Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The vasovagal nature of syncope, which remained unexplained despite full clinical and electrophysiologic investigation, was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (17 men and 13 women, mean age 65 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5) episodes of syncope of unknown origin were studied. Head-up tilt test was considered positive if syncope developed in association with hypotension, bradycardia, or both. During baseline head-up tilt 15 patients (50%) had a positive response. Ten patients had a vasodepressor response (marked hypotension without marked bradycardia) and 5 had a mixed response (marked hypotension with marked bradycardia). None of 8 control subjects became symptomatic during the test. Baseline head-up tilt test was positively reproducible in 10 of 14 patients (71%). Nine of these 10 patients underwent serial head-up tilt tests after drug administration to determine the pathogenesis of vasovagal syncope. Atropine prevented tilt-induced syncope in 3 of 8 patients (37.5%), propranolol in 2 of 8 (25%) and etilephrine in 7 of 7 (100%). Seven patients received long-term drug treatment with drugs selected on the basis of acute drug testing. One responder to atropine received transdermal scopolamine and 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 12 months. Head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vasovagal reaction in patients with syncope of unknown origin. Withdrawal of alpha-sympathetic stimulation is a principal mechanism responsible for vasodilation and syncope during head-up tilt.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study. 197 97

The vaso-vagal nature of syncopes which remained unexplained despite full clinical and electrophysiological investigation was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (16 men and 14 women, mean age 63.6 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5.1) episodes of syncope of unknown origin were studied together with 11 asymptomatic control subjects. Head-up tilt test was considered positive if syncope developed in association with hypotension and/or bradycardia. During baseline head-up tilt 15 patients (50%) showed a positive test, with vasodepressor response (marked hypotension without marked bradycardia) in 10 cases and with mixed response (marked hypotension with marked bradycardia) in 5 cases. None of the control subjects became symptomatic during the test. Mean time to syncope was 24.9 minutes. Baseline head-up tilt test was reproducibly positive in 10 out of 14 patients (71%). Eight of these 10 patients underwent serial head-up tilt tests after atropine (0.04 mg/Kg i.v. in 1 minute), propranolol (0.2 mg/Kg i.v. in 3 minutes) and etilefrin (15-30 mg/day orally for 2-3 days) to determine the pathogenesis of vaso-vagal syncope. Atropine prevented tilt-induced syncope in 3 out of 7 patients (43%), propranolol in 2 out of 7 (29%) and etilephrine in 6 out of 6 (100%). Seven patients were chronically treated with drugs selected on the basis of acute drug testing. One patient-responder to atropine received transdermal scopolamine and the other 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 7.7 months, except 1 who experienced another episode of syncope after having discontinued etilephrine 4 months before. These results suggest that: 1) head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vaso-vagal reaction in patients with syncope of unknown origin; 2) withdrawal of alpha-sympathetic stimulation is the principal mechanism responsible for vasodilation and syncope during head-up tilt; 3) alpha-sympathomimetic agents, such as etilephrine, are effective in preventing spontaneous episodes of vaso-vagal syncope during a short-term follow-up.
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PMID:[Syncope of undetermined nature after electrophysiologic study. Usefulness of the head-up tilt test in the diagnosis of vaso-vagal origin and in the choice of treatment]. 197 2

A 64-year-old man who complained of palpitations brought on by swallowing was found to have short runs of paroxysmal supraventricular tachycardia (SVT) induced by swallowing. Electrophysiology studies suggested that the SVT was an automatic atrial tachycardia. An esophageal manometric study demonstrated that the tachycardia was coincident with relaxation of the upper esophageal spincter and preceded peristaltic activity in the esophageal body. Atropine and bethanechol did not affect the swallow-induced tachycardia. The patient's symptoms were controlled by verapamil and quinidine. After five months, these medications were discontinued, with no recurrence of symptoms. Based on analysis of ten prior cases and the present case, it appears that swallow-induced SVT generally occurs in men between the ages of 45-75 years who have no evidence of structural heart disease or an esophageal disorder. The SVT is usually either a nonsustained automatic atrial tachycardia or atrial fibrillation. The mechanism is conjectural, but the most likely possibility is a vagally-mediated neural reflex, probably involving a neurotransmitter other than acetylcholine.
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PMID:Supraventricular tachycardia induced by swallowing: a case report and review of the literature. 243 58

