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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wide complex tachycardias present diagnostic challenges for emergency physicians. The history, physical examination, and ECG provide information required to arrive at the correct diagnosis. When a previous history of heart disease exists, VT should be suspected; however, no single clinical feature is sufficiently reliable for distinguishing VT from SVT. Patients with VT may tolerate their dysrhythmias for several hours and maintain hemodynamic stability. ECG analysis is the most useful process in differentiating SVT and VT. Characteristics suggestive of VT include evidence of AV dissociation, QRS duration of longer than 0.16 seconds, and QRS axis between -90 degrees +/- 180 degrees. Predictive QRS morphologic criteria also have been established for VT. A four-step approach to ECG analysis has been reported to accurately identify patients with VT, but prospective validation in an ED setting is lacking. The initial approach to treating patients with wide QRS tachycardias depends on hemodynamic stability. Until the identify of a dysrhythmia is certain, consider all patients to be suffering from VT. Unstable patients require immediate cardioversion. Acute treatment of stable patients includes lidocaine or procainamide. Adenosine is appropriate when wide QRS SVT is the diagnosis, and it also has been used as a diagnostic aid to identify dysrhythmias. Reports of complications with the use of adenosine as a diagnostic agent have not yet appeared but may occur after sufficient numbers of cases have accumulated. Magnesium sulfate may be useful in refractory cases of VT and torsades de pointes. Chronic treatment of patients prone to VT may include complex pharmacotherapy and AICDs. Development of new class III agents and enhancement of AICD technology may result in improved patient outcomes and the availability of more choices for emergent therapy of wide QRS tachycardias.
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PMID:Wide complex tachycardia. 758 95

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6-12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 +/- 20 years (range 18-82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 +/- 80 msecs (range 260-580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on beta-adrenergic stimulation are most likely to be terminated by adenosine.
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PMID:Adenosine-sensitive atrial tachycardia. 773 78

Adenosine has become the drug of choice for termination of regular, normal QRS tachycardia. Initial studies in adult and pediatric patients have shown that the drug is effective for tachycardias using the atrioventricular (AV) node as an integral part of the tachycardia circuit and has few serious side effects. Experience with adenosine administration in children was reviewed to examine the diagnostic and therapeutic usefulness, effective dose, and adverse effects of adenosine. Adenosine was administered to 38 children during 50 separate electrophysiologic evaluations. Eleven patients had structural or acquired heart disease. Tachycardia mechanisms included orthodromic-reciprocating tachycardia using an accessory AV connection (23 patients), primary atrial tachycardia (6 patients), AV node reentrant tachycardia (3 patients), ventricular tachycardia (2 patients), postoperative junctional tachycardia (1 patient), and antidromic-reciprocating tachycardia (1 patient). Adenosine successfully terminated 51 of 53 episodes (96%) of tachycardia using the AV node, 5 of 10 primary atrial tachycardias, 1 of 1 junctional tachycardia, and 1 of 3 ventricular tachycardias. Reinitiation of tachycardia was seen after 16 of 58 successful terminations (28%), reducing the effectiveness to 39 of 53 (74%) for tachycardia requiring the AV node. Average effective dose was 132 micrograms/kg, range 50 to 250 micrograms/kg, and was slightly higher for peripheral (147 micrograms/kg) than for central (120 micrograms/kg) administration. Significant complications occurred in 4 of 38 patients, including atrial fibrillation, accelerated ventricular tachycardia, apnea, and 1 minute of asystole. Although adenosine is useful therapeutically and diagnostically in children with tachycardia, its effectiveness is limited by tachycardia reinitiation and adverse effects. Higher doses may be required for peripheral intravenous administration.
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PMID:Therapeutic and diagnostic utility of adenosine during tachycardia evaluation in children. 802 80

The mechanism of ventricular tachycardia (VT) that occurs in the absence of structural heart disease ("idiopathic" VT) is unknown, but may involve triggered activity or reentry through calcium channel-mediated conduction pathways. It has been suggested that termination of VT by adenosine is specific to ventricular arrhythmias caused by cyclic adenosine monophosphate-mediated triggered activity. The effects of vagotonic maneuvers, and intravenous adenosine (up to 0.25 mg/kg in incremental doses) and verapamil (0.145 mg/kg) administered to 9 patients with "idiopathic" VT were studied during electrophysiologic study. Seven patients had inducible fascicular VT and 2 had incessant right ventricular outflow tract tachycardia. Vagal maneuvers did not have any effect on any VT. Adenosine interrupted both right ventricular outflow tract tachycardias for a period (2 to 15 seconds) that was dependent on the dose of adenosine, but had no effect on VT in any patient with fascicular VT. Verapamil produced stuttering termination of right ventricular outflow tract tachycardia with no preceding change in RR interval in patients with this arrhythmia. Administration of verapamil to patients with fascicular VT was followed by gradual slowing of the arrhythmia (cycle length increased from 397 +/- 45 to 506 +/- 86 ms; p < 0.01) in all 7 patients and by termination of VT in 6. In conclusion, the differential response of fascicular and right ventricular outflow tract tachycardias to both adenosine and verapamil suggests that: (1) These 2 forms of idiopathic VT have different mechanisms. (2) Fascicular VT is unlikely to be due to cyclic adenosine monophosphate-mediated triggered activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intravenous adenosine on verapamil-sensitive "idiopathic" ventricular tachycardia. 816 Jun 12

