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1. Full Text Mutations in Calmodulin Cause Ventricular Tachycardia and Sudden Cardiac Death
by Nyegaard, Mette and Overgaard, Michael T and Søndergaard, Mads T and Vranas, Marta and Behr, Elijah R and Hildebrandt, Lasse L and Lund, Jacob and Hedley, Paula L and Camm, A. John and Wettrell, Göran and Fosdal, Inger and Christiansen, Michael and Børglum, Anders D and Paediatrics (Lund) and Lund University and Lunds universitet and Pediatrik, Lund
The American Journal of Human Genetics, ISSN 0002-9297, 10/2012, Volume 91, Issue 4, pp. 703 - 712
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a devastating inherited disorder characterized by episodic syncope and/or sudden cardiac arrest... 
DIAGNOSIS | COMPLEX | CHANNEL | CPVT | MAPS | RYANODINE RECEPTOR | CA2+ RELEASE | FAMILIES | GENETICS & HEREDITY | CALCIUM-BINDING | TOOL | Amino Acid Sequence | Calmodulin - genetics | Genetic Predisposition to Disease | Syncope - genetics | Humans | Child, Preschool | Molecular Sequence Data | Male | Death, Sudden, Cardiac - etiology | Mutation, Missense | Young Adult | Ryanodine Receptor Calcium Release Channel - genetics | Adolescent | Tachycardia, Ventricular - genetics | Adult | Chromosomes, Human, Pair 14 | Female | Heterozygote | Calcium Channels - genetics | Child | Arrhythmias, Cardiac - genetics | Gene mutations | Cardiac arrest | Causes of | Ventricular tachycardia | Genetic aspects | Research | Health aspects | Calmodulin | Heart attacks | Exercise | Genetic disorders | Mutation | Calcium | Chromosomes | Report | Medicinsk genetik | Basic Medicine | Medical Genetics | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper
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2. Full Text Familial evaluation in arrhythmogenic right ventricular cardiomyopathy: Impact of genetics and revised task force criteria
by Quarta, Giovanni and Muir, Alison and Pantazis, Antonios and Syrris, Petros and Gehmlich, Katja and Garcia-Pavia, Pablo and Ward, Deirdre and Sen-Chowdhry, Srijita and Elliott, Perry M and McKenna, William J
Circulation, ISSN 0009-7322, 06/2011, Volume 123, Issue 23, pp. 2701 - 2709
Background-With recognition of disease-causing genes in arrhythmogenic right ventricular cardiomyopathy, mutation analysis is being applied. Methods and... 
arrhythmogenic right ventricular cardiomyopathy | desmosomes | family | genes | DIAGNOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | VARIANTS | PERIPHERAL VASCULAR DISEASE | PLAKOPHILIN-2 | MUTATIONS | HEMATOLOGY | DYSPLASIA/CARDIOMYOPATHY | Genetic Predisposition to Disease - genetics | Prevalence | Follow-Up Studies | Humans | Middle Aged | Risk Factors | Genotype | Male | Penetrance | Arrhythmogenic Right Ventricular Dysplasia - epidemiology | Arrhythmogenic Right Ventricular Dysplasia - diagnosis | Arrhythmogenic Right Ventricular Dysplasia - genetics | Point Mutation | Tachycardia, Ventricular - epidemiology | Pedigree | Tachycardia, Ventricular - diagnosis | Desmosomes - physiology | Electrocardiography | Tachycardia, Ventricular - genetics | Adult | Family | Female | Genetic Predisposition to Disease - epidemiology | Usage | Echocardiography | Gene mutations | Cardiomyopathy | Abnormalities | Analysis | Genetic aspects | Diagnosis | Heart diseases | Heart ventricle, Right
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3. Full Text Sudden cardiac death and genetic ion channelopathies: Long QT, Brugada, short QT, catecholaminergic polymorphic ventricular tachycardia, and idiopathic ventricular fibrillation
by Napolitano, Carlo and Bloise, Raffaella and Monteforte, Nicola and Priori, Silvia G
Circulation, ISSN 0009-7322, 04/2012, Volume 125, Issue 16, pp. 2027 - 2034
