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At least 19 recordsLinked to original sources
PubMed1979

Hypertrophic cardiomyopathy and human leukocyte antigen linkage: differentiation of two forms of hypertrophic cardiomyopathy.

To determine whether hypertrophic cardiomyopathy is associated with a human leukocyte antigen (HLA) phenotype, we tissue-typed 70 unrelated afflicted patients and 86 of their asymptomatic family members (from nine separate kindreds). Forty-five per cent of the white patients had B-12 antigen as compared to 23 per cent in matched control subjects; 69 per cent of black patients had a B-5-complex antigen as compared to 33 per cent in matched controls. Patients with a B-12 or B-5-complex antigen were nonhypertensive and had family members with the disease. Patients without these antigens were severely hypertensive and had no affected family members. Linkage analysis of six families revealed a lod score of 7.7 for asymmetric septal hypertrophy and the HLA region of chromosome 6. We conclude that there is a heritable, nonhypertensive form of hypertrophic cardiomyopathy linked to the HLA loci on chromosome 6 and that a sporadic form is associated with severe, systemic hypertension.

Adult↗
PubMed1979

Familial cardiomyopathy. Autosomally, dominantly inherited congestive cardiomyopathy with two cases of septal hypertrophy in one family.

A family with inherited congestive cardiomyopathy is presented. The diagnosis is based on clinical, morphological and laboratory evaluations. The first observed sign of the disease is arrhythmia and/or conduction defects. The onset of symptoms of pump failure is in adult life, and affected persons die within several years. Three persons have died suddenly. Septal hypertrophy was present in two affected persons. The mode of transmission is probably autosomal dominant. The recognition of arrhythmia as an early sign of the disease offers the opportunity of an early diagnosis.

Adult↗
PubMed2025

Polygenic Susceptibility in Peripartum, Alcohol-Induced, and Cancer Therapy-Related Cardiomyopathies.

IMPORTANCE: Rare monogenic variants linked to nonischemic dilated cardiomyopathy (DCM) are enriched among individuals with secondary cardiomyopathies, such as peripartum (PPCM), alcohol-induced (ACM), and cancer therapy-related (CCM) cardiomyopathies. However, it remains unclear whether a polygenic predisposition to DCM also contributes to these conditions. OBJECTIVE: To assess the association of a DCM polygenic score with PPCM, ACM, and CCM, and to evaluate the contributions of monogenic and polygenic susceptibilities to these secondary cardiomyopathies. DESIGN, SETTING, AND PARTICIPANTS: This was a retrospective genetic association analysis of data from the Mass General Brigham (MGB) Biobank (n&#x2009;=&#x2009;42&#x202f;137, 2008-2025), with replication in the UK Biobank (n&#x2009;=&#x2009;295&#x202f;160, 2005-2010), FinnGen (n&#x2009;=&#x2009;417&#x202f;950, 2017-2025), and the Veterans Affairs Million Veteran Program (n&#x2009;=&#x2009;516&#x202f;066, 2011-2025). In MGB Biobank, medical records were reviewed to ascertain secondary cardiomyopathy cases and antecedent clinical risk factors. EXPOSURES: DCM polygenic risk score and DCM monogenic variants. MAIN OUTCOMES AND MEASURES: The primary outcomes were the association of the DCM polygenic risk score with PPCM, ACM, and CCM and the prevalence of monogenic variants and a high polygenic score among individuals with cardiomyopathy. RESULTS: The mean (SD) age in the MGB Biobank was 55.7 (17.0) years at enrollment, and 24&#x202f;551 (58.3%) were female. Across the 4 study cohorts, 3414 individuals with secondary cardiomyopathy were identified, including 70 with PPCM, 2281 with ACM, and 1063 with CCM. The DCM polygenic score was associated with PPCM (odds ratio [OR], 1.82 per SD; 95% CI, 1.43-2.30), ACM (OR, 1.56; 95% CI,1.34-1.82), and CCM (OR, 1.64; 95% CI,1.24-2.15) (all with P&#x2009;<&#x2009;.001). Monogenic variants were enriched but present in 7 of 113 individuals with medical record-reviewed cardiomyopathy in MGB, while 66 had a high polygenic score, which conferred an approximately 3-fold increased odds of cardiomyopathy. Most individuals with cardiomyopathy lacked antecedent clinical risk factors. CONCLUSIONS AND RELEVANCE: In this cohort study, individuals with PPCM, ACM, and CCM were enriched for monogenic DCM variants and a high DCM polygenic score, suggesting a shared genetic susceptibility influenced by distinct environmental precipitants. These findings support a shared genetic architecture between secondary cardiomyopathies and DCM, although additional work with larger numbers of individuals with cardiomyopathy is needed to confirm these findings.

