Genetic Etiology for Alcohol-Induced Cardiac Toxicity
Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol. This study sought to evaluate the role of variation in cardiomyopathy-associated genes...
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| Published in | Journal of the American College of Cardiology Vol. 71; no. 20; pp. 2293 - 2302 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
22.05.2018
Elsevier Limited Elsevier Biomedical |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol.
This study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity.
The authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM.
Variants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10−5), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: −2.3% to −15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients.
TTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM.
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| AbstractList | Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol.
This study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity.
The authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM.
Variants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10−5), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: −2.3% to −15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients.
TTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM.
[Display omitted] Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol.BACKGROUNDAlcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol.This study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity.OBJECTIVESThis study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity.The authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM.METHODSThe authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM.Variants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10-5), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: -2.3% to -15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients.RESULTSVariants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10-5), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: -2.3% to -15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients.TTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM.CONCLUSIONSTTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM. AbstractBackgroundAlcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol. ObjectivesThis study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity. MethodsThe authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM. ResultsVariants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10 −5), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: −2.3% to −15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients. ConclusionsTTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM. Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol. This study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity. The authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM. Variants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10 ), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: -2.3% to -15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients. TTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM. BackgroundAlcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which factors determine cardiac toxicity on exposure to alcohol.ObjectivesThis study sought to evaluate the role of variation in cardiomyopathy-associated genes in the pathophysiology of ACM, and to examine the effects of alcohol intake and genotype on dilated cardiomyopathy (DCM) severity.MethodsThe authors characterized 141 ACM cases, 716 DCM cases, and 445 healthy volunteers. The authors compared the prevalence of rare, protein-altering variants in 9 genes associated with inherited DCM. They evaluated the effect of genotype and alcohol consumption on phenotype in DCM.ResultsVariants in well-characterized DCM-causing genes were more prevalent in patients with ACM than control subjects (13.5% vs. 2.9%; p = 1.2 ×10−5), but similar between patients with ACM and DCM (19.4%; p = 0.12) and with a predominant burden of titin truncating variants (TTNtv) (9.9%). Separately, we identified an interaction between TTN genotype and excess alcohol consumption in a cohort of DCM patients not meeting ACM criteria. On multivariate analysis, DCM patients with a TTNtv who consumed excess alcohol had an 8.7% absolute reduction in ejection fraction (95% confidence interval: −2.3% to −15.1%; p < 0.007) compared with those without TTNtv and excess alcohol consumption. The presence of TTNtv did not predict phenotype, outcome, or functional recovery on treatment in ACM patients.ConclusionsTTNtv represent a prevalent genetic predisposition for ACM, and are also associated with a worse left ventricular ejection fraction in DCM patients who consume alcohol above recommended levels. Familial evaluation and genetic testing should be considered in patients presenting with ACM. |