arrhythmias, cardiac | genetics, Brugada Syndrome | mutation | heart ventricles | long QT syndrome | CARDIAC & CARDIOVASCULAR SYSTEMS | STIMULATION | RISK STRATIFICATION | UNEXPLAINED DEATH | SCN5A MUTATIONS | FOLLOW-UP | INTERVAL DURATION | ARRHYTHMIA | CARRIERS | genetics, Brugada syndrome | CHANNEL | RYANODINE RECEPTOR | PERIPHERAL VASCULAR DISEASE | Brugada Syndrome - genetics | Ventricular Fibrillation - drug therapy | Channelopathies - physiopathology | Tachycardia, Ventricular - drug therapy | Brugada Syndrome - physiopathology | Humans | Male | Death, Sudden, Cardiac | Arrhythmias, Cardiac - physiopathology | Long QT Syndrome - physiopathology | Arrhythmias, Cardiac - drug therapy | Channelopathies - genetics | Tachycardia, Ventricular - physiopathology | Channelopathies - drug therapy | Brugada Syndrome - drug therapy | Long QT Syndrome - genetics | Tachycardia, Ventricular - genetics | Ventricular Fibrillation - genetics | Ventricular Fibrillation - physiopathology | Female | Long QT Syndrome - drug therapy | Arrhythmias, Cardiac - genetics | Usage | Gene mutations | Cardiac patients | Electrocardiogram | Electrocardiography | Long QT syndrome | Genetic aspects | Research | Health aspects | Heart attack | Risk factors
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4. Full Text Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Pathogenic Desmosome Mutations in Index-Patients Predict Outcome of Family Screening: Dutch Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Genotype-Phenotype Follow-Up Study
by Cox, Moniek G. P. J and van der Zwaag, Paul A and van der Werf, Christian and van der Smagt, Jasper J and Noorman, Maartje and Bhuiyan, Zahir A and Wiesfeld, Ans C. P and Volders, Paul G. A and van Langen, Irene M and Atsma, Douwe E and Dooijes, Dennis and van den Wijngaard, Arthur and Houweling, Arjan C and Jongbloed, Jan D. H and Jordaens, Luc and Cramer, Maarten J and Doevendans, Pieter A and de Bakker, Jacques M. T and Wilde, Arthur A. M and van Tintelen, J. Peter and Hauer, Richard N. W
Circulation, ISSN 0009-7322, 2011, Volume 123, Issue 23, pp. 2690 - U87
Background-Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an autosomal dominant inherited disease with incomplete penetrance and... 
desmosome | follow-up studies | arrhythmogenic right ventricular dysplasia | genetics | cardiomyopathy | CRITERIA | CARDIAC & CARDIOVASCULAR SYSTEMS | DYSPLASIA | DESMOCOLLIN-2 | PLAKOGLOBIN CAUSES | GENE | PLAKOPHILIN-2 MUTATIONS | DESMOGLEIN-2 | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | SLOW CONDUCTION | WAVE-FRONT CURVATURE | Predictive Value of Tests | Follow-Up Studies | Death, Sudden, Cardiac - epidemiology | Humans | Middle Aged | Netherlands - epidemiology | Male | Arrhythmogenic Right Ventricular Dysplasia - genetics | Desmosomes - pathology | Young Adult | Ventricular Fibrillation - pathology | Tachycardia, Ventricular - genetics | Ventricular Fibrillation - genetics | Adult | Female | Arrhythmogenic Right Ventricular Dysplasia - pathology | Risk Factors | Ventricular Fibrillation - mortality | Genotype | Asymptomatic Diseases - mortality | Arrhythmogenic Right Ventricular Dysplasia - mortality | Phenotype | Tachycardia, Ventricular - mortality | Adolescent | Tachycardia, Ventricular - pathology | Family | Dysplasia | Gene mutations | Cardiomyopathy | Abnormalities | Analysis | Genetic aspects | Diagnosis | Heart diseases | Heart ventricle, Right
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5. Full Text The RYR2-Encoded Ryanodine Receptor/Calcium Release Channel in Patients Diagnosed Previously With Either Catecholaminergic Polymorphic Ventricular Tachycardia or Genotype Negative, Exercise-Induced Long QT Syndrome A Comprehensive Open Reading Frame Mutational Analysis
by Medeiros-Domingo, Argelia and Bhuiyan, Zahurul A and Tester, David J and Hofman, Nynke and Bikker, Hennie and van Tintelen, J. Peter and Mannens, Marcel M. A. M and Wilde, Arthur A. M and Ackerman, Michael J
Journal of the American College of Cardiology, ISSN 0735-1097, 2009, Volume 54, Issue 22, pp. 2065 - 2074
Objectives This study was undertaken to determine the spectrum and prevalence of mutations in the RYR2-encoded cardiac ryanodine receptor in cases with... 
