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Morten S. Olesen - One of the best experts on this subject based on the ideXlab platform.
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Rare Variants in GJA5 Are Associated With Early-Onset Lone Atrial Fibrillation
The Canadian journal of cardiology, 2012Co-Authors: Ingrid E. Christophersen, Stig Haunso, Jesper Hastrup Svendsen, Javad Jabbari, Haya N. Holmegard, Arnljot Tveit, Morten S. OlesenAbstract:Abstract Background Genetic factors are believed to be important in early-onset Lone Atrial Fibrillation (AF). The gene GJA5 encodes the gap-junction protein Cx40, which together with Cx43 is responsible for the electrical coupling of the Atrial cardiomyocytes. The regulatory single nucleotide polymorphism rs10465885 in GJA5 was recently associated with early-onset Lone AF ( Methods The coding region and flanking intron sequences of GJA5 were resequenced in 342 patients with onset of Lone AF before the age of 50 (mean age at onset 34 ± 9 years), and in 216 controls. The single nucleotide polymorphism rs10465885 was genotyped in 342 patients and 534 control subjects and odds ratios were calculated for different genetic models. Results Genotyping of rs10465885 showed that the patients with early-onset Lone AF were more likely to carry the A allele compared with controls (odds ratio=1.30; P = 0.011). When resequencing GJA5 , we identified the mutation A96S, previously associated with Lone AF, which was not present in our control subjects or in any publicly available database or the National Heart, Lung, and Blood Institute Exome Variant Server (NHLBI EVS; 10,758 alleles). Conclusions We show a highly significant association between the A allele of rs10465885 and onset of Lone AF before age 50. This opposes a previous study, wherein the G allele was found to be associated with AF, and makes it impossible to exclude that the associations are coincidental.
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familial aggregation of Lone Atrial Fibrillation in young persons
Journal of the American College of Cardiology, 2012Co-Authors: Nina Oyen, Morten S. Olesen, Mattis F Ranthe, Lisbeth Carstensen, Heather A Boyd, Sorenpeter Olesen, Jan Wohlfahrt, Mads MelbyeAbstract:Objectives This study investigated whether an individual's risk of developing Lone Atrial Fibrillation (AF) before age 60 years is associated with Lone AF in relatives. Background Genetic factors may play a role in the development of Lone AF. Methods Using Danish national registers, a cohort was established of ∼4 million persons born between 1950 and 2008, and those with a family history of Lone AF (AF without preceding cardiovascular/endocrine diagnoses) were identified. Individuals were followed up until the first diagnosis of Lone AF. Poisson regression was used to estimate incidence rate ratios (IRRs). Results In ∼92 million person-years of follow-up, 9,507 persons were identified as having Lone AF. The IRRs for Lone AF given an affected first- or second-degree relative were 3.48 (95% confidence interval [CI]: 3.08 to 3.93) and 1.64 (95% CI: 1.04 to 2.59), respectively. IRRs were higher for men than for women but were not associated with the affected relative's sex. IRR for Lone AF was 6.24 (95% CI: 2.59 to 15.0), given at least 2 first-degree relatives affected with Lone AF. The IRR for Lone AF in persons aged Conclusions A family history of Lone AF is associated with substantial risk of Lone AF, with the strongest risks associated with young age at onset, multiple affected relatives, and in first-degree relatives. These results suggest routine evaluation of the families of at least certain types of patients with Lone AF.
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scn1bb r214q found in 3 patients 1 with brugada syndrome and 2 with Lone Atrial Fibrillation
Heart Rhythm, 2012Co-Authors: Stig Haunso, Jesper Hastrup Svendsen, Morten S. Olesen, Anders G. Holst, Jacob TfelthansenAbstract:Background SCN1Bb encodes the β-subunit of the sodium channel. A mutation in SCN1Bb R214Q has recently been shown both to increase the Kv4.3 current and to decrease the sodium current. The variant was suggested to increase the susceptibility to Brugada syndrome (BrS). Objective To sequence a population of BrS and early-onset Lone Atrial Fibrillation (AF) patients for the R214Q mutation in the SCN1Bb gene. Methods The coding sequence and splice junctions of SCN1Bb were bidirectionally sequenced by using Big Dye chemistry in 192 early-onset Lone AF patients and 22 BrS patients. Results Three probands carrying the R214Q variant were identified. No mutations were identified in genes previously associated with BrS or AF in these patients. Case 1 also had the onset of persistent Lone AF at the age of 39 years. Case 2 was a Lone AF case with onset at the age of 39 years and paroxysmal Lone AF. Case 3 was a BrS patient with a type 1 electrocardiogram and onset of disease at the age of 54 years. Both Lone AF patients had electrocardiograms that raised the suspicion of BrS, but intravenous flecainide testing was, in both cases, negative. R214Q was not present in the control group (n = 216) and has not previously been reported in conjunction to AF. Conclusion Three patients of 192 young Lone AF and 22 BrS patients carried the nonsynonymous R214Q mutations in SCN1Bb , thereby indicating that this variant increases the susceptibility to both BrS and AF.
