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At least 19 recordsLinked to original sources
PubMed1992

HLA and immunoglobulin polymorphisms in idiopathic dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is an idiopathic heart muscle disorder. The presence of circulating cardiac antibodies and the association with HLA-DR4 are consistent with autoimmune pathogenesis in a subset of patients. Sixty-eight DCM patients and 277 controls were typed for IgG heavy-chain constant region (Gm) and kappa light-chain (Km) allotypes. All patients and 210 of the 277 controls were HLA-DR typed. The Gm (1, 3, 17; 23; 5*, 21, 28) phenotype was overrepresented in DCM compared with controls (25% vs 13%, p = 0.0139, pc = NS, RR = 2.23). The frequency of this phenotype was higher in patients with younger age at onset, shorter symptom duration, and among those who were positive for cardiac as well as for non-organ-specific autoantibodies than in controls. A higher frequency of the Gm (1, +/- 2, 3, 17; +/- 23; 5*, 21, 28) heterozygous phenotypes was also found in DCM compared to controls (40.91% vs 26.89%; p = 0.02, pc = 0.04, RR = 1.88). The finding of Gm heterozygosity in DCM was associated with serum positivity for cardiac antibodies. A higher proportion of DCM patients were positive for both the Gm (1, 3, 17; 23; 5*, 21, 28) phenotype and HLA-DR4 compared to normals (3/68 vs 0/210; p = 0.04, RR = 22.50).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Relationship between left ventricular systolic function and the myocardial gray level distribution in patients with idiopathic dilated cardiomyopathy].

Dilated cardiomyopathy (DCM) is characterized by progressive left ventricular (LV) systolic dysfunction of nonspecific etiology. Fifty-nine DCM patients were serially observed by echocardiography for 4.5 +/- 2.6 years, and 7.3 +/- 3.4 times M-mode and two-dimensional echocardiography was performed during the observation period using SSH-11A (Toshiba). To assess LV systolic function, ejection fraction was calculated by Pombo's method. Myocardial gray level distribution shown by echocardiography was calculated to assess the myocardial tissue character. Two-dimensional echocardiographic images were obtained in the parasternal short-axis view, recorded on U-matic videotape, and transferred to an image processing computer system (MIPRON, Kontron). The images were digitized and stored on the computer. The regions of interest (ROI) were placed in the LV septum, posterior papillary muscle, posterior wall, anterior papillary muscle and entire LV wall. The gray level distributions in each ROI and its quantitative parameters (mean, SD, skewness, excess) were calculated. The corrected myocardial gray level of every ROI (CMD) was also calculated and expressed as the ratio to the mean gray level of the LV cavity. Seven patients exhibited significant decreases in ejection fraction (more than 10%) during the observation period (group A); the remainders showed less change (group B).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Dilated↗
PubMed2025

Epigenetic Regulation in Dilated Cardiomyopathy.

Dilated cardiomyopathy (DCM) is a nonischemic heart muscle disease characterized by impaired contractility, cardiac dilation, and heart failure, with both genetic and nongenetic causes. Emerging evidence highlights epigenetic mechanisms, including deoxyribonucleic acid methylation, histone modifications, chromatin remodeling, and noncoding RNAs, as critical regulators of gene expression in DCM pathogenesis. This article explores familial DCM linked to pathogenic variants in genes like lamin A/C and titin, as well as nongenetic forms such as diabetic and autoimmune DCM. By summarizing recent discoveries, it highlights the epigenetic factors in bridging genetic and environmental influences, offering potential biomarkers and therapeutic targets for improved DCM management.

Humans↗
PubMed2026

Clinical characteristics and prognostic impact of multiple pathogenic variants across the genetic spectrum of arrhythmogenic and dilated cardiomyopathies.