catecholaminergic polymorphic ventricular tachycardia | ryanodine receptor | sudden cardiac death | exertional syncope | SUDDEN UNEXPLAINED DEATH | GENE-MUTATIONS | ARRHYTHMIAS | CARDIAC & CARDIOVASCULAR SYSTEMS | FOLLOW-UP | IDENTIFICATION | 3-DIMENSIONAL STRUCTURE | DISEASE | RYR2 MUTATIONS | MOLECULAR AUTOPSY | SPECTRUM | Genetic Predisposition to Disease - genetics | Syncope - genetics | Catecholamines - metabolism | Humans | Genotype | Male | Death, Sudden, Cardiac - etiology | Open Reading Frames - genetics | Young Adult | Exercise Test | Ryanodine Receptor Calcium Release Channel - genetics | DNA Mutational Analysis | Long QT Syndrome - genetics | Tachycardia, Ventricular - genetics | Adult | Female | Mosaicism | Exercise - physiology | Calcium Channels - genetics | Cardiac arrhythmia | Mutation | Calcium | Mortality | Genes
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6. Full Text Age- and training-dependent development of arrhythmogenic right ventricular cardiomyopathy in heterozygous plakoglobin-deficient mice
by Kirchhof, Paulus and Fabritz, Larissa and Zwiener, Melanie and Witt, Henning and Schäfers, Michael and Zellerhoff, Stephan and Paul, Matthias and Athai, Timur and Hiller, Karl-Heinz and Baba, Hideo A and Breithardt, Günter and Ruiz, Patricia and Wichter, Thomas and Levkau, Bodo
Circulation, ISSN 0009-7322, 10/2006, Volume 114, Issue 17, pp. 1799 - 1806
Background - Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disorder that causes sudden death and right ventricular heart failure in... 
Conduction | Exercise | Arrhythmia | Cardiomyopathy | Desmosomes | Adherens junctions | Death, sudden | ARRHYTHMIAS | CARDIAC & CARDIOVASCULAR SYSTEMS | NAXOS-DISEASE | DYSPLASIA | exercise | RECEPTOR | death, sudden | adherens junctions | DELETION | arrhythmia | conduction | PLAKOPHILIN-2 MUTATIONS | EMBRYONIC HEART | WOOLLY HAIR | PERIPHERAL VASCULAR DISEASE | desmosomes | cardiomyopathy | HEMATOLOGY | EXPRESSION | DYSPLASIA/CARDIOMYOPATHY | Arrhythmogenic Right Ventricular Dysplasia - etiology | Ventricular Dysfunction, Right - genetics | Hypertrophy, Right Ventricular - etiology | Arrhythmogenic Right Ventricular Dysplasia - physiopathology | Arrhythmogenic Right Ventricular Dysplasia - genetics | Desmosomes - pathology | gamma Catenin - deficiency | Myocardium - metabolism | Electrocardiography | Tachycardia, Ventricular - genetics | Hypertrophy, Right Ventricular - pathology | Swimming | Arrhythmogenic Right Ventricular Dysplasia - pathology | Hypertrophy, Right Ventricular - genetics | Disease Models, Animal | Myocardium - ultrastructure | Physical Conditioning, Animal - adverse effects | Myocardial Contraction | Ventricular Premature Complexes - etiology | Genetic Predisposition to Disease | Models, Cardiovascular | Gene Expression Regulation | Tachycardia, Ventricular - etiology | gamma Catenin - genetics | Stress, Physiological - physiopathology | Arrhythmogenic Right Ventricular Dysplasia - epidemiology | Mice, Knockout | Phenotype | Animals | Aging - physiology | Ventricular Dysfunction, Right - etiology | Glucose - metabolism | Heterozygote | Mice | Ventricular Premature Complexes - genetics
