Original Article
Identification of a Genetic Locus for Familial Atrial Fibrillation
N Engl J Med 1997; 336:905-911March 27, 1997
- Abstract
Background
Atrial fibrillation, the most common sustained cardiac-rhythm disturbance, affects over 2 million Americans and accounts for one third of all strokes in patients over 65 years of age. The molecular basis for atrial fibrillation is unknown, and palliative therapy is used to control the ventricular rate and prevent systemic emboli. We identified a family of 26 members of whom 10 had atrial fibrillation that segregated as an autosomal dominant disease. We subsequently identified two additional families in which the disease was linked to the same locus.
Methods
We screened the human genome with 300 polymorphic dinucleotide-repeat markers using an unconventional strategy of pooling the DNA samples into two groups (affected and unaffected), which reduced the sample size by approximately 90 percent, before performing linkage analysis to map the locus. This made it possible to identify potential loci within a few weeks.
Results
The lod scores for markers D10S569 and D10S607, located at 10q22–q24, were 3.60 in Family 1. The disease locus in Families 2 and 3 was also linked to the same markers, with lod scores of 6.02 and 5.35 for markers D10S569 and D10S607, respectively, when data on all three families were combined. Haplotype analysis of the three families showed that the locus was between D10S1694 and D10S1786, an interval of 11.3 centimorgans.
Conclusions
Identification of the gene for familial atrial fibrillation will help to elucidate the molecular basis of the disease and provide insights into acquired forms. The strategy of pooling DNA samples for analysis is more time and cost effective than conventional screening and should accelerate the process of gene mapping in the future.
Media in This Article
Figure 3
Haplotypes and Recombination in Family 1.Figure 1
Pedigrees of Three Families with Familial Atrial Fibrillation.Article Activity
- Article
Atrial fibrillation, the most common sustained cardiac-rhythm disturbance,1 affects more than 2 million Americans,2 with an overall prevalence of 0.89 percent. The prevalence increases rapidly with age to 2.3 percent between the ages of 40 and 60 years and to 5.9 percent over the age of 65.2 Although the initial course of atrial fibrillation is often paroxysmal, it almost invariably progresses to a chronic sustained rhythm disturbance with manifestations ranging from palpitations to cardiac failure. The most dreaded complication is stroke; atrial fibrillation accounts for one third of all strokes in patients over the age of 65.3 Since there is currently no effective means of preventing or eliminating atrial fibrillation, therapy consists of controlling the ventricular rate and preventing systemic emboli with antiplatelet and anticoagulant therapy.4 The emotional and medical burdens imposed by long-term medical therapy and, in many cases, subsequent stroke are immense, with a total annual cost of $9 billion.
The molecular basis of atrial fibrillation has yet to be determined. One approach, which has been successful for metabolic disorders, is to identify the gene responsible for a familial form of the disease. Familial atrial fibrillation is probably very uncommon,5 but we located a small family in Spain in which atrial fibrillation segregates as an autosomal dominant trait. Only 10 living family members were affected; thus, to map the chromosomal locus by conventional genetic-linkage analysis would probably require analyzing DNA markers every 5 to 10 centimorgans (cM) throughout the human genome. The arduous task of analyzing DNA from each of the 26 family members for 300 to 600 markers would also be very costly. Accordingly, we adopted an unconventional strategy of pooling the DNA of the affected family members and comparing the results of the DNA analysis with those of an analysis of pooled DNA from unaffected family members at each marker locus to detect differences that would suggest segregation of a particular allele with the disease. This reduced the number of samples to be analyzed by more than 90 percent and enabled us to identify four potential loci within a few weeks.
Methods
Study Families and Diagnosis
We identified a family (Family 1) in which atrial fibrillation appears to be segregating as an autosomal dominant disease with high penetrance. The family consists of 26 living members spanning three generations, of whom 10 have atrial fibrillation. Two additional family members are known to have died of complications of the disease. We subsequently identified two other small families with a total of 17 living members, 9 of whom are affected. In these two families (Families 2 and 3) the defect mapped to the same locus as in the original family. The three pedigrees are shown in Figure 1Figure 1
Pedigrees of Three Families with Familial Atrial Fibrillation..Clinical Evaluation
After providing informed consent according to the guidelines of Baylor College of Medicine and Methodist Hospital, the subjects were evaluated by a detailed history taking, physical examination, 12-lead electrocardiography, and two-dimensional echocardiography. Criteria for diagnosis were based on the electrocardiographic findings. Other likely causes of atrial fibrillation in this population — such as hypertension, valvular disease, and thyroid disease — were ruled out at the time of diagnosis.
Preparation of DNA and Pooled Samples
Blood was collected from each member of the three families, DNA was extracted by the salting-out procedure,6 and lymphocytes were isolated for the development of transformed cell lines.7 For the pooled-sample analysis we used blood only from Family 1. Equimolar amounts of DNA from 10 affected members (Subjects II-2, II-3, III-1, III-3, III-5, III-11, IV-6, IV-7, IV-8, and IV-9) were combined into a single sample, as was DNA from 10 unaffected family members (Subjects II-1, II-4, II-6, III-4, III-6, III-8, III-9, III-10, III-12, and IV-5). Whenever possible, unaffected siblings and parents of affected subjects were chosen to provide samples for the unaffected pool in order to minimize the allelic differences between the two groups.
Marker Analysis
A total of about 300 polymorphic dinucleotide — (CA)n — repeat markers located approximately 15 to 20 cM apart were selected on the basis of their polymorphic information content primarily from the genetic maps of Genethon8 or the National Institutes of Health–Centre d'Etude du Polymorphisme Humain.9 For each microsatellite marker, primers annealing to the sense strand were end-labeled with [32P]γ-deoxyadenosine triphosphate with polynucleotide kinase (Pharmacia), and the DNA was amplified by the polymerase chain reaction under standard conditions for 30 cycles consisting of denaturation at 94°C for 45 seconds, annealing at 55°C for 30 seconds, and extension at 72°C for 30 seconds. Some markers required a higher annealing temperature. Initial denaturation was carried out at 95°C for five minutes. Each 50-μl reaction contained 150 pmol of specific primers, 0.3 U of Taq polymerase (Pharmacia), 200 μM 4-deoxynucleoside triphosphate, and 200 ng of genomic DNA for the analysis of either individual or pooled DNA samples. The amplified DNA products were analyzed by electrophoresis through 6 percent denaturing polyacrylamide–urea sequencing gels as previously described.10
After the 300 chromosomal markers were amplified from the two pooled DNA samples, the products were loaded side by side on a polyacrylamide gel and then subjected to electrophoresis. The electrophoretic pattern exhibited on the autoradiograph by each marker allele amplified from the pooled sample from the affected group was visually inspected, and the results were compared with those of the pooled sample from the unaffected group. The presence of a unique band or a band of greater intensity in the sample from the affected group suggested cosegregation of the marker allele with the disease allele.
Linkage Analysis
Two-point linkage analysis was carried out on a personal computer with version 5.2 of the Linkage program.11 Multipoint linkage analysis was conducted on a Vax computer with Fastlink. An autosomal dominant pattern of inheritance was assumed, and penetrance was set at 99 percent, on the basis of the observed high frequency of affected persons in sibships at risk in Family 1. The frequencies of the disease allele and the normal allele were assumed to be 0.0001 and 0.9999, respectively, and the allele frequencies of microsatellite markers were arbitrarily assigned a value of 1/n, where n refers to the number of alleles observed. Since the use of incorrect values for linkage parameters can cause false positive results, positive lod scores were tested for robustness with respect to variations in penetrance (from 60 to 99 percent), variations in the prevalence of phenocopies (from 0 to 5 percent), and marker-allele frequency with the use of published frequencies, when available, or the frequencies observed in this family.