Humans↗
PubMed2026

Physical Activity and Cardiovascular Outcomes in Phenotype-Negative Cardiomyopathy Variant Carriers.

IMPORTANCE: Exercise may lead to disease progression and higher risk of sudden death in individuals with genetic cardiomyopathies, but the effects of exercise among individuals carrying a cardiomyopathy-associated variant without clinical manifestations (G+P-) are unclear. OBJECTIVE: To examine whether the effects of moderate to vigorous physical activity (MVPA) on cardiovascular (CV) outcomes, cardiac structure and function, and risk of developing overt cardiomyopathy and malignant ventricular arrhythmias (VAs) vary by G+P- status. DESIGN, SETTING, AND PARTICIPANTS: UK Biobank participants with whole-genome sequencing providing 1 week of accelerometer-based physical activity data and without prevalent heart failure (HF), atrial fibrillation (AF), cardiomyopathy, VAs, or implantable cardioverter-defibrillators were included in this cohort study. The study was conducted at 22 assessment centers throughout the UK from February 2013 to December 2015 with a median follow-up of 8 years. Data were analyzed from March 2024 to June 2025. EXPOSURE: Accelerometer-measured MVPA (minutes/week). MAIN OUTCOMES AND MEASURES: Associations were analyzed between MVPA volume and future incidence of adverse CV outcomes (AF, HF, myocardial infarction [MI], and stroke), cardiac magnetic resonance (CMR)-based measures of cardiac remodeling, and surrogates for clinical cardiomyopathy onset (cardiomyopathy and VA). Associations were compared between G+P- carriers and noncarriers. RESULTS: Among 84&#x202f;699 individuals (mean [SD] age, 62 [8] years; 48&#x202f;353 [57%] women; 3979 G+P- carriers), greater MVPA was associated with a lower risk of adverse CV outcomes over a median (IQR) 8.0 (7.5-8.5) years, irrespective of genotype. In multivariable models, higher MVPA was broadly associated with lower risk of incident CV disease in G+P- carriers (hazard ratio [HR] at optimal MVPA level vs zero [95% CI], AF: 0.68 [0.58-0.79]; HF: 0.58 [0.47-0.71]; MI: 0.49, [0.24-1.00]; stroke: 0.35 [0.12-0.99]). For G+P- carriers, MVPA in the range of 100 to 400 minutes per week was generally associated with lowest risk. Among individuals with CMR imaging, MVPA was associated with a similar pattern and extent of cardiac remodeling (eg, left ventricular dilation and left ventricular hypertrophy) in G+P- carriers vs noncarriers. Among G+P- carriers, higher MVPA was associated with lower risk of incident cardiomyopathy (HR at optimal MVPA vs 0, 0.03; 95% CI, 0.00-0.98) with no increase in risk of VA (eg, HR at 400 minutes of MVPA vs 0, 0.98; 95% CI, 0.83-1.14). Findings were generally consistent across variants associated with dilated cardiomyopathy, hypertrophic cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy, although precision of estimates for arrhythmogenic right ventricular cardiomyopathy were limited. CONCLUSIONS AND RELEVANCE: In this cohort study, MVPA within the general range of guideline-based recommendations was associated with lower risk of adverse CV outcomes and similar degrees of cardiac remodeling for G+P- carriers compared to noncarriers. Findings support the appropriateness of guideline-based MVPA recommendations for G+P- carriers.

Humans↗
PubMed1978

Chronic alcoholic cardiomyopathy: fact or fiction?

