Cardiovascular status in young patients with insulin-dependent diabetes mellitus.

Kimball, Thomas R.; Daniels, Stephen R.; Khoury, Philip R.; Magnotti, Ralph A.; Turner, A M; Dolan, Lawrence M.

doi:10.1161/01.cir.90.1.357

Cited by 55 publications

(29 citation statements)

References 27 publications

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“…Contractility was assessed from the correlation between mean velocity of circumferential shortening (corrected for heart rate) and end-systolic wall stress in control subjects. The difference between measured and predicted mean velocity of circumferential shortening for the measured end-systolic wall stress served as an index of contractility (stroke velocity index) [2,9] . Left ventricular mass was calculated with the cube function formula, ASE-cube left ventricular mass=1·04((septal thickness in diastole+left ventricular internal diameter in diastole+left posterior wall thickness in diastole) 3 left ventricular internal diameter in diastole 3 ), that approximates the shape of the left ventricle as a prolate ellipsoid of regular configuration and a ratio of long-to short-axis lengths of 2:1.…”

Section: Echocardiographymentioning

confidence: 99%

“…They suggested that the increased systolic shortening was due to reduced afterload. Kimball et al [2] compared insulindependent diabetes mellitus patients who were a little older (mean age 17·6 years) with controls, and reported increased left ventricular performance measured as stroke volume, cardiac output, fractional shortening, and mean velocity of circumferential shortening, but no significant differences in preload or afterload. These data are in accordance with our data.…”

Section: Increased Left Ventricular Function In Iddm 1737mentioning

confidence: 99%

“…The abnormalities include increased left ventricular mass [2] , increased left ventricular contractility [2][3][4] , and impaired diastolic function [5,6] . These alterations could contribute to the renal hyperperfusion and elevated transglomerular filtration and be more directly involved in the development of microalbuminuria.…”

Section: Introductionmentioning

confidence: 99%

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Increased left ventricular systolic function in insulin dependent diabetic patients with normal albumin excretion

Christiansen¹

1998

European Heart Journal

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Alterations in cardiovascular function may be an aetiological factor for the development of microalbuminuria in patients with insulin-dependent diabetes mellitus. We studied cardiac function with echocardiography in relation to the degree of albuminuria in 27 insulin-dependent diabetes mellitus patients and 13 healthy subjects. Patients were grouped according to urinary albumin excretion: <20 g . min 1 (normoalbuminuric), and 20 to 200 g . min 1 (microalbuminuric). None were or had been treated with cardiovascular drugs. The normoalbuminuric patients had a higher heart rate, mean velocity of circumferential shortening, stroke velocity index (a measure of contractility), and aortic peak velocity than controls. No difference in diastolic function was present. In the microalbuminuric group, the stroke velocity index was comparable to values observed in healthy subjects. The increased systolic performance (heart rate and contractility) may contribute to the renal hyperperfusion and glomerular hyperfiltration observed in insulin-dependent diabetes mellitus patients before the development of micro-and in turn macroalbuminuria. The possible cause-effect mechanisms should be further studied, as preventive medical treatment of the hypercontractile heart is possible. In conclusion, cardiac contractility is increased in insulin-dependent diabetes mellitus patients with normoalbuminuria and returns to levels observed in healthy subjects when microalbuminuria develops.

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Section: Echocardiographymentioning

confidence: 99%

Section: Increased Left Ventricular Function In Iddm 1737mentioning

confidence: 99%

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Increased left ventricular systolic function in insulin dependent diabetic patients with normal albumin excretion

Christiansen¹

1998

European Heart Journal

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“…Other changes that are due to glucose induced activation of cPLA2, inhibition of Na + K + ATPase which could be involved in the regulation of vascular permeability, regulation of caldesmone and Another common problem observed in diabetic patients is cardiomyopathy. Up to 25 % of diabetic patients with congestive cardiac failure do not have significant angiographic evidence of coronary vessel disease and there is generally a greater prevalence of congestive heart failure in diabetic compared with non-diabetic patients [6,7]. This has been investigated using a transgenic mouse model which overexpresses PKCb isoform in the heart using a myosin heavy chain promoter to target the transgene to the myocardium.…”

mentioning

confidence: 99%

“…A new theory is postulated suggesting that insulin's activities on the vasculature can be divided into atherogenic and anti-atherogenic actions [7]. The anti-atherogenic actions include vasodilatation and release of nitric oxide (NO), inhibition of tumour necrosis factor (TNF) and angiotensin II actions, amino acid transport and conversion of glucose into glycogen.…”

