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 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Utilizing a Doppler ultrasonic flowmeter catheter, phasic instantaneous aortocoronary saphenous vein bypass blood velocity was recorded during various atrial arrhythmias in 17 patients. Atrial premature beats, supraventricular tachycardia and atrial fibrillation reduced peak bypass graft blood velocity in relation to the heart rate and diastolic cycle length. Such changes were more evident during the systolic fraction of bypass blood flow. In a single subject, systolic blood velocity alternans was observed during the course of atrial tachycardia. It is concluded that such study provides insight into the dynamics of bypass graft blood flow velocity during atrial arrhythmias.
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PMID:Effects of atrial arrhythmias on aortocoronary bypass graft blood velocity in man. 30 45

Seventy three infants who underwent neonatal anatomical correction for transposition of the great arteries with or without a ventricular septal defect were reviewed for evidence of conduction and rhythm abnormalities on preoperative and postoperative 12 lead electrocardiograms and during 24 hour Holter monitoring. There was a partial right bundle branch block pattern in 47% (29/62) of all patients and in 60% (24/40) of those with simple transposition. Complete right bundle branch block was noted in 21% including 5% with simple transposition. Holter monitoring showed sinus rhythm in all patients except three: one had episodes of supraventricular tachycardia, another an intermittent second degree heart block, and a third a complete heart block. Atrial extrasystoles were noted in 47% (29/62) of patients but were frequent in only three patients. Occasional unifocal ventricular extrasystoles were encountered in 37% (23/62) of patients and were frequent in a further 3% (2/62). Only one patient (2%) developed multifocal ventricular extrasystoles. The frequency of important cardiac arrhythmias after neonatal anatomical correction of transposition of the great arteries was 5%, significantly less than that reported after atrial inflow diversion for the same malformation.
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PMID:Cardiac conduction abnormalities and rhythm changes after neonatal anatomical correction of transposition of the great arteries. 155 42

The clinical characteristics of supraventricular tachyarrhythmias (SVTA) and their relation to left ventricular dysfunction were assessed in 208 consecutive patients with recent myocardial infarction. Arrhythmias were quantified on hospital discharge by 24 hour electrocardiographic recording. All the variables were evaluated between the second and the fourth week after infarction. SVTA occurred in 113 (54%) patients: Supraventricular premature beats (SVPB) in 49 (24%), frequent or repetitive SVPB in 37 (18%), atrial or junctional tachycardia in 23 (11%), atrial flutter or fibrillation in 4 (2%). Most of these arrhythmias occurred in the absence of symptoms, and the most complex forms were always selflimiting. No relation was found among the presence of different forms of SVTA and sex, coronary risk factors, previous history of ischemic heart disease, type or site of acute myocardial infarction, NYHA functional class. Age, left atrial dimension (LAD), cardio-thoracic ratio (CTR) and left ventricular ejection fraction (LVEF) at rest differed significantly among three groups of patients: those without SVTA, those with SVPB less than 100 per hour and those with frequent-repetitive SVPB or atrial-junctional tachycardia. The more SVTA complexity, the worse LAD, CTR, LVEF and the higher the age. Multivariate discriminant analysis showed that CTR was directly and LVEF inversely related to the occurrence of SVPB less than 100 per hour, while the presence of frequent-repetitive SVPB or supraventricular tachycardia was closely related to increasing age, LAD, CTR and decreasing LVEF. Patients with atrial fibrillation always showed the worst values of LAD, CTR, LVEF and age. The results of the present study show that different types of SVTA occurring at discharge from hospital after myocardial infarction are clinically benign, but always suggestive of different degrees of left ventricular dysfunction.
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PMID:The relation between supraventricular tachyarrhythmias and left ventricular dysfunction after acute myocardial infarction. 326 15