This study was designed to ascertain whether excessive prolonged alcohol intake itself may produce chronic cardiomyopathy. We reasoned that, since alcoholic cardiomyopathy is allegedly a chronic condition, asymptomatic or early symptomatic cases should be found in a large hospitalized alcoholic population. Two groups of patients were studied. The first group consisted of 292 chronic alcoholics whose hospital records were examined for evidence of early cardiomyopathy, according to predetermined criteria. The second group consisted of eight patients who died on the medical service ward and in whom one of the diagnoses listed in the autopsy report was alcoholic cardiomyopathy. In the first group hepatic and neurological complications of alcoholism were frequent; no patient was found to have early cardiomyopathy. In the second group the post-mortem records indicated that all eight patients had other illnesses causing the abnormal findings on which the diagnosis of alcoholic cardiomyopathy was made. We conclude that the concept of chronic alcoholic cardiomyopathy caused by the direct toxic effect of alcohol may not be valid.

Adolescent↗
PubMed1978

[Cardiomyopathies].

A) Definition and classification. Cardiomyopathy is defined as a dysfunction of cardiac muscle of unknown origin and classified according to genetic, morphological and functional criteria as follows: 1. cardiomyopathy of autosomal dominant inheritance with asymmetric septal hypertrophy (ASH) a) obstructive b) non obstructive 2. cardiomyopathy of autosomal dominant inheritance without ASH 3. cardiomyopathy of autosomal recessive inheritance 4. sporadic cardiomyopathy. It is assumed that at least the cardiomyopathies listed here are heterogeneous groups that have to be subdivided as soon as further discriminating findings--structural or enzymatic--are available. B) Diagnosis, prognosis, treatment. The diagnostic methods are evaluated, the prognosis and the treatment of the cardiomyopathies are reviewed.

Adrenergic beta-Antagonists↗
PubMed1977

[Application of non-invasive methods to assessment of left ventricular function in cardiomyopathy (author's transl)].

Left ventricular function in cardiomyopathy was studied by non-invasive methods. Various indices of left ventricular function were measured in patients with cardiomyopathy by mechanocardiography and echocardiography and were compared with indices in normal subjects and the following conclusions were obtained. 1) Patients with Congestive cardiomyopathy had high PEP/LVET, low mVcf, low EF, and low mPWV, suggesting depressed cardiac function. 2) Patients with Hypertrophic obstructive cardiomyopathy had characteristic findings, such as low DDR, high IVST/PWT, and SAM. 3) Patients with Hypertrophic non-obstructive cardiomyopathy had no characteristic changes in indices, however in some of the findings transition to Hypertrophic obstructive cardiomyopathy was suggested.

Cardiomyopathies↗
PubMed1978

Treatment of congestive cardiomyopathy.

Although the majority of patients with cardiomyopathy are in the category of primary or idiopathic cardiomyopathy, for which therapy is symptomatic and non-specific, there are a number of secondary forms of cardiomyopathy for which specific therapy is available, thus giving impetus to prompt and accurate diagnosis. Among inflammatory lesions, brucellosis, psittacosis and toxoplasmosis are examples. Treatable metabolic causes include thyrotoxicosis and thiamine deficiency, the latter as well as calorie-protein malnutrition are also preventable. There is presumptive evidence that the cardiomyopathy of haemochromatosis is benefited by repeated phlebotomies. Symptomatic relief of obstructive cardiomyopathy is achieved by beta-adrenergic blockade, although resection of obstructing myocardium still has a place. The therapeutic approach to the vast majority of cases of congestive cardiomyopathy is non-specific, comprising controlled activity, sodium restriction, digitalis and diuretics. Vasodilators and, occasionally, beta-adrenergic blockade may be beneficial. Pacemakers may be life-saving, whereas the place of anti-arrhythmics remains uncertain. Transplantation warrants further application. Valve replacement has little to offer. Primary prevention, comprising balanced nutrition, vaccines and genetic counselling, merits wider application. In individuals at risk or already afflicted, programmes of secondary prevention should include good nutrition, abstinence from alcohol and protection from drugs and toxins.

Cardiomyopathies↗
PubMed1977

[The problem of the cardiomyopathies].

The author criticizes the tendency to broaden continuously the notion of "cardiomyopathy" and the attempts to cover by this term almost all etiological and pathogenetic variants of myocardial lesions. Classification of these variants by two groups is proposed: 1) idiopathic cardiomyopathies, etiology of which are either not known, or not established yet; 2) symptomatic cardiomyopathies the causes of which are known. The first group comprises congestive and hypertrophic cardiomyopathies. Their essential clinico-anatomical features and considerations concerning pathogenesis are set forth. Every variant of the second group of cardiomyopathies (symptomatic) is analysed separately according to the character of the pathogenic agent. The need for comprehensive study of myocardial pathology in the so-called cardiomyopathies is emphasized.

