scholarly journals Diabetic cardiomyopathy

2009 ◽  
Vol 116 (10) ◽  
pp. 741-760 ◽  
Author(s):  
Omar Asghar ◽  
Ahmed Al-Sunni ◽  
Kaivan Khavandi ◽  
Ali Khavandi ◽  
Sarah Withers ◽  
...  

Diabetic cardiomyopathy is a distinct primary disease process, independent of coronary artery disease, which leads to heart failure in diabetic patients. Epidemiological and clinical trial data have confirmed the greater incidence and prevalence of heart failure in diabetes. Novel echocardiographic and MR (magnetic resonance) techniques have enabled a more accurate means of phenotyping diabetic cardiomyopathy. Experimental models of diabetes have provided a range of novel molecular targets for this condition, but none have been substantiated in humans. Similarly, although ultrastructural pathology of the microvessels and cardiomyocytes is well described in animal models, studies in humans are small and limited to light microscopy. With regard to treatment, recent data with thiazoledinediones has generated much controversy in terms of the cardiac safety of both these and other drugs currently in use and under development. Clinical trials are urgently required to establish the efficacy of currently available agents for heart failure, as well as novel therapies in patients specifically with diabetic cardiomyopathy.

2004 ◽  
Vol 107 (6) ◽  
pp. 539-557 ◽  
Author(s):  
Sajad A. HAYAT ◽  
Billal PATEL ◽  
Rajdeep S. KHATTAR ◽  
Rayaz A. MALIK

Independent of the severity of coronary artery disease, diabetic patients have an increased risk of developing heart failure. This clinical entity has been considered to be a distinct disease process referred to as ‘diabetic cardiomyopathy’. Experimental studies suggest that extensive metabolic perturbations may underlie both functional and structural alterations of the diabetic myocardium. Translational studies are, however, limited and only partly explain why diabetic patients are at increased risk of cardiomyopathy and heart failure. Although a range of diagnostic methods may help to characterize alterations in cardiac function in general, none are specific for the alterations in diabetes. Treatment paradigms are very much limited to interpretation and translation from the results of interventions in non-diabetic patients with heart failure. This suggests that there is an urgent need to conduct pathogenetic, diagnostic and therapeutic studies specifically in diabetic patients with cardiomyopathy to better understand the factors which initiate and progress diabetic cardiomyopathy and to develop more effective treatments.


2021 ◽  
Vol 21 ◽  
Author(s):  
Priyanka Mathur ◽  
Vibha Rani

: Risk of heart failure is 2-5 times higher in diabetic patients as compared to non-diabetic patients with similar comorbidities. Recent reports suggest that nearly half of the diabetic population remains undiagnosed making diabetic cardiomyopathy (DCM) a clinically relevant entity. In myocardium, chronic hyperglycemia elicits structural and functional abnormalities characterized by ventricular dilation, diastolic dysfunction, fibrosis, and hypertrophy leading to heart failure. Since diabetes is a multifactorial heterogeneous metabolic disorder which cannot be diagnosed or controlled along with coronary artery disease or hypertension, there is an urgent need to understand the underlying molecular mechanisms that leads to DCM and identify potential therapeutic targets. Small non-coding RNAs in particular microRNAs (miRNAs) have emerged as key regulators for several life threatening diseases including DCM. Recent studies have reported that miRNAs not only regulates the fundamental mechanisms of DCM such as insulin resistance, MAPK pathway, PI3K-AkT pathway, oxidative stress, inflammatory signaling but also possesses potential to be a therapeutic or diagnostic target. This review examines the role of critical miRNAs in the onset and pathogenesis of DCM which also depicts high potential as therapeutic and diagnostic in preclinical studies. Further, it highlights the completed and on-going clinical trials going around the globe for diabetes and miRNAs to provide a prospective about the upcoming miRNA therapeutics.


2008 ◽  
Vol 7 ◽  
pp. 19-19
Author(s):  
B PONIKOWSKA ◽  
E JANKOWSKA ◽  
K WEGRZYNOWSKATEODORCZYK ◽  
S POWIERZA ◽  
L BORODULINNADZIEJA ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
J. Fuentes-Antrás ◽  
B. Picatoste ◽  
A. Gómez-Hernández ◽  
J. Egido ◽  
J. Tuñón ◽  
...  

