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Recurrent Syncope (recurrent + syncope)

Distribution by Scientific Domains

Medical Sciences	81%
Life Sciences	18%

Selected Abstracts

Recurrent Syncope in a Patient After Myocardial Infarction

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4p1 2003
SUSANNE C. CREDNER
CREDNER, S.C., et al.: Recurrent Syncope in a Patient After Myocardial Infarction. A patient with ischemic cardiomyopathy presented with burning pain of his body surface with consecutive orthostatic intolerance and recurrent syncopes. A diagnosis of acute autonomic dysfunction was made and the patient was treated with midodrine, resulting in restoration of orthostatic tolerance after 6 weeks of therapy. (PACE 2003; 26[Pt. I]:920,921) [source]

A new approach to long QT syndrome mutation detection by Sequenom MassARRAY® system

ELECTROPHORESIS, Issue 10 2010
Catarina Allegue
Abstract Congenital long QT syndrome is an inherited cardiac disorder characterized by a prolonged QT interval and polymorphic ventricular arrhythmias that could result in recurrent syncope, seizures or sudden death as the most dramatic event. Until now QT interval mutations have been described in 12 genes, where the majority of mutations reside in three genes KCNQ1, KCNH2, and SCN5A. Diagnosis and prognosis are directly related with the gene and mutation involved. We have developed a diagnostic approach for long QT syndrome and Brugada syndrome based on published mutations and Sequenom MassArray® system. Three diagnostic tests have been developed, oriented to each of the three most prevalent genes in the long QT syndrome. A total of 433 mutations are analyzed in 38 multiplex reactions, allowing their detection in about 48,h. Tests were validated on 502 samples from individuals with different clinical conditions and family history. The average call rates obtained for each of the tests were 93, 83, and 73% in KCNQ1, KCNH2, and SCNA, respectively. Sequenom MassARRAY mutation detection is a reliable, highly flexible, and cost-efficient alternative to conventional methods for genetic testing in long QT syndrome and Brugada syndrome, facilitating flexible upgrades of the version of the test presented here with the inclusion of new mutations. [source]

Abnormal cardiovascular responses to carotid sinus massage also occur in vasovagal syncope , implications for diagnosis and treatment

EUROPEAN JOURNAL OF NEUROLOGY, Issue 8 2010
A. M. Humm
Background and purpose:, Carotid sinus massage (CSM) is commonly used to identify carotid sinus hypersensitivity (CSH) as a possible cause for syncope, especially in older patients. However, CSM itself could provoke classical vasovagal syncope (VVS) in pre disposed subjects. Methods:, Retrospective analysis of CSM, cardiovascular autonomic function tests (including tilt table testing) and medical history in 388 patients with recurrent syncope to identify and characterize patients in whom an abnormal response to CSM was more likely to reflect VVS than CSH. Results:, CSM was abnormal in 79 patients. In 53 patients (77.2 ± 8.7 years), CSH was the likely cause of syncope. VVS was the more likely diagnosis in 26 younger patients (59.7 ± 12.6 years) with longstanding syncope from youth, in whom fear or pain was as a trigger; 7/26 suffered from intense chronic or intermittent neck pain and one exacerbation of syncopal attacks followed a physical and emotional trauma to the neck. In VVS, 4/26 had spontaneous VVS during head-up tilt, another six after venepuncture (performed in 17/26). In 6/26, the abnormal response to CSM was delayed, occurring 62.8 ± 28.4 s after completion of CSM. The response to CSM was predominantly of the mixed type (20/26) and abnormal on both sides in 14/26. Conclusions:, An abnormal response to CSM may not indicate syncope caused by CSH and needs to be considered in the light of the patient's age, duration of syncopal episodes and detailed history of provocative stimuli. Differentiating CSH from VVS with an abnormal response to CSM has various implications from advice on driving to treatment strategies. [source]

Impairment of Coronary Microvascular Function in Patients with Neurally Mediated Syncope

