The additive effects of type 2 diabetes mellitus on left ventricular deformation and myocardial perfusion in essential hypertension: a 3.0 T cardiac magnetic resonance study

Abstract

Background Type 2 diabetes mellitus (T2DM) increases the risks of heart failure and mortality in patients with hypertension, however the underlying mechanism is unclear. This study aims to investigate the impact of coexisting T2DM on left ventricular (LV) deformation and myocardial perfusion in hypertensive individuals. Materials and methods Seventy hypertensive patients without T2DM [HTN(T2DM−)], forty patients with T2DM [HTN(T2DM+)] and 37 age- and sex-matched controls underwent cardiac magnetic resonance examination. Left ventricular (LV) myocardial strains, including global radial (GRPS), circumferential (GCPS) and longitudinal peak strain (GLPS), and resting myocardial perfusion indices, including upslope, time to maximum signal intensity (TTM), and max signal intensity (MaxSI), were measured and compared among groups by analysis of covariance after adjusting for age, sex, body mass index (BMI) and heart rate followed by Bonferroni’s post hoc test. Backwards stepwise multivariable linear regression analyses were performed to determine the effects of T2DM on LV strains and myocardial perfusion indices in patients with hypertension. Results Both GRPS and GLPS deteriorated significantly from controls, through HTN(T2DM−), to HTN(T2DM+) group; GCPS in HTN(T2DM+) group was lower than those in both HTN(T2DM−) and control groups. Compared with controls, HTN(T2DM−) group showed higher myocardial perfusion, and HTN(T2DM+) group exhibited lower perfusion than HTN(T2DM−) group and controls. Multiple regression analyses considering covariates of systolic blood pressure, age, sex, BMI, heart rate, smoking, indexed LV mass and eGFR demonstrated that T2DM was independently associated with LV strains (GRPS: p = 0.002, model R2= 0.383; GCPS: p < 0.001, model R2= 0.472; and GLPS: p = 0.002, model R2= 0.424, respectively) and perfusion indices (upslope: p < 0.001, model R2= 0.293; TTM: p < 0.001, model R2= 0.299; and MaxSI: p < 0.001, model R2= 0.268, respectively) in hypertension. When both T2DM and perfusion indices were included in the regression analyses, both T2DM and TTM were independently associated with GRPS (p = 0.044 and 0.017, model R2= 0.390) and GCPS (p = 0.002 and 0.001, model R2= 0.424), and T2DM but not perfusion indices was independently associated with GLPS (p = 0.002, model R2= 0.424). Conclusion In patients with hypertension, T2DM had an additive deleterious effect on subclinical LV systolic dysfunction and myocardial perfusion, and impaired myocardial perfusion by coexisting T2DM was associated with deteriorated LV systolic dysfunction.

Echocardiographic study of myocardial work in patients with type 2 diabetes mellitus

“…Essential hypertension and T2DM are two common chronic diseases. T2DM can aggravate LV diastolic dysfunction in patients with essential hypertension [ 38 , 39 ].…”

Effect of diabetes mellitus on the development of left ventricular contractile dysfunction in women with heart failure and preserved ejection fraction

“…The underlying mechanisms of the adverse effect of DM on LV systolic function are not fully understood. HFpEF comorbid with DM could induce a broad context of metabolic disorder, oxidative stress, and a systemic inflammatory state, resulting in excitation-contraction coupling impairment, extracellular matrix fibrosis, and microvasculature dysfunction, thereby promoting myocardial contractility impairment [ 3 , 23 , 26 ]. Based on the observation in our study that DM has a greater adverse effect on LV contractility in women than in men, the decline in the estrogen level at menopause together with the presence of DM may be responsible for this difference [ 27 ].…”

Additive Effects of Obesity on Myocardial Microcirculation and Left Ventricular Deformation in Essential Hypertension: A Contrast-Enhanced Cardiac Magnetic Resonance Imaging Study

“…Among these, microvascular abnormalities are an important disorder in both conditions with certain common pathological changes: endothelial dysfunction, microvascular remodeling and rarefaction ( 20 ). Some previous studies revealed no obvious difference in the resting myocardial perfusion between hypertensive and normotensive subjects ( 21 , 22 ), while other studies reported significantly increased resting myocardial perfusion in hypertensive patients due to an adaptive mechanism ( 23 , 24 ). Our results showed slightly increased resting myocardial perfusion in hypertensive patients without obesity compared with controls, but this difference did not reach statistical significance.…”