Diabetic cardiomyopathy entails a serious cardiac dysfunction induced by alterations in structure and contractility of the myocardium. This pathology is initiated by changes in energy substrates and occurs in the absence of atherothrombosis, hypertension, or other cardiomyopathies. Inflammation, hypertrophy, fibrosis, steatosis, and apoptosis in the myocardium have been studied in numerous diabetic experimental models in animals, mostly rodents. Type I and type II diabetes were induced by genetic manipulation, pancreatic toxins, and fat and sweet diets, and animals recapitulate the main features of human diabetes and related cardiomyopathy. In this review we update and discuss the main experimental models of diabetic cardiomyopathy, analysing the associated metabolic, structural, and functional abnormalities, and including current tools for detection of these responses. Also, novel experimental models based on genetic modifications of specific related genes have been discussed. The study of specific pathways or factors responsible for cardiac failures may be useful to design new pharmacological strategies for diabetic patients.


2021 ◽  
Vol 8 ◽  
Author(s):  
Sarah Kassab ◽  
Zainab Albalawi ◽  
Hussam Daghistani ◽  
Ashraf Kitmitto

A pathophysiological consequence of both type 1 and 2 diabetes is remodelling of the myocardium leading to the loss of left ventricular pump function and ultimately heart failure (HF). Abnormal cardiac bioenergetics associated with mitochondrial dysfunction occurs in the early stages of HF. Key factors influencing mitochondrial function are the shape, size and organisation of mitochondria within cardiomyocytes, with reports identifying small, fragmented mitochondria in the myocardium of diabetic patients. Cardiac mitochondria are now known to be dynamic organelles (with various functions beyond energy production); however, the mechanisms that underpin their dynamism are complex and links to motility are yet to be fully understood, particularly within the context of HF. This review will consider how the outer mitochondrial membrane protein Miro1 (Rhot1) mediates mitochondrial movement along microtubules via crosstalk with kinesin motors and explore the evidence for molecular level changes in the setting of diabetic cardiomyopathy. As HF and diabetes are recognised inflammatory conditions, with reports of enhanced activation of the NLRP3 inflammasome, we will also consider evidence linking microtubule organisation, inflammation and the association to mitochondrial motility. Diabetes is a global pandemic but with limited treatment options for diabetic cardiomyopathy, therefore we also discuss potential therapeutic approaches to target the mitochondrial-microtubule-inflammatory axis.


2016 ◽  
Vol 70 (3) ◽  
pp. 111-117
Author(s):  
Irena Mitevska ◽  
Marijan Bosevski

Abstract Cardiovascular disease is responsible for over 75% of deaths in diabetic patients, the majority caused by coronary artery disease (CAD) and heart failure. Cardiovascular morbidity and mortality in diabetic patients might be independently associated with other pathophysiologic mechanisms than coronary artery disease, epicardial and microvascular disease. There is an increasing notion that diabetic patients suffer from an additional cardiac condition named “diabetic cardiomyopathy”. There are several clinical, experimental, pathological and epidemiological researches that support the existence of a specific “diabetic cardiomyopathy”. This is assumed to be influenced by complex interaction of several metabolic changes that leads to both functional and structural alterations of the diabetic myocardium. In this review epidemiological aspects and clinical implications of this condition are presented.


2021 ◽  
Vol 8 ◽  
Author(s):  
Luca Alessandro Gondoni ◽  
Ferruccio Nibbio ◽  
Annamaria Titon

Aims: The number of elderly patients affected with multiple chronic diseases is constantly increasing. Even though multiple studies demonstrated a beneficial effect of cardiac rehabilitation, we do not have data on the outcomes in elderly patients with obesity and heart disease.Methods: We studied 772 consecutive obese subjects (275 women; 35.6%) aged ≥70 years, affected with coronary artery disease and/or heart failure. We conducted a symptom limited exercise test at the beginning and at the end of the program, which consisted of aerobic and strength physical activity, diet, and psychological counseling.Results: Mean body mass index (BMI) at baseline was 37.6 ± 4.4 kg/m2 and decreased to 36.4 ± 4.3 kg/m2 (P < 0.001). At baseline, attained metabolic equivalents (METs) were 4.7 ± 1.7, and by the end of the program, they were 5.6 ± 2.1 (P < 0.001). The mean improvement was 21.6 ± 21.7% (median, 17.6%; 95% CI, 20.0–23.1%). Patients over 80 years old had similar results compared to the younger ones. Diabetics did worse than non-diabetic patients: the improvement they reached was 19.4 ± 18.9% vs. 23.8 ± 23.9% (P = 0.005). The presence of heart failure was significantly related to both the baseline and final performance, but the attained improvement was significantly greater in heart failure patients: 24.3 ± 23.8% vs. 16.3 ± 15.4% (P < 0.001). No patient had adverse events related to the program.Conclusion: This study documents a significant improvement in exercise capacity in elderly obese patients affected with heart disease who underwent a rehabilitation program.


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