Subendocardial Systolic Dysfunction in Asymptomatic Normotensive Diabetic Patients

Abstract

Background: It remains uncertain whether diabetes itself causes specific echocardiographic features of myocardial morphology and function in the absence of hypertension or ischemic heart disease. The purpose of the present study was to determine the characteristics of pure diabetic cardiomyopathy-related echocardiographic morphology and function using layer-by-layer evaluation with myocardial strain echocardiography. Methods and Results:We enrolled 104 patients with poorly controlled type 2 diabetes mellitus (mean HbA1c level, 10%) with (n=74) or without (n=40) hypertension and 24 age-and sex-matched healthy volunteers. Patients with coronary artery stenosis or structural heart disease were excluded. Myocardial layer-specific strain was analyzed by speckle tracking echocardiography. Compared with the healthy control group, the normotensive diabetes group showed no significant difference in ejection fraction, left ventricular mass index, diastolic properties, left atrial volume index, or B-type natriuretic protein (BNP) level, but global longitudinal strain and subendocardial radial strain were significantly deteriorated. The deterioration of longitudinal strain correlated with body mass index (R=0.49, P<0.01) and blood pressure (R=0.36, P<0.01) in the normotensive diabetes group. Conclusions:Deterioration of left ventricular longitudinal shortening accompanied by decreased subendocardial wall thickening are the characteristic functional abnormalities of diabetic cardiomyopathy in patients without hypertrophy, diastolic dysfunction, or elevated BNP. Obesity and blood pressure may also play important roles in this strain abnormality in asymptomatic patients with type 2 diabetes. (Circ J 2015; 79: 1749 -1755

Impact of obesity and epicardial fat on early left atrial dysfunction assessed by cardiac MRI strain analysis

“…Diastolic dysfunction has been previously shown to correlate with duration of diabetes, HbA1c and obesity [24]. Previous reports of correlations between strains and BSA or BMI were limited to ventricle [25] and detailed LV strain contraction analysis highlight the rule of glycemic control [26]. In our study, we did not find an association between LA strain and duration of diabetes or HbA1c, possibly due to the early stage of diastolic dysfunction detected.…”

Mechanisms of Left Ventricular Dysfunction Assessed by Layer-Specific Strain Analysis in Patients With Repaired Tetralogy of Fallot

“…16 Yu et al showed that in anthracycline-treated survivors of childhood cancers, subendocardial circumferential deformation is sensitive to anthracycline. 17 In a rabbit model of DM, 25 and in patients with ischemia 15 or hypertension, 26 the vulnerability of the endocardial layers has been proposed. Although vulnerability of the endocardial layers in patients with rTOF has not been clarified physiologically or pathologically, the present study's findings demonstrated that potential myocardial damage occurs in the endocardial layers before the midmyocardial and epicardial layers in patients with rTOF when measured with layer-specific strain analysis, which is concordant with findings in reports on other diseases.…”

Prevalence, etiology, and clinical implications of reduced longitudinal systolic strain in renal transplant candidates

“…Recently, Enomoto et al. found that patients with poorly controlled DM had much worse GLS regardless of whether or not there was coexisting HTN . As of now, the exact pathophysiologic mechanism for this dysfunction is unknown, but there is some suspicion that microvasculopathy and inhibition of compensatory angiogenesis may be responsible via degeneration of myocardial fibers and reduced perfusion .…”

“…28 Recently, Enomoto et al found that patients with poorly controlled DM had much worse GLS regardless of whether or not there was coexisting HTN. 29,30 As of now, the exact pathophysiologic mechanism for this dysfunction is unknown, but there is some suspicion that microvasculopathy and inhibition of compensatory angiogenesis may be responsible via degeneration of myocardial fibers and reduced perfusion. 30 In addition, the extracellular matrix in diabetics is known to poorly adjust and compensate for progressively worsening cardiac demands to the point that longitudinal strain decreases.…”