Diabetic cardiomyopathy: How can cardiac magnetic resonance help?

Tadić, Marijana; Cuspidi, Cesare; Calicchio, Francesca; Mancia, Giuseppe

doi:10.1007/s00592-020-01528-2

Cited by 26 publications

(21 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Finally, the eGFR and uric acid were independently associated with LV PS in radial, circumferential, and longitudinal directions. In T2DM patients without CKD, our data revealed a reduction in radial PS, radial PSSR, radial PDSR, and circumferential PDSR compared to normal individuals, but no significant difference in LVEF was observed between these two groups, which was consistent with previous strain data regarding myocardial mechanics in DM [18][19][20][21][22]. The first 3-dimensional CMR strain study showed that longitudinal and circumferential PS as well as peak Fig.…”

Section: Discussionsupporting

confidence: 91%

The additive effects of kidney dysfunction on left ventricular function and strain in type 2 diabetes mellitus patients verified by cardiac magnetic resonance imaging

Zhang

Wang

Ren

et al. 2021

Cardiovasc Diabetol

View full text Add to dashboard Cite

Background Patients with type 2 diabetes mellitus (T2DM) are susceptible to coexisted with chronic kidney disease (CKD), which may increase cardiovascular mortality in these patients. The present study aimed to verify whether CKD aggravates the deterioration of left ventricular (LV) myocardial strain in T2DM patients and to explore the risk factors associated with LV strain. Materials and methods In total, 105 T2DM patients and 52 healthy individuals were included and underwent cardiac magnetic resonance examination. Patients were divided into the following two groups: T2DM with CKD (n = 33) and T2DM without CKD (n = 72). The baseline clinical and biochemical indices were obtained from hospital records before the cardiac magnetic resonance scan. Cine sequences, including long-axis views (2-chamber and 4-chamber) and short-axis views, were acquired. LV function and global strain parameters were measured based on cine sequences and compared among three groups. Pearson’s analysis was performed to investigate the correlation between LV strain parameters and clinical indices. Multiple linear regression analysis was used to identify the independent indicators of LV strain. Results Compared with normal controls, T2DM patients without CKD had a significantly decreased magnitude of peak strain (PS; radial), peak systolic strain rate (radial), and peak diastolic strain rate (radial and circumferential) (all P < 0.05). Furthermore, T2DM patients with CKD displayed markedly lower magnitudes of PS (radial, circumferential, and longitudinal) and peak diastolic strain rate (circumferential and longitudinal) than both normal controls and T2DM patients without CKD (all P < 0.05). The eGFR was positively associated with the magnitude of PS (R = radial, 0.392; circumferential, 0.436; longitudinal, 0.556), while uric acid was negatively associated with the magnitude of PS (R = radial, − 0.361; circumferential, − 0.391; longitudinal, − 0.460) (all P < 0.001). Multivariable linear regression indicated that the magnitude of PS was independently associated with eGFR (β = radial, 0.314; circumferential, 0.292; longitudinal, 0.500) and uric acid (β = radial, − 0.239; circumferential, − 0.211; longitudinal, − 0.238) (all P < 0.05). Conclusions Kidney dysfunction may aggravate the deterioration of LV strain in T2DM patients. LV strain is positively associated with the estimated glomerular filtration rate and negatively associated with uric acid, which may be independent risk factors for predicting reduction of LV strain.

show abstract

Section: Discussionsupporting

confidence: 91%

The additive effects of kidney dysfunction on left ventricular function and strain in type 2 diabetes mellitus patients verified by cardiac magnetic resonance imaging

Zhang

Wang

Ren

et al. 2021

Cardiovasc Diabetol

View full text Add to dashboard Cite

show abstract

“…This may be explained that the myocardial changes of T2DM patients without FMR are mainly manifested as the pathological process of simple diabetic cardiomyopathy. Sustained hyperglycaemia can cause oxidative stress, renin angiotensin system activation, vascular endothelial dysfunction, cytokine activation and cardiac autonomic nervous dysfunction, which may lead to myocardial extracellular matrix deposition, increased oxygen consumption of myocardial cells, myocardial hypertrophy, myocardial interstitial fibrosis and decreased myocardial compliance, ultimately resulting in cardiac dysfunction [ 18 , 19 ]. These results indicate that the variations in strain occur earlier and are more noticeable than LVEF, affirming that early detection of PS changes is important in constructive interventions and delaying the deterioration of the myocardium in T2DM patients.…”

Section: Discussionmentioning

confidence: 99%

Aggravation of functional mitral regurgitation on left ventricle stiffness in type 2 diabetes mellitus patients evaluated by CMR tissue tracking