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7. Full Text Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death
by Antzelevitch, Charles and Pollevick, Guido D and Cordeiro, Jonathan M and Casis, Oscar and Sanguinetti, Michael C and Aizawa, Yoshiyasu and Guerchicoff, Alejandra and Pfeiffer, Ryan and Oliva, Antonio and Wollnik, Bernd and Gelber, Philip and Bonaros Jr, Elias P and Burashnikov, Elena and Wu, Yuesheng and Sargent, John D and Schickel, Stefan and Oberheiden, Ralf and Bhatia, Atul and Hsu, Li-Fern and Haïssaguerre, Michel and Schimpf, Rainer and Borggrefe, Martin and Wolpert, Christian
Circulation, ISSN 0009-7322, 01/2007, Volume 115, Issue 4, pp. 442 - 449
Background - Cardiac ion channelopathies are responsible for an ever- increasing number and diversity of familial cardiac arrhythmia syndromes. We describe a... 
Electrophysiology | Genetics | Tachycardia | Fibrillation | Arrhythmia | CARDIAC & CARDIOVASCULAR SYSTEMS | VENTRICULAR-FIBRILLATION | QUINIDINE | SOCIETY | REPOLARIZATION | BRUGADA-SYNDROME | genetics | HERG | electrophysiology | GENE | arrhythmia | PERIPHERAL VASCULAR DISEASE | tachycardia | SCN5A | fibrillation | SUBUNIT | Cricetulus | Humans | Family Health | Male | Mutation, Missense | Death, Sudden, Cardiac | Calcium Channels - physiology | Electrocardiography | Tachycardia, Ventricular - genetics | Ventricular Fibrillation - genetics | Ventricular Fibrillation - physiopathology | Adult | Female | Registries | Calcium Channels - genetics | CHO Cells | Genetic Linkage | Tachycardia, Ventricular - ethnology | Cricetinae | European Continental Ancestry Group - genetics | Mutagenesis, Site-Directed | Calcium Channels, L-Type - physiology | Ventricular Fibrillation - ethnology | Patch-Clamp Techniques | Phenotype | Tachycardia, Ventricular - physiopathology | Animals | Calcium Channels, L-Type - genetics | Calcium channels | Electrocardiograph | Analysis | Physiological aspects | Development and progression | Genetic aspects | Equipment and supplies
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8. Full Text Risk Factors for Malignant Ventricular Arrhythmias in Lamin A/C Mutation Carriers A European Cohort Study
by van Rijsingen, Ingrid A. W and Arbustini, Eloisa and Elliott, Perry M and Mogensen, Jens and Hermans-van Ast, Johanna F and van der Kooi, Anneke J and van Tintelen, J. Peter and van den Berg, Maarten P and Pilotto, Anea and Pasotti, Michele and Jenkins, Sharon and Rowland, Camilla and Aslam, Uzma and Wilde, Arthur A. M and Perrot, Aneas and Pankuweit, Sabine and Zwinderman, Aeilko H and Charron, Philippe and Pinto, Yigal M
Journal of the American College of Cardiology, ISSN 0735-1097, 2012, Volume 59, Issue 5, pp. 493 - 500
Objectives The purpose of this study was to determine risk factors that predict malignant ventricular arrhythmias (MVA) in Lamin A/C (LMNA) mutation carriers.... 
