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Conduction Defect (conduction + defect)
Kinds of Conduction Defect Selected AbstractsSCN5A Mutation Associated with Cardiac Conduction Defect and Atrial ArrhythmiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2006PÄIVI J. LAITINEN-FORSBLOM Ph.D. Introduction: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias. Methods and Results: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms. Conclusions: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger. [source] Cardiac function and antiepileptic drug treatment in the elderly: A comparison between lamotrigine and sustained-release carbamazepineEPILEPSIA, Issue 8 2009Erik Saetre Summary Purpose:, To investigate the comparative effects of carbamazepine (CBZ) and lamotrigine (LTG) on electrocardiography (ECG) parameters in elderly patients with newly diagnosed epilepsy. Methods:,, The study was conducted in the Norwegian subcohort (n = 108) of an international randomized double-blind 40-week trial, which compared the efficacy and tolerability of LTG and sustained-release CBZ in patients aged 65 and older with newly diagnosed epilepsy. Target maintenance doses were 400 mg/day for CBZ and 100 mg/day for LTG, with adjustments based on clinical response. Patients with significant unpaced atrioventricular (AV) conduction defect were excluded. Resting 12-lead ECG recordings were made under standardized conditions at pretreatment (baseline) and at the 40-week study visit (treatment visit). Changes in QRS interval (primary endpoint), heart rate (HR), PQ, and QTc (HR-corrected QT) intervals were assessed and compared between groups. Results:, Of the 108 patients randomized, 33 discontinued prematurely because of adverse events (n = 24, none of which was cardiac) or other reasons (n = 9), and 15 were nonevaluable due to incomplete ECG data. None of the assessed ECG parameters differed significantly between groups at baseline. No significant ECG changes were recorded between baseline and treatment visit for QRS duration and QTc intervals, whereas HR fell and PQ intervals increased slightly on both treatments. However, there were no differences between groups in changes from baseline to treatment visit. There were no significant relationships between individual ECG changes and serum drug concentrations, except for QTc intervals, which decreased slightly with increasing CBZ concentrations. The proportion of patients with ECG parameters outside the normal range at treatment visit was similar to that recorded at baseline. Discussion:, Clinically significant ECG changes are not common during treatment with CBZ or LTG in elderly patients with no preexisting significant AV conduction defects. [source] Distribution and Correlates of Lipoprotein-Associated Phospholipase A2 in an Elderly Cohort: The Cardiovascular Health StudyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2008Curt D. Furberg MD OBJECTIVES: To determine whether high levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) are associated with prevalent cardiovascular disease (CVD) and to evaluate factors most influencing Lp-PLA2 levels in a community-based cohort of older adults. DESIGN: Cross-sectional. SETTING: The Cardiovascular Health Study (CHS), a population-based cohort study of men and women aged 65 and older. PARTICIPANTS: Five thousand five hundred thirty-one CHS participants. MEASUREMENTS: Levels of Lp-PLA2 activity were determined using stored blood samples from the baseline examination. RESULTS: Mean Lp-PLA2 was higher in participants with electrocardiographically determined ventricular conduction defect and major Q-wave abnormality and was positively correlated with left ventricular (LV) mass. It was high in those with echocardiographically determined abnormal LV ejection fraction, which persisted after adjustment. Mean Lp-PLA2 was also higher in participants with mild renal insufficiency and kidney disease. After multivariable adjustment, there was a modest but significant 27% greater risk of prevalent CHF per standard deviation increment of Lp-PLA2 and a modest but significant 12% greater risk of prevalent myocardial infarction. Lp-PLA2 was weakly but mainly most strongly correlated with cholesterol and lipoproteins, but those correlations were not especially strong. Lp-PLA2 was weakly positively correlated with soluble intercellular adhesion molecule-1 but not interleukin-6. In total, all factors considered could explain only 29% of Lp-PLA2 activity. CONCLUSION: Novel findings in the study are the associations, in those aged 65 and older, between Lp-PLA2 activity and LV dysfunction, CHF, and