Results
Clinical Characteristics
In Family 1 there were 10 living affected subjects (6 male and 4 female) whose age at diagnosis ranged from 2 to 35 years (average, 17.8). Nine family members had chronic atrial fibrillation, and one (Subject IV-6) had paroxysmal atrial fibrillation. Three had dyspnea on exertion (Subjects IV-6, II-2, and III-5), and seven were asymptomatic. Subject III-1 had pericarditis and atrial fibrillation at the time of diagnosis, but since the atrial fibrillation has persisted for 10 years, pericarditis was not considered the cause. Subject II-8 died of a cerebrovascular accident at the age of 68. Subject III-2, who was given a diagnosis of paroxysmal atrial fibrillation at the age of 20, died suddenly at the age of 36; no autopsy was performed. Electrocardioversion was attempted unsuccessfully in three of those with chronic atrial fibrillation. Subjects II-2 and III-5 had increased left ventricular internal diameters and ventricular ejection fractions of 51 and 54 percent, respectively. The remainder had no abnormalities on echocardiography, and the average ejection fraction was 69 percent.
In Families 2 and 3, all nine affected subjects had chronic atrial fibrillation, were asymptomatic, and had no echocardiographic abnormalities. The age at diagnosis in these two families ranged from 2 to 46 years.
DNA Analysis and Genetic Linkage
The 300 chromosomal markers used to screen the human genome were amplified from the pooled DNA samples from affected and unaffected subjects; the pooling procedure reduced the number of samples to be analyzed from 26 to 2. The electrophoretic pattern of the sample from the affected group differed from that of the unaffected group for 50 of the 300 marker alleles. These differences, which suggested potential loci for the gene responsible for atrial fibrillation, were identified within a few weeks. A typical example of a difference in a marker allele between the pooled samples is shown in Figure 2Figure 2
Results of Polyacrylamide-Gel Electrophoresis of Four DNA-Marker Loci Amplified from Pooled DNA.. In lanes 1 and 2 and lanes 3 and 4 of Figure 2, the electrophoretic pattern is similar, indicating that the two marker alleles are segregating at random with respect to the disease allele. In contrast, the intensity of the uppermost allele band in lane 6, showing the sample from the affected group, is greater than the intensity of the corresponding allele in lane 5, showing the sample from the unaffected group. A marker allele with greater intensity in the affected group, presumably due to an increased number of copies of the allele, suggests cosegregation with the disease.To confirm or rule out cosegregation, genetic-linkage analysis was necessary. This required genotyping of DNA from each of the 26 members of Family 1 for each of the 50 marker alleles. The resulting lod scores were at least -2 for all but four loci, for which low, positive scores were obtained that were consistent with the occurrence of cosegregation of the marker allele and the disease allele. Additional markers located in these four regions were amplified and analyzed, and the results ruled out three of these regions (4q, 7q, and 13q), but marker alleles (D10S569 and D10S607) in the region 10q22 cosegregated with the disease allele, with maximal two-point lod scores of 3.60, indicating genetic linkage. Lod scores for these markers remained above 3.0 despite variations in penetrance from 60 to 99 percent.
Since the estimated prevalence of atrial fibrillation in the general population below the age of 40 is less than 0.04 percent2 and the nonfamilial causes of atrial fibrillation at this young age are almost exclusively related to valvular heart disease or congenital defects, a phenocopy prevalence of even 1 percent is probably excessive. Nevertheless, lod scores for these markers remained significant even with a phenocopy prevalence of 5 percent. Similarly, lod scores were not sensitive to variations in the estimated frequencies of marker alleles.
We also typed a number of markers in Families 2 and 3 and determined that they had the same haplotype on the affected chromosome as Family 1 for all markers from D10S188 to D10S219, suggesting that the three families are distantly related. Markers outside this interval (D10S581, D10S1694, D10S1786, and D10S1686) were associated with different alleles in the other two families. A total of 27 markers were examined in an effort to define the precise boundaries of the region, but not all these markers were informative. Lod scores for the four most informative markers are presented in Table 1Table 1
Two-Point Lod Scores for Four Informative Markers Linked to 10q22–q24.. Multipoint analyses resulted in a peak lod score of 3.60 between markers D10S569 and D10S607 for Family 1 alone and 6.17 for all three families combined and contributed no new information with respect to the location of the gene for atrial fibrillation.Figure 3Figure 3
Haplotypes and Recombination in Family 1., Figure 4Figure 4
: Haplotypes and Recombination in Family 2., and Figure 5Figure 5
: Haplotypes and Recombination in Family 3. show the haplotypes for 11 informative markers in all three families and the positions of the recombination events that helped determine the location of the gene. In Family 1 crossovers were observed between the disease allele and D10S1786 in Subject III-1 and between the disease allele and D10S581 in Subject IV-6. Thus, on the basis of haplotype analysis, the gene causing atrial fibrillation in Family 1 lies between D10S581 and D10S1786, an interval of approximately 20.2 cM, on chromosome 10q22–q24. Family 3 had no crossovers in this region. In Family 2, either Subject II-2 or Subject II-3 had a crossover between D10S1694 and the disease allele, further limiting the region to one measuring 11.3 cM. Affected members of all three families had identical alleles for all markers tested from D10S188 through D10S219. Because the haplotype was conserved throughout such a large region, we conclude that these three families must be distantly related and have the same mutation at this locus, supporting the conclusion that the disease gene lies proximal to D10S1786 and distal to D10S1694, an interval of 11.3 cM.Discussion
We identified a small family in whom atrial fibrillation segregated as an autosomal dominant trait; this family consisted of 26 members, 10 of whom were affected and alive at the time of the study. Genetic-linkage analysis indicated that the gene responsible for atrial fibrillation in this family is located on chromosome 10q in the region of 10q22–q24, with two markers having maximal lod scores of 3.60. We identified regions containing potential loci for this gene within a few weeks by comparing the electrophoretic patterns exhibited by markers amplified from pooled DNA samples from the affected group with those observed in the pooled DNA samples from the unaffected parents and siblings, rather than by genotyping each marker in all 26 family members. This procedure reduced the number of samples in the genomic screen by 90 percent. Individual DNA analyses were performed for only 50 markers (a reduction of approximately 75 percent), resulting in the identification of the locus within a few weeks as opposed to several months to a year. The strategy gives rapid results and should be particularly useful in small families with a high penetrance of the disease gene. Subsequently, we identified two other families with atrial fibrillation that was also linked to 10q22–q24 (combined lod score for all three families, 6.02). The odds of genetic linkage of the disease in these families to the region of 10q22–q24 remained significant despite the wide range of values used for the variables in the linkage analyses — namely, a phenocopy prevalence of up to 5 percent and penetrance ranging from 60 to 99 percent. This analysis provides the first essential step in the identification of the responsible molecular defect.
