Additive effect of hypertension on left ventricular structure and function in patients with asymptomatic type 2 diabetes mellitus.

Objective We aimed to comprehensively determine the effects of hypertension on left ventricular (LV) structure, microcirculation, tissue characteristics, and deformation in type 2 diabetes mellitus (T2DM) using multiparametric cardiac magnetic resonance (CMR) imaging. Methods We prospectively enrolled 138 asymptomatic patients with T2DM (80 normotensive and 58 hypertensive individuals) and 42 normal glucose-tolerant and normotensive controls and performed multiparametric CMR examination to assess cardiac geometry, microvascular perfusion, extracellular volume (ECV), and strain. Univariable and multivariable linear analysis was performed to analyze the effect of hypertension on LV deformation in patients with T2DM. Results Compared with controls, patients with T2DM exhibited decreased strain, decreased microvascular perfusion, increased LV remodeling index, and increased ECV. Hypertension lead to greater deterioration of LV strain (peak strain-radial, P = 0.002; peak strain-longitudinal, P = 0.006) and LV remodeling index (P = 0.005) in patients with T2DM after adjustment for covariates; however, it did not affect microvascular perfusion (perfusion index, P = 0.469) and ECV (P = 0.375). In multivariable analysis, hypertension and diabetes were independent predictors of reduced LV strain, whereas hypertension is associated with greater impairment of diastolic function (P = 0.009) but not systolic function (P = 0.125) in the context of diabetes, independent of clinical factors and myocardial disorder. Conclusion Hypertension in the context of diabetes is significantly associated with LV diastolic function and concentric remodeling; however, it has little effect on systolic function, myocardial microcirculation, or fibrosis independent of covariates, which provide clinical evidence for understanding the pathogenesis of comorbidities and explaining the development of distinct heart failure phenotypes.