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Distinct arterial and cardiac remodelling patterns in hypertensive heart failure with a preserved ejection fraction
Marilet van Hoogland-van Heerden1, Pindile Mntla2, Odette Heyneke3
1Department of Physiology, School of Medicine, Sefako Makgatho Health Sciences University, Gauteng, South Africa. marilet.vanhoogland@smu.ac.za.
Abstract:
Hypertension (HTN) affects 30% of Africans, a driver of heart failure with preserved ejection fraction (HFpEF), particularly in older adults with arterial stiffness. Studies in sub-Saharan Africa report HFpEF in younger black South Africans. Black, older, and obese patients with HTN often show left ventricular hypertrophy (LVH), raising whether HFpEF presents distinct clinical and cardiac characteristics compared to HTN alone. This study used a matched case-control design with cross-sectional data from a South African community-based sample to examine HTN in Black participants with and without HFpEF. A total of 125 HFpEF cases and 510 controls were initially identified, including 95 hypertensive HFpEF cases and 256 hypertensive controls without HFpEF for final analysis. Clinically stable consenting adults (>18 years) were enrolled, and echocardiographic, anthropometric, haemodynamic, and pulse wave velocity (PWV) measurements were obtained. The mean age was ~58 years in both groups, and 80% were overweight or obese. Central diastolic blood pressure (DBPc) (p = 0.0295) and pulse pressure (PPc) (p = 0.0352) were lower in HFpEF, while PWV was higher (10.9 ± 4.8 vs 6.9 ± 3.9 m/s, p < 0.0001). Most HFpEF participants had concentric LVH (73%). Normal LV geometry was the most prevalent pattern among controls (45%); however, among controls with LVH, eccentric LVH was more prevalent than concentric LVH. Peripheral BP (BPp) was associated with the early to late ventricular filling velocities (E/A), while DBPp, PPp, and E/A correlated with HTN treatment. Heart failure with preserved ejection fraction was associated with greater arterial stiffness, concentric LVH, reduced renal function, higher heart rate, and elevated C-reactive protein and galectin-3, supporting adverse arterial-ventricular coupling and inflammatory-driven concentric remodelling in hypertensive HFpEF.