BACKGROUND: Arrhythmogenic and dilated cardiomyopathies (ACM and DCM, respectively) are genetically heterogeneous disorders of the right and/or left ventricles associated with an increased risk of major arrhythmic events (MAE) and end-stage heart failure (ESHF). In arrhythmogenic right ventricular cardiomyopathy (ARVC), the presence of >1 pathogenic or likely pathogenic (P/LP) variant is associated with worse outcomes. Whether this phenomenon occurs for non-desmosomal arrhythmogenic left ventricular cardiomyopathy (ALVC)/DCM genes is unknown. OBJECTIVE: This study aimed to evaluate the impact of single vs multiple P/LP variants on arrhythmic and heart failure outcomes across the ACM/DCM genetic spectrum. METHODS: We retrospectively analyzed 1054 genotype-positive patients with ≥1 P/LP variant in a definitive or strong evidence ARVC- or ALVC/DCM-causative gene. Primary endpoints were MAE (sustained ventricular tachycardia, ventricular fibrillation, aborted cardiac arrest, appropriate implantable cardioverter-defibrillator therapy, and sudden cardiac death) and ESHF (transplant or heart failure death). RESULTS: Of the 1054 patients, 27 (3%) harbored >1 P/LP variants (21 with ≥1 ALVC/DCM gene; 6 with >1 ARVC gene). MAE occurred in 20% of single-variant patients compared with 48% and 50% of those with >1 P/LP variants in ≥1 ALVC/DCM- and >1 ARVC-susceptibility gene(s), respectively. ESHF occurred in 9%, 29%, and 17% of patients, respectively. On adjusted analysis, >1 P/LP variants in ≥1 ALVC/DCM-susceptibility (MAE hazard ratio [HR], 2.46 [1.28-4.72]; P = .01 and ESHF HR, 3.15 [1.35-7.37], P = .01) and >1 ARVC-susceptibility gene(s) (MAE HR, 2.67 [1.28-8.72], P = .03) were independent predictors of the primary endpoints. CONCLUSION: Multiple P/LP variants confer an increased risk of arrhythmic events and heart failure across the ACM/DCM spectrum.

Arrhythmogenic cardiomyopathy↗
PubMed2026

Comparative whole-exome sequencing of ambulatory patients and transplant recipients with idiopathic dilated cardiomyopathy.

BACKGROUND: Idiopathic dilated cardiomyopathy (DCM) is a major cause of advanced heart failure and heart transplantation (HTx), yet the genetic correlates of progression to HTx and transplant-relevant arrhythmic phenotypes remain incompletely defined. We examined the genetics of idiopathic DCM in a Korean population, focusing on HTx/death and arrhythmic outcomes, to identify adverse outcome-linked genotype-phenotype associations. METHODS: Whole-exome sequencing was performed in 202 Korean patients with idiopathic DCM, including 56 HTx recipients and 146 ambulatory patients, and compared the findings with 1093 population-based controls. Genotype-phenotype correlations were analyzed for major clinical outcomes, including HTx, death, arrhythmias, and left ventricular functional recovery. RESULTS: Pathogenic/likely pathogenic variants were identified in 32% of patients (38% in HTx vs 30% in ambulatory patients). TTN was the most frequently affected gene overall (12%), but LMNA variants predominated in HTx recipients (20% vs 4%, p = 0.001). LMNA carriers showed substantially higher odds of HTx/death (OR 14.65, 95% CI 3.32-139.31; FDR p<0.001), and strong association with arrhythmias, including ventricular tachyarrhythmias and atrial fibrillation. Both missense and loss-of-function LMNA variants were associated with adverse outcomes. In contrast, TNNT2 variants were observed exclusively in ambulatory patients and identified a favorable functional-recovery phenotype, with a greater likelihood of LVEF recovery &#x2265;10 percentage points (OR 6.03, 95% CI 1.52-28.71; FDR p = 0.016). CONCLUSIONS: LMNA variants mark a high-risk transplant-trajectory phenotype in Korean idiopathic DCM. Genetic testing may aid early identification and management of candidates for advanced HF therapies, including HTx and durable MCS.

dilated cardiomyopathy↗
PubMed1978

Diagnosis and natural history of congested (dilated) cardiomyopathies.

The diagnosis of primary dilated cardiomyopathy depends on the recognition of a dilated poorly contracting left ventricle with increased end-diastolic and end-systolic volumes in the absence of a detectable cause. The diagnosis is made only after exclusion both of structural heart disease and of known causes of secondary heart muscle disorder. The natural history is still largely unknown and is probably as variable as the likely causes. The left ventricular disorder does not cause symptoms until heart failure supervenes except for occasional patients who develop an early atrial or ventricular dysrhythmia, conduction defect, chest pain or murmur of mitral regurgitation. This period of latency may be short, prolonged or even permanent since it is unlikely that all cases progess to the point of failure. A few patients recover normal or near-normal cardiac function. The interplay between high blood pressure, hypertensive heart failure and dilated cardiomyopathy is illustrated by patients who recover from heart failure to become hypertensive and vice versa and in current treatment with vasodilators and diuretics for patients at either end of the spectrum.

