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At least 19 recordsLinked to original sources
PubMed1978

Diabetic cardiomyopathy? An echocardiographic study of young diabetics.

An echocardiographic study was carried out on 23 young diabetics, 19 of whom had retinopathy. Their diastolic function was analysed by comparing the timing and pattern of mitral valve opening with the pattern of left ventricular wall movement. Only six patients had all their values within the normal range. Fourteen patients had abnormalities similar to those seen in patients with cardiomyopathy; the close time relation between mitral valve movement and wall movement was lost and mitral valve opening delayed in eight patients. Three other patients had considerable outward wall movement before mitral valve opening, which is characteristic of ischaemic heart disease. Although these studies provide no definite evidence of a cause, the abnormalities found may reflect a subclinical diabetic cardiomyopathy due to small-vessel disease.

Adolescent↗
PubMed2026

Racial outcomes in patients with diabetic cardiomyopathy treated with an aldose reductase inhibitor: the ARISE-HF trial.

BACKGROUND: Racial and ethnic differences in diabetic cardiomyopathy (DbCM) exist, with black and Hispanic participants showing poorer health status. It remains unclear whether these differences affect the natural progression of the disease. We aimed to evaluate disease progression in individuals with DbCM, as well as racial differences in the response to AT-001. METHODS: A total of 625 participants with DbCM were randomised to either placebo or AT-001 and followed for 15 months. The primary outcome was change in peak oxygen uptake (peak VO2) and secondary outcomes included Kansas City Cardiomyopathy Questionnaire (KCCQ) and Physical Activity Scale for the Elderly scores. Analyses were stratified by race and ethnicity (black, Hispanic, white). RESULTS: Black and Hispanic participants who received placebo experienced greater declines in peak VO2 (-0.74 and -1.67 mL/kg/min, respectively) compared with white participants (-0.23 mL/kg/min, p=0.005). AT-001 demonstrated a non-statistically significant trend towards slower declines in peak VO2 in black and Hispanic participants (-0.31 and -0.62 mL/kg/min, p=0.29, respectively). Black participants who received placebo had the largest declines in most KCCQ scores. CONCLUSION: Black and Hispanic participants with DbCM experienced faster disease progression, with black participants showing the most pronounced functional and quality of life declines. The effect of AT-001 on peak VO2 changes was not statistically significant with similar effects between racial and ethnic groups (NCT04083339). TRIAL REGISTRATION NUMBER: NCT04083339.

Aged↗
PubMed1977

Diabetic cardiomyopathy: the preclinical phase.

Left ventricular function was assessed by measuring sytolic time intervals in insulin-requiring diabetics with and without significant microangiopathy. The results were compared with those in normal controls. Significant microangiopathy was defined as proteinuria over 3 g/24 h or proliferative retinopathy. Left ventricular function was also assessed one and a half years later by echocardiography in four patients with microangiopathy. Patients with angina, previous myocardial infarction, hypertension, and alcoholism were excluded. All had normal electrocardiograms and chest radiographs. Diabetics with microangiopathy had impaired left ventricular function, whereas those with uncomplicated diabetes had normal function. This finding supports the existence of a specific diabetic cardiomyopathy due to microangiopathy rather than the metabolic defect. The association of microangiopathy and impaired left ventricular function may explain the high immediate mortality and the high incidence of cardiogenic shock and congestive heart failure after myocardial infarction in diabetics.

Adult↗
PubMed2025

Therapeutic Targeting of Decr1 Ameliorates Cardiomyopathy by Suppressing Mitochondrial Fatty Acid Oxidation in Diabetic Mice.