| Author | Lara-Pezzi, Enrique López-Garrido, Miguel A. Pantazis, Antonis Barton, Paul J. Amor-Salamanca, Almudena Wilk, Alicja Walsh, Roddy García-Pinilla, Jose Manuel Pascual-Figal, Domingo A. Whiffin, Nicola Buchan, Rachel J. Midwinter, William Manito, Nicolas Govind, Risha Nuñez, Julio Garcia-Pavia, Pablo Alonso-Pulpon, Luis Padron-Barthe, Laura Gonzalez-Vioque, Emiliano O’Regan, Declan P. Prasad, Sanjay Ware, James S. Guzzo-Merello, Gonzalo Tayal, Upasana Cook, Stuart A. Edwards, Elizabeth Bardaji, Alfredo Serrano, Isabel Salazar-Mendiguchía, Joel Baski, John |
| AuthorAffiliation | k Department of Cardiology, Hospital Universitario Virgen de la Arrixaca, IMIB-Arrixaca, University of Murcia, Murcia, Spain q University Francisco de Vitoria (UFV), Pozuelo de Alarcón, Madrid, Spain c MRC London Institute of Medical Sciences, Imperial College London, London, United Kingdom g Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Bellvitge, Barcelona, Spain j Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Virgen de la Victoria, IBIMA, Málaga, Spain n National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore h Genetics Department, Universidad Autónoma de Barcelona, Barcelona, Spain i CIBER in Cardiovascular Diseases, Madrid, Spain p Myocardial Biology Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain m Department of Biochemistry, Hospital Universitario Puerta de Hierro, Madrid, Spain e Institute of Psychiatry, Psychology and Neuroscience, Social Genet |
| AuthorAffiliation_xml | – name: c MRC London Institute of Medical Sciences, Imperial College London, London, United Kingdom – name: k Department of Cardiology, Hospital Universitario Virgen de la Arrixaca, IMIB-Arrixaca, University of Murcia, Murcia, Spain – name: n National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore – name: j Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Virgen de la Victoria, IBIMA, Málaga, Spain – name: i CIBER in Cardiovascular Diseases, Madrid, Spain – name: a National Heart and Lung Institute, Imperial College London, London, United Kingdom – name: p Myocardial Biology Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain – name: q University Francisco de Vitoria (UFV), Pozuelo de Alarcón, Madrid, Spain – name: m Department of Biochemistry, Hospital Universitario Puerta de Hierro, Madrid, Spain – name: g Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Bellvitge, Barcelona, Spain – name: f Department of Cardiology, Hospital Universitario de Tarragona Joan XXIII, IISPV, Rovira Virgili University, Tarragona, Spain – name: e Institute of Psychiatry, Psychology and Neuroscience, Social Genetic and Developmental Psychiatry Centre, King's College London, London, United Kingdom – name: o Division of Cardiovascular & Metabolic Disorders, Duke-National University of Singapore, Singapore – name: d Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain – name: h Genetics Department, Universidad Autónoma de Barcelona, Barcelona, Spain – name: b Cardiovascular Research Centre, Royal Brompton and Harefield NHS Foundation Trust London, London, United Kingdom – name: l Cardiology Department, Hospital Clínico Universitario, INCLIVA Universitat de Valencia, Valencia, Spain |
| Author_xml | – sequence: 1 givenname: James S. surname: Ware fullname: Ware, James S. organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 2 givenname: Almudena surname: Amor-Salamanca fullname: Amor-Salamanca, Almudena organization: Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain – sequence: 3 givenname: Upasana surname: Tayal fullname: Tayal, Upasana organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 4 givenname: Risha surname: Govind fullname: Govind, Risha organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 5 givenname: Isabel surname: Serrano fullname: Serrano, Isabel organization: Department of Cardiology, Hospital Universitario de Tarragona Joan XXIII, IISPV, Rovira Virgili University, Tarragona, Spain – sequence: 6 givenname: Joel surname: Salazar-Mendiguchía fullname: Salazar-Mendiguchía, Joel organization: Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Bellvitge, Barcelona, Spain – sequence: 7 givenname: Jose Manuel surname: García-Pinilla fullname: García-Pinilla, Jose Manuel organization: CIBER in Cardiovascular Diseases, Madrid, Spain – sequence: 8 givenname: Domingo A. surname: Pascual-Figal fullname: Pascual-Figal, Domingo A. organization: CIBER in Cardiovascular Diseases, Madrid, Spain – sequence: 9 givenname: Julio surname: Nuñez fullname: Nuñez, Julio organization: CIBER in Cardiovascular Diseases, Madrid, Spain – sequence: 10 givenname: Gonzalo surname: Guzzo-Merello fullname: Guzzo-Merello, Gonzalo organization: Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain – sequence: 11 givenname: Emiliano surname: Gonzalez-Vioque fullname: Gonzalez-Vioque, Emiliano organization: Department of Biochemistry, Hospital Universitario Puerta de Hierro, Madrid, Spain – sequence: 12 givenname: Alfredo surname: Bardaji fullname: Bardaji, Alfredo organization: Department of Cardiology, Hospital Universitario de Tarragona Joan XXIII, IISPV, Rovira Virgili University, Tarragona, Spain – sequence: 13 givenname: Nicolas surname: Manito fullname: Manito, Nicolas organization: Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Bellvitge, Barcelona, Spain – sequence: 14 givenname: Miguel A. surname: López-Garrido fullname: López-Garrido, Miguel A. organization: CIBER in Cardiovascular Diseases, Madrid, Spain – sequence: 15 givenname: Laura surname: Padron-Barthe fullname: Padron-Barthe, Laura organization: Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain – sequence: 16 givenname: Elizabeth surname: Edwards fullname: Edwards, Elizabeth organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 17 givenname: Nicola surname: Whiffin fullname: Whiffin, Nicola organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 18 givenname: Roddy surname: Walsh fullname: Walsh, Roddy organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 19 givenname: Rachel J. surname: Buchan fullname: Buchan, Rachel J. organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 20 givenname: William surname: Midwinter fullname: Midwinter, William organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 21 givenname: Alicja surname: Wilk fullname: Wilk, Alicja organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 22 givenname: Sanjay surname: Prasad fullname: Prasad, Sanjay organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 23 givenname: Antonis surname: Pantazis fullname: Pantazis, Antonis organization: Cardiovascular Research Centre, Royal Brompton and Harefield NHS Foundation Trust London, London, United Kingdom – sequence: 24 givenname: John surname: Baski fullname: Baski, John organization: Cardiovascular Research Centre, Royal Brompton and Harefield NHS Foundation Trust London, London, United Kingdom – sequence: 25 givenname: Declan P. surname: O’Regan fullname: O’Regan, Declan P. organization: MRC London Institute of Medical Sciences, Imperial College London, London, United Kingdom – sequence: 26 givenname: Luis surname: Alonso-Pulpon fullname: Alonso-Pulpon, Luis organization: Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain – sequence: 27 givenname: Stuart A. surname: Cook fullname: Cook, Stuart A. organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 28 givenname: Enrique surname: Lara-Pezzi fullname: Lara-Pezzi, Enrique organization: CIBER in Cardiovascular Diseases, Madrid, Spain – sequence: 29 givenname: Paul J. surname: Barton fullname: Barton, Paul J. email: p.barton@imperial.ac.uk organization: National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 30 givenname: Pablo surname: Garcia-Pavia fullname: Garcia-Pavia, Pablo email: pablogpavia@yahoo.es organization: Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29773157$$D View this record in MEDLINE/PubMed |
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| Keywords | alcohol titin genetics ExAC TTNtv variant LVEF ACM dilated cardiomyopathy DCM alcoholic cardiomyopathy left ventricular ejection fraction Exome Aggregation Consortium titin truncating variant |
| Language | English |
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| Snippet | Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown which... AbstractBackgroundAlcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely... BackgroundAlcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption. It is largely unknown... |
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| SubjectTerms | Adult Aged alcohol Alcohol use Alcoholic beverages Cardiology Cardiomyopathy Cardiomyopathy, Alcoholic - diagnosis Cardiomyopathy, Alcoholic - etiology Cardiomyopathy, Alcoholic - genetics Cardiotoxicity - diagnosis Cardiotoxicity - etiology Cardiotoxicity - genetics Cardiovascular Cardiovascular disease Cohort Studies Connectin Coronary vessels Dilated cardiomyopathy Ethnicity Etiology Family medical history Female Genetic Predisposition to Disease - etiology Genetic Predisposition to Disease - genetics Genetic screening genetics Genotype & phenotype Genotypes Heart Heart diseases Heart failure Heart surgery Humans Male Medical prognosis Middle Aged Multivariate analysis Patients Phenotypes Prospective Studies Recovery of function Self Report Survival analysis titin Toxicity Transplants & implants variant Ventricle |
| Title | Genetic Etiology for Alcohol-Induced Cardiac Toxicity |
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