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screening of kcnn3 in patients with early onset Lone Atrial Fibrillation
Europace, 2011Co-Authors: Javad Jabbari, Morten S. Olesen, Anders G. Holst, Jonas B. Nielsen, Daniel A Steinbruchel, Thomas JespersenAbstract:Aims The aim of this study was to screen KCNN3 encoding the small-conductance calcium-activated K+ channel (SK3) in Lone Atrial Fibrillation patients. Atrial Fibrillation (AF) is the most common cardiac arrhythmia. A genome-wide association study has recently associated an intronic single-nucleotide polymorphism (SNP) in KCNN3 with Lone AF. Methods and results We sequenced the coding region and splice junctions of KCNN3 in 209 early-onset Lone AF patients, screening for variations. A group of 208 healthy blood donors with normal ECGs and without cardiac symptoms were used as controls. All patients and controls were of Danish ethnicity. No mutations were found in the coding regions or splice sites of KCNN3 . We found one known exonic synonymous SNP (rs1131820) in KCNN3 that was associated with AF. Both the genotype distribution and allele frequencies of SNP rs1131820 were significantly different between the AF cases and controls ( P Genotype= 0.047 and P Allele= 0.027). Being a homozygous carrier of the major allele (GG) vs. the minor allele (AA) of rs1131820 was associated with an odds ratio of 2.85 (95% CI 1.13–7.18, P = 0.026) for Lone AF. Conclusions In this study of 209 young Lone AF patients, we found no mutations in the exons or splice sites of KCNN3 , but we found an association between the synonymous SNP rs1131820 in KCNN3 and Lone AF.
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Common polymorphisms in KCNJ5 [corrected] are associated with early-onset Lone Atrial Fibrillation in Caucasians.
The Cardiology, 2011Co-Authors: Javad Jabbari, Stig Haunso, Morten S. Olesen, Anders G. Holst, Jonas B. Nielsen, Jesper Hastrup SvendsenAbstract:Objectives: The aim of this study was to screen Lone Atrial Fibrillation (AF) patients for mutations in the genes KCNJ2 , KCNJ3 and KCN
Patrick T Ellinor - One of the best experts on this subject based on the ideXlab platform.
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does Atrial Fibrillation follow function ion channel mutations and Lone Atrial Fibrillation
Circulation-arrhythmia and Electrophysiology, 2015Co-Authors: Sebastian Clauss, Patrick T EllinorAbstract:In this issue of Circulation: Arrhythmia and Electrophysiology , Hayashi et al1 present an interesting study evaluating the role of rare genetic variants in cardiac ion channels in the development of Lone Atrial Fibrillation (AF). Article see p 1095 In recent years, compelling data has demonstrated that AF is heritable. Several studies have shown that mutations and rare variants, especially those located in genes encoding cardiac ion channels, are associated with AF. Additionally, genome-wide association studies have identified many common genetic variants that are associated with an increased risk for AF. Although most patients with AF present with comorbidities, such as hypertension, coronary artery disease, or heart failure, many younger patients have isolated or Lone AF.2 Given that these younger patients do not have an obvious cause for their arrhythmia, it has been assumed that genetics may play a significant role in the pathogenesis of Lone AF. Thus, many investigators have focused on individuals with Lone AF to obtain a unique window into the genetic basis of the arrhythmia. Over the last 10 years, many studies have considered individual candidate genes for AF and identified mutations in a wide range of genes encoding ion channels, signaling molecules, and transcription factors among others.3 These studies …
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Lone Atrial Fibrillation does it exist
Journal of the American College of Cardiology, 2014Co-Authors: George D Wyse, Patrick T Ellinor, Isabelle C Van Gelder, Jonathan M Kalman, Sanjiv M Narayan, Stanley Nattel, Ulrich Schotten, Michiel RienstraAbstract:The historical origin of the term "Lone Atrial Fibrillation" (AF) predates by 60 years our current understanding of the pathophysiology of AF, the multitude of known etiologies for AF, and our ability to image and diagnose heart disease. The term was meant to indicate AF in patients for whom subsequent investigations could not demonstrate heart disease, but for many practitioners has become synonymous with "idiopathic AF." As the list of heart diseases has expanded and diagnostic techniques have improved, the prevalence of Lone AF has fallen. The legacy of the intervening years is that definitions of Lone AF in the literature are inconsistent so that studies of Lone AF are not comparable. Guidelines provide a vague definition of Lone AF but do not provide direction about how much or what kind of imaging and other testing are necessary to exclude heart disease. There has been an explosion in the understanding of the pathophysiology of AF in the last 20 years in particular. Nevertheless, there are no apparently unique mechanisms for AF in patients categorized as having Lone AF. In addition, the term "Lone AF" is not invariably useful in making treatment decisions, and other tools for doing so have been more thoroughly and carefully validated. It is, therefore, recommended that use of the term "Lone AF" be avoided.