BACKGROUND: A significant increase in mitochondrial fatty acid oxidation (FAO) is now increasingly recognized as one of the metabolic alterations in diabetic cardiomyopathy (DCM). However, the molecular mechanisms underlying mitochondrial FAO impairment in DCM remain to be fully elucidated. METHODS: A type 2 diabetes (T2D) mouse model was established by a combination of high-fat diet (HFD) and streptozotocin (STZ) injection. Neonatal rat cardiomyocytes were treated with high glucose (HG) and palmitic acid (HP) to simulate diabetic cardiac injury. Gain- and loss-of-function approaches and RNA sequencing were utilized to investigate the role and mechanism of 2,4-dienoyl-CoA reductase 1 (Decr1) in DCM. RESULTS: By integrating the genomic data available in the Gene Expression Omnibus (GEO) with DCM rodents, we found that the transcriptional level of Decr1 was consistently upregulated in DCM (+255% for diabetic heart, p&#x2009;<&#x2009;0.0001; +281% for diabetic cells, p&#x2009;<&#x2009;0.0001). Cardiomyocytes-specific knockdown of Decr1 preserved cardiac function (+41% for EF, p&#x2009;<&#x2009;0.0001; +24% for FS, p&#x2009;=&#x2009;0.0052), inhibited cardiac hypertrophy (-34%, p&#x2009;<&#x2009;0.0001), fibrosis (-69%, p&#x2009;<&#x2009;0.0001), apoptosis (-56%, p&#x2009;<&#x2009;0.0001) and oxidative damage (-59%, p&#x2009;<&#x2009;0.0001) in DCM mice, while cardiomyocytes-specific overexpression of Decr1 aggravated DCM (-28% for EF, p&#x2009;=&#x2009;0.0347; -17% for FS, p&#x2009;=&#x2009;0.0014). Deletion of Decr1 prevented high glucose/palmitate (HG/HP)-induced hypertrophy (-22%, p&#x2009;=&#x2009;0.0006), mitochondrial dysfunction and apoptosis (-74%, p&#x2009;<&#x2009;0.0001) in cultured cardiomyocytes. Furthermore, RNA sequencing and functional analysis showed that Decr1 interacted with and upregulated pyruvate dehydrogenase kinase 4 (PDK4) in injured cardiomyocytes, and overexpression of PDK4 eliminated the benefits of Decr1 downregulation in DCM (-20% for EF, p&#x2009;=&#x2009;0.0071; -28% for FS, p&#x2009;=&#x2009;0.0022). Mechanistically, PDK4 acted as a kinase that induced phosphorylation and mitochondrial translocation of HDAC3. In the mitochondria, HDAC3 mediated the deacetylation of dehydrogenase trifunctional multienzyme complex &#x3b1; subunit (HADHA), contributing to excessive mitochondrial FAO and subsequent cardiac injury. From a screening of 256 natural products, we identified Atranorin and Kurarinone as potential inhibitors of Decr1, both demonstrating protective effects against DCM (Atranorin, +21% for EF, p&#x2009;=&#x2009;0.0134; +24% for FS, p&#x2009;=&#x2009;0.0006; Kurarinone, +20% for EF, p&#x2009;=&#x2009;0.0183; +27% for FS, p&#x2009;=&#x2009;0.0001). CONCLUSIONS: Our study delineates a molecular mechanism by which Decr1 potentiated higher mitochondrial lipid oxidation and cardiac damage by enhancing HADHA deacetylation through the PDK4/HDAC3 signalling pathway.

Animals↗
PubMed2026

Early Cardiomyopathy in Prediabetic NDPK-B-Deficient Mice Is Associated with Remodeling of the Mitochondrial O-GlcNAc Proteome.

Diabetic cardiomyopathy (DCM) is characterized by myocardial remodeling that may already be evident during prediabetes, yet the molecular alterations accompanying these early changes remain poorly understood. The present study examined mouse models of Nucleoside diphosphate kinase B (NDPK-B)-deficient prediabetes and streptozotocin-induced diabetes using O-GlcNAc-associated proteomic profiling to define stage-specific molecular alterations during the progression from prediabetic to diabetic cardiomyopathy. Both models exhibited increased left ventricular extracellular matrix deposition and impaired diastolic function, together with activation of the hexosamine biosynthesis pathway. Profiling of O-GlcNAc-associated proteins uncovered extensive remodeling of the mitochondrial proteome already at the prediabetic stage, with respiratory complex I among the most prominently altered targets, alongside changes in substrate metabolism and inflammatory signaling. In overt DCM, the putative O-GlcNAc proteomic profile was associated with a shift toward wider lipid-dependent metabolic reprogramming and remodeling of mitochondrial proteins. These findings identify early remodeling of the mitochondrial O-GlcNAc-associated proteome as a molecular signature of prediabetic cardiomyopathy and highlight respiratory complex I proteins as candidate targets for future mechanistic investigations.

