TY  - JOUR
AB  - BACKGROUND Mutations in SCN5A are rarely found in Thai patients with Brugada syndrome (BrS). Recent evidence suggested that common genetic variations may underlie BrS in a complex inheritance model.OBJECTIVE The purpose of this study was to find common and rare/low-frequency genetic variants predisposing to BrS in persons in Thailand.METHODS We conducted a genome-wide association study (GWAS) to explore the association of common variants in 154 Thai BrS cases and 432 controls. We sequenced SCN5A in 131 cases and 205 controls. Variants were classified according to current guidelines, and case-control association testing was performed for rare and low frequency variants.RESULTS Two loci were significantly associated with BrS. The first was near SCN5A/SCN10A (lead marker rs10428132; odds ratio [OR] 2.4; P = 3 x 10(-10)). Conditional analysis identified a novel independent signal in the same locus (rs6767797; OR 2.3; P = 2.7 x 10(-10)).The second locus was near HEY2 (lead marker rs3734634; OR 2.5; P = 7 x 10(-) (9)). Rare (minor allele frequency [MAF] <0.0001) coding variants in SCN5A were found in 8 of the 131 cases (6.1% in cases vs 2.0% in controls; P = .046; OR 3.3; 95% confident interval [CI] 1.0-11.1), but an enrichment of low-frequency (MAF 0.001 and 0.0001) variants also was observed in cases, with 1 variant (SCN5A: p.Arg965Cys) detected in 4.6% of Thai BrS patients vs 0.5% in controls (P = 0.015; OR 9.8; 95% CI 1.2-82.3).CONCLUSION The genetic basis of BrS in Thailand includes a wide spectrum of variant frequencies and effect sizes. As previously shown in European and Japanese populations, common variants near SCN5A and HEY2 are associated with BrS in the Thai population, confirming the transethnic transferability of these 2 major BrS loci.
AU  - Makarawate, P.*
AU  - Glinge, C.*
AU  - Khongphatthanayothin, A.*
AU  - Walsh, R.*
AU  - Mauleekoonphairoj, J.*
AU  - Amnueypol, M.*
AU  - Prechawat, S.*
AU  - Wongcharoen, W.*
AU  - Krittayaphong, R.*
AU  - Anannab, A.*
AU  - Lichtner, P.
AU  - Meitinger, T.
AU  - Tjong, F.V.Y.*
AU  - Lieve, K.V.V.*
AU  - Amin, A.S.*
AU  - Sahasatas, D.*
AU  - Ngarmukos, T.*
AU  - Wichadakul, D.*
AU  - Payungporn, S.*
AU  - Sutjaporn, B.*
AU  - Wandee, P.*
AU  - Poovorawan, Y.*
AU  - Tfelt-Hansen, J.*
AU  - Tanck, M.W.T.*
AU  - Tadros, R.*
AU  - Wilde, A.A.M.*
AU  - Bezzina, C.R.*
AU  - Veerakul, G.*
AU  - Nademanee, K.*
C1  - 60915
C2  - 49745
CY  - Ste 800, 230 Park Ave, New York, Ny 10169 Usa
SP  - 2145-2153
TI  - Common and rare susceptibility genetic variants predisposing to Brugada syndrome in Thailand.
JO  - Heart Rhythm
VL  - 17
IS  - 12
PB  - Elsevier Science Inc
PY  - 2020
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - BACKGROUND The efficacy of beta-blockers for treatment of patients with long QT syndrome type 3 (LQT3) has been repeatedly questioned, and it has been suggested that they might be detrimental for this genetic subgroup of patients with long QT syndrome (LQTS). The disquieting consequence has been that cardiologists confronted with LQT3 patients often do not even attempt pharmacologic therapy and implant cardioverter-defibrillators as first-choice treatment. However, the most recent clinical data indicate high efficacy of beta-Rocker therapy in LQT3 patients. OBJECTIVE The purpose of this study was to test the antiarrhythmic efficacy of beta-blockers in an established experimental model for LQT3. METHODS After phenotypic validation of 65 AKPQ-SCN5A knock-in transgenic (TG) mice compared to 32 wild-type (WT) mice, we tested the effect of the arrhythmogenic cholinergic muscarinic agonist carbachol in 19 WT and 39 TG anesthetized mice, with and without pretreatment with propranolol given intraperitoneally. RESULTS At the same heart rates, TG mice had a markedly longer QT interval than WT mice. Whereas carbachol had minor arrhythmic effects in the WT mice, it produced ventricular tachycardia (VT) and ventricular fibrillation (VF) in 55% of 20 TG mice. By contrast, in none of 19 TG mice pretreated with propranolol did VT/VF occur after carbachol injection. CONCLUSION These experimental data indicate that, contrary to previous reports, beta-blockade effectively prevents VT/VF in a validated LQT3 model. Together with the most recent clinical data, these findings indicate that there is no reason for not initiating protective therapy with beta-blockers in LQT3 patients.