The pooled-sample approach is based on the fact that each DNA marker has a unique and characteristic distribution of allele frequencies in the general population. When the DNA is pooled into two groups (affected and unaffected), each sample contains many alleles (rather than two, as is the case for a single subject), and thus, the intensity of the electrophoretic bands is dependent on the frequencies with which those alleles are represented in the pool. If a marker allele is segregating at random with respect to a disease, its distribution in the affected and unaffected subjects will be identical. If, on the other hand, a particular marker allele is cosegregating with the disease allele, then all the members of the affected pool will share this allele and DNA analysis will show a band of greater intensity than in the sample from the unaffected subjects or a unique band. The strategy of using pooled DNA samples to look for differences in allele distribution has been used to identify the locus of a recessive disease in a highly inbred population.12 Its lack of use in autosomal dominant diseases is probably due to the expectation that the inordinately high incidence of differences between affected and unaffected samples would represent false positive results. We minimized false positive results in our study by choosing as unaffected subjects in the pooled sample only parents and siblings, who were more likely to share alleles with the affected subjects.
Candidate genes that must be considered in the search for a genetic cause of atrial fibrillation include genes encoding channel or pore proteins and genes encoding the sympathetic or parasympathetic system that will influence cardiac conduction or automaticity, such as the β-adrenergic receptor or signaling proteins. The genes for the β-adrenergic receptor (ADRB1)13 and α-adrenergic receptor (ADRA2)14 are located on 10q23–q26, as is the gene for G-protein–coupled receptor kinase (GPRK5),15 which interacts with adrenergic receptors.
Mapping of the locus for atrial fibrillation provides the information necessary to identify the gene. Although atrial fibrillation is commonly associated with acquired heart disease, a substantial proportion of patients, particularly those with an early onset of disease, have no other forms of heart disease. It remains to be determined what percentage of the cases of atrial fibrillation in these patients is due to genetic defects. Thus, identification of the gene and elucidation of the molecular pathogenesis of atrial fibrillation should not only clarify the mechanism responsible for the familial form, but also shed light on the common acquired forms and eventually lead to more effective therapy. Identification of the gene and the responsible mutation is required to establish causality. The incidence of familial atrial fibrillation and the percentage of cases attributable to the 10q22–q24 locus remain to be determined. Nevertheless, families with familial atrial fibrillation can now be screened rapidly for genetic linkage to the 10q22–q24 region. For families in which the disease does not map to 10q22–q24, ruling out this locus will turn the search to other loci.
Supported in part by grants from the National Heart, Lung, and Blood Institute Specialized Centers of Research (P50-HL313-01); the National Heart, Lung, and Blood Institute Training Center in Molecular Cardiology (T32-HL-07706); and the American Heart Association Texas Affiliate (95R-1191).
We are indebted to Debora Weaver, Anna Zamora, and Che Rivers for their assistance in the preparation of the manuscript.
Source Information
From the Department of Cardiology, Baylor College of Medicine, Houston (R.B., T.T., G.Z.C., A.J.M., A.I., L.L.B., R.R.); the Cardiac Arrhythmia Service, Department of Cardiology, Hospital Clinic, University of Barcelona, Barcelona, Spain (L.M., J.B.); and the Department of Cardiology, Hospital Materno–Infantil Vall d'Hebron, Barcelona, Spain (J.G., A.D.).
Address reprint requests to Dr. Roberts at Baylor College of Medicine, 6550 Fannin, MS SM677, Houston, TX 77030.
- References
References
1
The National Heart, Lung, and Blood Institute Working Group on Atrial Fibrillation
CrossRef | Web of Science | Medline2
Feinberg WM ,Blackshear JL ,Laupacis A ,Kronmal R ,Hart RG . Prevalence, age distribution, and gender of patients with atrial fibrillation: analysis and implications. Arch Intern Med 1995;155:469-473
CrossRef | Web of Science | Medline3
Wolf PA ,Abbott RD ,Kannel WB . Atrial fibrillation: a major contributor to stroke in the elderly: the Framingham Study. Arch Intern Med 1987;147:1561-1564
CrossRef | Web of Science | Medline4
Albers GW . Atrial fibrillation and stroke: three new studies, three remaining questions. Arch Intern Med 1994;154:1443-1448
CrossRef | Web of Science | Medline5
Beyer F ,Paul T ,Luhmer I ,Bertram H ,Kallfelz HC . Familiäres idiopathisches Vorhofflimmern mit Bradyarrhythmie. Z Kardiol 1993;82:674-677
Medline6
Miller SA ,Dykes DD ,Polesky HF . A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res 1988;16:1215-1215
CrossRef | Web of Science | Medline7
Neitzel H . A routine method for the establishment of permanent growing lymphoblastoid cell lines. Hum Genet 1986;73:320-326
CrossRef | Web of Science | Medline8
Weissenbach J ,Gyapay G ,Dib C , et al. A second-generation linkage map of the human genome. Nature 1992;359:794-801
CrossRef | Web of Science | Medline9
NIH/CEPH Collaborative Mapping Group
CrossRef | Web of Science10
Durand JB ,Bachinski LL ,Bieling LC , et al. Localization of a gene responsible for familial dilated cardiomyopathy to chromosome 1q32. Circulation 1995;92:3387-3389
Web of Science | Medline11
Ott J. Analysis of human genetic linkage. Rev. ed. Baltimore: Johns Hopkins University Press, 1991.
12
Scott DA ,Carmi R ,Elbedour K ,Yosefsberg S ,Stone EM ,Sheffield VC . An autosomal recessive nonsyndromic-hearing-loss locus identified by DNA pooling using two inbred Bedouin kindreds. Am J Hum Genet 1996;59:385-391
Web of Science | Medline13
Hoehe M ,Berrettini W ,Leppert M , et al. Genetic mapping of adrenergic receptor genes. Am J Hum Genet 1989;45:Suppl:A143-A143 abstract.14
Yang-Feng TL ,Xue FY ,Zhong WW , et al. Chromosomal organization of adrenergic receptor genes. Proc Natl Acad Sci U S A 1990;87:1516-1520
CrossRef | Web of Science | Medline15
Bullrich F ,Druck T ,Kunapuli P , et al. Chromosomal mapping of the genes GPRK5 and GPRK6 encoding G protein-coupled receptor kinases GRK5 and GRK6. Cytogenet Cell Genet 1995;70:250-254
CrossRef | Medline
- Citing Articles (139)
Citing Articles
1
Poonam Velagapudi, Mohit K Turagam, Miguel A Leal, Abraham G Kocheril. (2012) Atrial Fibrillation and Acid Reflux Disease. Clinical Cardiologyn/a-n/a
CrossRef2
Babar Parvez, Dawood Darbar. (2011) The “missing” link in atrial fibrillation heritability. Journal of Electrocardiology 44:6, 641-644
CrossRef3
Junjie Xiao, Dandan Liang, Yi-Han Chen. (2011) The Genetics of Atrial Fibrillation: From the Bench to the Bedside. Annual Review of Genomics and Human Genetics 12:1, 73-96
CrossRef4
José Jalife, Maurits Allessie, Charles Antzelevitch, Yoshito Iesaka, Warren M. Jackman, Melvin M. Scheinman, Shih-Ann Chen. 2011. Pathophysiology of atrial fibrillation. , 20-34.