renal disease. CVD risk factors only minimally explain levels of Lp-PLA2. [source] SCN5A Mutation Associated with Cardiac Conduction Defect and Atrial ArrhythmiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2006PÄIVI J. LAITINEN-FORSBLOM Ph.D. Introduction: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias. Methods and Results: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms. Conclusions: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger. [source] Sudden Cardiac Death and Inherited Arrhythmia SyndromesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2005ANDREA SARKOZY M.D. Sudden cardiac death (SCD) at youth is rare and is often caused by inherited cardiac disorders. This review focuses on the genetic background of inherited primary electrical diseases, the so-called "channelopathies." Following a short clinical description of each syndrome, the recent findings in the genetics of long QT syndrome, short QT syndrome, isolated cardiac conduction defect, familial sick sinus syndrome, familial atrial fibrillation, cathecholaminergic polymorphic ventricular tachycardia, familial Wolff-Parkinson-White (WPW) syndrome, and Brugada syndrome are discussed. The currently proposed theoretical model of overlapping phenotypes in SCN5A sodium channel mutations is presented. The recent data indicate that advances in molecular genetics, experimental and clinical electrophysiology shed some light on the genetic background of primary electrical diseases. However, it is also becoming clear that the process from a mutation of a gene to the clinical presentation of a patient is currently only partially understood and extremely complex. [source] Transcatheter Closure of Congenital Ventricular Septal Defects: Experience with Various DevicesJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2003RAMESH ARORA D.M. Transcatheter closure of congenital ventricular septal defect (VSD) using various devices is gaining acceptance in selected cases of perimembranous and muscular defects, avoiding the inherent risks of cardiopulmonary bypass. The procedure was attempted in 137 patients having congenital defects using Rashkind Umbrella Device (RUD) in 29 patients, Amplatzer ventricular septal occluder (AVSO) in 107 patients, and Detachable Coil in one. All patients were selected using stringent criteria by detailed transthoracic echocardiography and/or transesophageal echocardiography. The location of VSD was perimembranous in 91 patients and was muscular trabecular in 46 patients. Seven patients had left ventricle (LV) to right atrium (RA) communication. Thirty-five patients with perimembranous and two with muscular VSD had aneurysm formation. The patients were 3 to 33 years old, and the diameter of VSD ranged from 3 to 12 mm. The pulmonary to systemic flow ratio was ,2:1 in 47 (34.3%) patients. The procedure was successful in 130 (94.8%) patients, with a success rate of 86.2% with RUD and 97.1% with AVSO. Residual shunt at 24 hours was seen in eight (32%) patients with RUD and in one patient (0.9%) with AVSO. Three (2.8%) developed transient bundle branch block, and two (1.9%) patients had complete heart block. New tricuspid stenosis and tricuspid regurgitation was observed in one patient each with AVSO. After immediate balloon dilatation, the mean pressure gradient across tricuspid valve decreased from 11 to 3 mmHg in the patient with tricuspid stenosis. On a follow-up of 1 to 66(mean 35.2 ± 10.7)months, the device was in position in all. None developed late conduction defect, aortic regurgitation, infective endocarditis, or hemolysis. At 9-month follow-up, the mean pressure gradient across the tricuspid valve was 3 mmHg in the patient with tricuspid stenosis. Complete occlusion of the shunt was achieved in 129 (99.2%) patients. One patient with RUD having persistent residual shunt underwent a second procedure with AVSO. Three out of 107 patients with AVSO had an unsuccessful procedure where the defect was perimembranous with a superior margin of defect less than 3 mm away from the aortic valve, and the specially designed perimembranous AVSO had to be retrieved because of hemodynamic compromise due to significant acute aortic regurgitation, whereas in all others, the defect was either ,3 mm away from the aortic valve or had aneurysm formation. All seven patients with LV to RA communication showed complete abolition of the shunt. Thus, in properly selected cases of perimembranous and muscular ventricular septal defects, the transcatheter closure is safe and efficacious using appropriate devices. The success rate is higher with AVSO compared with the previously