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Predictive role of connexin 40 in the pathogenesis of hereditary sick sinus syndrome  [cached]
S.Yu. Nikulina,A.A. Chernova,V.A. Shulman,T.S.Kukushkina
Rational Pharmacotherapy in Cardiology , 2011,
Abstract: Aim. To study the association of hereditary sick sinus syndrome (SSS) with connexin 40 gene (Cx40) polymorphism.Material and methods. 29 families with hereditary SSS were involved into prospective study. Probands were 20 women and 9 men (aged 58±0.15). Relatives, I-III degree of kinship, were 65 men and 68 women (aged 39±0.13). Clinical and instrumental examination was performed in all probands and their relatives. Diagnosis of SSS was verified by transesophageal atrial electrostimulation. Molecular genetic investigation of SSS patients and their relatives was carried out in laboratory of medical genetics of Research Institute of Therapy, Siberian Branch of Russian Academy of Medical Sciences.Results. 71 SSS patients, 44 their healthy relatives, I-III degree of kinship, 197 subjects of control group were genotyped for the polymorphism of 44G>A of gene Cx40. According to allele-specific polymerase chain reaction 3 types of genotypes ADRA2B (II — homozygous wild, ID — heterozygous, DD — homozygous mutant) were found in SSS patients, their relatives and healthy subjects of control group.Conclusion. Significant predominance of the heterozygous genotype 44G>A was found in SSS (45,07±5,9%) patients in comparison with subjects of the control group (29,44±3,2%).
Idiopathic sick sinus syndrome  [cached]
S.Y. Nikulina,V.A. Schulman,A.A. Chernova
Rational Pharmacotherapy in Cardiology , 2007,
Abstract: Aim. To evaluate changes in hereditary burden of sick sinus syndrome (SSS) in families of patients with SSS and assess heart rate variability (HRV) in patients with SSS.Results. 33 families of patients with SSS were examined. Clinical study, ECG-Holter monitoring, atropine test, transesophageal left atrial stimulation, echocardiography, veloergometry were fulfilled in all probands and their relatives in 1990 and 2005-2006. Cardiorhythmography was done in patients with SSS only in 2005-2006.Results. Increase in hereditary burden with SSS from 31 to 35% is registered during 15 years. Significant growth of patients with SSS was observed among daughters (from 50 to 71%), nephews (from 33 to 50%) and nieces (from 0 to 20%). HRV analysis shows prevalence of sympathetic system activity in patients with SSS.Conclusion. Growth of hereditary burden with SSS especially among female relatives is shown. HRV analysis can be used for SSS diagnostics.
Genetic predictors of idiopathic sick sinus syndrome  [cached]
A. A. Chernova,S. Yu. Nikulina,S. S. Tret'yakova
Rational Pharmacotherapy in Cardiology , 2012,
Abstract: Published data demonstrating genetic determination of sick sinus syndrome is presented. The definition of this pathology is presented; the main symptoms are described, as well as genes that influence the development of idiopathic sick sinus syndrome, their polymorphisms and role in disorders of the cardiovascular system.
S K Forouzannia,M h Abdollahi,S J Mirhosseini,S H Moshtaghion
Acta Medica Iranica , 2008,
Abstract: "nReports which describe sick sinus syndrome due to malignant lymphoma have been rare and only eight cases have been reported until now. This is a case of sick sinus syndrome and superior vena cava syndrome secondary to invasion of occult malignant lymphoma of the lung in a 60 years old male. There were no symptoms or signs of malignancy before the first presentation with sick sinus syndrome. Patient was treated with implantation of a permanent pacemaker. SA node involvement by lymphoma should be considered as an etiological factor when sick sinus syndrome of unknown cause is encountered.
Anaesthetic management of a patient with sick sinus syndrome for exploratory laparotomy
S Alex, JP Saneesh, R Rao, M Upadya
Southern African Journal of Anaesthesia and Analgesia , 2010,
Abstract: Sick sinus syndrome is a generalised abnormality of cardiac impulse formation that may be caused either by an intrinsic disease of the sinus node, which makes it unable to perform its pacemaking function, or by extrinsic factors. It commonly affects elderly persons. While the syndrome can have many causes, it usually is idiopathic. Abnormalities encompassed by this syndrome include sinus bradycardia, sinus arrest or exit block, combinations of sinoatrial and atrioventricular nodal conduction disturbances and atrial tachyarrhythmias. Diagnosis of sick sinus syndrome can be difficult because of its nonspecific symptoms and elusive findings on an electrocardiogram or a Holter monitor. Here, we present the perioperative management of an elderly patient with sick sinus syndrome with seminoma of undescended testis posted for exploratory laparotomy.
Atrial Size Independently Correlates with the Development of Paroxysmal Atrial Fibrillation in Patients with Sick Sinus Syndrome  [PDF]
Yu-Sheng Lin,G. Bih-Fang Guo,Yung-Lung Chen,Tzu-Hsien Tsai
Chang Gung Medical Journal , 2010,
Abstract: Background: Atrial fibrillation arises in 20-30% of patients with sick sinus syndrome,increasing the risk of systemic embolization and mortality. The aim of thisstudy was to examine the clinical determinants of development of paroxysmalatrial fibrillation in sick sinus syndrome patients before implantation of apacemaker.Methods: This case-control survey involved 144 patients (mean age
Pacemaker implantation in a patient with brugada and sick sinus syndrome  [cached]
Bjarke Risgaard,Henning Bundgaard,Reza Jabbari,Stig Hauns?
