Unravelling racial differences in hypertensive heart disease by multiparametric cardiovascular magnetic resonance: a phenotype-wide association study

Abstract

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dr Georgiopoulos was supported by the Onassis Foundation under the special grant & support program for scholars" association members Introduction – Black Afro-Caribbean hypertensives (BAHs) are exposed to a higher risk of heart failure (HF) than white hypertensives (WHs). Arterial afterload is higher in BAHs due to increased arterial stiffness and vascular volume; BAHs develop more often left ventricular (LV) hypertrophy, dilatation and systolic dysfunction than WHs. However, it is unclear whether other racial differences concur to the more pronounced LV remodelling in BAHs. Methods – This cross-sectional study included hypertensive patients undergoing cardiovascular magnetic resonance for their clinical work-up (1.5T Aera Siemens-Healthcare). Clinical history and haemodynamic parameters were collected in all participants; a subset of patients had complete bio-humoral assay of the renin-angiotensin-aldosterone system (RAAs). Arm cuff pressure was measured during CMR. The CMR protocol included: i) Arterial afterload / LV arterial-coupling - pulse-wave-velocity (PWV), aortic (Ea) and LV elastance (Ees) by aorta anatomic and phase-contrast velocity-encoding imaging; ii) ventricular remodelling and function - LV and right ventricular (RV) volumes, mass, EF, LV peak-filling rate by short-axis cine images; global circumferential and longitudinal strains by cine feature tracking; iii) left atrial (LA) remodelling volumes and reservoir, conduit and booster functions by long-axis cine images; iv) tissue characterisation: T2 and pre/post-contrast T1 relaxation times, extracellular volume (ECV) by single mid-ventricular short-axis T1/T2-mapping. Results – 34 BAHs and 35 WHs (52 ± 12 vs 45 ± 14 years, P < 0.05; 61% vs 65% males P = NS) were included in the study. Baseline features are summarised in the Table. LV systolic dysfunction was more prevalent in BAH than WHs (P = 0.038). Of note, BAHs tended to have greater LV volumes and significantly higher LV mass and septal thickness than WHs. In BAHs, but not in WHs, PWV was associated with increased septal thickness after correction for blood pressure and age (β-value: 0.447, P = 0.02). Normalised RV mass was greater in BHA than WHs; RV mass suits for the identification of racial or circulating factors predisposing to hypertrophy being largely unaffected by systemic afterload. In our study LV diastolic function and LA volumes were similar between BAHs and WHs, and none of the subjects had conditions associated with pre-capillary pulmonary hypertension. Hence, higher RV-mass in BAHs pinpoints a racial susceptibility to myocardial hypertrophy. Finally, in a subset of patients with RAAs assays (n = 43), the aldosterone/renin ratio was higher in BAHs than WHs (67.04 [IQR: 19.37-209.73] vs 13.77 [IQR: 7.47-40.43], P = 0.01). Conclusion – BAHs have heightened LV remodelling than WHs because of racial predisposition to develop hypertrophy which also encompasses derangements in RAAs. Altogether, these findings may account for the greater risk for HF in BAHs than WHs.