CrossRef5
Shinsuke Miyazaki, Ashok J. Shah, Daniel Scherr, Michel Haïssaguerre. (2011) Atrial fibrillation: Pathophysiology and current therapy. Annals of Medicine 43:6, 425-436
CrossRef6
Yi-Qing Yang, Mao-Ya Wang, Xian-Ling Zhang, Hong-Wei Tan, Hai-Feng Shi, Wei-Feng Jiang, Xin-Hua Wang, Wei-Yi Fang, Xu Liu. (2011) GATA4 loss-of-function mutations in familial atrial fibrillation. Clinica Chimica Acta 412:19-20, 1825-1830
CrossRef7
P. Kirchhof, G. Y. H. Lip, I. C. Van Gelder, J. Bax, E. Hylek, S. Kaab, U. Schotten, K. Wegscheider, G. Boriani, A. Brandes, M. Ezekowitz, H. Diener, L. Haegeli, H. Heidbuchel, D. Lane, L. Mont, S. Willems, P. Dorian, M. Aunes-Jansson, C. Blomstrom-Lundqvist, M. Borentain, S. Breitenstein, M. Brueckmann, N. Cater, A. Clemens, D. Dobrev, S. Dubner, N. G. Edvardsson, L. Friberg, A. Goette, M. Gulizia, R. Hatala, J. Horwood, L. Szumowski, L. Kappenberger, J. Kautzner, A. Leute, T. Lobban, R. Meyer, J. Millerhagen, J. Morgan, F. Muenzel, M. Nabauer, C. Baertels, M. Oeff, D. Paar, J. Polifka, U. Ravens, L. Rosin, W. Stegink, G. Steinbeck, P. Vardas, A. Vincent, M. Walter, G. Breithardt, A. J. Camm. (2011) Comprehensive risk reduction in patients with atrial fibrillation: emerging diagnostic and therapeutic options--a report from the 3rd Atrial Fibrillation Competence NETwork/European Heart Rhythm Association consensus conference. Europace
CrossRef8
D. Franco, A. Chinchilla, H. Daimi, J. N. Dominguez, A. Aranega. (2011) Modulation of conductive elements by Pitx2 and their impact on atrial arrhythmogenesis. Cardiovascular Research 91:2, 223-231
CrossRef9
2011. Inherited Heart Diseases. , 295-337.
CrossRef10
T. S. Potpara, G. Y. H. Lip. (2011) Lone atrial fibrillation: what is known and what is to come. International Journal of Clinical Practice 65:4, 446-457
CrossRef11
S. Mahida, S. A. Lubitz, M. Rienstra, D. J. Milan, P. T. Ellinor. (2011) Monogenic atrial fibrillation as pathophysiological paradigms. Cardiovascular Research 89:4, 692-700
CrossRef12
Robin Lemmens, Sylvia Hermans, Dieter Nuyens, Vincent Thijs. (2011) Genetics of Atrial Fibrillation and Possible Implications for Ischemic Stroke. Stroke Research and Treatment 2011, 1-7
CrossRef13
Y.-Q. Yang, X. Liu, X.-L. Zhang, X.-H. Wang, H.-W. Tan, H.-F. Shi, W.-F. Jiang, W.-Y. Fang. (2010) Novel connexin40 missense mutations in patients with familial atrial fibrillation. Europace 12:10, 1421-1427
CrossRef14
Qun-shan Wang, Yi-gang Li, Xing-dong Chen, Jie-fei Yu, Jun Wang, Jian Sun, Shang-biao Lu, Li Jin, Xiao-feng Wang. (2010) Angiotensinogen polymorphisms and acquired atrial fibrillation in Chinese. Journal of Electrocardiology 43:4, 373-377
CrossRef15
Robert Roberts, George A. Wells, Alexandre F. R. Stewart, Sonny Dandona, Li Chen. (2010) The Genome-Wide Association Study—A New Era for Common Polygenic Disorders. Journal of Cardiovascular Translational Research 3:3, 173-182
CrossRef16
M Khaled Sabeh, Calum A MacRae. (2010) The genetics of atrial fibrillation. Current Opinion in Cardiology 25:3, 186-191
CrossRef17
Oscar Campuzano, Pedro Beltrán-Álvarez, Anna Iglesias, Fabiana Scornik, Guillermo Pérez, Ramon Brugada. (2010) Genetics and cardiac channelopathies. Genetics in Medicine 12:5, 260-267
CrossRef18
Cordula M Wolf, Charles I Berul. 2010. Molecular Genetics of Cardiac Arrhythmias. .
CrossRef19
Cristina Chimenti, Matteo A. Russo, Angelo Carpi, Andrea Frustaci. (2010) Histological substrate of human atrial fibrillation. Biomedicine & Pharmacotherapy 64:3, 177-183
CrossRef20
Daniela Husser, Volker Adams, Christopher Piorkowski, Gerhard Hindricks, Andreas Bollmann. (2010) Chromosome 4q25 Variants and Atrial Fibrillation Recurrence After Catheter Ablation. Journal of the American College of Cardiology 55:8, 747-753
CrossRef21
Yi-Qing Yang, Xian-Ling Zhang, Xin-Hua Wang, Hong-Wei Tan, Hai-Feng Shi, Wei-Yi Fang, Xu Liu. (2010) Familial Aggregation of Lone atrial Fibrillation in the Chinese Population. Internal Medicine 49:22, 2385-2391
CrossRef22
Min Je Choi, Hye Won Shin, Sung Uk Choi, Ji Yong Park, Hye Won Lee, Hae Ja Lim, Suk Min Yoon, Seong Ho Chang. (2010) Paroxysmal atrial fibrillation developed during incomplete epidural anesthesia -A case report-. Korean Journal of Anesthesiology 59:Suppl, S58
CrossRef23
H. Le Marec, V. Probst. (2009) Génétique de la fibrillation auriculaire. Annales de Cardiologie et d'Angéiologie 58, S70-S72
CrossRef24
S.-M. Chaldoupi, P. Loh, R. N.W. Hauer, J. M.T. de Bakker, H. V.M. van Rijen. (2009) The role of connexin40 in atrial fibrillation. Cardiovascular Research 84:1, 15-23
CrossRef25
O. Campuzano, R. Brugada. (2009) Genetics of familial atrial fibrillation. Europace 11:10, 1267-1271
CrossRef26
QUN-SHAN WANG, XIAO-FENG WANG, XING-DONG CHEN, JIE-FEI YU, JUN WANG, JIAN SUN, SHANG-BIAO LU, MU-YAO SHEN, MING LU, YI-GANG LI, LI JIN. (2009) Genetic Polymorphism of KCNH2 Confers Predisposition of Acquired Atrial Fibrillation in Chinese. Journal of Cardiovascular Electrophysiology 20:10, 1158-1162
CrossRef27
