Echocardiographic evidence for impaired myocardial performance in children with type I diabetes mellitus

Friedman, Nancy; Levitsky, Lynne L.; Edidin, Deborah V.; Vitullo, Dolores A.; Lacina, Samuel J.; Chiemmongkoltip, Pipit

doi:10.1016/0002-9343(82)90775-6

Cited by 70 publications

(26 citation statements)

References 15 publications

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“…Friedman et al reported decreased left ventricular function assessed by ejection fraction, minor axis shortening, and velocity of circumferential fiber shortening in children and adolescents with type 1 diabetes. No correlations with duration of diabetes or metabolic control were found in their study [6]. This pattern has also been reported by other authors [9,11].…”

Section: Discussionsupporting

confidence: 90%

Echocardiographic load-independent indices of contractility in children and adolescents with type I diabetes: Effect of metabolic control and insulin on left ventricular performance

Schwingshandl¹,

Ward²,

Silink³

et al. 1995

Pediatr Cardiol

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A case-control study was carried out in a tertiary referral teaching hospital to evaluate left ventricular contractility in children and adolescents with type 1 diabetes and to study factors influencing left ventricular contractility. Thirty-four children and young adults with type 1 diabetes (age 10.8-21.8 years) were randomly selected from approximately 400 patients of the same age range in the outpatient department and compared with 16 non-diabetic controls (age 7.3-21.2 years). The relation of end-systolic wall stress to velocity of circumferential fiber shortening as a standard deviation score (SDS) from the normal range described by Colan et al. was used to assess left ventricular contractility. In the diabetic group the effect of age, duration of diabetes, metabolic control, insulin dose, and autonomic function on left ventricular contractility were studied. It was found that the end-systolic wall stress-velocity of circumferential fiber shortening relation was not different between diabetic subjects and controls [+0.52 (SEM 0.21) vs +0.90 (SEM 0.26) SDS, p = 0.3]. In the diabetic subjects, the end-systolic wall stress-velocity of circumferential fiber shortening relation was positively correlated with glycated hemoglobin (r = 0.37, p = 0.03) and insulin dose per kilogram of body weight (r = 0.36, p = 0.04). Those two variables together explained 24% of the variability in the end-systolic wall stress-velocity of circumferential fiber shortening relation. Twenty-eight of the diabetic subjects were also assessed for cardiac autonomic function. Disturbances of cardiac autonomic function were not associated with increased contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 90%

Echocardiographic load-independent indices of contractility in children and adolescents with type I diabetes: Effect of metabolic control and insulin on left ventricular performance

Schwingshandl¹,

Ward²,

Silink³

et al. 1995

Pediatr Cardiol

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“…Findings from echocardiographic and pathological studies demonstrated decreased systolic and diastolic functions. Myocardial hypertrophy and fibrosis are also common to diabetic cardiomyopathy (28)(29)(30)(31). There are some differences, however, such as myocardial necrosis and dystrophic calcification, which are generally not observed in diabetic cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Targeted overexpression of protein kinase C β2 isoform in myocardium causes cardiomyopathy

Wakasaki

Koya

Schoen

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

369

256

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Increased cardiovascular mortality occurs in diabetic patients with or without coronary artery disease and is attributed to the presence of diabetic cardiomyopathy. One potential mechanism is hyperglycemia that has been reported to activate protein kinase C (PKC), preferentially the ␤ isoform, which has been associated with the development of micro-and macrovascular pathologies in diabetes mellitus. To establish that the activation of the PKC␤ isoform can cause cardiac dysfunctions, we have established lines of transgenic mice with the specific overexpression of PKC␤2 isoform in the myocardium. These mice overexpressed the PKC␤2 isoform transgene by 2-to 10-fold as measured by mRNA, and proteins exhibited left ventricular hypertrophy, cardiac myocyte necrosis, multifocal fibrosis, and decreased left ventricular performance without vascular lesions. The severity of the phenotypes exhibited gene dose-dependence. Up-regulation of mRNAs for fetal type myosin heavy chain, atrial natriuretic factor, c-fos, transforming growth factor, and collagens was also observed. Moreover, treatment with a PKC␤-specific inhibitor resulted in functional and histological improvement. These findings have firmly established that the activation of the PKC␤2 isoform can cause specific cardiac cellular and functional changes leading to cardiomyopathy of diabetic or nondiabetic etiology.

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“…Friedman et al [67] demonstrated that diabetic patients had an increase in endsystolic diameter and volume, a diminished left ventricular ejection fraction (LVEF), and a decreased minor axis shortening and velocity of circumferential fiber shortening. In a similar study of 40 type 2 normotensive diabetic patients, 55% patients had systolic dysfunction, but only 7.5% had electrocardiographic changes compatible with cardiac ischemia; 40% patients were also found to have LV hypertrophy [130].…”

Section: Systolic Dysfunction In Diabetesmentioning

confidence: 99%

Diabetic cardiomyopathy: understanding the molecular and cellular basis to progress in diagnosis and treatment

2011

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Diabetes mellitus is an important and prevalent risk factor for congestive heart failure. Diabetic cardiomyopathy has been defined as ventricular dysfunction that occurs in diabetic patients independent of a recognized cause such as coronary artery disease or hypertension. The disease course consists of a hidden subclinical period, during which cellular structural insults and abnormalities lead initially to diastolic dysfunction, later to systolic dysfunction, and eventually to heart failure. Left ventricular hypertrophy, metabolic abnormalities, extracellular matrix changes, small vessel disease, cardiac autonomic neuropathy, insulin resistance, oxidative stress, and apoptosis are the most important contributors to diabetic cardiomyopathy onset and progression. Hyperglycemia is a major etiological factor in the development of diabetic cardiomyopathy. It increases the levels of free fatty acids and growth factors and causes abnormalities in substrate supply and utilization, calcium homeostasis, and lipid metabolism. Furthermore, it promotes excessive production and release of reactive oxygen species, which induces oxidative stress leading to abnormal gene expression, faulty signal transduction, and cardiomyocytes apoptosis. Stimulation of connective tissue growth factor, fibrosis, and the formation of advanced glycation end-products increase the stiffness of the diabetic hearts. Despite all the current information on diabetic cardiomyopathy, translational research is still scarce due to limited human myocardial tissue and most of our knowledge is extrapolated from animals. This paper aims to elucidate some of the molecular and cellular pathophysiologic mechanisms, structural changes, and therapeutic strategies that may help struggle against diabetic cardiomyopathy.

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Echocardiographic evidence for impaired myocardial performance in children with type I diabetes mellitus

Cited by 70 publications

References 15 publications

Echocardiographic load-independent indices of contractility in children and adolescents with type I diabetes: Effect of metabolic control and insulin on left ventricular performance

Echocardiographic load-independent indices of contractility in children and adolescents with type I diabetes: Effect of metabolic control and insulin on left ventricular performance

Targeted overexpression of protein kinase C β2 isoform in myocardium causes cardiomyopathy

Diabetic cardiomyopathy: understanding the molecular and cellular basis to progress in diagnosis and treatment

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