Animals↗
PubMed1979

The heart in diabetes mellitus. Part I. Biochemical basis for myocardial dysfunction.

The heart in acutely diabetic animals is subject to multiple inhibitions of glucose metabolism caused by enhanced metabolism of free fatty acids (FFA) and ketone bodies. Such metabolic changes may impair the reaction of the diabetic heart to oxygen lack. In chronically diabetic hearts the increased deposition of triglycerides in the heart and the formation of glycoproteins may underlie the newly recognized clinical entity of diabetic cardiomyopathy.

Alcoholism↗
PubMedDate not supplied

The WHO multinational study of vascular disease in diabetes: 2. Macrovascular disease prevalence.

14 national groups have collaborated under WHO auspices to select, from local defined populations of individuals with clinical diabetes, groups of approximately 500 within the age range 35--55 yr stratified by age, sex, and known duration of diabetes. In each center, the selected patients were submitted to a standardized study protocol, which included systematic inquiry (WHO questionnaire) for the presence of symptoms of angina pectoris, history of myocardial infarction, presence of intermittent claudication, and cigarette smoking history. Examination included standard biometry, blood pressure measurement, 12-lead (centrally Minnesota coded) electrocardiography, and central laboratory measurement of serum cholesterol and creatine. Ophthalmoscopic and urinary examinations were also included. The prevalence of arterial disease symptoms and electrocardiographic abnormalities show very large variation between countries, the lowest rates generally being found in the Oriental samples and the highest in the European. "Risk factors" for arterial disease (blood pressure, serum cholesterol, and cigarette smoking) also vary widely between diabetic groups. Although data are not yet complete, these differences appear unlikely to explain the variation in the atherosclerotic morbidity observed. Diabetic women were at least as vulnerable to arterial disease as diabetic men. A high prevalence of nonspecific abnormalities of the repolarization phase of the ECG was found, even in groups where ischemic abnormalities were rare. The origin of these is uncertain; they may represent variable local changes or possibly diabetic cardiomyopathy. This preliminary report confirms and quantifies previous indications that the impact of atherosclerotic disease on persons with diabetes varies considerably between national groups, in broad terms, running parallel with the variations in prevalence in the populations in general and suggesting that cultural and/or ethnic factors are more important determinants of atherosclerosis in diabetic individuals than is the diabetic state per se.

Adult↗
PubMed2026

Changes in cardiac myosin acetylation disrupt the super-relaxed state in genotype-negative hypertrophic cardiomyopathy with type 2 diabetes.

BACKGROUND: Patients with hypertrophic cardiomyopathy (HCM) and type 2 diabetes (T2D) have a more severe cardiac phenotype and worse clinical course than non&#x2011;diabetic patients. To identify how T2D aggravates the disease and whether the most abundant cardiac protein, myosin, is involved, we combined functional, structural and mass spectrometry analyses of human samples. METHODS: Left ventricular septal myectomy samples from genotype&#x2011;negative (G-) HCM patients without T2D (G-&#x2009;, N&#x2009;=&#x2009;19) and with T2D (G-T2D, N&#x2009;=&#x2009;15) were analyzed mainly using fluorescent ATP chase experiments, small&#x2011;angle X&#x2011;ray diffraction and targeted myosin heavy chain proteomics. RESULTS: Mant&#x2011;ATP chase measurements showed a lower fraction of myosin heads in the energy&#x2011;conserving super&#x2011;relaxed (SRX) state in G-T2D compared to non-diabetic myocardium. In parallel, X&#x2011;ray diffraction showed trends toward structural alterations in myosin organization in G-T2D tissue, consistent with altered OFF/ON state equilibrium. Targeted mass spectrometry identified hyperacetylation of several myosin lysine residues in G-T2D, including K847 within the S2 region. All&#x2011;atom molecular dynamics simulations indicated that K847 acetylation disrupts stabilizing electrostatic interactions in the interacting&#x2011;heads motif, which is associated with the OFF state. CONCLUSIONS: Disruption of myosin super&#x2011;relaxation emerges as a central cellular defect in G-T2D HCM myocardium and can be mechanistically linked to site&#x2011;specific myosin hyperacetylation at K847, providing a potential therapeutic target for genotype&#x2011;negative HCM with T2D.