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common variants in kcnn3 are associated with Lone Atrial Fibrillation
Nature Genetics, 2010Co-Authors: Patrick T Ellinor, Mina K Chung, Kathryn L Lunetta, Nicole L Glazer, Arne Pfeufer, Alvaro Alonso, Moritz F Sinner, Paul I W De BakkerAbstract:Atrial Fibrillation (AF) is the most common sustained arrhythmia. Previous studies have identified several genetic loci associated with typical AF. We sought to identify common genetic variants underlying Lone AF. This condition affects a subset of individuals without overt heart disease and with an increased heritability of AF. We report a meta-analysis of genome-wide association studies conducted using 1,335 individuals with Lone AF (cases) and 12,844 unaffected individuals (referents). Cases were obtained from the German AF Network, Heart and Vascular Health Study, the Atherosclerosis Risk in Communities Study, the Cleveland Clinic and Massachusetts General Hospital. We identified an association on chromosome 1q21 to Lone AF (rs13376333, adjusted odds ratio = 1.56; P = 6.3 x 10(-12)), and we replicated this association in two independent cohorts with Lone AF (overall combined odds ratio = 1.52, 95% CI 1.40-1.64; P = 1.83 x 10(-21)). rs13376333 is intronic to KCNN3, which encodes a potassium channel protein involved in Atrial repolarization.
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ace i d polymorphism associated with abnormal Atrial and atrioventricular conduction in Lone Atrial Fibrillation and structural heart disease implications for electrical remodeling
Heart Rhythm, 2009Co-Authors: Calum A Macrae, Patrick T Ellinor, Hiroshi Watanabe, Daniel W Kaiser, Seiko Makino, Brian S Wasserman, Prince J Kannankeril, Brian S Donahue, Dan M RodenAbstract:Background The angiotensin-converting enzyme (ACE) gene contains a common polymorphism based on the insertion (I) or deletion (D) of a 287-bp intronic DNA fragment. The D allele is associated with higher ACE activity and thus higher angiotensin II levels. Angiotensin II stimulates cardiac fibrosis and conduction heterogeneity. Objective The purpose of this study was to determine whether the ACE I/D polymorphism modulates cardiac electrophysiology. Methods Three different cohorts of patients were studied: 69 patients with paroxysmal Lone Atrial Fibrillation (AF), 151 patients with structural heart disease and no history of AF, and 161 healthy subjects without cardiovascular disease or AF. Patients taking drugs that affect cardiac conduction were excluded from the study. ECG parameters during sinus rhythm were compared among the ACE I/D genotypes. Results The ACE I/D polymorphism was associated with the PR interval and heart block in the Lone AF cohort. In multivariable linear regression models, the D allele was associated with longer PR interval in the Lone AF and heart disease cohorts (12.0-ms and 7.1-ms increase per D allele, respectively). P-wave duration showed a similar trend, with increase in PR interval across ACE I/D genotypes in the Lone AF and heart disease cohorts. Conclusion The ACE D allele is associated with electrical remodeling in patients with Lone AF and in those with heart disease, but not in control subjects. ACE activity may play a role in cardiac remodeling after the development of AF and heart disease.
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mutation in the s3 segment of kcnq1 results in familial Lone Atrial Fibrillation
Heart Rhythm, 2009Co-Authors: Seiko Makino, Marisa A Shea, Calum A Macrae, Yonathan F Melman, Sanjeev B Goyal, Anthony Rosenzweig, Patrick T EllinorAbstract:Background Mutations in several ion channel genes have been reported to cause rare cases of familial Atrial Fibrillation (AF). Objective The purpose of this study was to determine the genetic basis for AF in a family with autosomal dominant AF. Methods Family members were evaluated by 12-lead ECG, echocardiogram, signal-averaged P-wave analysis, and laboratory studies. Fourteen family members in AF-324 were studied. Six individuals had AF, with a mean age at onset of 32 years (range 16–59 years). Results Compared with unaffected family members, those with AF had a longer mean QRS duration (100 vs 86 ms, P = .015) but no difference in the corrected QT interval (423 ± 15 ms vs 421 ± 21 ms). The known loci for AF and other cardiovascular diseases were evaluated. Evidence of linkage was obtained with marker D11S4088 located within KCNQ1, and a highly conserved serine in the third transmembrane region was found to be mutated to a proline (S209P). Compared to the wild-type channel, the S209P mutant activates more rapidly, deactivates more slowly, and has a hyperpolarizing shift in the voltage activation curve. A fraction of the mutant channels are constitutively open at all voltages, resulting in a net increase in I Ks current. Conclusion We identified a family with Lone AF due to a mutation in the highly conserved S3 domain of KCNQ1, a region of the channel not previously implicated in the pathogenesis of AF.