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2p1 2003
JAW-WEN CHEN
CHEN, J.-W., et al.: Impairment of Coronary Microvascular Function in Patients with Neurally Mediated Syncope.Recent evidence suggests that myocardial ischemia may occur in patients with neurally mediated syncope and normal coronary angiograms. This study was conducted to evaluate if coronary microvascular function is impaired in such patients. Coronary hemodynamic studies and head-up tilt table tests (HUTs) were performed on 30 consecutive patients with normal coronary angiograms and recurrent syncope. Another ten subjects with atypical chest pain and no evidence of myocardial ischemia or syncope served as a control. Great cardiac vein flow (GCVF) and coronary sinus flow (CSF) were measured by the thermodilution method at baseline and after dipyridamole infusion (0.56 mg/kg IV for 4 minutes). Coronary flow reserve (CFR), derived from CSF and GCVF, was significantly lower in the 15 patients with positive HUT than in the other 15 patients with negative HUT (1.75 ± 0.48vs2.64 ± 0.8, P < 0.01and2.29 ± 0.45vs3.07 ± 0.63, P < 0.01, respectively). Ischemic-like ECG was noted during treadmill exercise test in 40% of the former and in 7% of the latter group(P = 0.01). There was no significant difference in CFR between patients with negative HUT and control subjects. Coronary microvascular function was impaired in syncopal patients with positive HUT and relatively preserved in those with negative HUT, suggesting the possible linkage between coronary microvascular dysfunction and the development of neurally mediated syncope. (PACE 2003; 26[Pt. I]:605,612) [source]

Electromagnetic Interference of an Implantable Loop Recorder by Commonly Encountered Electronic Devices

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2000
CAREL C. DE COCK
De COCK, C.C., et al.: Electromagnetic Interference of an Implantable Loop Recorder by Commonly Encountered Electronic Devices. Electromagnetic interference of pacemaker systems has been well established and can lead to an inappropriate function of these devices. Recently, an implantable loop recorder (ILR) (REVEAL, Medtronic Inc.) has been introduced to evaluate the possible arrhythmic etiology of patients with recurrent syncope. We evaluated the interference of this device in two patients with implantable ILR and in three nonimplanted ILRs with four electromagnetic sources: cellular phones (GSMs), electronic article surveillance systems (EASs), metal detector gates (MDGs), and magnetic resonance imaging (MRI). The GSM did not affect appropriate function of the ILR whereas radiofrequency (RF) EAS could interfere with normal function in implanted and nonimplanted systems. The MDG had no influence on ILR function. The magnetic field induced by the MRI resulted in an irreversible error in one nonimplanted ILR. Therefore, although interference between electromagnetic sources and ILRs appears to be rare in our study, physicians should be aware of possible malfunctioning of these devices. [source]

Epsilon-Like Electrocardiographic Pattern in a Patient with Brugada Syndrome

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009
Ozcan Ozeke M.D.
Both Brugada syndrome (BrS) and arrhythmogenic right ventricle dysplasia/cardiomyopathy (ARVD/C) can cause repolarization abnormalities in right precordial leads and predispose to sudden cardiac death (SCD) due to ventricular arrhythmias. Although there is controversy over whether BrS is distinct from ARVD/C, it is believed that both are different clinical entities with respect to both the clinical presentation and the genetic predisposition. The coexistence of these two relatively rare clinical entities is also reported, but, some hypothesized that it is more possible that disease of the right ventricular muscle might accentuate the Brugada electrocardiographic pattern. In clinic practice, there may be cases where the dividing line is not so clear. We report a 33-year-old male presenting with recurrent syncope, who has a peculiar pattern of coved-type ST-segment elevation (ST-SE) with epsilon-like wave in right precordial leads. [source]