lamin A/C | risk factors | sudden cardiac death | cardiomyopathy | implantable cardioverter-defibrillator | GENE-MUTATIONS | LAMINOPATHIES | FAMILIAL DILATED CARDIOMYOPATHY | CARDIAC & CARDIOVASCULAR SYSTEMS | CONDUCTION-SYSTEM DISEASE | SUDDEN-DEATH | DREIFUSS MUSCULAR-DYSTROPHY | Severity of Illness Index | Genetic Predisposition to Disease | Follow-Up Studies | Humans | Middle Aged | Risk Factors | Europe - epidemiology | Male | Lamin Type A - metabolism | Incidence | DNA - genetics | Tachycardia, Ventricular - epidemiology | DNA Mutational Analysis | Lamin Type A - genetics | Tachycardia, Ventricular - metabolism | Tachycardia, Ventricular - genetics | Adult | Female | Retrospective Studies | Mutation
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9. Full Text Compound and Digenic Heterozygosity Predicts Lifetime Arrhythmic Outcome and Sudden Cardiac Death in Desmosomal Gene–Related Arrhythmogenic Right Ventricular Cardiomyopathy
by Rigato, Ilaria and Bauce, Barbara and Rampazzo, Alessandra and Zorzi, Alessandro and Pilichou, Kalliopi and Mazzotti, Elisa and Migliore, Federico and Marra, Martina Perazzolo and Lorenzon, Alessandra and De Bortoli, Marzia and Calore, Martina and Nava, Andrea and Daliento, Luciano and Gregori, Dario and Iliceto, Sabino and Thiene, Gaetano and Basso, Cristina and Corrado, Domenico
Circulation: Cardiovascular Genetics, ISSN 1942-325X, 12/2013, Volume 6, Issue 6, pp. 533 - 542
BACKGROUND—Mutations in genes encoding for desmosomal proteins are the most common cause of arrhythmogenic right ventricular cardiomyopathy (ARVC). We assessed... 
Cardiomyopathies | Genetics | Death sudden cardiac | CARDIAC & CARDIOVASCULAR SYSTEMS | MANAGEMENT | death | FOLLOW-UP | PLAKOPHILIN-2 | CLINICAL-FEATURES | PLAKOGLOBIN CAUSES | IMPACT | genetics | sudden | IN-VIVO | GENETICS & HEREDITY | MUTATIONS | cardiomyopathies | TASK-FORCE CRITERIA | cardiac | DYSPLASIA/CARDIOMYOPATHY | Prognosis | Humans | Middle Aged | Male | Death, Sudden, Cardiac | Arrhythmogenic Right Ventricular Dysplasia - physiopathology | Arrhythmogenic Right Ventricular Dysplasia - genetics | Young Adult | Desmoplakins - genetics | Time Factors | Tachycardia, Ventricular - genetics | Ventricular Fibrillation - genetics | Ventricular Fibrillation - physiopathology | Adult | Female | Desmocollins - genetics | Desmoglein 2 - genetics | Plakophilins - genetics | Risk Factors | Kaplan-Meier Estimate | Genotype | Tachycardia, Ventricular - physiopathology | Desmosomes - genetics | Sex Factors | Heterozygote | Mutation
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10. Full Text Incidence and risk factors of arrhythmic events in catecholaminergic polymorphic ventricular tachycardia
by Hayashi, Meiso and Denjoy, Isabelle and Extramiana, Fabrice and Maltret, Alice and Buisson, Nathalie Roux and Lupoglazoff, Jean-Marc and Klug, Didier and Hayashi, Miyuki and Takatsuki, Seiji and Villain, Elisabeth and Kamblock, Joël and Messali, Anne and Guicheney, Pascale and Lunardi, Joël and Leenhardt, Antoine
Circulation, ISSN 0009-7322, 05/2009, Volume 119, Issue 18, pp. 2426 - 2434
Background-The pathophysiological background of catecholaminergic polymorphic ventricular tachycardia is well understood, but the clinical features of this... 
