DOI: 10.1093/eurheartj/ehag785.1003 ISSN: 0195-668X

Exercise capacity in arterial hypertension: left ventricular posterior wall thickness as a structural determinant of reduced peak oxygen consumption in preserved ejection fraction phenotype

V Pires Kassab, S V Villela Daniel, L G O Oldra, G S Milanesi, F R de Souza, L A Bortolotto, R Kalil Filho, M J N N Alves

Abstract

Introduction

Arterial hypertension (AH) is associated with left ventricular hypertrophy (LVH) and cardiac remodelling, characterized by increased septum wall thickness (SWT), which are recognized markers of hypertensive heart disease, and may impair exercise capacity even in patients with preserved ejection fraction. Peak oxygen consumption (peak VO2) is a key marker of functional capacity, but its relationship with echocardiographic structural parameters in AH patients remains unclear.

Purpose

To evaluate the association between peak VO2 and echocardiographic measurements in AH patients with preserved ejection fraction and LVH.

Methods

This retrospective study analysed a cohort of 8,423 patients with AH (blood pressure >140mmHg), from which 47 patients with ejection fraction ≥55%, and SWT and LVPW >9mm on Doppler echocardiography, were selected. Peak VO2 was obtained by cardiopulmonary exercise testing and analysed in relation to clinical and echocardiographic variables. Spearman correlation and multivariable linear regression analyses were performed.

Results

Peak VO2 showed a significant negative correlation with age (R = −0.322, p=0.027), and LVPW (R = −0.363, p=0.012) indicating lower exercise capacity. Positive correlations were observed with height (R=0.551, p<0.001), body surface area (R=0.375, p=0.009), aortic root diameter (R=0.328, p=0.024), and left ventricular end-diastolic diameter (R=0.307; p=0.036). No correlations were found for weight (p=0.276), LA size (p=0.186), left ventricle (LV) (p=0.914), SWT (p=0.359), LV systolic volume (p=0.084), and fractional shortening (p=0.612), and LV mass index (p=0.648). Final multivariable model explained 46.7% of the variability in peak VO2 (R²=0.467). In linear regression, age (B = -0.296; ß = -0.406; 95% CI: -0.460 to -0.133; p=0.001), height (B = 27.316; ß = 0.326; 95% CI: 6.549 tô 48.083; p=0.011), aortic root diameter (B = 0.702; ß = 0.260; 95% CI: 0.034 to 1.371; p=0.040), and LVPW (B = -1.736; ß = -0.278; 95% CI: -3.115 to -0.357; p=0.015) remained independently associated with peak VO2. Notably, greater LVPW was independently associated with lower peak VO2, indicating a consistent and robust negative association with exercise capacity. Additionally, the interaction between LVPW and sex was significant (LVPW × SEX: B = -2.585; p=0.010), with the model including SEX and LVPW × SEX explaining R=0.575, R 2=0.330, and F=10.84, p<0.001, indicating a stronger negative impact of LVPW on exercise capacity in women compared to men.

Conclusion

LVPW emerged as an independent determinant of lower peak VO2 in AH patients with LVH and preserved ejection fraction. The negative impact of LVPW on exercise capacity was more pronounced in women, highlighting sex-specific functional consequences of concentric remodelling. These findings reinforce the role of structural cardiac alterations as contributors to exercise limitation even in the absence of systolic dysfunction.

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