Cardiomegaly↗
PubMed2026

Alpha protein kinase 3 gene therapy restores heart function in mouse and human models of cardiomyopathy.

Truncating variants in the ALPK3 gene (encoding alpha protein kinase 3) cause severe cardiomyopathy for which no curative treatment exists1-3. Here we establish an adeno-associated virus (AAV)-mediated gene replacement therapy to deliver full-length human ALPK3. AAV-ALPK3 prevented disease in neonatal Alpk3-mutant mice and reversed established pathology in adults, with proteomic analysis demonstrating reversal of more than 95% of the molecular disease signature. Beyond ALPK3 deficiency, we explored broader therapeutic potential based on ALPK3's regulatory role in proteostasis, a pathway commonly disrupted across cardiomyopathies. ALPK3 expression is reduced in cardiomyocytes with TTN-truncating variants, the most prevalent cause of dilated cardiomyopathy, and the encoded titin protein has a protein quality control network in common with ALPK3. AAV-ALPK3 restored contractile function in human cardiac organoids with an ALPK3- or TTN-truncating variant. These findings provide proof of concept for ALPK3 gene therapy in patients with ALPK3 cardiomyopathy and reveal potential for indication expansion to cardiomyopathies associated with TTN-truncating variants, which are not amenable to gene replacement therapy due to size limitations.

Animals↗
PubMed2022

Mortality Among Patients With Early-Onset Atrial Fibrillation and Rare Variants in Cardiomyopathy and Arrhythmia Genes.

IMPORTANCE: Patients with early-onset atrial fibrillation (AF) are enriched for rare variants in cardiomyopathy and arrhythmia genes. The clinical significance of these rare variants in patients with early-onset AF is unknown. OBJECTIVE: To assess the association between rare variants in cardiomyopathy and arrhythmia genes detected in patients with early-onset AF and time to death. DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study included participants with AF diagnosed before 66 years of age who underwent whole-genome sequencing through the National Heart, Lung and Blood Institute's Trans-Omics for Precision Medicine program. Participants were enrolled from November 23, 1999, to June 2, 2015. Data were analyzed from February 26 to September 19, 2021. EXPOSURES: Rare variants identified in a panel of 145 genes that are included in cardiomyopathy and arrhythmia panels used by commercial clinical genetic testing laboratories. MAIN OUTCOMES AND MEASURES: The primary study outcome was time to death and was adjudicated from medical records and the National Death Index. Multivariable Cox proportional hazards regression was used to evaluate the association of disease-associated variants with risk of death after adjustment for age at AF diagnosis, sex, race, body mass index, left ventricular ejection fraction, and an interaction term of age at AF diagnosis and disease-associated variant status. RESULTS: Among 1293 participants (934 [72%] male; median age at enrollment, 56.0 years; IQR, 48.0-61.0 years), disease-associated (pathogenic or likely pathogenic) rare variants were found in 131 (10%). During a median follow-up of 9.9 years (IQR, 6.9-13.2 years), 219 participants (17%) died. In univariable analysis, disease-associated variants were associated with an increased risk of mortality (hazard ratio, [HR], 1.5; 95% CI, 1.0-2.1; P&#x2009;=&#x2009;.05); the association remained significant in multivariable modeling when adjusted for age at AF diagnosis, sex, race, body mass index, left ventricular ejection fraction, and an interaction term between disease-associated variant status and age at AF diagnosis. The interaction demonstrated that disease-associated variants were associated with a significantly higher risk of mortality compared with no disease-associated variant when AF was diagnosed at a younger age (P&#x2009;=&#x2009;.008 for interaction). Higher body mass index (per IQR: HR, 1.4; 95% CI, 1.2-1.6; P&#x2009;<&#x2009;.001) and lower left ventricular ejection fraction (per IQR: HR, 0.8; 95% CI, 0.7-0.8; P&#x2009;<&#x2009;.001) were associated with higher mortality risk. There were 73 cardiomyopathy-related deaths, 40 sudden deaths, and 10 stroke-related deaths. Mortality among patients with the most prevalent genes with disease-associated variants was 26% (10 of 38 patients) for TTN, 33% (6 of 18) for MYH7, 22% (2 of 9) for LMNA, 0% (0 of 10) for MYH6, and 0% (0 of 8) for KCNQ1. CONCLUSIONS AND RELEVANCE: The findings suggest that rare variants in cardiomyopathy and arrhythmia genes may be associated with increased risk of mortality among patients with early-onset AF, especially those diagnosed at a younger age. Genetic testing may provide important prognostic information for patients with early-onset AF.