Calum A Macrae - One of the best experts on this subject based on the ideXlab platform.
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ace i d polymorphism associated with abnormal Atrial and atrioventricular conduction in Lone Atrial Fibrillation and structural heart disease implications for electrical remodeling
Heart Rhythm, 2009Co-Authors: Calum A Macrae, Patrick T Ellinor, Hiroshi Watanabe, Daniel W Kaiser, Seiko Makino, Brian S Wasserman, Prince J Kannankeril, Brian S Donahue, Dan M RodenAbstract:Background The angiotensin-converting enzyme (ACE) gene contains a common polymorphism based on the insertion (I) or deletion (D) of a 287-bp intronic DNA fragment. The D allele is associated with higher ACE activity and thus higher angiotensin II levels. Angiotensin II stimulates cardiac fibrosis and conduction heterogeneity. Objective The purpose of this study was to determine whether the ACE I/D polymorphism modulates cardiac electrophysiology. Methods Three different cohorts of patients were studied: 69 patients with paroxysmal Lone Atrial Fibrillation (AF), 151 patients with structural heart disease and no history of AF, and 161 healthy subjects without cardiovascular disease or AF. Patients taking drugs that affect cardiac conduction were excluded from the study. ECG parameters during sinus rhythm were compared among the ACE I/D genotypes. Results The ACE I/D polymorphism was associated with the PR interval and heart block in the Lone AF cohort. In multivariable linear regression models, the D allele was associated with longer PR interval in the Lone AF and heart disease cohorts (12.0-ms and 7.1-ms increase per D allele, respectively). P-wave duration showed a similar trend, with increase in PR interval across ACE I/D genotypes in the Lone AF and heart disease cohorts. Conclusion The ACE D allele is associated with electrical remodeling in patients with Lone AF and in those with heart disease, but not in control subjects. ACE activity may play a role in cardiac remodeling after the development of AF and heart disease.
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mutation in the s3 segment of kcnq1 results in familial Lone Atrial Fibrillation
Heart Rhythm, 2009Co-Authors: Seiko Makino, Marisa A Shea, Calum A Macrae, Yonathan F Melman, Sanjeev B Goyal, Anthony Rosenzweig, Patrick T EllinorAbstract:Background Mutations in several ion channel genes have been reported to cause rare cases of familial Atrial Fibrillation (AF). Objective The purpose of this study was to determine the genetic basis for AF in a family with autosomal dominant AF. Methods Family members were evaluated by 12-lead ECG, echocardiogram, signal-averaged P-wave analysis, and laboratory studies. Fourteen family members in AF-324 were studied. Six individuals had AF, with a mean age at onset of 32 years (range 16–59 years). Results Compared with unaffected family members, those with AF had a longer mean QRS duration (100 vs 86 ms, P = .015) but no difference in the corrected QT interval (423 ± 15 ms vs 421 ± 21 ms). The known loci for AF and other cardiovascular diseases were evaluated. Evidence of linkage was obtained with marker D11S4088 located within KCNQ1, and a highly conserved serine in the third transmembrane region was found to be mutated to a proline (S209P). Compared to the wild-type channel, the S209P mutant activates more rapidly, deactivates more slowly, and has a hyperpolarizing shift in the voltage activation curve. A fraction of the mutant channels are constitutively open at all voltages, resulting in a net increase in I Ks current. Conclusion We identified a family with Lone AF due to a mutation in the highly conserved S3 domain of KCNQ1, a region of the channel not previously implicated in the pathogenesis of AF.
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c reactive protein in Lone Atrial Fibrillation
American Journal of Cardiology, 2006Co-Authors: Patrick T Ellinor, Kristen K Patton, Marisa A Shea, Adrian F Low, Calum A MacraeAbstract:An inflammatory cause of Atrial Fibrillation (AF) has been proposed on the basis of the presence of lymphocytic infiltrates in the biopsy results of patients with Lone AF, alterations of C-reactive protein (CRP) and interleukin-6 levels in subjects with AF, and the time course of postoperative AF. Many previous studies exploring inflammatory factors in AF have been confounded by concomitant medical illnesses. Subjects with Lone AF provide a unique opportunity to eliminate the effects of associated conditions. We therefore sought to determine CRP levels in homogenous cohorts of patients with Lone AF or AF and hypertension. One hundred twenty-one subjects with Lone AF, 52 subjects with AF and hypertension, and 75 control subjects were enrolled and studied. Plasma CRP levels were determined using a commercially available immunoassay. There was no significant difference in CRP levels between subjects with Lone AF and controls (1.34 vs 1.21 mg/L, p = 0.18). CRP levels in subjects with AF and hypertension were elevated compared with those of controls and those of subjects with Lone AF, although this difference was attributable to increased body mass indexes. CRP levels were not elevated in subjects with Lone AF compared with controls. In conclusion, these findings clarify previous observations of elevations in CRP levels in subjects with AF and suggest that this marker of systemic inflammation is associated not with the arrhythmia per se, but rather with underlying cardiovascular disease.