AU  - Calvillo, L.*
AU  - Spazzolini, C.*
AU  - Vullo, E.*
AU  - Insolia, R.*
AU  - Crotti, L.
AU  - Schwartz, P.J.*
C1  - 29118
C2  - 33684
SP  - 126-132
TI  - Propranolol prevents life-threatening arrhythmias in LQT3 transgenic mice: Implications for the clinical management of LQT3 patients.
JO  - Heart Rhythm
VL  - 11
IS  - 1
PB  - Elsevier Science Inc
PY  - 2014
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - BACKGROUND There is limited information on genetic factors OBJECTIVE To assess the association of common variation in associated with sudden cardiac arrest (SCA). genes in fatty acid pathways with SCA risk. METHODS We selected 85 candidate genes and 1155 single nucleotide poLymorphisms (SNPs) tagging common variation in each gene. We investigated the SNP associations with SCA in a population-based case-control study. Cases (n = 2160) were from a repository of SCA in the greater Seattle area. Controls (n = 2615), frequency-matched on age and sex, were from the same area. We used Linear Logistic regression to examine SNP associations with SCA. We performed permutation-based p-min tests to account for multiple comparisons within each gene. The SNP associations with a corrected P value of <.05 were then examined in a meta-analysis of these SNP associations in 9 replication studies totaling 2129 SCA cases and 23,833 noncases. RESULTS Eight SN Ps in or near 8 genes were associated with SCA risk in the discovery study, one of which was nominally significant in the replication phase (rs7737692, minor allele frequency 36%, near the CPCAT1 gene). For each copy of the minor allele, rs7737692 was associated with 13% Lower SCA risk (95% confidence interval 21% to 5%) in the discovery phase and 9 /a lower SCA risk ( 9 5 % confidence interval 16% to 1%) in the replication phase. CONCLUSIONS While none of the associations reached significance with Bonferroni correction, a common genetic variant near LPCAT1, a gene involved in the remodeling of phospholipids, was nominally associated with incident SCA risk. Further study is needed to validate this observation
AU  - Lemaitre, R.N.*
AU  - Johnson, C.O.*
AU  - Hesselson, S.*
AU  - Sotoodehnia, N.*
AU  - McKnight, B.*
AU  - Sitlani, C.M.*
AU  - Rea, T.D.*
AU  - King, I.B.*
AU  - Kwok, P.*
AU  - Mak, A.*
AU  - Li, G.*
AU  - Brody, J.*
AU  - Larson, E.*
AU  - Mozaffarian, D.*
AU  - Psaty, B.M.*
AU  - Huertas-Vazquez, A.*
AU  - Tardif, J.-C.*
AU  - Albert, C.M.*
AU  - Lyytikaeinen, L.*
AU  - Arking, D.E.*
AU  - Kääb, S.*
AU  - Huikuri, H.V.*
AU  - Krijthe, B.P.*
AU  - Eijgelsheim, M.*
AU  - Wang, Y.A.*
AU  - Reinier, K.*
AU  - Lehtimaeki, T.*
AU  - Pulit, S.L.*
AU  - Brugada, R.*
AU  - Müller-Nurasyid, M.
AU  - Newton-Cheh, C.H.*
AU  - Karhunen, P.J.*
AU  - Stricker, B.H.*
AU  - Goyette, P.*
AU  - Rotter, J.I.*
AU  - Chugh, S.S.*
AU  - Chakravarti, A.*
AU  - Jouven, X.*
AU  - Siscovick, D.S.*
C1  - 30920
C2  - 34019
CY  - New York
SP  - 471-477
TI  - Common variation in fatty acid metabolic genes and risk of incident sudden cardiac arrest.