Alcoholism↗
PubMed1992

Cardiac persistence of cardioviral RNA detected by polymerase chain reaction in a murine model of dilated cardiomyopathy.

BACKGROUND: In our model of dilated cardiomyopathy (DCM), cardiac dilatation and hypertrophy developed after inoculation of encephalomyocarditis virus (EMCV), but the infectious virus was isolated only early after infection. In this study, we investigated whether viral RNA could be detected at later times using the polymerase chain reaction (PCR). METHODS AND RESULTS: In the in vitro study, FL (human amnion) cells infected with EMCV were harvested for RNA extraction, and viral cDNA was synthesized by reverse transcription with random hexamers. Using oligonucleotide primers with homology to the 5' noncoding region of EMCV, we enzymatically amplified a 121-base pair band, which was homologous to a probe specific for EMCV as demonstrated by Southern blot hybridization. The sensitivity of this PCR technique was at the level of about 10(2)-10(3) copies of viral RNA genome. In the in vivo study, four-week-old DBA/2 mice were inoculated with EMCV intraperitoneally (10 pfu/mouse) and killed on days 1,2,3,5,7,10,14,18,28,60, and 90. The hearts were divided into three parts for purification of total RNA, histopathological examination, and to culture for infectious virus. The infectious virus was isolated from the heart after the second day but never after the 14th day. The viral genome was detectable by PCR on the second day, when very little mononuclear cell infiltration around the blood vessels was histologically visible. Positive PCR signals were observed in all hearts through day 14. Viral RNA was also detected in four of six 28-day samples, four of six 60-day samples, and two of seven 90-day samples when diffuse myocardial fibrosis was prominent, but myocardial necrosis or cellular infiltration had disappeared. CONCLUSIONS: The persistence of EMCV RNA was shown by PCR in the chronic stage of EMCV-induced myocarditis, a time when the inflammatory reaction had largely subsided. The PCR is a potentially useful method to test possible viral etiologies in idiopathic heart muscle disease or DCM.

Animals↗
PubMed1992

Assessment of immune modulation of beta-adrenergic pathways in human dilated cardiomyopathy: influence of methodologic factors.

Sera from patients with dilated cardiomyopathy contain autoantibodies modifying cardiac beta-adrenergic pathways. The influence of the methodology used to determine the prevalence of these antibodies was examined by comparing in 51 patients with idiopathic dilated cardiomyopathy the results of three assays: (1) isoproterenol-sensitive adenylate cyclase; (2) ligand binding inhibition; (3) enzyme-linked immunoassay (ELISA) of beta-receptor peptides. In 20% of the patients, all three tests gave positive results, while the concordance of the adenylate cyclase assay with either of the other two tests was 65%. ELISA was positive for a beta 1-receptor peptide corresponding to the second extracellular loop, but negative for a beta 2-receptor peptide. The results suggest that autoantibodies in dilated cardiomyopathy sera interact with several components of the beta-receptor-adenylate cyclase, and therefore a combination of methodologic approaches is needed to evaluate the prevalence and consequences of beta-receptor autoimmunity.

Adenylyl Cyclases↗
PubMed1992

Respiratory chain defect of myocardial mitochondria in idiopathic dilated cardiomyopathy of Doberman pinscher dogs.

Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause. We tested the hypothesis that IDCM was associated with a myocardial metabolic defect by determining a comprehensive biochemical profile of metabolite concentrations and enzyme activities for the major metabolic pathways of the myocardium. We used the Doberman pinscher breed as a naturally occurring canine model of IDCM and compared its myocardial profile with that of healthy adult mongrels. Compared with controls, myocardium in IDCM had markedly reduced mitochondrial electron transport activity and myoglobin concentration, in association with acidosis and energy depletion following anoxic challenge: 60% decreased NADH dehydrogenase and 50% decreased ATP synthetase activities; 90% decreased myoglobin concentration; and 30% reduced ATP and 50% increased lactate and proton concentrations. Sarcoplasmic reticulum Ca(2+)-transport ATPase was decreased by 42%. There was a 15% compensatory increase in fatty acid oxidation and Krebs cycle activity. Other biochemical changes were mild by comparison with the mitochondrial defects. We conclude that IDCM is associated with a marked impairment of mitochondrial production of ATP, arising from decreased activity of the mitochondrial electron transport system, including myoglobin. These changes may be secondary to an underlying genetic defect or may indicate a deficiency of the mitochondrial respiratory chain that predisposes this breed to heart failure.

ATP Synthetase Complexes↗
PubMed1992

Similar prevalence of enteroviral genome within the myocardium from patients with idiopathic dilated cardiomyopathy and controls by the polymerase chain reaction.

OBJECTIVE: To assess the prevalence and significance of enteroviral genome within myocardial biopsy specimens taken from patients with idiopathic dilated cardiomyopathy and from controls. DESIGN: Prospective evaluation of myocardial tissue for the presence of an enteroviral genome by the polymerase chain reaction. SETTING: A tertiary referral centre for patients with idiopathic dilated cardiomyopathy. PATIENTS: Tissue for the study came from 50 consecutive patients with dilated cardiomyopathy, 41 with other forms of heart disease and 34 from coroners' necropsy cases. RESULTS: Enteroviral genome was detected in 6/50 (12%) patients with dilated cardiomyopathy and 13/75 (17%) of the controls (not significant). No differences were seen between dilated cardiomyopathy patients with or without myocardial enteroviral genome in respect of age; duration of symptoms; proportion of patients with a premorbid acute viral illness, excess alcohol consumption, or hypertension; New York Heart Association functional class; measures of left ventricular function; or endomyocardial histology. Within the control group enteroviral genome was detected in 3/15 (20%) patients with ischaemic heart disease, 2/19 (10.5%) with valvar heart disease, 1/5 (20%) with specific heart muscle disease, 0/2 (0%) with congenital heart disease, and 7/34 (20.6%) cases of sudden death. During 2-52 month follow up (mean 22) 15/44 (34%) patients without myocardial enteroviral genome and 2/6 (33%) with myocardial enteroviral genome died suddenly or required orthotopic heart transplantation for progressive heart failure. CONCLUSIONS: These findings do not support the hypothesis that persistent enteroviral infection is of pathogenic or prognostic importance in dilated cardiomyopathy but they are consistent with enterovirus being a common environmental pathogen.

Adolescent↗
PubMed2025

Identification of Biomarkers for Right Ventricular Dysfunction in Idiopathic Dilated Cardiomyopathy Via Urinary Proteomics and Machine Learning.

BACKGROUND: Right ventricular dysfunction (RVD) is a common complication of idiopathic dilated cardiomyopathy linked to poor outcomes. However, reliable noninvasive biomarkers for RVD remain lacking. This study aimed to identify urinary proteomic markers using mass spectrometry and machine learning. METHODS: In this prospective cohort, patients with idiopathic dilated cardiomyopathy were classified by cardiac magnetic resonance imaging into groups with RVD (RV ejection fraction <45%) and without RVD groups. Baseline urine samples were profiled by data-independent acquisition mass spectrometry. Differentially expressed proteins were identified and selected by least absolute shrinkage and selection operator regression to build a diagnostic model, developed in a training set, and validated in a test set. The primary end point was a composite of cardiovascular death, heart failure rehospitalization, left ventricular assist device implantation, or heart transplantation. RESULTS: The study enrolled 147 patients with idiopathic dilated cardiomyopathy (64 with RVD, 83 without), with a median follow-up of 19.3&#x2009;months. Of 3579 quantified urinary proteins, 46 were differentially expressed between groups. A 3-protein panel (RARRES1 [retinoic acid receptor responder protein 1], MVB12B [multivesicular body subunit 12B], GSK3A [glycogen synthase kinase 3 alpha]) was identified and showed excellent diagnostic accuracy (training area under the curve 0.946; validation area under the curve0.935), outperforming both NT-proBNP (N-terminal pro-brain natriuretic peptide) and tricuspid annular plane systolic excursion. The risk score derived from this panel effectively stratified patients, with the high-risk group exhibiting significantly worse outcomes than the low-risk group (hazard ratio, 3.24 [95% CI, 1.56-6.71], P=0.002). CONCLUSIONS: The urinary proteomic panel developed in this study demonstrates diagnostic and prognostic potential for identifying RVD in idiopathic dilated cardiomyopathy, providing a promising noninvasive tool for precise detection and clinical risk stratification.