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reduced apelin levels in Lone Atrial Fibrillation
European Heart Journal, 2006Co-Authors: Patrick T Ellinor, Adrian F Low, Calum A MacraeAbstract:Aims Apelin is an endogenous peptide hormone that appears to have a physiological role in counter-regulation of the angiotensin and vasopressin systems. This peptide has been reported to be down-regulated in subjects with acute heart failure, but has not been studied in other cardiovascular conditions. We studied apelin levels in 73 subjects with Lone Atrial Fibrillation (AF). Methods and results Study subjects had electrocardiographic evidence of paroxysmal or chronic AF and a structurally normal heart on echocardiography. Subjects were excluded if they had a history of coronary artery disease, rheumatic heart disease, cardiomyopathy, significant valvular disease, hyperthyroidism, or antecedent hypertension. Controls were recruited from a healthy outpatient population. Plasma apelin levels were determined using a commercially available immunoassay. Seventy-three subjects with Lone AF and 73 healthy controls were enrolled and studied. Mean levels of apelin were significantly lower in subjects with Lone AF when compared with controls (307 vs. 648 pg/mL, P <0.00005). Conclusion Reduced apelin levels were observed in this homogenous population of Lone AF subjects and may represent an underlying diathesis predisposing to this common arrhythmia.
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Familial aggregation in Lone Atrial Fibrillation
Human Genetics, 2005Co-Authors: Patrick T Ellinor, Jeremy N Ruskin, Danita M. Yoerger, Calum A MacraeAbstract:Atrial Fibrillation (AF) is the most common clinical arrhythmia and a major risk factor for stroke. To investigate the role of genetic factors in a typical clinical population, we determined the extent of familial aggregation in patients with Lone AF. To estimate the relative risk to family members, the prevalence of AF for each class of relative was compared to the prevalence in the comparable age and sex group from the general population. Family members had an increased relative risk of AF compared to the general population (risk ratio; 95% confidence intervals): sons (8.1; 2.0–32), daughters (9.5; 1.3–67), brothers (70; 47–102), sisters (34; 14–80), mothers (4.0; 2.5–6.5) and fathers (2.0; 1.2–3.6). Relatives of probands with Lone AF are at a substantially increased risk of developing this arrhythmia suggesting a Mendelian genetic contribution to the etiology of this common trait.
Stig Haunso - One of the best experts on this subject based on the ideXlab platform.
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Rare Variants in GJA5 Are Associated With Early-Onset Lone Atrial Fibrillation
The Canadian journal of cardiology, 2012Co-Authors: Ingrid E. Christophersen, Stig Haunso, Jesper Hastrup Svendsen, Javad Jabbari, Haya N. Holmegard, Arnljot Tveit, Morten S. OlesenAbstract:Abstract Background Genetic factors are believed to be important in early-onset Lone Atrial Fibrillation (AF). The gene GJA5 encodes the gap-junction protein Cx40, which together with Cx43 is responsible for the electrical coupling of the Atrial cardiomyocytes. The regulatory single nucleotide polymorphism rs10465885 in GJA5 was recently associated with early-onset Lone AF ( Methods The coding region and flanking intron sequences of GJA5 were resequenced in 342 patients with onset of Lone AF before the age of 50 (mean age at onset 34 ± 9 years), and in 216 controls. The single nucleotide polymorphism rs10465885 was genotyped in 342 patients and 534 control subjects and odds ratios were calculated for different genetic models. Results Genotyping of rs10465885 showed that the patients with early-onset Lone AF were more likely to carry the A allele compared with controls (odds ratio=1.30; P = 0.011). When resequencing GJA5 , we identified the mutation A96S, previously associated with Lone AF, which was not present in our control subjects or in any publicly available database or the National Heart, Lung, and Blood Institute Exome Variant Server (NHLBI EVS; 10,758 alleles). Conclusions We show a highly significant association between the A allele of rs10465885 and onset of Lone AF before age 50. This opposes a previous study, wherein the G allele was found to be associated with AF, and makes it impossible to exclude that the associations are coincidental.