JO  - Heart Rhythm
VL  - 11
IS  - 3
PB  - Elsevier Science Inc
PY  - 2014
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - BACKGROUND: The debate on the diagnostic value of high intercostal spaces (ICSs) and of the number of diagnostic leads in the Brugada syndrome (BrS) has been settled by a recent expert consensus statement. OBJECTIVE: We have tested the validity of the new ECG diagnostic criteria using echocardiographic, molecular and clinical evidence in one clinical BrS study population. METHODS: We analyzed 114 BrS patients with a spontaneous or drug-induced type 1 pattern recorded in one or more right precordial leads in 4(th), 3(rd) and 2(nd) ICS. The right ventricular outflow tract (RVOT) was localized by echocardiography. All probands were screened on the SCN5A gene. RESULTS: The percentage of mutation carriers (MCs) and the event rate were similar regardless of the diagnostic ICS (4(th) vs high ICSs: MCs 23% vs 19%; event rate 22% vs 28%) and of the number of diagnostic leads (1 vs ≥ 2: MCs 20% vs 22%; event rate 22% vs 27%).The concordance between RVOT anatomical location and the diagnostic ICSs was 86%. The percentage of diagnostic ECG pattern recorded was significantly increased by the exploration of the ICSs showing RVOT at echocardiography (echo-guided vs conventional approach 100% vs 43% p<0.001). CONCLUSION: The high ICSs are not inferior to the standard 4(th) ICS for the ECG diagnosis of BrS and the interindividual variability depends on anatomical location of the RVOT as assessed by echocardiography. This approach significantly increases diagnostic sensitivity without decreasing specificity and fully supports the recently published new diagnostic criteria.
AU  - Savastano, S.*
AU  - Rordorf, R.*
AU  - Vicentini, A.*
AU  - Petracci, B.*
AU  - Taravelli, E.*
AU  - Castelletti, S.*
AU  - D'Errico, A.*
AU  - Torchio, M.*
AU  - Dossena, C.*
AU  - Novara, P.*
AU  - Dagradi, F.*
AU  - Landolina, M.*
AU  - Spazzolini, C.*
AU  - Crotti, L.
AU  - Schwartz, P.J.*
C1  - 31054
C2  - 34146
CY  - New York
SP  - 1176-1183
TI  - A comprehensive electrocardiographic, molecular and echocardiographic study of the Brugada Syndrome: Validation of the 2013 diagnostic criteria.
JO  - Heart Rhythm
VL  - 11
IS  - 7
PB  - Elsevier Science Inc
PY  - 2014
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - BACKGROUND Less than 30% of the cases of Brugada syndrome (BrS) have an identified genetic cause. Of the known BrS-susceptibility genes, loss-of-function mutations in SCN5A or CACNA1C and their auxiliary subunits are most common. On the basis of the recent demonstration that fibroblast growth factor(FGF) homologous factors(FHFs; FGF11-FGF14) regulate cardiac Na+ and Ca2+ channel currents, we hypothesized that FHFs are candidate BrS loci. OBJECTIVE The goal of this study was to test whether FGF12 is a candidate BrS locus. METHODS We used quantitative polymerase chain reaction to identify the major FHF expressed in the human ventricle and then queried a phenotype-positive, genotype-negative BrS biorepository for FHF mutations associated with BrS. We queried the effects of an identified mutant with biochemical analyses combined with electrophysiological assessment. We designed a novel rat ventricular cardiomyocyte system in which we swapped the endogenous FHF with the identified mutant and defined its effects on multiple ionic currents in their native milieu and on the cardiac action potential. RESULTS We identified FGF12 as the major FHF expressed in the human ventricle. In 102 individuals in the biorepository, we identified a single missense mutation in FGF12-B (Q7R-FGF12). The mutant reduced binding to the Na(V)1.5 C terminus, but not to junctophilin-2. In adult rat cardiac myocytes, Q7R-FGF12, but not wild-type FGF12, reduced Na+ channel current density and availability without affecting Ca2+ channel function. Furthermore, the mutant, but not wild-type FGF12, reduced action potential amplitude, which is consistent with amutant-induced loss of Na+ channel function. CONCLUSIONS These multilevel investigations strongly suggest that Q7R-FGF12 is a disease-associated BrS mutation. Moreover, these data suggest for the first time that FHF effects on Na+ and Ca2+ channels are separable. Most significantly, this study establishes a new method to analyze effects of human arrhythmogenic mutations on cardiac ionic currents.