Humans↗
PubMed2024

SLC40A1-related hemochromatosis associated with a p.Y333H mutation in mainland China: a pedigree report and literature review.

BACKGROUND: Haemochromatosis is a genetic disease characterized by the excessive deposition of iron in various tissues and organs, eventually results in organ damage including cirrhosis, diabetes, cardiomyopathy, etc. SLC40A1-related haemochromatosis is associated with gain-of-function mutations in the SLC40A1 gene, which encodes ferroportin. While sporadic reports of this condition exist in mainland China, the understanding of the phenotype and genetic pattern associated with the SLC40A1 p.Y333H mutation remains incomplete. CASE PRESENTATION: We report a pedigree with heterozygous p.Y333H mutation in Chinese Han population. The proband is a 64-year-old man complaining of persistent abnormality of liver enzyme levels for 1 year, with a history of knee joint pain, diabetes and skin pigmentation. He displayed markedly elevated serum ferritin level and transferrin saturation. Magnetic resonance imaging showed iron deposition in the liver, spleen, and pancreas, along with cirrhosis and splenomegaly. Whole exome sequencing identified a heterozygous allelic variant c.997T&#x2009;>&#x2009;C (p.Y333H). Genetic screening of family members identified four first-degree relatives and three second-degree relatives having the same mutation. Additional cases with this mutation from two published studies were included. Among the probands and screened relatives, all eight males aged over 30 y had ferritin level&#x2009;>&#x2009;1000&#xa0;&#xb5;g/L, transferrin saturation&#x2009;>&#x2009;90%. Four patients with organ damage in the present study received therapeutic phlebotomy, alleviating clinical symptoms and improving in transferrin saturation and serum ferritin. CONCLUSIONS: This study reports the largest pedigree with heterozygous SLC40A1 p.Y333H mutation in the Chinese population to date. In Chinese families, males over 30 years old with hemochromatosis due to SLC40A1 p.Y333H mutation exhibit severe iron overload phenotypes.

Humans↗
PubMed2025

Distinct immune-metabolic phenotypes underlie poor coronary collateral circulation.

BACKGROUND: Coronary collateral circulation (CCC) significantly impacts myocardial perfusion and clinical outcomes in coronary artery disease patients, yet the underlying molecular heterogeneity remains inadequately characterized. OBJECTIVE: To identify distinct molecular phenotypes in patients with poor CCC, validate these phenotypes using clinical parameters, and evaluate their prognostic implications. METHODS: This study enrolled 149 patients (80 with good CCC and 69 with poor CCC) for high-throughput proteomic profiling. Unsupervised consensus clustering identified molecular subtypes within poor CCC patients, followed by differential expression analysis and KEGG pathway enrichment. Boruta feature selection was implemented, and multiple machine learning algorithms were tested on clinical data, with XGBoost optimization (accuracy 80.0%, F1-score 80.31%) and SHAP value interpretation. External validation was performed using the MIMIC database. Kaplan-Meier analysis and Cox regression models assessed major adverse cardiovascular events (MACE). RESULTS: Two distinct phenotypes emerged among poor CCC patients: Cluster 1 (n&#x2009;=&#x2009;39, Complement-Driven Vascular Remodeling [CDVR]) and Cluster 2 (n&#x2009;=&#x2009;30, Immuno-Thrombotic Myocardial Dysfunction [ITMD]). An XGBoost model incorporating fasting glucose, eosinophil percentage, and HbA1c achieved excellent discrimination (AUC&#x2009;>&#x2009;0.91). External validation confirmed the phenotype-specific clinical patterns. Notably, Cluster 2 demonstrated significantly higher MACE incidence compared to Cluster 1 (Log-rank p&#x2009;<&#x2009;0.05), with KEGG analysis revealing significant upregulation of platelet activation, diabetic cardiomyopathy, and metabolic pathways in the ITMD phenotype. CONCLUSION: Poor CCC encompasses distinct immune-metabolic phenotypes that can be accurately classified using integrated proteomic-clinical modeling. This classification enables more precise risk stratification and may guide personalized therapeutic strategies for coronary artery disease patients with inadequate collateralization.

