Early diastolic impairment of diabetic heart: The significance of right ventricle

Karamitsos, Theodoros D; Karvounis, Haralambos; Dalamanga, E.; Papadopoulos, Christodoulos; Didangellos, T.P.; Karamitsos, Dimitrios T.; Parharidis, Georgios E.; Louridas, Georgios E.

doi:10.1016/j.ijcard.2006.02.003

Cited by 90 publications

(78 citation statements)

References 28 publications

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“…In our study, we did not find evidence of any significant difference in Sm between the 2 groups throughout the whole experiment. This result was in accordance with the report by Karamitsos et al (18).…”

Section: Discussionsupporting

confidence: 94%

“…However, there were no significant differences of RV wall thickness and internal dimensions in the 2 groups at the 12th week after the STZ injection. Karamitsos et al described a similar finding by demonstrating RV dysfunction prior to the structural abnormality in type 1 diabetic patients (18). However, as the experiment continued, the changes in the structure of the myocardium became visible.…”

Section: Discussionmentioning

confidence: 65%

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Diastolic function of the right ventricle is impaired in experimental type 2 diabetic rat models

Miao¹,

Zhang²,

Yuan³

et al. 2014

Turk J Med Sci

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 65%

Diastolic function of the right ventricle is impaired in experimental type 2 diabetic rat models

Miao¹,

Zhang²,

Yuan³

et al. 2014

Turk J Med Sci

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“…In contrast, increasing PI3K (p110α) activity utilising caPI3K-Tg mice provided protection against diastolic dysfunction and myocardial remodelling in a diabetes model. LV diastolic dysfunction is one of the earliest manifestations of diabetic cardiomyopathy, presenting prior to the onset of systolic dysfunction [26,31,32]. Diastolic dysfunction is characterised by abnormal LV relaxation and filling, associated with elevated LVEDP, a depressed E/A ratio and increased deceleration time [25].…”

Section: Discussionmentioning

confidence: 99%

Enhanced phosphoinositide 3-kinase(p110α) activity prevents diabetes-induced cardiomyopathy and superoxide generation in a mouse model of diabetes

et al. 2012

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Aims/hypothesis Diabetic cardiomyopathy is characterised by diastolic dysfunction, oxidative stress, fibrosis, apoptosis and pathological cardiomyocyte hypertrophy. Phosphoinositide 3-kinase (PI3K)(p110α) is a cardioprotective kinase, but its role in the diabetic heart is unknown. The aim of this study was to assess whether PI3K(p110α) plays a critical role in the induction of diabetic cardiomyopathy, and whether increasing PI3K(p110α) activity in the heart can prevent the development of cardiac dysfunction in a setting of diabetes.Methods Type 1 diabetes was induced with streptozotocin in adult male cardiac-specific transgenic mice with increased PI3K(p110α) activity (constitutively active PI3K [p110α], caPI3K] or decreased PI3K(p110α) activity (dominantnegative PI3K [p110α], dnPI3K) and non-transgenic (Ntg) mice for 12 weeks. Cardiac function, histological and molecular analyses were performed. Results Diabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C β2 (PKCβ2), p22 phox and apoptosis signalregulating kinase 1 (Ask1) expression. Diabetic dnPI3K mice displayed an exaggerated cardiomyopathy phenotype compared with diabetic Ntg mice. In contrast, diabetic caPI3K mice were protected against diastolic dysfunction, pathological cardiomyocyte hypertrophy, fibrosis and apoptosis. Protection in diabetic caPI3K mice was associated with attenuation of left ventricular superoxide generation, attenuated Anp, Bnp, PKCβ2, Ask1 and p22 phox expression, and elevated AKT. Further, in cardiomyocyte-like cells, increased PI3K(p110α) activity suppressed high glucose-induced superoxide generation and enhanced mitochondrial function. Conclusions/interpretation These results demonstrate that reduced PI3K activity accelerates the development of diabetic cardiomyopathy, and that enhanced PI3K(p110α) activity can prevent adverse cardiac remodelling and dysfunction in a setting of diabetes.

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“…LV diastolic dysfunction has been reported to be the earliest detectable functional defect in diabetic cardiomyopathy (Fang et al, , 2005Karamitsos et al, 2007;Valle et al, 2006) and is characterized by increased LV end-diastolic pressure and a decreased LV enddiastolic volume (Hamblin et al, 2007a;Regan et al, 1977). The higher filling pressures are a result of reduced diastolic ventricular compliance which thereby alters diastolic filling and HF ensues.…”

Section: Functional Alterations 321 Diastolic Dysfunctionmentioning

confidence: 99%

“…Diabetic Cardiomyopathy: Cardiac Changes, Pathophysiological Mechanisms, Biologic Markers, and the Available Therapeutic Armamentarium 489 diabetic cardiomyopathy is impaired diastolic function (Fang et al, , 2005Karamitsos et al, 2007), owing to reduced elasticity of the diabetic myocardium as a result of interstitial collagen deposition. The reduced diastolic function early in the time course of DM is followed by late decreases in systolic performance (Devereux et al, 2000;Fang et al, 2003;Mildenberger et al, 1984;Raev, 1994;Von Bibra et al, 2005).…”

mentioning

confidence: 99%

Diabetic Cardiomyopathy: Cardiac Changes, Pathophysiological Mechanisms, Biologic Markers, and the Available Therapeutic Armamentarium

Hill¹

2012

Cardiomyopathies - From Basic Research to Clinical Management

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Early diastolic impairment of diabetic heart: The significance of right ventricle

Cited by 90 publications

References 28 publications

Diastolic function of the right ventricle is impaired in experimental type 2 diabetic rat models

Diastolic function of the right ventricle is impaired in experimental type 2 diabetic rat models

Enhanced phosphoinositide 3-kinase(p110α) activity prevents diabetes-induced cardiomyopathy and superoxide generation in a mouse model of diabetes

Diabetic Cardiomyopathy: Cardiac Changes, Pathophysiological Mechanisms, Biologic Markers, and the Available Therapeutic Armamentarium

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