Atrial Fibrillation↗
PubMed2026

Desmoplakin Mutations in Cardiac Fibroblasts Cause TGF&#x3b2;1-Mediated Pathological Fibrogenesis in Desmoplakin Cardiomyopathy Via Beclin-1 Regulation.

BACKGROUND: Pathological fibrosis is a major finding in cardiovascular diseases and can result in arrhythmia and heart failure. Desmosome gene mutations can lead to arrhythmogenic cardiomyopathy. Among arrhythmogenic cardiomyopathies, pathogenic DSP (desmoplakin) variants cause a distinctive cardiomyopathy with excessive cardiac fibrosis that could precede ventricular dysfunction. DSP variants are also linked to other fibrotic diseases. Whether DSP plays any role in pathological fibrosis remains unknown. METHODS: Mesenchymal stromal cells (MSCs) are resident fibroblast-like cells that are responsible for fibrogenesis in most organs, including the heart. We first used RNA-seq genome-wide analyses to generate cardiac fibroblast-like, induced pluripotent stem cell-derived MSCs from normal donors and patients with arrhythmogenic cardiomyopathy and DSP mutations. We then studied the fibrogenic responses of cardiac MSCs to TGF&#x3b2;1 (transforming growth factor &#x3b2;1) using Western/Co-IP, autophagy assays, gene knockdowns/over-expressions, genomic analyses, mouse DSP knockdown models, immunostaining, and qPCR. RESULTS: TGF&#x3b2;1 induced excessive accumulation of VIM (vimentin)/fibrillar collagens and over-activated fibrotic genes in DSP-mutant MSCs when compared with normal MSCs. In normal MSCs, VIMs bind to wild-type DSP during normal fibrogenesis after TGF&#x3b2;1. DSP-mutant MSCs exhibited a haplo-insufficient phenotype with increased DSP-unbound VIMs that sequestered BECN1 (beclin-1) from activating autophagy and CAV1 (caveolin-1)-mediated endocytosis. Decreased autophagy caused collagen accumulation, and diminished CAV1 endocytosis resulted in abnormal CAV1 plaque formation that over-activated fibrotic genes (COL1A1, COL3A1, and fibronectin [FN]) via heightened p38 activity after TGF&#x3b2;1. Genome-wide analysis and DSP knockdown in mouse fibroblasts confirmed this novel role of DSP mutations in pathological fibrosis. Overexpression of VIM-binding domains of DSP could suppress pathological fibrosis by increasing collagen autophagic degradation and decreasing fibrotic gene expression. CONCLUSIONS: Our data reveal that DSP deficiency in MSCs/fibroblasts leads to exaggerated fibrogenesis in DSP-cardiomyopathy by decreasing BECN1 availability for autophagy and CAV1-endocytosis. Overexpression of VIM binding domains of DSP could be a new strategy to treat pathological fibrosis.

Animals↗
PubMed2026

Arrhythmia and cardiomyopathy risk in Taiwan with complementary biobank evidence on thyroid genetic susceptibility: an integrative population-based framework.