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scn1bb r214q found in 3 patients 1 with brugada syndrome and 2 with Lone Atrial Fibrillation
Heart Rhythm, 2012Co-Authors: Stig Haunso, Jesper Hastrup Svendsen, Morten S. Olesen, Anders G. Holst, Jacob TfelthansenAbstract:Background SCN1Bb encodes the β-subunit of the sodium channel. A mutation in SCN1Bb R214Q has recently been shown both to increase the Kv4.3 current and to decrease the sodium current. The variant was suggested to increase the susceptibility to Brugada syndrome (BrS). Objective To sequence a population of BrS and early-onset Lone Atrial Fibrillation (AF) patients for the R214Q mutation in the SCN1Bb gene. Methods The coding sequence and splice junctions of SCN1Bb were bidirectionally sequenced by using Big Dye chemistry in 192 early-onset Lone AF patients and 22 BrS patients. Results Three probands carrying the R214Q variant were identified. No mutations were identified in genes previously associated with BrS or AF in these patients. Case 1 also had the onset of persistent Lone AF at the age of 39 years. Case 2 was a Lone AF case with onset at the age of 39 years and paroxysmal Lone AF. Case 3 was a BrS patient with a type 1 electrocardiogram and onset of disease at the age of 54 years. Both Lone AF patients had electrocardiograms that raised the suspicion of BrS, but intravenous flecainide testing was, in both cases, negative. R214Q was not present in the control group (n = 216) and has not previously been reported in conjunction to AF. Conclusion Three patients of 192 young Lone AF and 22 BrS patients carried the nonsynonymous R214Q mutations in SCN1Bb , thereby indicating that this variant increases the susceptibility to both BrS and AF.
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Common polymorphisms in KCNJ5 [corrected] are associated with early-onset Lone Atrial Fibrillation in Caucasians.
The Cardiology, 2011Co-Authors: Javad Jabbari, Stig Haunso, Morten S. Olesen, Anders G. Holst, Jonas B. Nielsen, Jesper Hastrup SvendsenAbstract:Objectives: The aim of this study was to screen Lone Atrial Fibrillation (AF) patients for mutations in the genes KCNJ2 , KCNJ3 and KCN
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abnormal Atrial activation in young patients with Lone Atrial Fibrillation
Europace, 2011Co-Authors: Fredrik Holmqvist, Stig Haunso, Morten S. Olesen, Arnljot Tveit, Steve Enger, Jari Tapanainen, Raija Jurkko, Rasmus HavmollerAbstract:Aims Patients with a history of Atrial Fibrillation (AF) have previously been shown to have altered Atrial conduction, as seen non-invasively using signal-averaged P-wave analysis. However, little is known about the P-wave morphology in patients in the early phases of AF with structurally normal hearts. Methods and results Thirty-six patients with Lone AF were included before the age of 40 years (34 ± 4 years, 34 men) and compared with age- and gender-matched control subjects. Standard 12-lead electrocardiogram (ECG) was recorded for at least 10 s. P-wave morphology and duration were estimated using signal-averaged P-wave analysis. Echocardiography was performed in association with the ECG recording. Heart rate (67 ± 13 vs. 65 ± 7 b.p.m., P = 0.800) and PQ-interval (163 ± 16 vs. 164 ± 23 ms, P = 0.629) were similar in AF cases and controls, as was P-wave duration (136 ± 13 vs. 129 ± 13 ms, P = 0.107). The distribution of P-wave morphology differed between the AF cases and controls [33/58/0/8 vs. 75/25/0/0% (Type 1/Type 2/Type 3/atypical), P = 0.001], with a larger proportion of patients with AF exhibiting signs of impaired interAtrial conduction. Conclusion A significant difference in P-wave morphology distribution was seen between patients with early-onset, Lone paroxysmal AF and age- and gender-matched healthy control subjects. This finding indicates that alterations in Atrial electrophysiology are common in the early stage of the arrhythmia, and since it occurs in young patients without co-morbidity may well be the cause rather than the consequence of AF. (Less)
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kcne3 mutation v17m identified in a patient with Lone Atrial Fibrillation
Cellular Physiology and Biochemistry, 2008Co-Authors: Alicia Lundby, Stig Haunso, Jesper Hastrup Svendsen, Sorenpeter Olesen, Lasse Steen Ravn, Nicole SchmittAbstract:Background: Atrial Fibrillation (AF) is the most common cardiac rhythm disorder with a lifetime risk for development of 25 % for people aged 40 or older [1]. In this study we aim for the functional as
Jos G Maessen - One of the best experts on this subject based on the ideXlab platform.