Tachycardia | Clinical genetics | Ventricular | Beta-blocker | Death | Sudden | Mutation | Follow-up studies | CARDIAC & CARDIOVASCULAR SYSTEMS | beta-blocker | SUDDEN-DEATH | FOLLOW-UP | death, sudden | tachycardia, ventricular | CHILDREN | mutation | follow-up studies | IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR | GENE | FAMILIES | clinical genetics | RYR2 MUTATIONS | PERIPHERAL VASCULAR DISEASE | SPECTRUM | Follow-Up Studies | Death, Sudden, Cardiac - epidemiology | Humans | Middle Aged | Child, Preschool | Family Health | Male | Calsequestrin - genetics | Incidence | Young Adult | Exercise Test | Tachycardia, Ventricular - genetics | Adult | Female | Child | Adrenergic beta-Antagonists - therapeutic use | Syncope - genetics | Risk Factors | Kaplan-Meier Estimate | Syncope - mortality | Tachycardia, Ventricular - prevention & control | Polymorphism, Genetic | Tachycardia, Ventricular - mortality | Ryanodine Receptor Calcium Release Channel - genetics | Adolescent | Arrhythmia | Physiological aspects | Ventricular tachycardia | Development and progression | Catecholamines | Research | Risk factors | Ryanodine Receptor Calcium Release Channel | Adrenergic beta-Antagonists | Death, Sudden, Cardiac | Life Sciences | Tachycardia, Ventricular | Syncope | Cardiology and cardiovascular system | Calsequestrin | Human health and pathology | Kaplan-Meiers Estimate
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11. Full Text Ventricular arrhythmias and sudden cardiac death
by John, Roy M, Dr and Tedrow, Usha B, MD and Koplan, Bruce A, MD and Albert, Christine M, MD and Epstein, Laurence M, MD and Sweeney, Michael O, MD and Miller, Amy Leigh, MD and Michaud, Gregory F, MD and Stevenson, William G, Prof
Lancet, The, ISSN 0140-6736, 2012, Volume 380, Issue 9852, pp. 1520 - 1529
Summary Management strategies for ventricular arrhythmias are guided by the risk of sudden death and severity of symptoms. Patients with a substantial risk of... 
Internal Medicine | MEDICINE, GENERAL & INTERNAL | HEART-DISEASE | RESYNCHRONIZATION THERAPY | HYPERTROPHIC CARDIOMYOPATHY | IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR | MYOCARDIAL-INFARCTION | CATHETER ABLATION | AMERICAN-COLLEGE | ASSOCIATION TASK-FORCE | PROPHYLACTIC IMPLANTATION | GUIDELINES WRITING COMMITTEE | Tachycardia, Ventricular - therapy | Tachycardia, Ventricular - complications | Brugada Syndrome - physiopathology | Humans | Catheter Ablation | Death, Sudden, Cardiac - etiology | Arrhythmogenic Right Ventricular Dysplasia - therapy | Arrhythmogenic Right Ventricular Dysplasia - physiopathology | Long QT Syndrome - therapy | Long QT Syndrome - physiopathology | Arrhythmogenic Right Ventricular Dysplasia - genetics | Cardiopulmonary Resuscitation | Tachycardia, Ventricular - physiopathology | Defibrillators, Implantable | Ventricular Fibrillation - complications | Electrocardiography | Tachycardia, Ventricular - genetics | Ventricular Fibrillation - genetics | Ventricular Fibrillation - physiopathology | Ventricular Fibrillation - therapy | Brugada Syndrome - therapy | Prevention | Care and treatment | Arrhythmia | Risk factors | Cardiac arrest | Cardiac arrhythmia | Cardiovascular disease | Heart attacks | Mutation | Womens health
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12. Full Text Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans
by Watanabe, Hiroshi and Chopra, Nagesh and Laver, Derek and Hwang, Hyun Seok and Davies, Sean S and Roach, Daniel E and Duff, Henry J and Roden, Dan M and Wilde, Arthur A. M and Knollmann, Björn C
Nature medicine, ISSN 1078-8956, 2009, Volume 15, Issue 4, pp. 380 - 383
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially lethal inherited arrhythmia syndrome in which drug therapy is often ineffective.... 