Saumya Das, Seiko Makino, Yonathan F. Melman, Marisa A. Shea, Sanjeev B. Goyal, Anthony Rosenzweig, Calum A. MacRae, Patrick T. Ellinor. (2009) Mutation in the S3 segment of KCNQ1 results in familial lone atrial fibrillation. Heart Rhythm 6:8, 1146-1153
CrossRef28
Guiscard Seebohm. (2009) Kv7.1 in atrial fibrillation. Heart Rhythm 6:8, 1154-1155
CrossRef29
Yiqing Yang, Jun Li, Xiaoping Lin, Yanzong Yang, Kui Hong, Lei Wang, Jinqiu Liu, Li Li, Dinghong Yan, Dandan Liang, Junjie Xiao, Hongmei Jin, Jie Wu, Yangyang Zhang, Yi-Han Chen. (2009) Novel KCNA5 loss-of-function mutations responsible for atrial fibrillation. Journal of Human Genetics 54:5, 277-283
CrossRef30
Julia Heisler Indik, Joseph S. Alpert. (2009) The Patient with Atrial Fibrillation. The American Journal of Medicine 122:5, 415-418
CrossRef31
Óscar Campuzano, Georgia Sarquella-Brugada, Ramón Brugada, Pedro Brugada, Josep Brugada. (2009) Bases genéticas de las arritmias malignas y las miocardiopatías. Revista Española de Cardiología 62:4, 422-436
CrossRef32
Concepción Moro Serrano, Antonio Hernández-Madrid. (2009) Fibrilación auricular: ¿estamos ante una epidemia?. Revista Española de Cardiología 62:1, 10-14
CrossRef33
S. Kaab, D. Darbar, C. van Noord, J. Dupuis, A. Pfeufer, C. Newton-Cheh, R. Schnabel, S. Makino, M. F. Sinner, P. J. Kannankeril, B. M. Beckmann, S. Choudry, B. S. Donahue, J. Heeringa, S. Perz, K. L. Lunetta, M. G. Larson, D. Levy, C. A. MacRae, J. N. Ruskin, A. Wacker, A. Schomig, H.-E. Wichmann, G. Steinbeck, T. Meitinger, A. G. Uitterlinden, J. C.M. Witteman, D. M. Roden, E. J. Benjamin, P. T. Ellinor. (2008) Large scale replication and meta-analysis of variants on chromosome 4q25 associated with atrial fibrillation. European Heart Journal 30:7, 813-819
CrossRef34
L. Mont, R. Elosua, J. Brugada. (2008) Endurance sport practice as a risk factor for atrial fibrillation and atrial flutter. Europace 11:1, 11-17
CrossRef35
T. Jared Bunch, Douglas L. Packer, Arshad Jahangir, G. Richard Locke, Nicholas J. Talley, Bernard J. Gersh, Ranjini R. Roy, David O. Hodge, Samuel J. Asirvatham. (2008) Long-Term Risk of Atrial Fibrillation With Symptomatic Gastroesophageal Reflux Disease and Esophagitis. The American Journal of Cardiology 102:9, 1207-1211
CrossRef36
Eric Schulze-Bahr. (2008) Susceptibility genes & modifiers for cardiac arrhythmias. Progress in Biophysics and Molecular Biology 98:2-3, 289-300
CrossRef37
Sanjay Kharche, Clifford J. Garratt, Mark R. Boyett, Shin Inada, Arun V. Holden, Jules C. Hancox, Henggui Zhang. (2008) Atrial proarrhythmia due to increased inward rectifier current (IK1) arising from KCNJ2 mutation – A simulation study. Progress in Biophysics and Molecular Biology 98:2-3, 186-197
CrossRef38
Dawood Darbar. (2008) Cardiac sodium channel variants: Action players with many faces. Heart Rhythm 5:10, 1441-1443
CrossRef39
LIN Y. CHEN, KATHLEEN J. HERRON, BEE C. TAI, TIMOTHY M. OLSON. (2008) Lone Atrial Fibrillation: Influence of Familial Disease on Gender Predilection. Journal of Cardiovascular Electrophysiology 19:8, 802-806
CrossRef40
Robert Roberts. (2008) The human genome and prospects for management of cardiovascular disease. Canadian Journal of Cardiology 24, 11C-14C
CrossRef41
Hodgson-Zingman, Denice M., Karst, Margaret L., Zingman, Leonid V., Heublein, Denise M., Darbar, Dawood, Herron, Kathleen J., Ballew, Jeffrey D., de Andrade, Mariza, Burnett, John C. Jr., Olson, Timothy M., . (2008) Atrial Natriuretic Peptide Frameshift Mutation in Familial Atrial Fibrillation. New England Journal of Medicine 359:2, 158-165
Full Text42
Chia-Ti Tsai, Ling-Ping Lai, Juey-Jen Hwang, Jiunn-Lee Lin, Fu-Tien Chiang. (2008) Molecular Genetics of Atrial Fibrillation. Journal of the American College of Cardiology 52:4, 241-250
CrossRef43
Gregory M. Marcus, Lisa M. Smith, Eric Vittinghoff, Zian H. Tseng, Nitish Badhwar, Byron K. Lee, Randall J. Lee, Melvin M. Scheinman, Jeffrey E. Olgin. (2008) A first-degree family history in lone atrial fibrillation patients. Heart Rhythm 5:6, 826-830
CrossRef44
Michael H. Gollob. (2008) Begetting atrial fibrillation: Connexins and arrhythmogenesis. Heart Rhythm 5:6, 888-891
CrossRef45
PETER J. MOHLER, MARK E. ANDERSON. (2008) New Insights into Genetic Causes of Sinus Node Disease and Atrial Fibrillation. Journal of Cardiovascular Electrophysiology 19:5, 516-518
CrossRef46
MARGARET L. KARST, KATHLEEN J. HERRON, TIMOTHY M. OLSON. (2008) X-Linked Nonsyndromic Sinus Node Dysfunction and Atrial Fibrillation Caused by Emerin Mutation. Journal of Cardiovascular Electrophysiology 19:5, 510-515
CrossRef47
Ali Andalib, Ramon Brugada, Stanley Nattel. (2008) Atrial fibrillation: evidence for genetically determined disease. Current Opinion in Cardiology 23:3, 176-183
CrossRef48
Nicolas Doll, Alexander M. Fabricius, Virginia Dietel, Piotr Suwalski, Thomas Walther, Jan F. Gummert, Friedrich W. Mohr. 2008. Perioperative Complications During Surgical Treatment of Atrial Fibrillation: Tips and Pitfalls. , 235-244.
CrossRef49
Robert A. Byrne, Kieran Daly. 2008. Pathophysiology of Atrial Fibrillation. , 21-29.
CrossRef50
Ramon Brugada. 2008. Genetics of Atrial Fibrillation. , 31-35.
