Diastolic dysfunction is not related to changes in glycaemic control over 6 months in type 2 (non-insulin-dependent) diabetes mellitus

Gough, Stephen; Smyllie, J. H.; Barker, Madeleine; Berkin, K E; Rice, P.; Grant, Peter J.

doi:10.1007/bf00569568

Cited by 29 publications

(14 citation statements)

References 37 publications

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“…13 However, other studies have demonstrated no significant association between glycemic control and cardiac function. [21][22][23][24][25] The lack of correlation between systolic and diastolic function with HbA1c at baseline in our patients may have been because of by guest on May 9, 2018 http://circimaging.ahajournals.org/ Downloaded from the selection criteria: our patients were selected into the study as they all had poor glycemic control.…”

Section: Systolic and Diastolic Function In Diabetes Mellitusmentioning

confidence: 96%

Impact of Improved Glycemic Control on Cardiac Function in Type 2 Diabetes Mellitus

Leung

Wong

Hudson

et al. 2016

Circ: Cardiovascular Imaging

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Background— Patients with type 2 diabetes mellitus are at risk of heart failure. Specific therapeutic interventions for diabetic heart disease are still elusive. We aimed to examine the impact of improved glycemic control on left ventricular (LV) function in these patients. Methods and Results— A total of 105 subjects with type 2 diabetes mellitus (aged 54±10 years) and poor glycemic control received optimization of treatment for blood glucose, blood pressure, and cholesterol to recommended targets for 12 months. LV systolic and diastolic function, measured by LV global longitudinal strain (GLS) and septal e′ velocities, were compared before and after optimization. At baseline, patients had impaired LV systolic (GLS −14.9±3.2%) and diastolic function (e′ 6.2±1.7 cm/s). After 12 months, glycated hemoglobin (HbA1c) decreased from 10.3±2.4% to 8.3±2.0%, which was associated with significant relative improvement in GLS of 21% and septal e′ of 24%. There was a progressively greater improvement in GLS as patients achieved a lower final HbA1c. Patients achieving an HbA1c of <7.0% had the largest improvement. The 15 patients whose HbA1c worsened experienced a decline in GLS. Patients who improved their HbA1c by ≥1.0% had a significantly higher relative improvement in e′ than those who did not (32% versus 8%; P =0.003). Baseline GLS, decrease in body mass index, and treatment with metformin were additional independent predictors of GLS improvement. Conclusions— Improvements in glycemic control over a 12-month period led to improvements in LV systolic and diastolic function. This may have long-term prognostic implications.

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Section: Systolic and Diastolic Function In Diabetes Mellitusmentioning

confidence: 96%

Impact of Improved Glycemic Control on Cardiac Function in Type 2 Diabetes Mellitus

Leung

Wong

Hudson

et al. 2016

Circ: Cardiovascular Imaging

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“…In addition to revealing a prevalence of LVDD of Ͼ50%, this study also unmasked a significant number of subjects (28%) with a pseudonormal pattern of diastolic filling that has yet to be recognized in previous studies (4)(5)(6)(7)(8)(9)(10)(11). In these studies, the Valsalva maneuver and pulmonary venous recordings were not used.…”

Section: Transmitral and Pulmonary Venous Doppler Flow Velocity Recormentioning

confidence: 99%

“…However, other studies have found no such correlation (4,6,11,18). It has been suggested that LVDD is secondary to microvascular disease because an association with retinopathy has been described (7,8).…”

mentioning

confidence: 98%

Diastolic Dysfunction in Normotensive Men with Well-Controlled Type 2 Diabetes

Poirier¹,

Bogaty²,

Garneau³

et al. 2001

Diabetes Care

558

282

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Abbreviations: CAD, coronary artery disease; IVRT, isovolumetric relaxation time; LVDD, left ventricular diastolic dysfunction; MET, metabolic equivalent; PST, posterior wall thickness; PVa, pulmonary reversed A wave velocity; PVd, pulmonary D wave velocity; PVs, pulmonary S wave velocity.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Diastolic Dysfunction in Normotensive Men With Well-Controlled Type 2 DiabetesImportance of maneuvers in echocardiographic screening for preclinical diabetic cardiomyopathyOBJECTIVE -Because a pseudonormal pattern of ventricular filling has never been considered in studies that reported a prevalence of left ventricular diastolic dysfunction (LVDD) between 20 and 40%, our aim was to more completely evaluate the prevalence of LVDD in subjects with diabetes.RESEARCH DESIGN AND METHODS -We studied 46 men with type 2 diabetes who were aged 38-67 years; without evidence of diabetic complications, hypertension, coronary artery disease, congestive heart failure, or thyroid or overt renal disease; and with a maximal treadmill exercise test showing no ischemia. LVDD was evaluated by Doppler echocardiography, which included the use of the Valsalva maneuver and pulmonary venous recordings to unmask a pseudonormal pattern of left ventricular filling.RESULTS -LVDD was found in 28 subjects (60%), of whom 13 (28%) had a pseudonormal pattern of ventricular filling and 15 (32%) had impaired relaxation. Systolic function was normal in all subjects, and there was no correlation between LVDD and indexes of metabolic control.CONCLUSIONS -LVDD is much more common than previously reported in subjects with well-controlled type 2 diabetes who are free of clinically detectable heart disease. The high prevalence of this phenomenon in this high-risk population suggests that screening for LVDD in type 2 diabetes should include procedures such as the Valsalva maneuver and pulmonary venous recordings to unmask a pseudonormal pattern of ventricular filling.