mentioning

confidence: 99%

Cardiovascular complications of diabetes

et al. 1997

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Cardiovascular complications are the leading causes of mortality in both insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The severity of this problem is clearly illustrated by the finding that IDDM patients suffer from mortality rates many times higher than of the general population [1]. In spite of the gravity of this complication, there is a relative paucity of data specifically on the pathogenesis, prevention and the treatment of the cardiovascular lesions in diabetes. The goal of this article is to highlight certain areas which are pertinent to diabetic cardiovascular complications and to suggest research goals which will bring understanding of the pathogenesis of this grave complication and its potential treatments.George L. King: Hyperglycaemia and insulin resistance: how do they increase cardiovascular risk in diabetic patients?A major cause of morbidity and mortality in diabetic patients is macrovascular disease affecting the heart and large vessels. In diabetes there is an acceleration of atherosclerosis with excessive extracellular matrix thickening. In the heart, the major pathology is atherosclerosis of the coronary arteries, and the fibrosis, and hypertrophy of the myocardium. Hyperglycaemia, hyperlipidaemia and insulin resistance are some of the recognized risk factors [2,3]. The basic abnormalities are in glucose metabolism and insulin action which can lead to a whole range of vascular changes in the areas of coagulation, contractility, leukocyte adhesions, and smooth muscle cell proliferation. The mechanisms by which hyperglycaemia causes vascular dysfunction are probably multiple. These mechanisms include non-enzymatic glycation, oxidative stress, polyol-myoinositol alteration, and activation of diacylglycerol (DAG) and protein kinase C (PKC) pathways. The role of the DAG and PKC pathways which regulate many vascular functions were discussed since this is the newest of the four main theories.Studies over the last 7 years have shown that there is an increase in DAG levels and activation of PKC activities in vascular cells from the retina, glomeruli, aorta and the heart when exposed to high glucose levels in culture or in the diabetic state in vivo [4]. Increased glycolysis can elevate DAG which in turn activates protein kinase C in the vascular cells. The b I and II isoforms of PKC are predominantly increased in the vascular cells induced by diabetes and hyperglycaemia involving PKCbI in the renal glomeruli and PKCbII in the rest of the vasculature.The increase in DAG levels and activation of PKCb isoforms have been associated with a variety of biochemical, cellular and physiological changes in the vasculature. These changes lead to an increase in the transcription rate of transforming growth factor b (TGFb)which regulates increases in the synthesis of extra-cellular matrix protein such as type IV and VI collagen, and fibronectin resulting in capillary basement membrane thickening which is observed in all diabetic animals and patients [5]. The abnormal amount of base...

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Epidemiology of Macrovascular Disease and Hypertension in Diabetes Mellitus

Tuomilehto

Rastenytė²,

Qiao

et al. 2003

International Textbook of Diabetes Mellitus

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Macrovascular diseases—atherosclerosis, coronary heart disease, cerebrovascular disease or stroke, and peripheral vascular disease—are major causes of morbidity, mortality, and severe disability among diabetic persons. Hypertension is a major contributor to macrovascular disease in diabetic patients. Although late macrovascular complications are common in both type 1 diabetes mellitus and type 2 diabetes mellitus, a somewhat different etiology has been suggested for these two types of diabetes. A number of studies have attempted to answer the basic questions of the epidemiology of hypertension and macrovascular disease in diabetes: (1) What is the occurrence of these disorders in diabetic patients? (2) Are they more common in diabetic patients compared with the general population? (3) Are the risk factors for these disorders the same in diabetic patients as in the general population? (4) Is asymptomatic hyperglycemia an independent risk factor for macrovascular disease? Our ability to diagnose different late complications of diabetes vary. For instance, we may be able to detect retinopathy and increased urinary albumin excretion earlier than clinical macrovascular disease (for which usually 75% stenosis is needed for clinical effects). In addition, the occurrence of macrovascular disease shows a very large geographical variation in the general population. This may also be reflected in between‐population variation in the prevalence of hypertension and macrovascular complications of diabetes. Therefore, the risk of macrovascular disease in diabetic patients must always be interpreted in relation to the risk in the background population. The risk can be expressed in different ways: (1) absolute risk, i.e. as the excess number of cases or excess in the frequency of these complications between diabetic and nondiabetic subjects; (2) relative risk (rate ratio), i.e. ratio of the frequency between diabetic and nondiabetic subjects; (3) population attributable risk, i.e. the proportion of cases of these complications that can be attributed to diabetes, and thereby could possibly be prevented by measures targeted to primary and secondary prevention of diabetes.

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Cardiovascular status in young patients with insulin-dependent diabetes mellitus.

Cited by 55 publications

References 27 publications

Increased left ventricular systolic function in insulin dependent diabetic patients with normal albumin excretion

Increased left ventricular systolic function in insulin dependent diabetic patients with normal albumin excretion

Cardiovascular complications of diabetes

Epidemiology of Macrovascular Disease and Hypertension in Diabetes Mellitus

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