Humans↗
PubMed1992

An experimental model for dilated cardiomyopathy after rabbit coronavirus infection.

A rabbit model for coronavirus-induced dilated cardiomyopathy is described. Acute rabbit coronavirus infection results in virus-induced myocarditis and congestive heart failure. Of the survivors of rabbit coronavirus infection, 41% had increased heart weight and heart weight-to-body weight ratios, biventricular dilation, myocyte hypertrophy, myocardial fibrosis, and myocarditis consistent with the development of dilated cardiomyopathy. These changes were also seen in the remaining 59% of the survivors, except that the degree of myocyte hypertrophy was reduced and only right ventricular dilation was present. In most survivors, myocarditis was usually mild (1-5 foci/transverse section), but in some cases it was severe (> 20 foci/transverse section). Interstitial and replacement fibrosis was more pronounced in the papillary muscles. These data suggest that rabbit coronavirus infection may progress to dilated cardiomyopathy.

Animals↗
PubMed1992

Detection of enteroviral RNA in idiopathic dilated cardiomyopathy and other human cardiac tissues.

Enteroviruses have been considered to be a possible cause of idiopathic dilated cardiomyopathy. We used a polymerase chain reaction methodology for the identification of enteroviral RNA in an attempt to provide evidence of a role for enteroviruses in the pathogenesis of idiopathic dilated cardiomyopathy. The methodology was shown to identify a wide variety of enteroviruses with a sensitivity up to 0.1-1 plaque-forming units/gram of tissue. 5 of 11 cases (45%) of idiopathic dilated cardiomyopathy, as well as 9 of 24 cases (38%) of a wide variety of other cardiac conditions (including normal heart), were positive for enteroviral nucleic acid sequences; all eight control cases of breast carcinoma tested were negative. These results suggest that both the normal and abnormal heart may represent a site of latent or low-grade persistent enteroviral infection, and that the mere presence of enteroviral nucleic acid sequences is not specifically associated with idiopathic dilated cardiomyopathy.

Cardiomyopathy, Dilated↗
PubMed1992

Genomic detection of enteroviruses in the myocardium--studies on animal hearts with coxsackievirus B3 myocarditis and endomyocardial biopsies from patients with myocarditis and dilated cardiomyopathy.

We examined myocardial tissues for the presence of enteroviral RNA in animal models with experimental coxsackievirus B3 myocarditis and in endomyocardial biopsy samples obtained from patients clinically diagnosed as having dilated cardiomyopathy or myocarditis using polymerase chain reaction (PCR) gene amplification with enterovirus-generic primers and/or coxsackievirus B3-specific primers. In animal models, coxsackievirus B3 was detected in myocardial tissues up to 28 days, 56 days and 180 days after inoculation, in C3H/He mice, A/J mice and Syrian golden hamsters, respectively. The viral genomes were identified by in situ hybridization in myocardial cells and some interstitial cells in and around the myocarditic lesions in animals. In human endomyocardial biopsy samples, enteroviral RNA sequences were detected in 8 (32%) out of 25 patients with clinical dilated cardiomyopathy and in 3 (33%) out of 9 patients with clinical myocarditis. The patients showing histologic findings of myocarditis and clinical features resembling dilated cardiomyopathy had a high incidence (83%) of positive PCR result for enteroviral RNA sequences. Additionally, 25% of patients with dilated cardiomyopathy showing no histologic findings of myocarditis had positive PCR result. This study supports a link between viral myocarditis and dilated cardiomyopathy.

Adult↗
PubMed1992

Virus infection and dilated cardiomyopathy.

