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)

Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.
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PMID:Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug. 173 70

Thirty-five patients with bundle branch block (BBB) and unexplained syncope underwent electrophysiologic study (EPS) including programmed ventricular stimulation and ajmaline administration (1 mg/kg, IV) to induce infra-His block. A prolonged HV interval (greater than 55 ms) was present in 16 of the 35 patients. Ajmaline-induced HV block occurred in 12 patients (complete HV block in 10, and 2:1 HV block in two). Monomorphic ventricular tachycardia (VT) was inducible in nine (25.7%) and polymorphic VT in two patients (5.7%). Left ventricular ejection fraction (LVEF) was less than 40% in five patients (45.5%) with inducible VT. Two patients had an unexpected co-existence of inducible HV block and VT. The remaining 14 patients (40%) had no detectable abnormality. The incidence of inducible VT was higher (45% vs 13.3%), and the presence of negative studies was lower (30% vs 53.3%) in patients with structural heart disease (n = 20), when compared to those with no significant heart disease (n = 15) (differences not significant [NS]). During a mean follow-up period of 16.5 +/- 9.2 months, all the patients with inducible HV block have been asymptomatic after having received permanent pacemakers. Patients with inducible monomorphic VT (except one with poor left ventricular function who died suddenly) have also been asymptomatic on antiarrhythmic drugs. Of the remaining patients, seven with normal EPS, two with prolonged HV intervals but no inducible HV block (despite being given permanent pacemakers) and one patient with polymorphic VT on antiarrhythmic drugs continue to have recurrent syncope. Approximately 60% of patients with BBB and unexplained syncope have clinically significant electrophysiologic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of patients with bundle branch block and "unexplained" syncope: a study based on comprehensive electrophysiologic testing and ajmaline stress. 245 15

The clinical, ECG and electrophysiological data of 37 patients (28 males and 9 females) with spontaneous intra-hisian block are reported. Of these patients, 11 had hypertensive heart disease and 5 had ischemic heart disease with previous myocardial infarction; in 21 patients, clinical signs of heart disease were not evident. In 18 patients, a single or recurrent episode of syncope had occurred. One patient had junctional rhythm and 36 sinus rhythm; among these, 12 patients presented PR greater than 200 msec (7 with a narrow and 5 with a wide QRS); 12 patients had a single or bilateral bundle branch block; 12 had a normal ECG. The electrophysiological study showed a split H-H1 in 22 patients, a wide His deflection (H greater than 25 msec) in 4 and HV greater than 65 msec with narrow QRS in 11. In 17 patients a more or less marked sinoatrial node and/or atrioventricular node dysfunction was present. Atrial pacing, performed in all, induced 2nd degree Mobitz 2 intra-hisian block in 9 patients. Ajmaline was used in 16 patients but induced a complete intra-hisian block in only one. In 28 patients a preventive pacemaker was implanted after electrophysiological study. During the follow-up (mean 25 months/pt.), 38% of the patients developed complete atrioventricular block. No recurrence of syncope occurred in the paced patients. Comparison of patients who developed atrioventricular block and those who maintained normal atrioventricular conduction did not show differences as far as heart disease, previous syncope, ECG pattern and results were concerned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous grade I bundle of His block. Clinical, electrocardiographic and electrophysiological studies in 37 patients]. 274 10

The efficacy of ajmaline (50-75 mg i.v.) or lidocaine (100-200 mg i.v.) in terminating persistent, haemodynamically stable ventricular tachycardia (VT) was compared in a prospective, randomized trial of 31 patients. There were no significant differences as to age, underlying heart disease, ejection fraction and rate of ventricular tachycardia between the two treatment groups. Ajmaline terminated VT in 10 of the 15 patients receiving it, lidocaine in only 2 of 16 (P less than 0.01). The frequency of VT was not significantly changed by lidocaine, while mean cycle length during VT changed under ajmaline from 369 +/- 82 ms to 452 +/- 11 ms (P less than 0.01). In contrast to lidocaine, QRS duration under ajmaline lengthened from 166 +/- 18 ms to 200 ms +/- 28 ms (P less than 0.01), but return cycles after tachycardia termination were similar (ajmaline, 863 +/- 296 ms; lidocaine, 917 +/- 367 ms). Both drugs were equally well tolerated, but in this series ajmaline was more effective in the acute treatment of persistent VT.
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PMID:[Emergency therapy of ventricular tachycardias: lidocaine versus ajmaline]. 304 23

A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (MAPs) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. Ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial MAPs may demonstrate regionally different action potential changes that may contribute to the ECG changes in Brugada syndrome.
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PMID:Transient local changes in right ventricular monophasic action potentials due to ajmaline in a patient with Brugada Syndrome. 1041 81

We report about a 20-year old patient suffering cardiopulmonary resuscitation due to ventricular fibrillation. We diagnosed Brugada syndrome after exclusion structural heart disease and a positive Ajmalin test and implanted an ICD. In that there is a 20-30% familiar disposition, it was necessary that all family members undergo a cardiac examination. It was found that one brother and one sister presented the beginning of a right ventricular dilatation and a fibrolipomatous area in the anterior wall segment of the right ventricle. This result is compatible with a "concealed" arrhythmogenic right ventricular dysplasia (ARVD). As a prognostic indication we decided to implant an ICD prophylactically. The case report demonstrates the value of familiar examination of patients with an unclear ventricular arrhythmogenic event.
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PMID:[Brugada syndrome or ARVD (arrhythmogenic right ventricular dysplasia) or both? Significance and value of right precordial ECG changes]. 1213 89

Brugada syndrome (BrS) represents an inherited disorder associated with risk of sudden cardiac death due to VF in patients without structural heart disease. Currently, BrS is diagnosed by typical cove-shaped ST-segment elevation >2 mm in >1 RV precordial lead V1, V2 occurring spontaneously or after a sodium-channel blocker provocation test without any further evidence of malignant arrhythmias. An ICD should always be implanted in symptomatic BrS patients to prevent sudden death, despite high rates of complications with these devices. In asymptomatic people, an electrophysiological study should be performed to evaluate the need for an ICD. The recent discovery of a functional substrate has revolutionised our approach to the pathophysiology and management of BrS. Promising new therapeutic options have emerged in the last 3 years. Ajmaline is able to determine the extension of the substrate by prolonging the duration and fragmentation of abnormal epicardial electrograms. Substrate ablation results in the disappearance of both coved-type ECG and ventricular tachycardia/VF inducibility. These findings are clinically relevant, suggesting that epicardial ablation guided by ajmaline infusion may be an effective therapeutic option in BrS, potentially removing the need for ICD implantation.
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PMID:Brugada Syndrome: Progress in Diagnosis and Management. 3091 62