AU  - Hennessey, J.A.*
AU  - Marcou, C.A.*
AU  - Wang, C.*
AU  - Wei, E.Q.*
AU  - Wang, C.J.*
AU  - Tester, D.J.*
AU  - Torchio, M.*
AU  - Dagradi, F.*
AU  - Crotti, L.
AU  - Schwartz, P.J.*
AU  - Ackerman, M.J.*
AU  - Pitt, G.S.*
C1  - 28837
C2  - 30325
SP  - 1886-1894
TI  - FGF12 is a candidate Brugada syndrome locus.
JO  - Heart Rhythm
VL  - 10
IS  - 12
PB  - Elsevier Science
PY  - 2013
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - no abstract
AU  - Crotti, L.
C1  - 7668
C2  - 30140
SP  - 1097-1098
TI  - Gene expression and arrhythmic risk.
JO  - Heart Rhythm
VL  - 9
IS  - 7
PB  - Elsevier Science Inc.
PY  - 2012
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - Although QT prolongation following myocardial infarction (MI) is generally moderate, cases with marked QT prolongation leading to life-threatening torsades de pointes (TdP) have been described. OBJECTIVE: To investigate the genetic substrate of this phenomenon. METHODS: We studied 13 patients who developed TdP in the subacute phase of MI (2-11 days) and a group of 133 ethnically matched controls with uncomplicated MI. Long QT syndrome genes and the KCNH2-K897T polymorphism were screened by using denaturing high-performance liquid chromatography plus direct sequencing and a specific TaqMan assay, respectively. RESULTS: Two of the 13 patients (15%) who presented with QT prolongation and TdP were found to carry long QT syndrome mutations (KCNH2-R744X and SCN5A-E446K). Nine of the remaining 11 patients (82%) carried the KCNH2-K897T polymorphism, which was present in 35% of the controls (P = .0035). Thus, patients with an acute MI carrying the KCNH2-K897T polymorphism had an 8-fold greater risk of experiencing TdP compared with controls (95% confidence interval = 2-40). CONCLUSIONS: Our data suggest that the common K897T polymorphism is associated with an increased risk of TdP developing in the subacute phase of MI. Our findings support the concept that the electrical remodeling associated with this healing phase of MI may unmask a genetic substrate predisposing to a time-limited development of life-threatening arrhythmias. They also provide the first line of evidence in support of the hypothesis that a common polymorphism, previously described as a modifier of the severity of LQTS, may increase the risk of life-threatening arrhythmias in a much more prevalent cardiac disease such as myocardial infarction.
AU  - Crotti, L.
AU  - Hu, D.*
AU  - Barajas-Martínez, H.*
AU  - de Ferrari, G.M.*
AU  - Oliva, A.*
AU  - Insolia, R.*
AU  - Pollevick, G.D.*
AU  - Dagradi, F.*
AU  - Guerchicoff, A.*
AU  - Greco, F.*
AU  - Schwartz, P.J.*
AU  - Viskin, S.
AU  - Antzelevitch, C.*
C1  - 7669
C2  - 30141
SP  - 1104-1112
TI  - Torsades de pointes following acute myocardial infarction: Evidence for a deadly link with a common genetic variant.
JO  - Heart Rhythm
VL  - 9
IS  - 7
PB  - Elsevier Science Inc.
PY  - 2012
SN  - 1547-5271
ER  - 

TY  - JOUR
AU  - Crotti, L.
AU  - Schwartz, P.J.*
C1  - 11503
C2  - 30726
SP  - 1983-1985
TI  - When genetic screening for your patient with long QT syndrome comes back negative, don't always take a no for a no.