Adenosine has been reported to cause polymorphic VT in patients with congenital or acquired prolonged QT intervals and to cause pause dependent VT in a patient with a normal QT interval. There have been no previous reports of adenosine causing nonpause dependent polymorphic VT in patients without structural heart disease. We report two patients, with normal hearts and normal QT intervals, who developed nonsustained polymorphic VT that was not pause dependent. Adenosine induced polymorphic VT does not appear to be a marker of the long QT syndrome, but may be an uncommon yet not unexpected pharmacological response to drug administration.
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PMID:Adenosine induced polymorphic ventricular tachycardia in adults without structural heart disease. 908 May 5

Tachyarrhythmias are common rhythm disturbances in infants and children. Despite the availability of diagnostic criteria arrhythmias are sometimes commonly misdiagnosed. Recent reports suggest that an endogenous purine nucleoside, adenosine, has a diagnostic effect in narrow QRS complex tachycardias, in addition to terminating supraventricular tachycardia involving the atrioventricular node. This report reviews the authors' experience with the use of adenosine for diagnosis of narrow and wide complex tachyarrhythmias in children. Adenosine was administered to 43 patients with several types of tachyarrhythmias (mean age, 8.3 +/- 5.24 years). Nineteen patients had structural or acquired heart disease. Of the 43 patients there were 28 (65%) several different types of narrow QRS complex tachycardia and 14 (33%) ventricular arrhythmias. One patient (2%) had long QT. Adenosine terminated supraventricular tachycardia, in 11 of 12 patients (92%), ventricular tachycardia in five of eight patients (63%), and transiently terminated premature ventricular contractions in two of six patients (33%). The diagnostic ability of adenosine was perfect in eight supraventricular tachycardia. In these eight cases the tachycardia mechanism was unclear before the administration of adenosine, which demonstrated three cases of sinus tachycardia, three of atrial flutter, one of atrial fibrillation and one of atrial fibrilloflutter. Confirmation of the primary diagnosis by adenosine was perfect in five tachyarrhythmias including three cases of atrial flutter, one of atrial fibrillation and one of ectopic atrial tachycardia. The average effective dose of adenosine was 212 micrograms/kg (range, 100-400 micrograms/kg). There were no serious side-effects except transient dyspnea, chest pain and flushing. These findings demonstrate adenosine to be helpful and safe in the diagnosis of tachyarrhythmias.
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PMID:Role of adenosine in the diagnosis and treatment of tachyarrhythmias in pediatric patients. 936 55

Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23+/-5 to 11+/-3 ms, P<0.01), to values similar to S, latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P<0.05). Adenosine had no effect on S, latency (9+/-2 vs. 9+/-2 ms) but decreased monophasic action potential duration from 202+/-37 to 158+/-38 ms (P<0.01). Adenosine was also given to 10 patients with S2 introduced at a coupling interval 40-50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than Si latency (21+/-12 vs. 9+/-2 ms, P<0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.
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PMID:Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli. 1052 20

