Hemodynamic changes in blood pressure and estimated pulse wave velocity following LVOT obstruction relief with mavacamten
M E Koilakou, D Terentes-Printzios, A Kasiakogias, A S Antonopoulos, V Gardikioti, F E Kourti, A Kourountzoglou, T Tsampras, T Katsimichas, P Alexiou, E Georgousi, A Miliou, G Lazaros, K Tsioufis, C VlachopoulosAbstract
Background/Introduction
In obstructive hypertrophic cardiomyopathy (oHCM), dynamic left ventricular outflow tract (LVOT) obstruction limits effective blood flow and alters systemic hemodynamics. Mavacamten reduces myocardial contractility and relieves LVOT gradients. While its effects on obstruction and symptoms are well established, the impact on systemic blood pressure (BP) and arterial stiffness remains insufficiently characterized.
Purpose
To assess changes in BP, mean arterial pressure (MAP), and estimated pulse wave velocity (ePWV) following initiation of mavacamten, and to determine whether pharmacological relief of LVOT obstruction is associated with changes in systemic arterial load and stiffness during short-term follow-up.
Methods
Thirty-six consecutive patients with oHCM were assessed at baseline and after a mean follow-up of 6 months following mavacamten initiation. Patients maintained stable vasoactive medications. ePWV was calculated using a validated equation based on age and MAP. Office systolic BP (OSBP), diastolic BP (ODBP), MAP, and ePWV were compared using paired-sample t-tests.
Results
LVOT gradients decreased significantly (Valsalva: 85.5±29.3 to 29.3±18.5 mmHg; Δ−56.2 mmHg; p<0.001), accompanied by parallel improvement in functional status, with most patients improving by at least one NYHA class (p<0.001). OSBP was significantly higher compared with baseline (mean paired difference was 8.1 mmHg; 95% CI 2.8 to 13.4; p=0.004). MAP also increased significantly (5.1 mmHg; 95% CI 0.9 to 9.3; p=0.02). ODBP showed a non-significant increase (3.1 mmHg; 95% CI 1.0 to 7.2;p=0.13). ePWV increased significantly at follow-up (baseline–follow-up 0.39 m/s; 95% CI 0.08 to 0.70; p=0.015), indicating higher estimated arterial stiffness values after treatment initiation. When stratified by mavacamten dose (>5mg vs <=5 mg), mean increases were numerically higher in the second group (10mg/15mg of mavacamten, ΔePWV 0.68 vs 0.26 m/s; ΔOSBP 14.1 vs 5.4 mmHg; ΔMAP 9.1 vs 3.4 mmHg), suggesting a possible dose-related effect, although between-group differences did not reach statistical significance.
Conclusion(s)
In patients with oHCM, initiation of mavacamten was associated with significant increases in systolic BP, MAP, and ePWV over 6 months. These findings suggest that systemic BP and arterial stiffness indices may increase following pharmacological relief of LVOT obstruction. The observed rise in ePWV highlights the potential impact of treatment on vascular load and central hemodynamics, emphasizing the need for BP monitoring after therapy initiation. Reassessment of antihypertensive therapy during follow-up may be required to maintain optimal vascular control.