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Cardiovascular disease is the most common cause of death in the diabetic population and is currently one of the leading causes of death in the United States and other industrialized countries. The health care expenses associated with cardiovascular disease are staggering, reaching more than 350 billion dollars in 2003. The risk factors for cardiovascular disease include high fat/cholesterol levels, alcoholism, smoking, genetics, environmental factors and hypertension, which are commonly used to gauge an individual's risk of cardiovascular disease and to track their progress during therapy. Most recently, these factors have become important in the early prevention of cardiovascular diseases. Oxidative stress, the imbalance between reactive oxygen species production and breakdown by endogenous antioxidants, has been implicated in the onset and progression of cardiovascular diseases such as congestive heart failure and diabetes-associated heart dysfunction (diabetic cardiomyopathy). Antioxidant therapy has shown promise in preventing the development of diabetic heart complications. This review focuses on recent advances in oxidative stress theory and antioxidant therapy in diabetic cardiomyopathy, with an emphasis on the stress signaling pathways hypothesized to be involved. Many of these stress signaling pathways lead to activation of reactive oxygen species, major players in the development and progression of diabetic cardiomyopathy.
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PMID:Oxidative stress and stress signaling: menace of diabetic cardiomyopathy. 1603 22

In this study we examined diabetes- and hypertension-induced changes in cardiac structure and function in an animal model of type 2 diabetes, the Goto-Kakizaki (GK) rat. We hypothesized that treatment with omapatrilat, a vasopeptidase inhibitor, which causes simultaneous inhibition of angiotensin converting enzyme and neutral endopeptidase, provides additional cardioprotective effects, during normal- as well as high sodium intake, compared to treatment with enalapril, a selective inhibitor of angiotensin converting enzyme. Fifty-two GK rats were randomized into 6 groups to receive either normal-sodium (NaCl 0.8%) or high-sodium (NaCl 6%) diet and enalapril, omapatrilat or vehicle for 12 weeks. The GK rats developed hypertension, cardiac hypertrophy and overexpression of cardiac natriuretic peptides and profibrotic connective tissue growth factor compared to nondiabetic Wistar rats. The high dietary sodium further increased the systolic blood pressure, and changed the mitral inflow pattern measured by echocardiography towards diastolic dysfunction. Enalapril and omapatrilat equally decreased the systolic blood pressure compared to the control group during normal- as well as high-sodium diet. Both drugs had beneficial cardioprotective effects, which were blunted by the high dietary sodium. Compared to enalapril, omapatrilat reduced the echocardiographically measured left ventricular mass during normal-sodium diet and improved the diastolic function during high-sodium diet in GK rats. Furthermore, omapatrilat reduced relative cardiac weight more effectively than enalapril during high sodium intake. Our results suggest that both the renin-angiotensin and the neutral endopeptidase system are involved in the pathogenesis of diabetic cardiomyopathy since vasopeptidase inhibition was shown to provide additional benefits in comparison with selective angiotensin converting enzyme inhibition alone.
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PMID:Vasopeptidase inhibition has beneficial cardiac effects in spontaneously diabetic Goto-Kakizaki rats. 1613 72

Fifty type 2 diabetes patients (25 of them being hypertensive) who had no cardiac symptoms had their left ventricular function assessed. There were 24 female and 26 male diabetes patients evaluated, along with a control group of 50 healthy subjects. The patients and controls underwent full clinical evaluation, which included physical examination, blood biochemistry (urea and electrolyte; creatinine, creatinine clearance; fasting blood and two-hour postprandial glucose levels, lipid profile), electrocardiograph, chest radiograph, and echocardiograph. The hypertensive diabetes patients had higher cholesterol levels, and 50% had levels >5.0 mmol/L. Sixteen patients had cataracts, 14 had background retinopathy, 12 had peripheral neuropathy, and 7 had peripheral vascular disease. The subjects had significantly lower ejection fraction than controls, and fractional shortening showed a similar pattern. Eight patients had ejection fraction <50% compared to none of the controls. Sixty-six percent of the subjects and 30% of the controls had diastolic dysfunction (reverse E/A ratio, prolonged deceleration time, and lower deceleration rate), respectively, but the diabetes patients did not show any difference. Diastolic dysfunction correlated significantly with age, fasting blood glucose, and two-hour postprandial glucose. The subjects had higher left ventricular mass (LVM) than controls. The LVM correlated significantly positively with diastolic blood pressure, systolic blood pressure, and pulse pressure. Subclinical diabetic cardiomyopathy exists in our patients; in addition, other risk factors for cardiomyopathy and coronary artery disease exist, including hypertension, hypercholesterolemia, and obesity.
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PMID:Left ventricular function in type 2 diabetes patients without cardiac symptoms in Zaria, Nigeria. 1626 87