The implication of virus infection in the pathogenesis of dilated cardiomyopathy has been strengthened by a number of studies demonstrating a progression from myocarditis to this condition. In this context a histological diagnosis from endomyocardial biopsy is mandatory. Serological studies have provided only circumstantial evidence. The development and clinical application of enterovirus group-specific hybridization probes and the polymerase chain reaction has allowed the detection of enteroviral RNA sequences in endomyocardial biopsy samples from patients in all stages of the disease. The persistence of enteroviral RNA within the myocardium of patients with dilated cardiomyopathy appears to indicate an adverse prognosis for the patient. Preliminary data, however, suggest that disappearance of the virus may be associated with clinical improvement, offering the hope that future antiviral agents may alter the natural history of the disease.

Biopsy↗
PubMed1992

Pharmacotherapy of dilated cardiomyopathy: current status and future directions.

The current status and future directions of the pharmacotherapy of dilated cardiomyopathy are reviewed. The Japanese multicenter study on the effect of beta-blockers revealed significant improvement of NYHA functional classification, LV end-diastolic dimension, ejection fraction, and exercise tolerance time in patients with dilated cardiomyopathy. From our study using normal rabbits, metoprolol augmented adenylate cyclase activity without upregulation of the beta-adrenergic receptor number. Carteolol, a beta-adrenergic blocker with intrinsic sympathomimetic action, prevented the development of dilatation and hypertrophy of the heart in the chronic stage following murine encephalomyocarditis (EMC) viral myocarditis. Metoprolol exerted no such effect. Animal experiments indicated that immunosuppressive treatment for inflammatory myocarditis may aggravate the clinical course of the disease. However, immunosuppressive treatment in acute myocarditis should be reevaluated with the use of newly developed antiviral agents. A new synthetic immunoactive peptide FK 565, given before or simultaneously with viral inoculation, proved effective in inhibiting myocardial virus replication and myocardial damage in murine EMC viral myocarditis. Beneficial effects of captopril on survival rate and myocardial injury were demonstrated dose dependently in murine EMC viral myocarditis, even when the treatment was started around the peak of virus replication, namely, on day 4-14 after inoculation. Captopril may be promising for the treatment of acute myocarditis, and hopefully for prevention of the progression from myocarditis to dilated cardiomyopathy.

Adrenergic beta-Antagonists↗
PubMed2026

Dysregulated Ribonucleoprotein Granules Impair Mitochondrial Function in RBM20-Related Dilated Cardiomyopathy.

BACKGROUND: Pathogenic variants in RBM20 cause severe dilated cardiomyopathy. Loss-of-function variants disrupt splicing; neomorphic gain-of-function (GoF) variants also mislocalize RBM20 to cytoplasmic ribonucleoprotein granules and are associated with more aggressive disease. The mechanism by which RBM20 mislocalization drives cardiac dysfunction remains unknown. METHODS: We investigated the effects of Rbm20 GoF and loss-of-function (LoF) variants using proteomic profiling, protein solubility assays, mitochondrial respiration and calcium flux analyses, and ultrastructural imaging in mouse models. Human induced pluripotent stem cell-derived cardioids were used to validate variant-specific phenotypes. RESULTS: Rbm20 GoF, but not LoF, variants caused posttranscriptional downregulation of soluble mitochondrial proteins, including the calcium efflux regulator TMEM65 (transmembrane protein 65), and reduced solubility of mitochondrial membrane proteins. Electron microscopy revealed enlarged mitochondria with cristae disorganization. Functional assays confirmed impaired oxidative phosphorylation, reduced mitochondrial membrane potential, and abnormal calcium handling in Rbm20 GoF models. Human cardioids reproduced these findings, demonstrating that cytoplasmic mislocalization, rather than splicing deficiency, drives mitochondrial dysfunction. CONCLUSIONS: Cytoplasmic mislocalization of RBM20 disrupts mitochondrial function by reducing mitochondrial protein abundance, leading to oxidative phosphorylation failure and abnormal mitochondrial calcium handling. This mechanism distinguishes RBM20 GoF from LoF variants and may explain the more severe heart failure phenotype observed in patients with RBM20 GoF variants. These insights advance the mechanistic understanding of RBM20-related cardiomyopathy and identify mitochondrial mRNA/protein regulation as a key node in cardiac energetics.

cardiomyopathy, dilated↗