Aetiologic and clinical characteristics of syncope in Chinese children

ACTA PAEDIATRICA, Issue 10 2007
Li Chen
Abstract Aim: This study aimed to improve diagnostic efficacy of syncope in children by analyzing the aetiology and clinical characteristics of syncope in Chinese children. Methods: We retrospectively analyzed the causes of syncope and diagnostic workup in 154 consecutive children seen in the Department of Pediatrics, Peking University First Hospital, China, because of a syncope-related event. Results: In all patients with transient loss of consciousness (TLOC), there were 136 (88.31%) patients attributing to syncope, and 18 (11.69%) belonging to nonsyncopal cases. Neurally mediated syncope (NMS) was the most common cause of syncope (99 cases; 64.3%), with cardiac causes ranking second (10 cases; 6.5%). Other nonsyncopal causes included psychiatric problems and neurological and metabolic disorders. In 25 cases (16.2%), the cause was uncertain. Cases of NMS often had clear inducement of syncope and prodromes. Children with cardiac syncope often had a history of cardiac disease, were often younger than those with NMS, and showed exercise-related syncope, syncope spells in any body position or at an early age, or sudden death in family members but no prodromes. Neurological disorder was suspected in cases of TLOC with seizures, TLOC spells in any position, postictal phase of disorientation or abnormal neurological signs. A metabolic cause is suspected with a history of metabolic disease, prolonged anger, or violent vomiting and diarrhoea. Children with psychiatric disorders were adolescent girls, with prolonged TLOC spells, who had more frequent TLOC. Although many tests were used in diagnosis, most were not goal directed. Now, electrocardiography is recommended in almost all children with syncope. Neurological testing, including electroencephalography and computed tomography were rarely helpful unless with evidence of neurological signs and symptoms. Head-up tilt test (HUTT) was most useful in children with recurrent syncope in whom heart disease was not suspected. Conclusion: NMS was the most common cause of syncope. We recommended HUTT as the important basis of the TLOC workup. [source]

Coronary Slow Flow Phenomenon and Risk for Sudden Cardiac Death Due to Ventricular Arrhythmias: A Case Report and Review of Literature

CLINICAL CARDIOLOGY, Issue 8 2008
Dr. Shoaib Saya
Abstract We report a case of coronary slow flow phenomenon (CSFP) in a patient who underwent coronary angiography due to anginal chest pain and recurrent syncope with complete normalization of flow after intracoronary adenosine. He was noted to have multiple episodes of nonsustained ventricular tachycardia on holter monitor and increased QTc dispersion on surface electrocardiogram (EKG). He responded very well to oral dipyridamole therapy with complete resolution of his symptoms and no episodes of ventricular tachycardia on the event recorder at 3 months. We review the diagnosis and clinical features of CSFP and its association with increased QTc dispersion and the role of oral dipyridamole therapy in this condition. Copyright © 2007 Wiley Periodicals, Inc. [source]

Effective long-term control of cardiac events with ,-blockers in a family with a common LQT1 mutation

CLINICAL GENETICS, Issue 3 2004
H Wedekind
The congenital long QT syndrome (LQTS) is characterized by a prolonged QT interval on the surface electrocardiogram and an increased risk of recurrent syncope and sudden cardiac death. Mutations in seven genes have been identified as the molecular basis of LQTS. ,-blockers are the treatment of choice to reduce cardiac symptoms. However, long-term follow-up of genotyped families with LQTS has been rarely reported. We have clinically followed a four-generation family with LQTS being treated with , - blocker therapy over a period of 23 years. Seven family members were carriers of two amino acid alterations in cis (V254M-V417M) in the cardiac potassium channel gene KCNQ1. Voltage-clamp recordings of mutant KCNQ1 protein in Xenopus oocytes showed that only the V254M mutation reduced the IKs current and that the effect of the V417M variant was negligible. The family exhibited the complete clinical spectrum of the disease, from asymptomatic patients to victims of sudden death before ,-blocker therapy. There was no significant reduction in QTc (556 ± 40 ms½ before therapy, 494 ± 20 ms½ during 17 years of treatment; n = 5 individuals). Of nine family members, one female died suddenly before treatment, three females of the second generation were asymptomatic, and four individuals of the third and fourth generation were symptomatic. All mutation carriers were treated with ,-blockers and remained asymptomatic for a follow-up up to 23 years. Long-term follow-up of a LQT1 family with a common mutation (V254M) being on ,-blocker therapy was effective and safe. This study underscores the importance of long-term follow-up in families with specific LQT mutations to provide valuable information for clinicians for an appropriate antiarrhythmic treatment. [source]