MEDICINE, RESEARCH & EXPERIMENTAL | MYOCYTES | RYANODINE RECEPTOR | CA2+ RELEASE | INCREASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CASQ2 | MECHANISMS | DEATH | SARCOPLASMIC-RETICULUM | MUTATIONS | CELL BIOLOGY | Arrhythmias, Cardiac - prevention & control | Humans | Male | Ryanodine Receptor Calcium Release Channel - drug effects | Anti-Arrhythmia Agents - therapeutic use | Tachycardia, Ventricular - prevention & control | Syndrome | Polymorphism, Genetic | Heart Rate - drug effects | Animals | Calcium - physiology | Tachycardia, Ventricular - genetics | Mice | Child | Flecainide - therapeutic use | Ryanodine Receptor Calcium Release Channel - physiology | Prevention | Usage | Control | Animal models in research | Arrhythmia | Physiological aspects | Ventricular tachycardia | Research | Flecainide | Health aspects | Genetic polymorphisms | Cardiac arrhythmia | Medical research | Pharmacology | Molecular biology | Rodents
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13. Full Text Truncating FLNC Mutations Are Associated With High-Risk Dilated and Arrhythmogenic Cardiomyopathies
by Ortiz-Genga, Martín F., MD and Cuenca, Sofía, MD, PhD and Dal Ferro, Matteo, MD and Zorio, Esther, MD, PhD and Salgado-Aranda, Ricardo, MD and Climent, Vicente, MD and Padrón-Barthe, Laura, PhD and Duro-Aguado, Iria, MD and Jiménez-Jáimez, Juan, MD, PhD and Hidalgo-Olivares, Víctor M., MD and García-Campo, Enrique, MD and Lanzillo, Chiara, MD, PhD and Suárez-Mier, M. Paz, MD, PhD and Yonath, Hagith, MD and Marcos-Alonso, Sonia, MD, PhD and Ochoa, Juan P., MD and Santomé, José L., BSc and García-Giustiniani, Diego, MD and Rodríguez-Garrido, Jorge L., MD and Domínguez, Fernando, MD and Merlo, Marco, MD and Palomino, Julián, MD, PhD and Peña, María L., MD and Trujillo, Juan P., MD, PhD and Martín-Vila, Alicia, PharmD and Stolfo, Davide, MD and Molina, Pilar, MD, PhD and Lara-Pezzi, Enrique, PhD and Calvo-Iglesias, Francisco E., MD, PhD and Nof, Eyal, MD and Calò, Leonardo, MD and Barriales-Villa, Roberto, MD, PhD and Gimeno-Blanes, Juan R., MD, PhD and Arad, Michael, MD, PhD and García-Pavía, Pablo, MD, PhD and Monserrat, Lorenzo, MD, PhD
JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2016, Volume 68, Issue 22, pp. 2440 - 2451
Abstract Background Filamin C (encoded by the FLNC gene) is essential for sarcomere attachment to the plasmatic membrane. FLNC mutations have been associated... 
Cardiovascular | Internal Medicine | ventricular arrhythmia | filaminopathy | sudden death | filamin C | prognosis | genotype | FILAMIN C CAUSE | DOMAIN | CARDIAC & CARDIOVASCULAR SYSTEMS | ISOFORMS | MUSCLE | MYOPATHY | ACTIN-BINDING PROTEIN | Immunohistochemistry | Prognosis | Humans | Middle Aged | Child, Preschool | Infant | Male | Cardiomyopathies - etiology | Young Adult | Cardiomyopathies - genetics | DNA Mutational Analysis | Tachycardia, Ventricular - metabolism | Tachycardia, Ventricular - genetics | Adult | Female | Retrospective Studies | Filamins - genetics | Child | Tachycardia, Ventricular - complications | Risk Factors | Genotype | DNA - genetics | Filamins - metabolism | Cardiomyopathies - metabolism | Adolescent | Aged | Mutation | Heart failure | Genetic aspects | Cardiology | Genetic screening | Proteins | Laboratories | Cardiomyopathy | Genes | Index Medicus | Abridged Index Medicus
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