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

Having observed 18 cases, the authors describe a syndrome of recurrent paroxysmal atrial arrhythmia which was very homogeneous from the clinical and ECG point of view. It was usually found in middle aged males, with no demonstrable underlying heart disease, whose disorder of intra-atrial conduction occurred during sinus rhythm. The condition developed slowly over the course of years towards a maximum incidence of several short daily attacks of an arrhythmia which alternated between an atrial fibrillation and atrial flutter. Vagal overactivity is the precipitating cause of these attacks which are usually not completely nocturnal. The condition never progressed to sino-atrial block nor to permanent fibrillation. The beginning of each attack, often heralded by atrial coupling with a long enough interval to cause re-entry, is accompanied by slowing of the sinus rate down to the threshold level. The vagal effect of shortening the action potential and refractory period is recognised to be non-homogeneous in the atrial wall, and suggests a re-entry mechanism rather than hyper-excitability. This would explain the usual resistance of atrial arrhythmias of vagal origin to digitalis, beta blockers and quinidine. Amiodarone alone is usually effective because of the prolongation of the action potential which it causes. In 5 particularly resistant cases a good clinical result was obtained by the insertion of an atrial pacemaker with a fairly rapid rate.
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PMID:[The atrial arrhythmia syndrome of vagal origin]. 2 9

The authors report 6 cases of acute respiratory failure complicating chronic bronchial and lung disease admitted to hospital with the diagnosis of: heart disease, 3 cases, pulmonary oedema, pulmonary embolism, atrial flutter; status asthmaticus : one case; neuro-psychiatric disease : 2 cases (toxic coma and agitation). The authors emphasize the frequency of chronic bronchial disease and recall the signs of acute decompensation discussing the possible difficulties in diagnosis and the therapeutic implications.
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PMID:[Deceptive and revealing clinical forms of acute respiratory insufficience in chronic bronchopneumopathies]. 19 94

The experience of three institutions in the management of atrial flutter in infants under 2 years of age without associated heart disease is reviewed. Five babies with neonatal onset were treated with digoxin and had uncomplicated resolution of their arrhythmia, although one continued to have episodes of paroxysmal supraventricular tachycardia for six years. Two of the three older infants required DC cardioversion for complications after quinidine was substituted for digoxin therapy. Digoxin continues to be the preferred initial therapy for non-acutely ill patients; those showing signs of cardiac decompensation should be converted with DC countershock.
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PMID:Idiopathic atrial flutter in infancy: a review of eight cases. 26 74

Disturbances of heart rhythm, observed during 700 heart catheterizations in infants and children, are discussed. Paroxysmal supraventricular tachycardia has been observed in 25 investigations (3,6%), sinus bradycardia in 18 (2,6%), junctional rhythm in 10 (1,4%), second degree AV-block in 9 (1,3%), ventricular fibrillation in 8 (1,1%), sinus tachycardia in 7 (1%), complete block in 7 (1%), asystole and atrial flutter in 2 (0,3%) each, and ventricular tachycardia in 1 (0,15%). Supraventricular tachycardia occurred equally in all ages without preference of a special malformation. The two patients with WPW-syndrome, however, showed this disorder in each of three catheterizations. Propranolol and verapamil succeeded in terminating the attacks. Junctional rhythm and sinus tachycardia presented equal behavior and benignity. Sinus bradycardia, second and third degree AV-block, and especially ventricular fibrillation occurred mostly in neonates and infants, many of them cyanotic and suffering from complex malformations and therefore needing multiple catheter manipulations. Bradycardia was in two, asystole in one of the very sick neonates associated with subsequent death within 24 hours. Once asystole resulted in immediate death after pulmonary angiography in a child with severe pulmonary hypertension. Ventricular fibrillation could be terminated promptly by DC countershock in all patients, but three of the children died subsequently. Complete block occurred only in children with systemic right ventricular pressure, 4 of the 7 patients having pulmonary hypertension, too. In two instances the block subsided spontaneously, the rest could successfully be treated with orciprenaline (Alupent R). Life threatening arrhythmias became less frequent as a consequence of earlier investigation, if severe heart disease was suspected, and by closer control of cyanosis, acidosis and temperature before, during, and after catheterization.
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PMID:[The risks involved in the heart catheter examination. A retrospective evaluation of the complications after 700 examination. III. Irregularities of heart (author's transl)]. 53 Jul 27

The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil.
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PMID:Effects of intravenous verapamil on cardiac arrhythmias and on the electrocardiogram. 116 42

Out of a pacemaker population of 392 patients, 90 (23%) have been found to have sinoatrial syndrome. Their ages ranged from 22 to 86 years, and averaged 66 for men and 70 for women. The male-to-female ratio was 1:1.6. Before pacemaker implantation, syncopal attacks had occurred in 54%, dizziness without syncope in 31% and tachyarrhythmias in 57%. Atrial or paroxysmal supraventricular tachycardia had been recorded in 33%, atrial fibrillation or flutter in 28%, and ventricular tachycardia in 11%. First and/or second degree AV block was found in 36%. Coronary heart disease was present in 61% and 20% had had myocardial infarction. Cardiomyopathy and previous carditis were other associated heart diseases. Sinoatrial syndrome was the only manifestation of heart disease in 20%. Follow-up time after pacemaker implantation ranged from 3 months to 7 years, mean 23 months. Syncopal attacks were stopped in 48 of 49 patients, dizziness was relieved in all 28 patients and tachyarrhythmias were controlled by combined drug treatment in 43 of 51 patients. Nineteen patients died during the follow-up, most of them of cerebrovascular events or myocardial infarction. Associated coronary heart disease was especially frequent in this group. The death of one patient was caused by a run-away pacemaker. Other pacing failures were due to electrode movement or premature battery exhaustion. There was no mortality associated with pacemaker implantations or replacements. These results strongly support the view that pacemaker treatment most effectively controls symptoms of sinoatrial syndrome when drug treatment fails.
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PMID:Treatment of sinoatrial syndrome with permanent cardiac pacing in 90 patients. 119 8