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effectiveness and safety of simultaneous hybrid thoracoscopic and endocardial catheter ablation of Lone Atrial Fibrillation
Annals of cardiothoracic surgery, 2014Co-Authors: Laurent Pison, Sandro Gelsomino, Fabiana Luca, Jos G Maessen, Orlando Parise, Harry J G M Crijns, Mark La MeirAbstract:Background: We evaluated the safety and effectiveness of the hybrid thoracoscopic endocardial epicardial technique for the treatment of Lone Atrial Fibrillation (LAF). Methods: Between 2009 and 2012, a cohort of 78 consecutive patients (median age 60.5 years, 77% male) underwent ablation of Atrial Fibrillation (AF) as a stand-aLone procedure using a thoracoscopic, hybrid epicardial-endocardial technique. All patients underwent continuous 7-day Holter monitoring (HM) at 3 months, 6 months, 1 year and yearly thereafter. All patients reached 1-year follow-up. Median follow-up was 24 months [interquartile range (IQR) 12-36]. Results: No death or conversion to cardiopulmonary bypass occurred. No patient demonstrated paralysis of the phrenic nerve. Overall, the incidence of perioperative complications was 8% (n=6). At the end of follow-up sixty-eight patients (87%) were in sinus rhythm (SR) with no episode of AF, Atrial flutter (AFL) or Atrial tachycardia (AT) lasting longer than 30 seconds and off antiarrhythmic drugs (ADD). Among patients with long-standing persistent AF, 15 (100%) were in SR and off AAD. Success rates were 82% (n=28) in persistent and 76% (n=22) in paroxysmal AF (P=0.08). No patient died and no thromboembolic/bleeding events or procedure-related complications occurred during the follow-up. Conclusions: Thoracoscopic hybrid epicardial endocardial technique proved to be effective and safe in the treatment of LAF and to represent an important new suitable option to treat stand-aLone AF. Our findings need to be confirmed by further larger studies.
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minimally invasive surgical treatment of Lone Atrial Fibrillation early results of hybrid versus standard minimally invasive approach employing radiofrequency sources
International Journal of Cardiology, 2013Co-Authors: Mark La Meir, Sandro Gelsomino, Fabiana Luca, Gian Franco Gensini, Laurant Pison, Francis Wellens, Orlando Parise, Harry J G M Crijns, Andrea Colella, Jos G MaessenAbstract:Abstract Background We compared short-term results of a hybrid versus a standard surgical bilateral thoracoscopic approach employing radiofrequency (RF) sources in the surgical treatment of Lone Atrial Fibrillation (LAF). Methods Between January 2008 and July 2010 sixty-three consecutive patients with LAF underwent minimally invasive surgery. Thirty-five (55.5%) underwent surgery with the hybrid approach whereas 28 (45.5%) underwent bilateral thoracoscopic standard procedure (no-hybrid group). All patients underwent continuous 7-day Holter Monitoring (HM) at 3months, 6months and 1year. Results At 1year, 91.4% and 82.1% (time-related prevalence 5.2% vs.6.0% [ p =0.56]) of the patients were free of AF and AAD. The hybrid group yielded better results in long standing persistent AF (8.2% [time related prevalence 81.8% vs. 44.4%, p =0.001] vs.14.9%, p =0.04). One-year success rates were 87.5% vs. 100% ( p =0.04) in persistent [time related prevalence 3.8% vs. 0%, p p =0.04) in paroxysmal AF [time related prevalence 3.2% vs. 0%, p One-year prevalence of Warfarin use was significantly higher in the hybrid group (29.0% [26.2–33.1] and 13.4% [9.9–16.3]) with no difference by AF type. LA reverse remodeling occurred in 81.7% ( n =30) of hybrid patients and 67.8% ( n =19) of no-hybrid patients at latest control ( p =0.02). Left Atrial emptying fraction increased in both groups (50±14%, p p =0.004 in hybrid and no-hybrid, respectively) without differences between groups ( p =0.6). Conclusions The hybrid procedure yielded excellent results in long-standing persistent AF. Our findings need to be confirmed by further larger studies.