World Journal of Cardiology , 2013, DOI: 10.4330/wjc.v5.i3.65
Abstract: Brugada syndrome (BrS) is a rare and inherited primary arrhythmic syndrome characterized by ST-segment elevations in the right precordial leads (V1-V3) with an increased risk of sudden cardiac death (SCD). Arrhythmias in BrS are often nocturne, and brady-arrhythmias are often seen in patients with loss-of-function mutations in SCN5A. In this case-report we present a 75-year old woman referred to our outpatient clinic for inherited cardiac diseases for a familial clinical work-up. Since childhood she had suffered from dizziness, absence seizures, and countless Syncope’s. In 2004 sick sinus syndrome was suspected and she was treated with implantation of a pacemaker (PM) at another institution. An inherited cardiac disease was one day suddenly suspected, as the patient had a 61-year old brother who was diagnosed with symptomatic BrS, and treated with an implantable cardioverter defibrillator (ICD) after aborted SCD. A mutation screening revealed a SCN5A [S231CfsX251 (c.692-693delCA)] loss-of-function mutation not previously reported, and as a part of the cascade screening in relatives she was therefore referred to our clinic. In the 7 year period after PM implantation she had experienced no cardiac symptoms, although her electrocardiogram changes now were consistent with a BrS type 1 pattern. A genetic test confirmed that she had the same mutation in SCN5A as her brother. In this case-report we present a loss-of function mutation in SCN5A not previously associated with BrS nor presented in healthy controls. Sinus node dysfunction has previously been documented in patients with symptomatic BrS, which suggests it is not a rare concomitant. The only accepted treatment of BrS is today implantation of an ICD. In the future studies should evaluate if PM in some cases of symptomatic BrS can be used instead of ICDs in patients with a loss-of-function SCN5A mutations
Promoter Polymorphism G-6A, which Modulates Angiotensinogen Gene Expression, Is Associated with Non-Familial Sick Sinus Syndrome  [PDF]
Jan-Yow Chen, Ying-Ming Liou, Hong-Dar Isaac Wu, Kuo-Hung Lin, Kuan-Cheng Chang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0029951
Abstract: Background It is well known that familial sick sinus syndrome (SSS) is caused by functional alterations of ion channels and gap junction. Limited information is available on the mechanism of age-related non-familial SSS. Although evidence shows a close link between arrhythmia and the renin-angiotensin system (RAS), it remains to be determined whether the RAS is involved in the pathogenesis of non-familial SSS. Methods In this study, 113 patients with documented non-familial SSS and 125 controls were screened for angiotensinogen (AGT) and gap junction protein-connexin 40 (Cx40) promoter polymorphisms by gene sequencing, followed by an association study. A luciferase assay was used to determine the transcriptional activity of the promoter polymorphism. The interaction between nuclear factors and the promoter polymorphism was characterized by an electrophoretic mobility shift assay (EMSA). Results Association study showed the Cx40 -44/+71 polymorphisms are not associated with non-familial SSS; however, it indicated that four polymorphic sites at positions -6, -20, -152, and -217 in the AGT promoter are linked to non-familial SSS. Compared to controls, SSS patients had a lower frequency of the G-6A AA genotype (OR 2.88, 95% CI 1.58–5.22, P = 0.001) and a higher frequency of the G allele at -6 position (OR 2.65, 95% CI 1.54–4.57, P = 0.0003). EMSA and luciferase assays confirmed that nucleotide G at position -6 modulates the binding affinity with nuclear factors and yields a lower transcriptional activity than nucleotide A (P<0.01). Conclusion G-6A polymorphism, which modulates the transcriptional activity of the AGT promoter, may contribute to non-familial SSS susceptibility.
Anesthetic Management of a Patient with Sick Sinus Syndrome during General Anesthesia for Maxillofacial Surgery  [PDF]
Kenichi Satoh, Atsumi Ishizuka, Ayako Ohashi, Miho Kumagai, Shigeharu Joh
Open Journal of Anesthesiology (OJAnes) , 2015, DOI: 10.4236/ojanes.2015.54011
Abstract: Sick sinus syndrome (SSS) is a generalized abnormality of cardiac impulse formation. Patients with SSS occasionally need temporary pacing during general anesthesia. The most common issue arising in the perioperative period is electromagnetic interference with device function. We report a case of a 66-year-old man who required temporary cardiac pacing during maxillary cyst extirpation using electrocautery.
Multiple Loss-of-Function Mechanisms Contribute to SCN5A-Related Familial Sick Sinus Syndrome  [PDF]
Junhong Gui,Tao Wang,Richard P. O. Jones,Dorothy Trump,Thomas Zimmer,Ming Lei
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010985
Abstract: To identify molecular mechanisms underlying SCN5A-related sick sinus syndrome (SSS), a rare type of SSS, in parallel experiments we elucidated the electrophysiological properties and the cell surface localization of thirteen human Nav1.5 (hNav1.5) mutant channels previously linked to this disease.
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