CrossRef51
Lasse S. Ravn, Yoshiyasu Aizawa, Guido D. Pollevick, Jacob Hofman-Bang, Jonathan M. Cordeiro, Ulrik Dixen, Gorm Jensen, Yuesheng Wu, Elena Burashnikov, Stig Haunso, Alejandra Guerchicoff, Dan Hu, Jesper H. Svendsen, Michael Christiansen, Charles Antzelevitch. (2008) Gain of function in IKs secondary to a mutation in KCNE5 associated with atrial fibrillation. Heart Rhythm 5:3, 427-435
CrossRef52
Dawood Darbar, Amanda Hardy, Jonathan L. Haines, Dan M. Roden. (2008) Prolonged Signal-Averaged P-Wave Duration as an Intermediate Phenotype for Familial Atrial Fibrillation. Journal of the American College of Cardiology 51:11, 1083-1089
CrossRef53
Barry London. (2008) An Irregularly Irregular Inheritance
Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.. Journal of the American College of Cardiology 51:11, 1090-1091
CrossRef54
Patrick T. Ellinor, B. Alexander Yi, Calum A. MacRae. (2008) Genetics of Atrial Fibrillation. Medical Clinics of North America 92:1, 41-51
CrossRef55
Alicia Lundby, Lasse Steen Ravn, Jesper Hastrup Svendsen, Stig Haunsø, Søren-Peter Olesen, Nicole Schmitt. (2008) KCNE3 Mutation V17M Identified in a Patient with Lone Atrial Fibrillation. Cellular Physiology and Biochemistry 21:1-3, 047-054
CrossRef56
Patrick T. Ellinor, Edwin G. Nam, Marisa A. Shea, David J. Milan, Jeremy N. Ruskin, Calum A. MacRae. (2008) Cardiac sodium channel mutation in atrial fibrillation. Heart Rhythm 5:1, 99-105
CrossRef57
Atul Khasnis, Ranjan K. Thakur. (2008) Atrial Fibrillation: A Historical Perspective. Medical Clinics of North America 92:1, 1-15
CrossRef58
Alicia Lundby, Lasse Steen Ravn, Jesper Hastrup Svendsen, Søren-Peter Olesen, Nicole Schmitt. (2007) KCNQ1 mutation Q147R is associated with atrial fibrillation and prolonged QT interval. Heart Rhythm 4:12, 1532-1541
CrossRef59
Ryan G. Aleong, Calum A. MacRae, Patrick T. Ellinor. (2007) Heritability and genetics of atrial fibrillation. Current Cardiovascular Risk Reports 1:5, 414-419
CrossRef60
Arun Kalyanasundaram, Glenn S Gerhard, Kimberly A Skelding. (2007) Genomics, haplotypes and cardiovascular disease. Future Cardiology 3:6, 601-610
CrossRef61
Robyn Otway, Jamie I. Vandenberg, Diane Fatkin. (2007) Atrial Fibrillation—A New Cardiac Channelopathy. Heart, Lung and Circulation 16:5, 356-360
CrossRef62
Robert Roberts, Alexandre F.R. Stewart, George A. Wells, Kathryn A. Williams, Nihan Kavaslar, Ruth McPherson. (2007) Identifying genes for coronary artery disease: An idea whose time has come. Canadian Journal of Cardiology 23, 7A-15A
CrossRef63
Dawood Darbar, Alison A. Motsinger, Marylyn D. Ritchie, James V. Gainer, Dan M. Roden. (2007) Polymorphism modulates symptomatic response to antiarrhythmic drug therapy in patients with lone atrial fibrillation. Heart Rhythm 4:6, 743-749
CrossRef64
A. Diegeler. (2007) Chirurgische Therapie bei Vorhofflimmern. Herzschrittmachertherapie & Elektrophysiologie 18:2, 77-82
CrossRef65
Sumeet S. Chugh. (2007) Confronting the genetic complexity of atrial fibrillation: This too shall pass. Heart Rhythm 4:4, 476-477
CrossRef66
Paul G.A. Volders, Qian Zhu, Carl Timmermans, Petra M.H. Eurlings, Xiaoyan Su, Yvonne H. Arens, Li Li, Roselie J. Jongbloed, Min Xia, Luz-Maria Rodriguez, Yi Han Chen. (2007) Mapping a novel locus for familial atrial fibrillation on chromosome 10p11-q21. Heart Rhythm 4:4, 469-475
CrossRef67
Lin Y. Chen, Win-Kuang Shen. (2007) Epidemiology of atrial fibrillation: A current perspective. Heart Rhythm 4:3, S1-S6
CrossRef68
Kristen K Patton, Richard L Page. (2007) Pharmacological therapy of atrial fibrillation. Expert Opinion on Investigational Drugs 16:2, 169-179
CrossRef69
Zhiyu Zeng, Chen Tan, Siyong Teng, Jianhong Chen, Shaoyong Su, Xiaoyang Zhou, Fangzheng Wang, Shu Zhang, Dongfeng Gu, Jonathan C. Makielski, Jielin Pu. (2007) The Single Nucleotide Polymorphisms of <i>I</i><sub>Ks</sub> Potassium Channel Genes and Their Association with Atrial Fibrillation in a Chinese Population. Cardiology 108:2, 97-103
CrossRef70
L Y Chen, J D Ballew, K J Herron, R J Rodeheffer, T M Olson. (2007) A Common Polymorphism in SCN5A is Associated with Lone Atrial Fibrillation. Clinical Pharmacology & Therapeutics 81:1, 35-41
CrossRef71
Naomasa Makita, Hiroyuki Tsutsui. (2007) Genetic Polymorphisms and Arrhythmia Susceptibility. Circulation Journal 71:SupplementA, A54-A60
CrossRef72
Arthur AM Wilde, Hanno L Tan. (2007) Inherited Arrhythmia Syndromes. Circulation Journal 71:SupplementA, A12-A19
CrossRef73
(2006) ACC/AHA/ESC: Guías de Práctica Clínica 2006 para el manejo de pacientes con fibrilación auricular. Versión resumida. Revista Española de Cardiología 59:12, 1329.e1-1329.e64
CrossRef74
Jerónimo Farré. (2006) Siete reflexiones sobre un primer episodio de fibrilación auricular solitaria. Revista Española de Cardiología 59:11, 1093-1095
CrossRef75
Patrick T Ellinor, Subbarao Choudry, Calum A MacRae. (2006) Genetics of atrial fibrillation. Future Cardiology 2:5, 579-584
CrossRef76
DANIEL R. FRISCH, KEVIN F. KWAKU, DOMINIC J. ALLOCCO, PETER J. ZIMETBAUM. (2006) Atrioventricular Nodal Reentrant Tachycardia in Two Siblings with Wolfram Syndrome. Journal of Cardiovascular Electrophysiology 17:9, 1029-1031
CrossRef77
Valentin Fuster, Lars E. Rydén, David S. Cannom, Harry J. Crijns, Anne B. Curtis, Kenneth A. Ellenbogen, Jonathan L. Halperin, Jean-Yves Le Heuzey, G. Neal Kay, James E. Lowe, S. Bertil Olsson, Eric N. Prystowsky, Juan Luis Tamargo, Samuel Wann. (2006) ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation. Journal of the American College of Cardiology 48:4, e149-e246
CrossRef78
Enrico Flossmann. (2006) Genetics of ischaemic stroke; single gene disorders. International Journal of Stroke 1:3, 131-139
CrossRef79
Valentin Fuster, Lars E. Rydén, David S. Cannom, Harry J. Crijns, Anne B. Curtis, Kenneth A. Ellenbogen, Jonathan L. Halperin, Jean-Yves Le Heuzey, G. Neal Kay, James E. Lowe, S. Bertil Olsson, Eric N. Prystowsky, Juan Luis Tamargo, Samuel Wann. (2006) ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation—Executive Summary. Journal of the American College of Cardiology 48:4, 854-906
CrossRef80
