Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q96S42 (nodal)
 22,877 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient in whom syncopal episodes occurred following an inferior myocardial infarction is described. Electrocardiographic monitoring revealed periods of profound sinus bradycardia and AV block during syncope. In addition, transient spontaneous prolongations of the PR interval due to AV nodal delay and episodes of atrial fibrillation also occurred. Sinus node recovery time following atrial overdrive was within normal limits. Symptoms disappeared following the insertion of a permanent, demand pacemaker. The onset of symptoms following myocardial infarction suggests that dysfunction of the sino-atrial and AV nodes may have been the result of ischemic damage during the infarction.
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PMID:Sinus and A-V nodal dysfunction following myocardial infarction. 115 53

A case of Romano-Ward syndrome effectively treated by both propranolol and atrial pacing is reported. A 33 year-old female, who had experienced syncopal episodes since she was 20 years old, had a family history showing her son with QTc 0.46. Her QT-U interval and QTc were both 0.6 second when propranolol was not administered. It shortened to 0.28 second and 0.39 respectively under exercise stress testing, and also shortened to 0.41 second and 0.43 respectively when left satellite ganglion block was used. Electrophysiologic study demonstrated that both sinus and atrioventricular nodal functions were normal, but the refractory periods of right and left ventricle differed significantly, and nonsustained ventricular tachycardia was induced. Her QT-U and QTc intervals shortened to 0.37 seconds and 0.43 respectively through both the treatment of 80 bpm atrial pacing, and the administration of 80mg propranolol. She has never experienced a syncopal episode.
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PMID:[A case of Romano-Ward syndrome effectively treated by propranolol and atrial pacing]. 206 94

In this report we present the case of a patient with recurrent syncopal episodes. During one of the attacks the patient was monitored by telemetry and the ECG lead showed asystole for more than 7 seconds. As in cases of the cardioinhibitory type of hypersensitive carotid sinus syndrome (HCSS), asystole may represent suppression of the sinus node or suppression of both sinus and atrioventricular (AV) node. Unfortunately, in contrast to HCSS, there is no maneuver that can reproducibly induce episodes of asystole. Consequently, very little is known about the occurrence of AV block in the presence of sinus arrest. In the patient described in this report, we were able to demonstrate that suppression of sinus and AV nodes occurred simultaneously. It is interesting to note that in this type of syncope data from noninvasive and invasive techniques in assessing sinus nodal and AV nodal conduction may not be conclusive. In the group of patients with this type of syncope, permanent atrial demand pacing is contraindicated.
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PMID:Reflex cardiac asystole. 243 92

There is little data on cardiac electrophysiological assessment and long term follow-up of unexplained syncope from Australasia. We present 94 patients with unexplained syncope who underwent such assessment and followup for an average of 52 months in 92 patients. Of the 94 investigated 57 were male, the average age was 61 years and average number of syncopal episodes prior to study was 8 (minimum 2). Forty-two patients had heart disease. Patients were divided into 3 groups on results of electro physiological testing. Normal (31 patients), group 1 with intermediate abnormalities of sinus node function or atrioventricular conduction (37 patients) and group 2 in whom the abnormalities were felt likely to represent the cause of syncope (26 patients). Abnormalities detected in group 2 were sinus node dysfunction in 12, abnormal atrioventricular nodal conduction in 8, abnormal infranodal conduction in 2, vagal hypersensitivity in 3 and ventricular tachycardia in two. Follow-up for a mean of 52 months was obtained in 92 patients. Recurrent syncope occurred in 37% of the patients. Treatment reduced recurrent syncope to a level approaching statistical significance in group 2 patients (50% to 13%; 0.01 greater than p greater than 0.05) but had little influence on recurrent syncope in group 1 or normal patients. There were 14 deaths over the follow-up period. Mortality was predicted by group 2 electrophysiological abnormality (p less than 0.02) and the presence of heart disease (p less than 0.05) and was not reduced by specific therapy. Sudden death occurred in 3 patients, all with heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac electrophysiological assessment and the natural history of unexplained syncope. 338 Apr 45

Paroxysmal complete atrioventricular (AV) block without associated electrocardiographic (ECG) abnormality is not a well recognized entity. A mother and her daughter had recurrent syncopal episodes, but a normal ECG. The episodes were preceded by nausea and vomiting. ECG during these episodes revealed complete heart block. In the mother, one episode was promptly reversed by atropine. Electrophysiological evaluation of the sinus and AV nodal function and atrial and ventricular effective refractory periods before and after autonomic blockade was normal. Provocative manoeuvres failed to induce AV block. Paroxysmal AV block was vagally mediated in one of the patients, as indicated by prompt response to atropine. In the second case, the vagal dependence could not be proved but appears to be the most likely explanation. It thus appears that paroxysmal, vagally mediated complete AV block should be seriously considered in patients with unexplained syncope.
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PMID:Paroxysmal vagally mediated AV block with recurrent syncope. 400 43

An 82 year old man presented with multiple syncopal episodes. Since his ECG showed LBBB (left bundle branch block) with first degree AV block, he was advised permanent pacemaker implantation. However, a wide QRS tachycardia on the Holter raised the possibility of tachycardia-mediated syncope. EP (electrophysiological) studies revealed easily and repeatedly inducible short lasting slow-fast AVNRT (atrioventricular nodal reentry tachycardia) with severe hypotension. After RF ablation of the slow pathway, he is asymptomatic at six month follow-up.
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PMID:All that glitters is not gold ... all that faints is not slow. 1619 Jan 37

Escape-capture bigeminy is a bigeminal rhythm in which each escape beat is followed by a captured beat. This dysrhythmia is very rare, because its manifestation requires the sinus interval to be longer than the escape interval. This is possible only with severe sinus nodal disease, where the intrinsic sinus rate is extremely low, or with a sinus rhythm associated with an accelerated junctional rhythm. The authors review the case of a 75-year-old man who presented with occasional dizziness and near-syncopal episodes. He was diagnosed with escape-capture bigeminy and subsequently underwent pacemaker placement.
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PMID:The great escape: junctional escape-capture bigeminy. 1708 32