Prior studies have demonstrated that sympathetic tone may influence the effects of adenosine on His-Purkinje automaticity, and that enhanced vagal tone may influence its effects on the sinus node. However, the interaction between autonomic tone and the effects of adenosine on the sinus node in humans remains unknown. Therefore, this study was designed to investigate the interaction between different states of autonomic tone and the bradycardiac response of the sinus node to adenosine. In 11 patients without structural heart disease who underwent a clinically indicated electrophysiology procedure, the sinus cycle length was measured before and after a 12-mg bolus of adenosine in the baseline state, during an infusion of 2 mcg/min of isoproterenol, after the administration of 0.2 mg/kg of propranolol, and again after the administration of 0.04 mg/kg of atropine. Adenosine significantly lengthened the sinus cycle length in the baseline state (760 +/- 165 vs 909 +/- 188 ms, P < 0.05), during isoproterenol infusion (516 +/- 67 vs 766 +/- 146 ms, P < 0.05), after propranolol (850 +/- 153 vs 914 +/- 143 ms, P < 0.05) and after the combination of propranolol and atropine (662 +/- 76 vs 801 +/- 121 ms, P < 0.05). The degree of lengthening in sinus cycle length was significantly greater (P < 0.05) during isoproterenol infusion (253 +/- 157 ms, or 51% +/- 40%) than in the baseline state (149 +/- 85 ms, or 20% +/- 12%), after propranolol (68 +/- 53 ms, or 8% +/- 8%), and after propranolol and atropine (140 +/- 110 ms, or 21% +/- 18%). The negative chronotropic effect of adenosine is influenced by autonomic tone. The effect of adenosine on the sinus node is accentuated by beta-adrenergic stimulation and unaffected by beta-adrenergic blockade or combined beta-adrenergic and cholinergic blockade.
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PMID:Interaction between autonomic tone and the negative chronotropic effect of adenosine in humans. 1064 33

Sudden infant death syndrome (SIDS) occurs silently usually during sleep and, though remaining unexplained after autopsy, leaves footprints creating a pattern analogous to that which follows a flood of nitric acid (NO). These footprints in SIDS are associated with serious pathological changes, viz. elevated hepatic iron, bone marrow hyperplasia, hypomyelinated respiratory control centres, elevated lung immunoglobulins, cerebral hypoperfusion resembling lesions induced by chronic hypoxemia, ischemia, congenital heart disease and congenital myopathy. Hypoxia stimulates the immune response and the over-arousal of the immune response triggers a flood of NO. Adenosine triggers sleep. NO and adenosine are additive as dilators of coronary blood vessels. Blood pressure collapses. Selenium increases the activity of the enzyme ferrochelatase during incorporation of heme into cytochrome oxidase. NO binds to cytochrome oxidase, inhibiting respiration. When NO reaches dangerous levels, the cell turns on production of heme oxygenase. Heme is broken down to iron (Fe) carbon monoxide (CO) and bile pigments. NO has a huge affinity for hemoglobin which catalyses NO degradation to nitrate. Furthermore, NO is a product of smoke and SIDS incidence is higher in smoking mothers.
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PMID:Association of sudden infant death syndrome with grossly deranged iron metabolism and nitric oxide overload. 1079 Jul 39

Supraventricular tachycardias are the most frequent forms of symptomatic tachyarrhythmias in infants, children and adolescents. Clinical symptoms depend on age and underlying cardiac anatomy. Newborn babies and infants with paroxysmal atrioventricular reentrant tachycardias usually present with signs of congestive heart failure due to rapid heart rate. In older children and adolescents, palpitations are the leading symptom. Patients with chronic-permanent tachycardias (i.e., atrial ectopic tachycardia, permanent form of junctional reciprocating tachycardia) often develop a secondary form of dilated cardiomyopathy, the so-called "tachymyopathy". Adenosine has evolved as the drug of choice in any age group for the termination of atrioventricular reentrant tachycardia of any origin. In addition, it serves as a diagnostic tool in primary atrial tachycardias. Long-term management of atrioventricular reentrant tachycardia in infancy and childhood is age dependent. In newborn babies and infants, pharmacological therapy is advised due to the high spontaneous cessation rate of those tachycardias at the end of the first year of life. In contrast to this, the probability of spontaneous cessation of tachycardia in children > 1 year of age is very low. Therefore, radiofrequency catheter ablation of the anatomical substrate of the tachycardia is a rational alternative to long-lasting antiarrhythmic therapy. Results in children with a structurally normal heart are comparable to those achieved in adults. In patients with congenital heart disease and supraventricular tachycardias, catheter ablation during preoperative cardiac catheterization is recommended. Atrial reentrant tachycardias have been identified as one major risk factor for late postoperative morbidity and mortality in young patients. Pharmacological therapy is often not sufficient to control the tachycardia. In addition, underlying sinus node dysfunction may be aggravated in a considerable portion of the patients affected. Catheter ablation based on conventional endocardial mapping techniques by multipolar electrode catheters with the aim of identifying the critical region of the reentrant circuit is associated with an impaired success rate and a considerable recurrence rate. It may be assumed that, using the modern mapping techniques currently available (electroanatomical mapping and non-contact mapping), results of radiofrequency catheter ablation of atrial reentrant tachycardias after surgical correction of congenital heart disease will be significantly improved within the next few years.
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PMID:[Supraventricular tachycardia in infants, children and adolescents: diagnosis, drug and interventional therapy]. 1092 40


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