribed to a blood pressure-independent effect of the dual RAS blockade. This therapy should be recomended in patients with evidence of PPM after AVR.