Diabetes mellitus is a worldwide epidemic. Cardiovascular disease remains the major cause of morbidity and mortality in people with diabetes. Studies have suggested that increased risk of cardiovascular disease is not restricted to type II or type I diabetes mellitus, but extends to prediabetic stages such as impaired fasting glucose, impaired glucose tolerance, metabolic syndrome, and obesity. Insulin resistance, impaired fasting glucose, impaired glucose tolerance, and diabetes mellitus form a continuous sequence of risk for cardiovascular disease. Therefore, cardiovascular disease mortality and morbidity within the diabetes epidemic grow into vast proportions. Evidence also exists that diabetic patients have a high prevalence of heart failure or impaired diastolic and systolic cardiac function subsequent to the combination of coronary artery disease, hypertension, and diabetic cardiomyopathy. In view of the proportions of this new epidemic, prevention of diabetes and its prediabetic states is likely to be the most effective strategy to prevent serious cardiovascular events.
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PMID:Epidemiology of the diabetic heart. 1634 Apr 2

Diabetes has emerged as a major threat to worldwide health. The increasing incidence of diabetes in young individuals is particularly worrisome given that the disease is likely to evolve over a period of years. In 1972, the existence of a diabetic cardiomyopathy was proposed based on the experience with four adult diabetic patients who suffered from congestive heart failure in the absence of discernible coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. The exact mechanisms underlying the disease are unknown; however, an important component of the pathological alterations observed in these hearts includes the accumulation of extracellular matrix (ECM) proteins, in particular collagens. The excess deposition of ECM in the heart mirrors what occurs in other organs such as the kidney and peritoneum of diabetics. Mechanisms responsible for these alterations may include the excess production, reduced degradation, and/or chemical modification of ECM proteins. These effects may be the result of direct or indirect actions of high glucose concentrations. This article reviews our state of knowledge on the effects that diabetes-like conditions exert on the cells responsible for ECM production as well as relevant experimental and clinical data.
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PMID:The pathogenesis of myocardial fibrosis in the setting of diabetic cardiomyopathy. 1648 30

In patients with diabetes, an increased risk of symptomatic heart failure usually develops in the presence of hypertension or ischemic heart disease. However, a predisposition to heart failure might also reflect the effects of underlying abnormalities in diastolic function that can occur in asymptomatic patients with diabetes alone (termed diabetic cardiomyopathy). Evidence of cardiomyopathy has also been demonstrated in animal models of both Type 1 (streptozotocin-induced diabetes) and Type 2 diabetes (Zucker diabetic fatty rats and ob/ob or db/db mice). During insulin resistance or diabetes, the heart rapidly modifies its energy metabolism, resulting in augmented fatty acid and decreased glucose consumption. Accumulating evidence suggests that this alteration of cardiac metabolism plays an important role in the development of cardiomyopathy. Hence, a better understanding of this dysregulation in cardiac substrate utilization during insulin resistance and diabetes could provide information as to potential targets for the treatment of cardiomyopathy. This review is focused on evaluating the acute and chronic regulation and dysregulation of cardiac metabolism in normal and insulin-resistant/diabetic hearts and how these changes could contribute toward the development of cardiomyopathy.
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PMID:Role of changes in cardiac metabolism in development of diabetic cardiomyopathy. 1675 Dec 93