Gollob, Michael H., Jones, Douglas L., Krahn, Andrew D., Danis, Lynne, Gong, Xiang-Qun, Shao, Qing, Liu, Xiaoqin, Veinot, John P., Tang, Anthony S.L., Stewart, Alexandre F.R., Tesson, Frederique, Klein, George J., Yee, Raymond, Skanes, Allan C., Guiraudon, Gerard M., Ebihara, Lisa, Bai, Donglin, . (2006) Somatic Mutations in the Connexin 40 Gene (GJA5) in Atrial Fibrillation. New England Journal of Medicine 354:25, 2677-2688
Full Text81
M. F. Sinner, A. Pfeufer, S. Kääb. (2006) Genetik von Vorhofflimmern: seltene Mutationen, häufige Genvarianten und klinische Relevanz?. Herzschrittmachertherapie & Elektrophysiologie 17:2, 95-105
CrossRef82
Robert Roberts. (2006) Mechanisms of Disease: genetic mechanisms of atrial fibrillation. Nature Clinical Practice Cardiovascular Medicine 3:5, 276-282
CrossRef83
Stephen M. Modell, Michael H. Lehmann. (2006) The long QT syndrome family of cardiac ion channelopathies: A HuGE review*. Genetics in Medicine 8:3, 143-155
CrossRef84
Torsten K. Roepke, Geoffrey W. Abbott. (2006) Pharmacogenetics and cardiac ion channels. Vascular Pharmacology 44:2, 90-106
CrossRef85
Mihai V. Podgoreanu, Debra A. Schwinn. (2005) New Paradigms in Cardiovascular Medicine. Journal of the American College of Cardiology 46:11, 1965-1977
CrossRef86
Patrick T. Ellinor, Danita M. Yoerger, Jeremy N. Ruskin, Calum A. MacRae. (2005) Familial aggregation in lone atrial fibrillation. Human Genetics 118:2, 179-184
CrossRef87
Richard L. Page, Dan M. Roden. (2005) Drug therapy for atrial fibrillation: where do we go from here?. Nature Reviews Drug Discovery 4:11, 899-910
CrossRef88
Akiko Shiroshita-Takeshita, Bianca J. J. M. Brundel, Stanley Nattel. (2005) Atrial Fibrillation: Basic Mechanisms, Remodeling and Triggers. Journal of Interventional Cardiac Electrophysiology 13:3, 181-193
CrossRef89
ANDREA SARKOZY, PEDRO BRUGADA. (2005) Sudden Cardiac Death and Inherited Arrhythmia Syndromes. Journal of Cardiovascular Electrophysiology 16:s1, S8-S20
CrossRef90
Andres Ricardo Perez Riera, Celso Ferreira, Sergio J Dubner, Edgardo Schapachnik, Joaquim D. Soares, Johnson Francis. (2005) Brief Review of the Recently Described Short QT Syndrome and Other Cardiac Channelopathies. Annals of Noninvasive Electrocardiology 10:3, 371-377
CrossRef91
Min Xia, Qingfeng Jin, Saïd Bendahhou, Yusong He, Marie-Madeleine Larroque, Yiping Chen, Qinshu Zhou, Yiqing Yang, Yi Liu, Ban Liu, Qian Zhu, Yanting Zhou, Jie Lin, Bo Liang, Li Li, Xiongjian Dong, Zhiwen Pan, Rongrong Wang, Haiying Wan, Weiqin Qiu, Wenyuan Xu, Petra Eurlings, Jacques Barhanin, Yihan Chen. (2005) A Kir2.1 gain-of-function mutation underlies familial atrial fibrillation. Biochemical and Biophysical Research Communications 332:4, 1012-1019
CrossRef92
KRISTEN K. PATTON, ERAN S. ZACKS, JOSEPH Y. CHANG, MARISA A. SHEA, JEREMY N. RUSKIN, CALUM A. MACRAE, PATRICK T. ELLINOR. (2005) Clinical Subtypes of Lone Atrial Fibrillation. Pacing and Clinical Electrophysiology 28:7, 630-638
CrossRef93
Gerardo Moreno, Concepción Moro. (2005) Ablación de fibrilación auricular familiar. Buena evolución a largo plazo. Revista Española de Cardiología 58:7, 878-879
CrossRef94
Dawood Darbar, Dan M. Roden. (2005) Symptomatic burden as an endpoint to evaluate interventions in patients with atrial fibrillation. Heart Rhythm 2:5, 544-549
CrossRef95
Joseph S. Alpert. (2005) Atrial fibrillation: Now one of the most common causes for hospitalization. Current Cardiology Reports 7:3, 149-150
CrossRef96
RAMON BRUGADA. (2005) Is Atrial Fibrillation a Genetic Disease?. Journal of Cardiovascular Electrophysiology 16:5, 553-556
CrossRef97
JUN OTOMO, SHIGEO KURE, TOMOKO SHIBA, AKIHIKO KARIBE, TSUYOSHI SHINOZAKI, TETSUO YAGI, HIROSHI NAGANUMA, FUMIAKI TEZUKA, MASAETSU MIURA, MEIICHI ITO, JUN WATANABE, YOICHI MATSUBARA, KUNIO SHIRATO. (2005) Electrophysiological and Histopathological Characteristics of Progressive Atrioventricular Block Accompanied by Familial Dilated Cardiomyopathy Caused by a Novel Mutation of Lamin A/C Gene. Journal of Cardiovascular Electrophysiology 16:2, 137-145
CrossRef98
Ashish Agarwal, Meghan York, Bharat K. Kantharia, Michael Ezekowitz. (2005) Atrial Fibrillation: Modern Concepts and Management. Annual Review of Medicine 56:1, 475-494
CrossRef99
G Michael Vincent, Li Zhang. (2005) The Role of Genotyping in Diagnosing Cardiac Channelopathies. Molecular Diagnosis 9:3, 105-118
CrossRef100
Page, Richard L., . (2004) Newly Diagnosed Atrial Fibrillation. New England Journal of Medicine 351:23, 2408-2416
Full Text101
Yiqing Yang, Min Xia, Qingfeng Jin, Saïd Bendahhou, Jingyi Shi, Yiping Chen, Bo Liang, Jie Lin, Yi Liu, Ban Liu, Qinshu Zhou, Dongwei Zhang, Rong Wang, Ning Ma, Xiaoyan Su, Kaiya Niu, Yan Pei, Wenyuan Xu, Zhaopeng Chen, Haiying Wan, Jianmin Cui, Jacques Barhanin, Yihan Chen. (2004) Identification of a KCNE2 Gain-of-Function Mutation in Patients with Familial Atrial Fibrillation. The American Journal of Human Genetics 75:5, 899-905
CrossRef102
Edward P. Havranek, Frederick A. Masoudi. (2004) What we're talking about when we talk about race. Journal of the American College of Cardiology 43:3, 436-437
CrossRef103
NABIL EL-SHERIF, GHAYATH BAROUDI. (2004) Atrial Fibrillation:. Molecular Biology Has Yet to Impact Management. Journal of Cardiovascular Electrophysiology 15:2, 224-225
CrossRef104
BORYS SURAWICZ. (2004) Brief History of Cardiac Arrhythmias Since the End of the Nineteenth Century:. Journal of Cardiovascular Electrophysiology 15:1, 101-111
CrossRef105
CHARLES ANTZELEVITCH. (2003) Molecular Genetics of Arrhythmias and Cardiovascular Conditions Associated with Arrhythmias. Journal of Cardiovascular Electrophysiology 14:11, 1259-1272
CrossRef106
Paul A Gould, John Power, Archer Broughton, David M Kaye. (2003) Review of the current management of atrial fibrillation. Expert Opinion on Pharmacotherapy 4:11, 1889-1899
CrossRef107
CHARLES ANTZELEVITCH. (2003) Molecular Genetics of Arrhythmias and Cardiovascular Conditions Associated with Arrhythmias. Pacing and Clinical Electrophysiology 26:11, 2194-2208
CrossRef108