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“…Diabetic cardiomyopathy is characterized by an early diastolic dysfunction and a late systolic one, with intracellular retention of calcium and sodium and loss of potassium. The mechanism of diastolic dysfunction remains unknown, but it does not appear to be due to changes in blood pressure, microvascular complications, or elevated circulating glycated hemoglobin levels (15,16). We tested whether the impairment of cardiac function in diabetes is dependent upon the activation of the PARP pathway within the heart.…”

mentioning

confidence: 99%

The Role of Poly(ADP-Ribose) Polymerase Activation in the Development of Myocardial and Endothelial Dysfunction in Diabetes

et al. 2002

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Patients with diabetes exhibit a high incidence of diabetic cardiomyopathy and vascular complications, which underlie the development of retinopathy, nephropathy, and neuropathy and increase the risk of hypertension, stroke, and myocardial infarction. There is emerging evidence that the activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) importantly contributes to the development of endothelial dysfunction in a streptozotocin-induced model of diabetes. We investigated the role of PARP activation in the pathogenesis of cardiac dysfunction in streptozotocin-induced and genetic (nonobese diabetic) models of diabetes in rats and mice. Development of diabetes was accompanied by hyperglycemia, cardiac PARP activation, a selective loss of endothelium-dependent vasodilation in the thoracic aorta, and an early diastolic dysfunction of the heart. Treatment with a novel potent phenanthridinonebased PARP inhibitor, PJ34, starting 1 week after the onset of diabetes, restored normal vascular responsiveness and significantly improved cardiac dysfunction, despite the persistence of severe hyperglycemia. The beneficial effect of PARP inhibition persisted even after several weeks of discontinuation of the treatment. Thus, PARP activation plays a central role in the pathogenesis of diabetic cardiovascular (cardiac as well as endothelial) dysfunction. PARP inhibitors may exert beneficial effects against the development of cardiovascular complications in diabetes. Diabetes 51:514 -521, 2002 P oly(ADP ribose) polymerase (PARP), also known as poly(ADP ribose) synthetase (PARS), is an abundant nuclear enzyme of eukaryotic cells that participates in DNA repair in response to genotoxic stress. When activated by DNA single-strand breaks, PARP initiates an energy-consuming cycle by transferring ADP ribose units from NAD ϩ to nuclear proteins. This process results in rapid depletion of the intracellular NAD ϩ and ATP pools, slowing the rate of glycolysis and mitochondrial respiration, eventually leading to cellular dysfunction and death (1-7). Overactivation of PARP represents an important mechanism of tissue damage in various pathological conditions associated with oxidant stress, including myocardial reperfusion injury (4), stroke (3), shock (7,8), and autoimmune ␤-cell destruction (5,6). Recently, we reported that the activation of PARP importantly contributes to the development of endothelial dysfunction in a streptozotocin (STZ)-induced model of diabetes in mice (9,10).Cardiovascular complications are the most common cause of morbidity and mortality in diabetic patients. The presence of myocardial dysfunction independent of coronary artery disease in diabetes, known as "diabetic cardiomyopathy," has been well documented in both humans and animals (11-15). Diabetic cardiomyopathy is characterized by an early diastolic dysfunction and a late systolic one, with intracellular retention of calcium and sodium and loss of potassium. The mechanism of diastolic dysfunction remains unknown, but it does not appear to be due to cha...

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Diastolic dysfunction is not related to changes in glycaemic control over 6 months in type 2 (non-insulin-dependent) diabetes mellitus

Cited by 29 publications

References 37 publications

Impact of Improved Glycemic Control on Cardiac Function in Type 2 Diabetes Mellitus

Impact of Improved Glycemic Control on Cardiac Function in Type 2 Diabetes Mellitus

Diastolic Dysfunction in Normotensive Men with Well-Controlled Type 2 Diabetes

The Role of Poly(ADP-Ribose) Polymerase Activation in the Development of Myocardial and Endothelial Dysfunction in Diabetes

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