Tricyclic antidepressant drugs are known to cause often electrocardiographic abnormalities and to induce sometimes cardiac rhythm disturbances. We report a case of a patient on antidepressant therapy (Desipramine Hydrochloride, 50 mg/die, and Dothiepin Hydrochloride, 150 mg/die), without any underlaying heart disease, admitted to our Coronary Care Unit for recurrent syncopal episodes. An ECG on admission showed Sinus Tachycardia with Ectopic Ventricular Beats and recurrent runs of Torsade de Pointes, a distinctive form of Ventricular Tachycardia. Lignocaine i.v. was only transiently effective. Both Isoprenaline and Atropine Sulphate i.v. were uneffective. Ventricular Fibrillation occurred and cardioversion was achieved by a single DC shock. Amiodarone i.v. and electrical overdrive only temporarily suppressed ventricular arrhythmias. Magnesium Sulphate i.v. (bolus + infusion) induced a definitive suppression of Torsades de Pointes. One day later no more arrhythmias were present.
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PMID:[Torsade de pointes caused by tricyclic antidepressive agents. Description of a clinical case]. 355 44

Congenital or idiopathic complete A-V block with no detectable heart disease may be complicated by near syncope, syncope or sudden death. The proposed predictive "risk factors" of these events have not proved sufficiently reliable so far. This study was undertaken in order to re-evaluate the correlation between symptoms and clinical and electrophysiological data with particular regard to the junctional recovery time in 10 patients (4 M; 6 F; mean age 24.4 +/- 9.6 at our first observation) with congenital or idiopathic complete A-V block. Patients were divided into 2 groups: group A (3 M; 3 F; mean age 27.8 +/- 10.6 at our first observation) with patients who complained of vertigo, near syncope or syncope before our study; group B (1 M; 3 F; mean age 19.2 +/- 4.1 at first observation) without cardiovascular symptoms before our study. In group A, Holter monitoring revealed periods of asystole longer than 3000 ms in 2, and ectopic ventricular arrhythmias mainly during effort in 2; ergometric stress test performed in 3 patients demonstrated ectopic ventricular arrhythmias in 2 (those who had ectopic ventricular arrhythmias at rest). In all patients the site of the block was suprahisian (demonstrated by electrophysiologic endocavitary study) with a normal H-V interval; mean junctional recovery time was 4.600 +/- 1.620 ms and corrected junctional recovery time was 3.088 +/- 1.500. Four patients had vertigo during the electrophysiologic endocavitary study. After Atropine 0.02 mg/Kg i.v. junctional recovery time and corrected junctional recovery time decreased respectively to 1052 +/- 238 and 166 +/- 38 ms (the measurement was made in 5 patients). In group B Holter monitoring revealed periods of asystole longer than 3000 ms in 1 case. All patients had ectopic ventricular arrhythmias, confirmed by the stress test. In this group too, the block was suprahisian (electrophysiologic endocavitary study) with normal H-V. Mean junctional recovery time was 5162 +/- 2408 ms; and corrected junctional recovery time 3687 +/- 2202. Two patients complained of dizziness during the electrophysiologic endocavitary study. After Atropine 0.02 mg/Kg i.v., junctional recovery time and corrected junctional recovery time decreased respectively to 1300 +/- 356 and 260 +/- 145 ms. Four group A and 1 group B patients received a permanent pacemaker and have remained asymptomatic since.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinico-electrophysiologic relations in isolated complete atrioventricular block, congenital or idiopathic]. 637 52