used devices, as well as more successful for the muscular defects than those that are perimembranous in location. (J Interven Cardiol 2003;16:83,91) [source] C-Peptide Deficiency: An Important Pathogenetic Factor In Type 1 Diabetic NeuropathyJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000Aaf Sima Background: C-peptide has insulin-like effects and ameliorates the acute nerve conduction defect (NCD) in experimental and human type 1 diabetic neuropathy (DN). Methods: In this study, diabetic BB/Wor-rats were treated with rat C-peptide (75 ng/kg) from onset of diabetes for 8 months (prevention-group, PG). In a separate experiment, 5-mo untreated diabetic BB/Wor-rats were started on the same C-peptide treatment continued to 8 mo of diabetes (intervention group, IG). Results: In the PG, the NCD was significantly decreased (p < 0.001) compared to untreated BB/Wor-rats and was similar to that of normo-C-peptidemic and isohyperglycemic type 2 BBZ rats. This effect was associated with significant preventions of nodal changes (p < 0.001) including axo-glial dysjunction (p < 0.001), which was not different from non-diabetic control rats. Axonal atrophy and Wallerian degeneration were significantly prevented (both p < 0.05). In the IG, the NCD decreased significantly (p < 0.01) during the 3 mo treatment period. Associated with the functional improvement, nodal changes improved significantly (p < 0.001) as did axonal degenerative changes (p < 0.01). C-peptide treatment in the IG resulted in a significant increase in the frequency of regenerating fibers (p < 0.001) compared with untreated 5 mo diabetic rats. Conclusion: These studies demonstrate that C-peptide replacement in type 1 diabetes prevents the chronic NCD and structural changes. Furthermore, C-peptide treatment significantly improves the already established functional and structural abnormalities of DN. This is the first demonstration of a therapeutic improvement of established neuropathy in experimental diabetes. We conclude that C-peptide deficiency in type 1 diabetes is an important pathogenetic component of DN and that its replacement may provide a valuable adjunct to intensive insulin treatment. [source] Manometric study in Kearns,Sayre syndromeDISEASES OF THE ESOPHAGUS, Issue 1 2001K. H. Katsanos Although swallowing difficulties have been described in patients with Kearns,Sayre syndrome (KSS), the spectrum of manometric characteristics of dysphagia is not yet well known. Moreover, it is conceivable that a combination of various degrees of swallowing difficulties with different patterns in manometric studies exist, each playing a major role in the prognosis, natural history, and quality of life of KSS patients. An 18-year-old girl diagnosed at the age of 5 years with KSS (muscle biopsy) was admitted to our department with an upper respiratory tract infection and dysphagia. Clinical examination revealed growth retardation, external ophthalmoplegia, pigmentary retinopathy, impaired hearing, and ataxia. An electrocardiogram revealed cardiac conduction defects (long Q-T), and brain magnetic resonance imaging showed abnormalities in the cerebellar hemispheres. A manometric and motility study for dysphagia was conducted and the pharynx and upper esophageal sphincter (UES) resting pressures were similar to control group values, but the swallowing peak contraction pressure of the pharynx and the closing pressure of the UES were very low and could not promote effective peristaltic waves. Relaxation and coordination of the UES were not affected although pharyngeal and upper esophagus peristaltic waves proved to be very low and, consequently, were practically ineffective. The patient was started on treatment comprising a diet rich in potassium, magnesium, and calcium, and oral administration of vitamin D and co-enzyme Q10 100 mg daily; she was discharged 6 days later with apparent clinical improvement. [source] Cardiac function and antiepileptic drug treatment in the elderly: A comparison between lamotrigine and sustained-release carbamazepineEPILEPSIA, Issue 8 2009Erik Saetre Summary Purpose:, To investigate the comparative effects of carbamazepine (CBZ) and lamotrigine (LTG) on electrocardiography (ECG) parameters in elderly patients with newly diagnosed epilepsy. Methods:,, The study was conducted in the Norwegian subcohort (n = 108) of an international randomized double-blind 40-week trial, which compared the efficacy and tolerability of LTG and sustained-release CBZ in patients aged 65 and older with newly diagnosed epilepsy. Target maintenance doses were 400 mg/day for CBZ and 100 mg/day for LTG, with adjustments