JO  - Heart Rhythm
VL  - 9
IS  - 12
PB  - Elsevier
PY  - 2012
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - BACKGROUND: Cardiac sodium channel β-subunit mutations have been associated with several inherited cardiac arrhythmia syndromes. OBJECTIVE: To identify and characterize variations in SCN1Bb associated with Brugada syndrome (BrS) and sudden infant death syndrome (SIDS). METHODS: All known exons and intron borders of the BrS-susceptibility genes were amplified and sequenced in both directions. Wild type (WT) and mutant genes were expressed in TSA201 cells and studied using co-immunoprecipitation and whole-cell patch-clamp techniques. RESULTS: Patient 1 was a 44-year-old man with an ajmaline-induced type 1 ST-segment elevation in V1 and V2 supporting the diagnosis of BrS. Patient 2 was a 62-year-old woman displaying a coved-type BrS electrocardiogram who developed cardiac arrest during fever. Patient 3 was a 4-month-old female SIDS case. A R214Q variant was detected in exon 3A of SCN1Bb (Na(v)1B) in all three probands, but not in any other gene previously associated with BrS or SIDS. R214Q was identified in 4 of 807 ethnically-matched healthy controls (0.50%). Co-expression of SCN5A/WT + SCN1Bb/R214Q resulted in peak sodium channel current (I(Na)) 56.5% smaller compared to SCN5A/WT + SCN1Bb/WT (n = 11-12, P<0.05). Co-expression of KCND3/WT + SCN1Bb/R214Q induced a Kv4.3 current (transient outward potassium current, I(to)) 70.6% greater compared with KCND3/WT + SCN1Bb/WT (n = 10-11, P<0.01). Co-immunoprecipitation indicated structural association between Na(v)β1B and Na(v)1.5 and K(v)4.3. CONCLUSION: Our results suggest that R214Q variation in SCN1Bb is a functional polymorphism that may serve as a modifier of the substrate responsible for BrS or SIDS phenotypes via a combined loss of function of sodium channel current and gain of function of transient outward potassium current.
AU  - Hu, D.*
AU  - Barajas-Martínez, H.*
AU  - Medeiros-Domingo, A.*
AU  - Crotti, L.
AU  - Veltmann, C.*
AU  - Schimpf, R.*
AU  - Urrutia, J.*
AU  - Alday, A.*
AU  - Casis, O.*
AU  - Pfeiffer, R.*
AU  - Burashnikov, E.*
AU  - Caceres, G.*
AU  - Tester, D.J.*
AU  - Wolpert, C.*
AU  - Borggrefe, M.*
AU  - Schwartz, P.
AU  - Ackerman, M.J.*
AU  - Antzelevitch, C.*
C1  - 7507
C2  - 29766
SP  - 760-769
TI  - A novel rare variant in SCN1Bb linked to Brugada syndrome and SIDS by combined modulation of Nav1.5 and Kv4.3 channel currents.
JO  - Heart Rhythm
VL  - 9
IS  - 5
PB  - Elsevier
PY  - 2012
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - BACKGROUND The early repolarization pattern (ERP) is common and associated with risk of sudden cardiac death. ERP is heritable, and mutations have been described in syndromatic cases. OBJECTIVE To conduct a meta-analysis of genome-wide association studies to identify common genetic variants influencing ERP. METHODS We ascertained ERP on the basis of electrocardiograms in 3 large community-based cohorts from Europe and the United States: the Framingham Heart Study, the Health 2000 Study, and the KORA F4 Study. We analyzed genome-wide association studies in participants with and without ERP by logistic regression assuming an additive genetic model and meta-analyzed individual cohort results. We then sought to strengthen support for findings that reached P <= 1 x 10(-5) in independent individuals by direct genotyping or in-silico analysis of genome-wide data. We meta-analyzed the results from both stages. RESULTS Of 7482 individuals in the discovery stage, 452 showed ERP (ERP positive: mean age 46.9 +/- 8.9 years, 30.3% women; ERP negative: 47.5 +/- 9.4 years, 54.2% women). After meta-analysis, 8 single nucleotide polymorphisms reached P <= 1 x 10(-5): The most significant finding was intergenic rs11653989 (odds ratio 0.47; 95% confidence interval 0.36-0.61; P = 6.9 x 10(-9)). The most biologically relevant finding was intronic to KCND3: rs17029069 (odds ratio 1.46; 95% confidence interval 1.25-1.69; P = 8.5 x 10(-7)). In the replication step (7151 individuals), none of the 8 variants replicated, and combined meta-analysis results failed to reach genome-wide significance. CONCLUSIONS In a genome-wide association study, we were not able to reliably identify genetic variants predisposing to ERP, presumably due to insufficient statistical power and phenotype heterogeneity. The reported heritability of ERP warrants continued investigation in larger well-phenotyped populations.
AU  - Sinner, M.F.*
AU  - Porthan, K.*
AU  - Noseworthy, P.A.*
AU  - Havulinna, A.S.*
AU  - Tikkanen, J.T.*
AU  - Müller-Nurasyid, M.
AU  - Peloso, G.*
AU  - Ulivi, S.*
AU  - Beckmann, B.M.*
AU  - Brockhaus, A.C.
AU  - Cooper, R.R.*
AU  - Gasparini, P.*
AU  - Hengstenberg, C.*
AU  - Hwang, S.-J.*
AU  - Iorio, A.*
AU  - Junttila, M.J.*
AU  - Klopp, N.