Diabetes mellitus increases by 2.5 to 5 the relative risk of congestive heart failure. Besides the classical risk factors of congestive heart failure such as obesity, arterial hypertension and coronary artery disease that are frequently associated to type 2 diabetes, a diabetic cardiomyopathy plays also a role. This specific complication is related to metabolic factors and oxidative stress, leading to muscular cell apoptosis and fibrosis. The management of a diabetic patient with congestive heart failure has several specificities not only concerning the treatment of cardiac insufficiency but most importantly concerning antidiabetic therapy. The relationship between glitazones, peripheral oedema and risk of congestive heart failure is currently raising much interest and controversies.
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PMID:[Diabetes mellitus and congestive heart failure: physiopathology and treatment]. 1697 38

The present article analyses the intimate relationship between diabetes mellitus and congestive heart failure. This relationship is indeed "bidirectional". On the one hand, it is well known that diabetes mellitus, especially type 2 diabetes, predisposes to congestive heart failure due to intricated mechanisms. In most cases, there is a combination of various well-known risk factors, such as obesity, arterial hypertension and coronary heart disease, with a specific diabetic cardiomyopathy, whose pathophysiology is complex. On the other hand, several studies showed that congestive heart failure increases the risk of new type 2 diabetes, probably due to decreased muscular perfusion and excessive neurohumoral response. Remarkably, such a risk could be reduced by a drug capable of inhibiting the renin-angiotensin system, as previously reported in patients with arterial hypertension. The recent launch and the increasing use of thiazolidinediones (glitazones) raise the interest for congestive heart failure in diabetic patients. Indeed, because of their positive effect on insulin resistance and various pleiotropic effects, glitazones may exert some cardiovascular protection; however, both rosiglitazone and pioglitazone are associated with fluid retention, which could reveal or aggravate episodes of congestive heart failure.
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PMID:[Congestive heart failure and diabetes mellitus: an intricated relationship]. 1746 1

Type 1 and type 2 diabetic patients are at increased risk of cardiomyopathy and heart failure is a major cause of death for these patients. Cardiomyopathy in diabetes is associated with a cluster of features including decreased diastolic compliance, interstitial fibrosis and myocyte hypertrophy. The mechanisms leading to diabetic cardiomyopathy remain uncertain. Diabetes is associated with most known risk factors for cardiac failure seen in the overall population, including obesity, dyslipidemia, thrombosis, infarction, hypertension, activation of multiple hormone and cytokine systems, autonomic neuropathy, endothelial dysfunction and coronary artery disease. In light of these common contributing pathologies it remains uncertain whether diabetic cardiomyopathy is a distinct disease. It is also uncertain which factors are most important to the overall incidence of heart failure in diabetic patients. This review focuses on factors that can have direct effects on diabetic cardiomyocytes: hyperglycemia, altered fuel use, and changes in the activity of insulin and angiotensin. Particular attention is given to the changes these factors can have on cardiac mitochondria and the role of reactive oxygen species in mediating injury to cardiomyocytes.
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PMID:Causes and characteristics of diabetic cardiomyopathy. 1748 34

Diabetic cardiomyopathy is a myocardial disease caused by diabetes mellitus unrelated to vascular and valvular pathology or systemic arterial hypertension. Clinical and experimental studies have shown that diabetes mellitus causes myocardial hypertrophy, necrosis, and apoptosis, and increases interstitial tissue. The pathophysiology of diabetic cardiomyopathy is incompletely understood. It appears that metabolic perturbations such as hyperlipidemia, hyperinsulinemia, hyperglycemia, and changes in cardiac metabolism are involved in cellular consequences leading to increased oxidative stress, interstitial fibrosis, myocyte death, and altered intracellular ions transient and calcium homeostasis. Clinically, an early detection of asymptomatic diastolic dysfunction is possible. When patients develop signals and symptoms of heart failure, isolated diastolic dysfunction is usually detected. Systolic dysfunction is a late finding. Treatment of heart failure due to diabetic cardiomyopathy is not different from myocardiopathies of other etiologies and must follow the guidelines according to ventricular function, whether diastolic or diastolic and systolic impairment.
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PMID:[Diabetic cardiomyopathy]. 1750 22


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