Introduction: The European Society of Cardiology classified hypertensive heart disease (HHD) into 4 left ventricular (LV) phenotypes by indexed LV mass (LVM), mass : volume ratio (M:V) and indexed end diastolic volume (EDV) (Table 1). All forms of HHD carry varying degrees of adverse cardiovascular prognosis, but their underlying mechanisms are poorly understood. We sought to investigate the presence and extend of ultra–structural myocardial changes and variation in central aortic function using CMR relaxometry and voxel–tracking myocardial strain techniques.Methods: 88 hypertensive patients (49 ± 14 years, 57% male, SBP: 167 ± 30mmHg, DBP: 96 ± 14 mmHg) underwent CMR (1.5T) and were compared with 29 age–and sex–matched normotensive controls (47 ± 14years, 59% male, SBP: 128 ± 12mmHg, DBP: 79 ± 10mmHg). Native and post–contrast T1–mapping was performed. Circumferential myocardial strain was calculated with voxel–tracking software. Aortic compliance and distensibility were also estimated.Results: Please see Figure 1. At a structural level, increased LV mass in eccentric LVH and concentric LVH resulted from: i) significantly increased myocardial cell volume (eccentric LVH: 78 ± 19 vs concentric LVH: 73 ± 15 vs remodeling: 55 ± 9 respectively, P < 0.05) and ii) significantly increased interstitial volume (eccentric LVH: 33 ± 10 vs concentric LVH: 30 ± 10 vs remodeling: 19 ± 2 respectively, P < 0.05). Functionally, eccentric LVH and concentric LVH were associated with significantly impaired peak circumferential strain (eccentric LVH: –12.8 ± 4.6 vs concentric LVH: – 15.5 ± 3.1 vs remodeling: –17.1 ± 3.2 vs controls: –17.4 ± 2.6% respectively, P < 0.05), with evidence of systolic and diastolic strain rate impairment. Despite similar BP severity as LVH phenotypes, LV remodeling was not associated with significant intracellular/interstitial expansion (native T1: 1029 ± 45 vs 1024 ± 41ms, P = 0.67) or myocardial dysfunction compared to normotensive controls but was associated with reduced aortic compliance and distensibility.Conclusions: The extent of interstitial fibrosis is different across hypertensive heart disease phenotypes. LVH, in particular eccentric LVH, is associated with significant myocardial interstitial fibrosis and systolic/diastolic strain impairment. LV remodeling is associated with normal myocardial, but abnormal aortic, function. Our results may explain the poor cardiovascular prognosis with hypertensive LVH.(Equation is included in full-text article.)(Equation is included in full-text article.)Figure 1.