based on clinical response. Patients with significant unpaced atrioventricular (AV) conduction defect were excluded. Resting 12-lead ECG recordings were made under standardized conditions at pretreatment (baseline) and at the 40-week study visit (treatment visit). Changes in QRS interval (primary endpoint), heart rate (HR), PQ, and QTc (HR-corrected QT) intervals were assessed and compared between groups. Results:, Of the 108 patients randomized, 33 discontinued prematurely because of adverse events (n = 24, none of which was cardiac) or other reasons (n = 9), and 15 were nonevaluable due to incomplete ECG data. None of the assessed ECG parameters differed significantly between groups at baseline. No significant ECG changes were recorded between baseline and treatment visit for QRS duration and QTc intervals, whereas HR fell and PQ intervals increased slightly on both treatments. However, there were no differences between groups in changes from baseline to treatment visit. There were no significant relationships between individual ECG changes and serum drug concentrations, except for QTc intervals, which decreased slightly with increasing CBZ concentrations. The proportion of patients with ECG parameters outside the normal range at treatment visit was similar to that recorded at baseline. Discussion:, Clinically significant ECG changes are not common during treatment with CBZ or LTG in elderly patients with no preexisting significant AV conduction defects. [source] SCN5A Mutation Associated with Cardiac Conduction Defect and Atrial ArrhythmiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2006PÄIVI J. LAITINEN-FORSBLOM Ph.D. Introduction: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias. Methods and Results: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms. Conclusions: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger. [source] Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiographyJOURNAL OF INTERNAL MEDICINE, Issue 5 2002C. M. Sköld Abstract. Sköld CM, Larsen FF, Rasmussen E, Pehrsson SK, Eklund AG (Karolinska Hospital and Institutet, Stockholm, Sweden). Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiography. J Intern Med 2002; 252: 465,471. Objectives. To elucidate whether cardiac magnetic resonance imaging (MRI) could be useful in disclosing structural changes in the myocardium in sarcoidosis patients and to relate echo-Doppler derived indices of left ventricular function to electrocardiogram (ECG) findings. Design. The MRI was performed in 18 consecutive patients with sarcoidosis. Left ventricular ejection fraction (LVEF), i.e. systolic function, was estimated echocardiographically by Simpson's two-dimensional method (n = 16). Diastolic function was estimated by age-corrected Doppler-derived indices: isovolumetric relaxation time (IVRT), deceleration time (DT) and early filling/atrial contraction ratio (E/A ratio). Results. Eleven patients had conduction defects or dysrhythmias (ECG+) whilst seven patients had a normal ECG (ECG,). In two patients, high signalling, contrast-enhanced, isolated regions, suggestive of deposits, were seen in the left ventricular myocardium on MRI. Both these patients had abnormal ECGs and signs of systolic and/or diastolic dysfunction on echocardiography. LVEF was subnormal in seven of 10 of the ECG+ patients and in two of six of the ECG,. Signs of diastolic dysfunction were found in 59% and 56% of the measurements in the ECG+ and ECG, patients, respectively. Conclusion. We conclude (i) that myocardial deposits on MRI in sarcoidosis patients have a high specificity for cardiac involvement but a rather low sensitivity; (ii) that a substantial proportion of sarcoidosis patients with abnormal ECGs have echocardiographic signs of systolic and/or diastolic dysfunction. [source] Location and Clinical Implications of High-Degree Atrioventricular Block During Dipyridamole Infusion: A Case ReportANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2002Mazen Alakhras M.D. We describe a patient with bifascicular block, who developed transient high-degree atrioventricular block during dipyridamole infusion. This patient was subsequently found to have significant His-Purkinje disease at electrophysiology study, and underwent permanent pacemaker implantation. Spontaneous atrioventricular block was documented during follow-up. This case report raises the issue of dipyridamole safety in patients with intraventricular conduction defects, and contributes an additional mechanism to the possible explanation of dipyridamole-induced atrioventricular block. A.N.E. 2002;7(2):174,176 [source] | ||||||||||||||||||||||