AU  - Kähönen, M.*
AU  - Laaksonen, M.A.*
AU  - Lehtimäki, T.*
AU  - Lichtner, P.
AU  - Lyytikäinen, L.-P.*
AU  - Martens, E.*
AU  - Meisinger, C.
AU  - Meitinger, T.
AU  - Merchant, F.M.*
AU  - Nieminen, M.S.*
AU  - Peters, A.
AU  - Pietila, A.*
AU  - Perz, S.
AU  - Oikarinen, L.*
AU  - Raitakari, O.*
AU  - Reinhard, W.*
AU  - Silander, K.*
AU  - Thorand, B.
AU  - Wichmann, H.-E.
AU  - Sinagra, G.*
AU  - Viikari, J.*
AU  - O'Donnell, C.J.*
AU  - Ellinor, P.T.*
AU  - Huikuri, H.V.*
AU  - Kääb, S.*
AU  - Newton-Cheh, C.*
AU  - Salomaa, V.*
C1  - 10621
C2  - 30406
SP  - 1627-1634
TI  - A meta-analysis of genome-wide association studies of the electrocardiographic early repolarization pattern.
JO  - Heart Rhythm
VL  - 9
IS  - 10
PB  - Elsevier
PY  - 2012
SN  - 1547-5271
ER  - 

TY  - JOUR
AB  - Atrial fibrillation (AF) is the most common sustained arrhythmia and has a substantial heritable component. Numerous associations between single nucleotide polymorphisms (SNPs) and AF have been described, but few have been replicated. We sought to systematically replicate SNPs that are reported to be associated with AF in two large study samples of European descent. METHODS: We searched PubMed for studies reporting associations between SNPs and AF published before July 1, 2007. SNPs were genotyped in two independent case-control samples from Germany and the United States. Associations between SNPs and AF were assessed using logistic regression models adjusting for age, sex, and hypertension. A meta-analysis of the results from the two studies was performed. RESULTS: We identified 21 SNPs and the angiotensin-converting enzyme insertion/deletion polymorphism that were reported to be associated with AF in the literature. Nine of these genetic variants were not represented on common genome-wide SNP arrays. We successfully genotyped 21 of these 22 variants in 2,145 cases with AF from the German Competence Network for Atrial Fibrillation and 4,073 controls from the KORA S4 study and 16 variants in 790 cases and 1,330 controls from the Massachusetts General Hospital. None of the SNPs replicated in independent populations with AF. CONCLUSION: Our results suggest that previously reported associations to AF were likely false positives and highlight the need for systematic replication of genetic associations in large, independent cohorts to accurately detect variants associated with disease.
AU  - Sinner, M.F.*
AU  - Lubitz, SA.*
AU  - Pfeufer, A.
AU  - Makino, S.*
AU  - Beckmann, B.M.*
AU  - Lunetta, K.L.*
AU  - Steinbeck, G.*
AU  - Perz, S.
AU  - Rahman, R.*
AU  - Sonni, A.*
AU  - Greenberg, S.M.*
AU  - Furie, K.L.*
AU  - Wichmann, H.-E.
AU  - Meitinger, T.
AU  - Peters, A.
AU  - Benjamin, E.J.*
AU  - Rosand, J.*
AU  - Ellinor, P.T.*
AU  - Kääb, S.*
C1  - 3673
C2  - 27854
SP  - 403-409
TI  - Lack of replication in polymorphisms reported to be associated with atrial fibrillation.
JO  - Heart Rhythm
VL  - 8
IS  - 3
PB  - Elsevier Science Inc.
PY  - 2011
SN  - 1547-5271
ER  - 

TY  - JOUR
AU  - Hinterseer, M.*
AU  - Beckmann, B.-M.*
AU  - Thomsen, B.*
AU  - Pfeufer, A.*
AU  - Perz, S.
AU  - Wichmann, H.-E.
AU  - Steinbeck, G.*
AU  - Vos, M.A.*
AU  - Kääb, S.*
C1  - 4518
C2  - 25025
SP  - S269-S270
TI  - Beat-to-beat variability of QT intervals is increased in drug-induced and congenital long-QT syndromes.
JO  - Heart Rhythm
VL  - 3
IS  - 5
PB  - Elsevier
PY  - 2006
SN  - 1547-5271
ER  -