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Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
A cardiomyopathy is a primary myocardial disorder. It is different than structural cardiac disorders, including congenital heart disorders, coronary artery disease, or valvular disorders. There are three main types of cardiomyopathies which include dilated, hypertrophic, and restrictive cardiomyopathies. Dilated cardiomyopathy is myocardial dysfunction that results in HF, with ventricular dilation and systolic dysfunction. Hypertrophic cardiomyopathy is a congenital or acquired disorder, with extreme ventricular hypertrophy and diastolic dysfunction, lacking increased afterload – it may be caused by coarctation of the aorta, systemic hypertension, or valvular aortic stenosis. Restrictive cardiomyopathy involves noncompliant ventricular walls, which resist diastolic filling. When one ventricle is affected it is usually the LV. However, both ventricles can be affected. An ischemic cardiomyopathy can occur with severe CAD, with or without infarction. It is not a primary myocardial disorder. Cardiomyopathies are signified by signs and symptoms of HF, based on systolic, diastolic, or combined dysfunction. Diabetic cardiomyopathy is cardiac dysfunction with structural, functional, and metabolic alterations even though coronary artery disease may be absent.
Diabetes
Published in Awanish Kumar, Ashwini Kumar, Diabetes, 2020
The Madras Diabetes Research Foundation (India) and Indian Diabetes Research Foundation (India) independently conducted various studies in India and concluded that Indians, especially the south Indian population, are at high risk of developing diabetes, insulin resistance and related cardiovascular complications. The primary risk factors observed in these studies, involving wide age group subjects, were low level of high-density lipoprotein (low HDL) and high triglyceride (TG) level, contributing to an increased risk of metabolic syndrome [21–23]. Diabetic cardiomyopathy can be defined as myocardial dysfunction in diabetic patients in the absence of coronary artery disease (CAD), hypertension and valve defects. The development of diabetic cardiomyopathy is attributed to various factors viz. insulin resistance, hyperlipidaemia and cardiac autonomic dysfunction. Insulin resistance and hyperlipidaemia are two major ingredients of a collective complication known as metabolic syndrome (MS). Hyperglycaemia, hyperinsulinaemia and elevated free fatty acid (FFA) are the major factors that lead to cardiac steatosis. Brain natriuretic peptide (BNP), biomolecule released from cardiac ventricles, was also found to be elevated in patients who suffered heart failure. The gene expression of BNP was also found to be upregulated in animal models of insulin resistance (hyperinsulinaemia) along with other symptoms such as LVH [24].
Caloric Restriction in Obesity and Diabetic Heart Disease
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Edith Hochhauser, Maayan Waldman, Michael Arad
Diabetes promotes adverse myocardial remodeling which is aggravated in the presence of hypertension (Paul 2003; Patel and Mehta 2012). In patients with aortic stenosis, diabetes was associated with increased myocardial fibrosis, increased LV mass and reduced systolic function despite similar aortic value gradients and independent of coexisting coronary artery diseases (Falcao-Pires, Hamdani et al. 2011; Lindman, Arnold et al. 2011). Diabetic cardiomyopathy is defined as a defect in ventricular contractile function occurring independently of CAD and hypertension (Hayat, Patel et al. 2004). The term now includes diastolic dysfunction that is now considered as an early feature of diabetic cardiomyopathy, usually preceding the development of systolic dysfunction (Schannwell, Schneppenheim et al. 2002; Varga, Giricz et al. 2015). The etiology of diabetic cardiomyopathy includes the two main defects in diabetes such as insulin resistance and hyperglycemia triggering a cascade of specific myocyte abnormalities. There is intrinsic myocyte stiffening, characterized by increased diastolic tension. This is followed by interstitial fibrosis, collagen cross-linking by advanced glycosylation products and eventual systolic dysfunction (Paul 2003). Thus, diabetic myocardial remodeling appears to have significant impact on the evolution of HF, irrespective of the etiology (Eguchi, Kario et al. 2005).
Restorative Effect of Semecarpus Anacardium on Altered Energy Metabolism in Type-2 Diabetes Mellitus–Induced Cardiac Dysfunction in Rats
Published in Journal of Dietary Supplements, 2020
Suganthi Subramani, Haseena Banu Hedyathullah Khan, Shanthi Palanivelu, Sachidanandam Thiruvaiyaru Panchanadham
Reduction of glucose metabolism is believed to be an important mechanism in diabetic cardiomyopathy (Belke et al. 2000), and restoration of cardiac glucose metabolism improves diabetic heart function. Defective glycolysis in the heart of diabetic patients and in experimental diabetic animal models has been reported (Rodrigues and McNeill 1992). In type 2 diabetes mellitus (T2DM), hyperglycemia results from both lack of suppression of hepatic glucose production in the absorptive state and excessive glucose production in the postabsorptive state. Significant decreases in the activities of glycolytic enzymes hexokinase, phosphoglucoisomerase, and aldolase were observed in CVD-induced diabetic rats consistent with those of other studies (Radhika and Krishnakumari Sudarsanam 2010).
Type 2 diabetes mellitus and cardiovascular disease: focus on the effect of antihyperglycemic treatments on cardiovascular outcomes
Published in Expert Review of Cardiovascular Therapy, 2020
Ravi Choxi, Sumon Roy, Angeliki Stamatouli, Stéphanie B Mayer, Ion S Jovin
There are many complex mechanisms underlying diabetic cardiomyopathy. Accumulation of advanced glycation end products leads to the crosslinking of collagen in the myocardium and development of diastolic dysfunction [20]. Insulin resistance leads to impaired glucose utilization and degradation of lipids to free fatty acids. Lipid accumulation in the cardiomyocyte leads to lipotoxicity and myocardial apoptosis [21]. Additionally, there is activation of the local renin-angiotensin-aldosterone system within the myocardium that leads to increased production of angiotensin II in cardiomyocytes leading to myocardial remodeling [22]. There are also several metabolic disturbances such as the generation of reactive oxygen species leading to oxidative stress in the cardiomyocyte, increased levels of free fatty acids, changes in mitochondrial metabolism, and generalized inflammation that lead to myocardial apoptosis and scarring [20]. Taken together, these different mechanisms contribute to diabetic cardiomyopathy, which can progress to clinical symptoms of overt heart failure. Diastolic dysfunction is correlated with the degree of hyperglycemia and improving hyperglycemia can lead to an improvement in diabetic cardiomyopathy as demonstrated in rat experiements [23]. Biologic plausibility for this is demonstrated by findings that insulin replacement ameliorates systemic and cardiac markers of diabetic cardiomyopathy in rats [23]. The array of different mechanistic metabolic dysfunction in uncontrolled diabetes together leads to changes in the myocardium increasing the propensity of heart failure. Figure 2 summarizes the pathophysiological effects DM2 has on the development of heart failure.
Ameliorative effect of apelin on streptozotocin-induced diabetes and its associated cardiac hypertrophy
Published in Alexandria Journal of Medicine, 2018
Diabetic cardiomyopathy has been defined as a ventricular dysfunction that occurs in diabetic patients independent of a recognized cause, such as coronary artery disease or hypertension.2 The hallmark characteristic of diabetic cardiomyopathy is a subclinical phase associated with cellular structural abnormalities including cardiomyocyte hypertrophy, cardiac inflammation, fibrosis and increased apoptosis which lead initially to diastolic dysfunction, later to systolic dysfunction and eventually to heart failure.3