PATRICK T. ELLINOR, CALUM A. MACRAE. (2003) The Genetics of Atrial Fibrillation. Journal of Cardiovascular Electrophysiology 14:9, 1007-1009
CrossRef109
P Charron. (2003) Aspects génétiques de la fibrillation auriculaire. Annales de Cardiologie et d'Angéiologie 52:4, 254-257
CrossRef110
Luisa Mestroni. (2003) Genomic medicine and atrial fibrillation. Journal of the American College of Cardiology 41:12, 2193-2196
CrossRef111
Dawood Darbar, Kathleen J Herron, Jeffrey D Ballew, Arshad Jahangir, Bernard J Gersh, Win-K Shen, Stephen C Hammill, Douglas L Packer, Timothy M Olson. (2003) Familial atrial fibrillation is a genetically heterogeneous disorder. Journal of the American College of Cardiology 41:12, 2185-2192
CrossRef112
Eric Schulze-Bahr, Axel Neu, Patrick Friederich, U. Benjamin Kaupp, Günter Breithardt, Olaf Pongs, Dirk Isbrandt. (2003) Pacemaker channel dysfunction in a patient with sinus node disease. Journal of Clinical Investigation 111:10, 1537-1545
CrossRef113
Robert Roberts, Ramon Brugada. (2003) Genetics and Arrhythmias. Annual Review of Medicine 54:1, 257-267
CrossRef114
Nicholas S Peters, Richard J Schilling, Prapa Kanagaratnam, Vias Markides. (2002) Atrial fibrillation: strategies to control, combat, and cure. The Lancet 359:9306, 593-603
CrossRef115
Robert Roberts, Ramon Brugada. (2001) Genetic aspects of arrhythmias. American Journal of Medical Genetics 97:4, 310-318
CrossRef116
Valentin Fuster, Lars E. Rydén, Richard W. Asinger, David S. Cannom, Harry J. Crijns, Robert L. Frye, Jonathan L. Halperin, G.Neal Kay, Werner W. Klein, Samuel Lévy, Robert L. McNamara, Eric N. Prystowsky, L.Samuel Wann, D.George Wyse, Raymond J. Gibbons, Elliott M. Antman, Joseph S. Alpert, David P. Faxon, Valentin Fuster, Gabriel Gregoratos, Loren F. Hiratzka, Alice K. Jacobs, Richard O. Russell, Sidney C. Smith, Werner W. Klein, Angeles Alonso-Garcia, Carina Blomström-Lundqvist, Guy De Backer, Marcus Flather, Jaromir Hradec, Ali Oto, Alexander Parkhomenko, Sigmund Silber, Adam Torbicki. (2001) ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation. Journal of the American College of Cardiology 38:4, 1266
CrossRef117
Falk, Rodney H., . (2001) Atrial Fibrillation. New England Journal of Medicine 344:14, 1067-1078
Full Text118
Sumeet S Chugh, Joseph L Blackshear, Win-Kuang Shen, Stephen C Hammill, Bernard J Gersh. (2001) Epidemiology and natural history of atrial fibrillation: clinical implications. Journal of the American College of Cardiology 37:2, 371-378
CrossRef119
Robert Roberts. (2000) A perspective: the new millennium dawns on a new paradigm for cardiology—molecular genetics. Journal of the American College of Cardiology 36:3, 661-667
CrossRef120
Karla R. Bowles, Sherin E. Abraham, Ramon Brugada, Carmelann Zintz, James Comeaux, Dan Sorajja, Shinichi Tsubata, Hua Li, Lois Brandon, Richard A. Gibbs, Steve E. Scherer, Neil E. Bowles, Jeffrey A. Towbin. (2000) Construction of a High-Resolution Physical Map of the Chromosome 10q22–q23 Dilated Cardiomyopathy Locus and Analysis of Candidate Genes. Genomics 67:2, 109-127
CrossRef121
Duanxiang Li, Paula Burch, Oscar Gonzalez, Catherine D. Kashork, Lisa G. Shaffer, Linda L. Bachinski, Robert Roberts. (2000) Molecular Cloning, Expression Analysis, and Chromosome Mapping of WDR6, a Novel Human WD-Repeat Gene. Biochemical and Biophysical Research Communications 274:1, 117-123
CrossRef122
Douglas P. Zipes. (2000) A century of cardiac arrhythmias. Journal of the American College of Cardiology 35:5, 38B-44B
CrossRef123
S. Nattel, D. Li, L. Yue. (2000) Basic Mechanisms of Atrial Fibrillation—Very New Insights into Very Old Ideas. Annual Review of Physiology 62:1, 51-77
CrossRef124
JEFFREY A. TOWBIN, MATTEO VATTA. (2000) The Genetics of Cardiac Arrhythmias. Pacing and Clinical Electrophysiology 23:1, 106-119
CrossRef125
DAN M. RODEN, PETER M. SPOONER. (1999) Inherited Long QT Syndromes:.. Journal of Cardiovascular Electrophysiology 10:12, 1664-1683
CrossRef126
Jan Nemec, Win-Kuang Shen. (1999) Pharmacotherapy of atrial fibrillation. Expert Opinion on Pharmacotherapy 1:1, 81-96
CrossRef127
Elizabeth Goldmuntz. (1999) Recent advances in understanding the genetic etiology of congenital heart disease. Current Opinion in Pediatrics 11:5, 437-444
CrossRef128
Y. Romero, G. R. Locke. (1999) Is There a GERD Gene?. The American Journal of Gastroenterology 94:5, 1127-1129
CrossRef129
Ramon Brugada, Robert Roberts. (1999) Molecular biology and atrial fibrillation. Current Opinion in Cardiology 14:3, 269
CrossRef130
Dan M Roden. (1999) An Overview of Contemporary Approaches to Antiarrhythmic Therapy. Japanese Circulation Journal 63:9, 655-658
CrossRef131
Howard Feit, Alice Silbergleit, Lori B. Schneider, Jorge A. Gutierrez, Reine-Paule Fitoussi, Cécile Réyès, Guy A. Rouleau, Bernard Brais, Charles E. Jackson, Jacques S. Beckmann, Eric Seboun. (1998) Vocal Cord and Pharyngeal Weakness with Autosomal Dominant Distal Myopathy: Clinical Description and Gene Localization to 5q31. The American Journal of Human Genetics 63:6, 1732-1742
CrossRef132
Ramon Brugada, Robert Roberts. (1998) The molecular genetics of arrhythmias and sudden death. Clinical Cardiology 21:8, 553-560
CrossRef133
SUMA A. THOMAS, RICHARD B. SCHUESSLER, JEFFREY E. SAFFITZ. (1998) Connexins, Conduction, and Atrial Fibrillation. Journal of Cardiovascular Electrophysiology 9:6, 608-611
CrossRef134
Ludwig Thierfelder. (1998) Genetik der dilatativen Kardiomyopathie. Medizinische Klinik 93:4, 210-214
CrossRef135
Members of the Sicilian Gambit. (1998) The Search for Novel Antiarrhythmic Strategies. Japanese Circulation Journal 62:9, 633-648
CrossRef136
Klaus Kattenbeck, Hans-Joachim Trappe. (1998) Supraventrikuläre Tachykardien Teil I: Vorhofflimmern — Vorhofflattern: Diagnostik und Therapie. Medizinische Klinik 93:1, 47-48
CrossRef137
Sanjiv M Narayan, Michael E Cain, Joseph M Smith. (1997) Atrial fibrillation. The Lancet 350:9082, 943-950
CrossRef138
(1997) Familial Atrial Fibrillation. New England Journal of Medicine 337:5, 350-350
Full Text139
Allessie, Maurits A., . (1997) Is Atrial Fibrillation Sometimes a Genetic Disease?. New England Journal of Medicine 336:13, 950-952
Full Text
- Letters