Humans↗
PubMed1979

[Cardiomyopathy in juvenile diabetics? (author's transl)].

Report on a cardiologic study conducted in 26 juvenile diabetics with insulin deficiency, in whom the disease had lasted for more than ten years. Electrocardiograms, vectorcardiograms and echocardiograms were recorded. The investigations did not indicate the presence of a subclinical cardiomyopathy as a sign of an early diabetic microangiopathy of the myocardium. Hence the findings by Riff and Riff (1974) as well as those by Sanderson et al (1978) have not been confirmed.

Adolescent↗
PubMed1979

The natural history of hypertrophic cardiomyopathy in infants of diabetic mothers.

Eleven infants of diabetic mothers with hypertrophic cardiomyopathy have been followed for 30 to 40 months. All infants presented with cardiorespiratory distress and were found to have disproportionate septal hypertrophy on echocardiogram. Cardiac catheterization was done in four infants; three had significant subaortic obstruction. One infant had remarkable improvement after treatment with propranolol. Two infants who received digoxin did poorly and responded favorably to cessation of therapy. The natural history of HCM-IDM appears to be benign, with a resolution of symptoms within two to four weeks and a resolution of septal hypertrophy within two to 12 months. Most of the infants need only supportive care; if pharmacologic intervention is deemed necessary, propranolol appears to be the drug of choice. The natural history of this entity is that of spontaneous regression of symptoms and septal hypertrophy irrespective of therapy.

Angiocardiography↗
PubMed1979

Hereditary and acquired cardiomyopathies in experimental animals: mechanical, biochemical, and structural features.

Evidence has been presented regarding alterations of contractile behavior muscle biochemistry, and ulstrastructure during the course of the hereditary hamster cardiomyopathy. Also, preliminary structural and mechanical data were presented on the acquired cardiomyopathy of diabetes mellitus in experimental animals. In the hamster model, contractile performance, measured as isometric tension and rate of tension development, was shown to be depressed throughout the course of the disease, whereas normalized force-velocity relationships returned to normal only during the compensated stages of hypertrophy. Force-frequency relationships were depressed in myopathic muscles, indicating the presence of alterations in the muscle activation system, namely, the biochemical and functional integrity of the sarcoplasmic reticulum. Analysis of the contractile proteins in myopathic muscle has revealed depressions of Ca2+ activity in purified myosin in addition to an independently increased neutral protease activity that results in the specific degradation of LC2 of myosin. Sympathetic time and norepinephrine turnover increase progressively during the course of the disease. These changes are accompanied by decreasing tissue levels of neorepinephrine and increasing levels of dopamine, indicating a shift in the rate-limiting step for norepinephrine synthesis. Alterations were also noted in nuclear protein composition and serotonin levels. Microscopically, the myolytic and calcification changes that characterize the hamster cardiomyopathy have been confirmed. In addition, contraction bands and lysosomal changes have been observed that may relate to cateholamine hypersensitivity. In the experimental model of diabetic cardiomyopathy, a significant alteration in relaxation process was demonstrated despite the fact that peak tension development and its rate of development were unaltered. Also, the length dependence of contractile behavior was altered when compared to that of age-matched controls, indicating a potential loss of contractility reserve. When animals with combined hypertension and diabetes were studied, bothe contraction and relaxation processes were affected to a greater degree.

Actomyosin↗