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the hybrid approach for the surgical treatment of Lone Atrial Fibrillation one year results employing a monopolar radiofrequency source
Journal of Cardiothoracic Surgery, 2012Co-Authors: Mark La Meir, Sandro Gelsomino, Fabiana Luca, Roberto Lorusso, Gian Franco Gensini, Francis Wellens, Laurent Pison, Orlando Parise, Jos G MaessenAbstract:The hybrid technique combines a mono or bilateral epicardial approach with a percutaneous endocardial ablation in a single-step procedure. We present our early results with this technique employing a monopolar radiofrequency source through a right thoracoscopy in patients with Lone Atrial Fibrillation (LAF). Between June 2009 and December 2010 nineteen consecutive patients (mean 60.8 ± 8.6 years, 84.2% male) underwent right unilateral minimally invasive hybrid procedure for LAF at our Institution. Ten patients (52.6.6%) had long-standing persistent AF while four (21.1%) had persistent and five (26.3%) paroxysmal AF. All patients were followed-up according the Heart Rhythm Society/European Heart Rhythm Association/European Cardiac Arrhythmia Society (HRS/EHRA/ECA) and Society of Thoracic Surgeon (STS) guidelines. There were neither early nor late deaths. It was possible to complete all the procedures as planned without any conversion to cardiopulmonary bypass. No patient died during the follow up. At one year, 7/19 (36.8%) patients were in sinus rhythm with no episode of AF and off antiarrhythmic drugs (AAD). Time-related prevalence of postoperative AF peaked at 44.4% (41.3–47.4) at two weeks, was 30.4% (27.3–34.9) at three months, fell to 14.2% (11.6–18.1) by 6 months and was 13.3% (11.0–17.4) at 12 months Among patients with long-standing persistent (LSP) AF, 20% (2/10) were in Sinus rythm and off AAD. One-year success rates were 50% (2/4) in persistent and 60% (3/5) in paroxysmal AF. At 12 months estimated prevalence of antyarrhythmic drugs and Warfarin use were 26% (22.4–33.1) and 48% (37.2–53.2), respectively. One year results combining the percutaneous endocardial with the right thoracoscopic epicardial technique were, in our experience, not satisfactory, particularly in patients with LSP and persistent AF. Our findings need to be confirmed by larger studies.
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treatment of Lone Atrial Fibrillation a look at the past a view of the present and a glance at the future
European Journal of Cardio-Thoracic Surgery, 2012Co-Authors: Sandro Gelsomino, Mark La Meir, Fabiana Luca, Roberto Lorusso, Gian Franco Gensini, Elena Crudeli, Ludovico Vasquez, Jos G MaessenAbstract:Summary Despite its proven efficacy, the Cox–Maze III procedure did not gain widespread acceptance for the treatment of Lone Atrial Fibrillation (LAF) because of its complexity and technical difficulty. Surgical ablation for LAF can now be successfully performed utilizing minimally invasive techniques. This article provides an overview of the current state of the art in the surgical treatment of LAF. A brief review of pathophysiology, pharmacological treatment as well as catheter ablation is also provided. The most widely employed minimally invasive approach to LAF has been the video-assisted bilateral mini-thoracotomy or thoracoscopic pulmonary vein island creation and left Atrial appendage removal or exclusion, usually with ganglionic plexi evaluation and destruction. Recently, a hybrid approach has been introduced, which combines a mono or bilateral epicardial approach with a percutaneous endocardial ablation in a single-step procedure to limit the shortcomings of both techniques. Suboptimal results of both catheter ablation and surgery suggest that success in the treatment of LAF will probably rely on a close collaboration between the surgeon and the electrophysiologist. Further studies are warranted to determine whether the hybrid approach is effective, especially in patients with long-standing persistent and persistent LAF.
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minimally invasive thoracoscopic hybrid treatment of Lone Atrial Fibrillation early results of monopolar versus bipolar radiofrequency source
Interactive Cardiovascular and Thoracic Surgery, 2012Co-Authors: Mark La Meir, Sandro Gelsomino, Fabiana Luca, Roberto Lorusso, Gian Franco Gensini, Laurant Pison, Francis Wellens, Jos G MaessenAbstract:We compare results of a hybrid monopolar vs. a hybrid bipolar thoracoscopic approach employing radiofrequency (RF) sources for the surgical treatment of Lone Atrial Fibrillation (LAF). From January 2008 to June 2010, 19 patients (35.1%) underwent RF monopolar/monolateral RF ablation, whereas 35 (64.9%) had RF bipolar/bilateral thoracoscopic ablation. One-year time-related prevalence of postoperative AF was 13.3 (11.0-17.4) and 5.2% (4.2-6.7), in monopolar and bipolar groups, respectively (P < 0.001). It was 21.1 (17.6-24.9) vs. 8.2% (5.1-11.6) in long standing persistent (P < 0.001), 13.2 (10.6-17.8) vs. 3.8% (1.4-6.9) in persistent (P < 0.001) and 5.6 (2.8-8.3) vs. 3.2% (1.0-6.5) in paroxysmal AF (P = 0.64). At 12 months, estimated prevalence of anti-arrhythmic drugs was 26 (22.4-30.1) and 18.0% (15.5-21.7, P = 0.04), whereas prevalence of warfarin use was 48.2 (44.2-52.2) and 29.0% (26.2-33.1, P < 0.001) in the monopolar and bipolar groups, respectively. Left Atrial (LA) reverse remodelling occurred in 47.3% of monopolar patients (n = 9) and in 77.1% of bipolar patients (P = 0.03). The hybrid bilateral approach with a bipolar device for the treatment of LAF showed a good 1-year success rate independently of the AF type and seems to be the better choice for longstanding persistent and persistent LAF.