In 20 children needing treatment for symptomatic sick sinus syndrome, the average age at presentation was 7.1 years and ranged from 9 months to 18 years. Symptoms were never precise but, in retrospect, 5 children had syncope, 7 had a rapid heart action, 6 had dyspnoea or tachypnoea, 2 had nonspecific chest pains, 2 had pale spells, and 1 had a sudden hemiplegia. Symptoms followed cardiac surgery in 15 cases and were related to unoperated congenital heart disease in 2 and to myocarditis in 2. The aetiology was unknown in 1 case. The type of cardiac surgery resulting in the development of the sick sinus syndrome was predominantly related to atrial suturing. Both tachy- and bradydysrhythmias were found, including wandering atrial pacemaker (9 cases), junctional rhythm (19 cases), supraventricular tachycardia (9 cases), atrial flutter (11 cases), and atrial fibrillation (2 cases). Both atrial (8 cases) and ventricular (7 cases) premature beats were seen. All patients were given trials of drug therapy but difficulties were encountered. Cardioversion was used for tachyarrhythmias in 11 cases without serious problems. Six children had permanent cardiac pacemakers inserted with good results. Recognition of the sick sinus syndrome in childhood is important and treatment must be regulated by the severity of symptoms.
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PMID:Sick sinus syndrome. Symptomatic cases in children. 121 60

Atrial flutter is a common and usually benign but symptomatic supraventricular tachycardia. There is a striking similarity between patients with atrial flutter suggesting a common substrate despite the presence or absence of underlying heart disease. In man, the mechanism is a single reentrant circuit originating in the right atrium whose center appears to be functional within the anatomical constraints of the right atrium. The reentrant circuit of atrial flutter contains an area of slow conduction in the inferior right atrium but the size and exact location is uncertain. Drug therapy directed at terminating and preventing atrial flutter has been available for many years. The efficacy and safety of this therapy is not as well tested as is the same therapy for atrial fibrillation. The most effective way to terminate atrial flutter is a nonpharmacological approach. Several nonpharmacological methods provide new treatment options in the management of patients with drug resistant or hemodynamically unstable atrial flutter. The use of anticoagulation for this disorder is still evolving. There is a risk of clinically apparent thromboemboli in some patients with atrial flutter although the risk appears less than that for atrial fibrillation. In the future, refinements and improvements in therapy for atrial flutter will likely be derived from a better understanding of its mechanism.
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PMID:Atrial flutter--update on the mechanism and treatment. 128 52

We describe, to the best of our knowledge for the first time, the occurrence of idiopathic atrial flutter (AF) in two male children of a family. The two brothers are the third and sixth of seven children, and the only males. The parents do not suffer from any heart disease. The first sister died in Turkey at the age of twenty days. The parents do not know the cause of death. The fourth sister died at de age of five years, also in Turkey, probably because of meningitis. Electrocardiograms of the parents and the other three sisters are normal. Besides the unique familial occurrence, the AF themselves offer some unusual features. In the first patient, the AF could not be converted to sinus rhythm. In the second patient, the AF occurred paroxysmally, and in addition to the AF, the electrocardiogram tracings revealed paroxysmal atrial tachycardia.
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PMID:[Familial manifestation of idiopathic atrial flutter]. 137 70

Flecainide (100 mg twice daily) was used for prevention of paroxysmal atrial fibrillation (PAF) in 52 patients with frequent symptomatic attacks that were resistant or intolerant to quinidine (600-900 mg/day). Underlying heart disease was present in only 8 cases and left ventricular ejection fraction was always greater than 30%. No patient had had a myocardial infarction. Vagally induced PAF was clinically documented in 35 patients. Amiodarone, previously used and ineffective, was combined with flecainide in 33 patients. After 1-5.8 years of follow-up, complete disappearance of PAF was observed in 38 patients (73%). The success rate was slightly higher in patients with vagally induced PAF (p = 0.07). Extracardiac side effects necessitated withdrawal in only 3 cases. Permanent pacemaker was needed in 7 patients on amiodarone and flecainide because of excessive sinus bradycardia. Two patients, with previously documented atrial flutter, experienced presyncopal episodes of atrial flutter with 1:1 atrioventricular (AV) conduction and wide QRS complex. No death occurred during the follow-up. In this series, quinidine proved to be unsuccessful in 46 patients and it was withdrawn in 6. We concluded that flecainide is efficient and well tolerated for long-term prevention of PAF in patients resistant to quinidine. The possibility of 1:1 AV conduction during atrial flutter may suggest the use of verapamil or beta blockers in combination with flecainide in patients with previously documented atrial flutter.
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PMID:Flecainide in quinidine-resistant atrial fibrillation. 151 1


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