BACKGROUND: Arrhythmia-induced cardiomyopathy (AiCM) is a potentially reversible cause of ventricular dysfunction; however, only a subset of patients with arrhythmia develop cardiomyopathy. Emerging evidence suggests that endocrine factors, particularly thyroid dysfunction with genetic susceptibility, may contribute to inter-individual variability in arrhythmia-related myocardial outcomes. METHODS: We performed a dual-cohort population-based study using the National Health Insurance Research Database (NHIRD, 2000-2015) and the Taiwan Biobank (TWB). In NHIRD, we examined the association between newly diagnosed arrhythmia and incident cardiomyopathy using Cox proportional hazards models. In TWB, genome-wide data, thyroid-stimulating hormone (TSH), polygenic risk scores (PRSs), lifestyle factors, and metabolic comorbidities were analyzed using multivariable regression and interaction models to assess determinants of thyroid dysfunction. RESULTS: In the NHIRD cohort, arrhythmia was associated with a significantly increased risk of incident cardiomyopathy (adjusted hazard ratio (aHR): 2.49, 95% CI: 1.94-2.96), with atrial fibrillation showing the strongest association among arrhythmia subtypes. In the TWB cohort, a higher thyroid polygenic risk score was strongly associated with thyroid dysfunction (adjusted odds ratio (aOR): 6.64, 95% CI: 5.86-7.52). The association between genetic susceptibility and thyroid dysfunction was further modified by metabolic and lifestyle factors, including diabetes, hyperlipidemia, and dietary patterns. Genome-wide analysis identified multiple loci associated with thyroid-stimulating hormone regulation, consistent with a polygenic architecture of thyroid endocrine traits. CONCLUSION: Arrhythmia was associated with an increased risk of cardiomyopathy in a nationwide cohort, while thyroid genetic susceptibility was strongly associated with thyroid dysfunction in a biobank cohort and modified by metabolic and lifestyle factors. These findings provide complementary population-level evidence of parallel cardiovascular and endocrine-genetic associations. Because the two cohorts were not individually linked, causal inference cannot be established. The results support a systems-level framework of endocrine-cardiac interaction and suggest that integrated clinical and genetic risk assessment may help identify individuals who warrant closer monitoring.

arrhythmia↗
PubMed1975

Cardiomyopathy in the dog.

Medical records of 12 dogs determined at necropsy as having had cardiomyopathy and of 5 live dogs with clinical, electrocardiographic and radiographic evidence of the disease were reviewed. Congestive cardiomyopathy was the most common form of the disease, affecting 15 of the 17 dogs. The dogs were primarily of large breeds and ranged in age from 2 to 8 years. Clinical findings included right and left congestive heart failure presenting as pulmonary congestion and edema, pleural effusion, hepatomegaly, and ascites. Thoracic radiographs showed moderate severe enlargement of all cardiac chambers and evidence of congestive heart failure. Atrial fibrillation was the predominant rhythmn; ventricular premature contractions and left ventricular hypertrophy were sometimes noted. At necropsy, biventricular dilation including dilation of the atrioventricular annular rings and accompanying massive atrial dilation was observed. Myocardial contractility was poor and had resulted in dilation of the heart chambers with minimal hypertrophic responses. The atrioventricular valve leaflets and chordae tendinae were usually near normal. Medical treatment included rest, digoxin, and diuretics, Medical or electrical cardioversion of atrial fibrillation to normal sinus rhythm was also attempted. Prognosis for congestive cardiomyopathy is very poor. The average survival time after onset of signs is 6-12 months; 1 dog in our study survived for 20 months. In contrast to congestive cardiomyopathy, the hypertrophic form is rare in the dog. Only two of the dogs studied had hypertrophic cardiomyopathy; one case was diagnosed at necropsy and one by angiocardiography. Both had features of idiopathic hypertrophic subaortic stenosis (IHSS) as reported in man.

Angiocardiography↗
PubMed1976

[Alcoholic Cardiomyopathy (author's transl)].

Alcoholic cardiomyopathy is a consequence of toxic effects of ethyl alcohol. Acute effects must be distinguished from chronic effects over many years. Chronic abuse of alcohol of 1.5-2 g ethyl alcohol per kg body weight (i.e. about 100-150 g/70 kg) per day for years can cause congestive cardiomyopathy in predisposed persons, usually between 30 and 50 years of age. The diagnosis is associated with some criteria for exclusion, i.e. coronary heart disease, hypertension, valvular heart disease, in addition all obstructive and restrictive cardiomyopathy must be excluded. On the other hand, a specific constellation of findings can be considered characteristic of alcoholic cardiomyopathy, namely the coincidence of a radiologically established cardiomegaly in the form of a congestive cardiomyopathy with a raised serum concentration of immunoglobulin A and a negative myocardial immunofluorescence test. Therapeutically, in addition to the classical principles of the treatment of heart failure, absolute abstention from alcohol and physical stress seemed to be effective.

Acute Disease↗