Zhang

Yan

Jiang

et al. 2021

Cardiovasc Diabetol

View full text Add to dashboard Cite

Background Functional mitral regurgitation (FMR) is one of the most common heart valve diseases in diabetes and may increase left ventricular (LV) preload and aggravate myocardial stiffness. This study aimed to investigate the aggravation of FMR on the deterioration of LV strain in type 2 diabetes mellitus (T2DM) patients and explore the independent indicators of LV peak strain (PS). Materials and methods In total, 157 T2DM patients (59 patients with and 98 without FMR) and 52 age- and sex-matched healthy control volunteers were included and underwent cardiac magnetic resonance examination. T2DM with FMR patients were divided into T2DM patients with mild (n = 21), moderate (n = 19) and severe (n = 19) regurgitation. LV function and global strain parameters were compared among groups. Multivariate analysis was used to identify the independent indicators of LV PS. Results The T2DM with FMR had lower LV strain parameters in radial, circumferential and longitudinal direction than both the normal and the T2DM without FMR (all P < 0.05). The mild had mainly decreased peak diastolic strain rate (PDSR) compared to the normal. The moderate had decreased peak systolic strain rate (PSSR) compared to the normal and PDSR compared to the mild and the normal. The severe FMR group had decreased PDSR and PSSR compared to the mild and the normal (all P < 0.05). Multiple linear regression showed that the regurgitation degree was independent associated with radial (β = − 0.272), circumferential (β = − 0.412) and longitudinal (β = − 0.347) PS; the months with diabetes was independently associated with radial (β = − 0.299) and longitudinal (β = − 0.347) PS in T2DM with FMR. Conclusion FMR may aggravate the deterioration of LV stiffness in T2DM patients, resulting in decline of LV strain and function. The regurgitation degree and months with diabetes were independently correlated with LV global PS in T2DM with FMR.

show abstract

“…Diabetic cardiomyopathy is one of the main complications of diabetes and one of the largest causes of mortality in patients with diabetes ( 25 ). Moreover, its pathogenesis is complex and has not been fully defined ( 26 ). In recent years, studies have reported that excessive ERS lead to the apoptosis of cardiomyocytes ( 27-29 ).…”

Section: Discussionmentioning

confidence: 99%

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Wang

et al. 2021

Exp Ther Med

View full text Add to dashboard Cite

Diabetic cardiomyopathy is a common complication of diabetes, in which endoplasmic reticulum stress (ERS) serves an important role. Rutin can treat the myocardial dysfunction of diabetic rats. However, to the best of our knowledge, studies on the effects of Rutin on myocardial injury caused by diabetes from the perspective of ERS have not previously been reported. In the present study, the role of rutin in the regulation of ERS in myocardial injury was assessed. Different high glucose concentrations were used to treat H9C2 myoblast cells to establish a myocardial damage model. A cell counting kit-8 assay was used to determine cell viability. A lactate dehydrogenase kit was used to detect cytotoxicity. Apoptosis levels were determined using a TUNEL assay. Western blotting was used to determine the expression levels of apoptosis-related proteins and ERS-related proteins, including heat shock protein A family member 5, inositol-requiring enzyme-1α, X-box binding protein 1, activating transcription factor 6, C/EBP-homologous protein (CHOP), cleaved caspase-12 and caspase-12. The anti-apoptotic and anti-ERS effects of Rutin on H9C2 cardiac cells induced by high glucose were examined after the administration of the ERS activator thapsigargin (TG). The results indicated that rutin could dose-dependently inhibit the level of apoptosis and ERS induced by high glucose in H9C2 cells. After administration of the ERS activator TG, it was demonstrated that TG could reverse the anti-apoptotic and anti-ERS effects of rutin on H9C2 cells stimulated with high glucose. Collectively, the present results suggested that rutin may alleviate cardiomyocyte model cell injury induced by high glucose through the inhibition of apoptosis and ERS.

show abstract

Diabetic cardiomyopathy: How can cardiac magnetic resonance help?

Cited by 26 publications

References 27 publications

The additive effects of kidney dysfunction on left ventricular function and strain in type 2 diabetes mellitus patients verified by cardiac magnetic resonance imaging

The additive effects of kidney dysfunction on left ventricular function and strain in type 2 diabetes mellitus patients verified by cardiac magnetic resonance imaging

Aggravation of functional mitral regurgitation on left ventricle stiffness in type 2 diabetes mellitus patients evaluated by CMR tissue tracking

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Contact Info

Product

Resources

About