Atrial ectopic tachycardia is an uncommon life-threatening supraventricular tachycardia in children and is resistant to usual antiarrhythmic drugs. Whereas the cellular mechanism of atrial ectopic tachycardia is unknown, atrial ectopic tachycardia may be due to a form of automaticity. Moricizine HCl has been used primarily for ventricular rhythm disturbances; the drug depresses abnormal automaticity and delayed after-depolarizations but has little effect on normal automaticity. Because of this property, we have used moricizine HCl in 4 patients with atrial ectopic tachycardia. As evidenced by continuous 24-hour Holter monitoring, moricizine HCl was successful in suppressing atrial ectopic tachycardia in each patient. During a limited follow-up (6 months) no side effects have occurred. Moricizine HCl is a promising primary drug for atrial ectopic tachycardia.
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PMID:Ethmozine (moricizine HCl): a promising drug for "automatic" atrial ectopic tachycardia. 331 May 91

In an attempt to narrow the definition of normal ventilatory response to hypercapnia (SVE), we studied 105 healthy Caucasians, aged from 18 to 80 years and living at sea level. The mean and SD of SVE were 2.18 +/- 0.77 1 X min-1 X mmHg-1 in males and 1.70 +/- 0.74 in females, narrower than the ranges previously reported. The 95% tolerance limits were 0.491-3.735 and 0.241-2.963 respectively. SVE was correlated with height, body surface area, static and dynamic lung volumes (p less than 0.01), age and weight (p less than 0.05). A prediction formula for SVE was derived on the basis of FEV1, which of the above parameters best correlated with SVE. The separate measurement of the tidal volume and frequency changes (SVT, Sf and SVT/Sf) showed that the SVT and SVT/Sf were significantly higher in males than in females even after adjustment for lung volume (p less than 0.01 and p less than 0.02 respectively), suggesting a different pattern of response to hypercapnia between the sexes.
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PMID:Ventilatory response and pattern of breathing during hypercapnia. 369 40

Fetal arrhythmias were detected in 33/198 high risk pregnancies from 21 weeks to term. Using the two-dimensional echocardiographic image of the fetal heart as a guide, the M-mode beam was directed to define the motion of the ventricular and atrial walls and atrioventricular valve or semilunar valves. Atrial contraction was defined either by the atrial wall motion or from the A-point of the atrioventricular valve. Ventricular contraction was defined by closure of the atrioventricular valve (C-point), the onset of ventricular wall contraction, or from the semilunar valve opening. Ladder diagrams of the sequence of atrial and ventricular activation were constructed to define the temporal sequence of these events. Premature atrial contractions were present in 12. In one fetus this arrhythmia converted into supraventricular tachycardia while in the other 11 fetuses the course was benign. Two fetuses had premature ventricular contractions. Supraventricular tachycardia was noted in five fetuses. One with hydrops at 29 weeks returned to sinus rhythm following maternal administration of procainamide. A second hydropic fetus with paroxysmal atrial tachycardia and hydrops failed to respond to digitalis, propranolol, procainamide, verapamil, or amiodarone, and died shortly after cesarean section. Two mature fetuses had tachycardia close to term and were treated after cesarean section. One fetus with runs of atrial tachycardia died in utero. Three fetuses had complete heart block, two of whom were from mothers with connective tissue diseases. In four fetuses, there was bradycardia of less than 100/minute lasting more than 30 seconds, but these episodes disappeared in 2 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recognition of fetal arrhythmias by echocardiography. 392 48

A total of 114 children (age range 4 months to 18 years) underwent definitive operation for life-threatening or incessant tachydysrhythmias resulting from accessory conduction pathways (Kent bundle) (79), atrial ectopic foci (18), or ventricular ectopic foci (17). Of the patients with the accessory pathway type of supraventricular tachycardia, 63.3% (50/79) had classical Wolff-Parkinson-White syndrome whereas 36.7% (29/79) had retrograde conduction only across the pathway. Locations of the pathways were as follows: left posterior 48.1% (38/79), right anterior or lateral 27.8% (22/79), posterior septal 16.5% (13/79), anterior septal 3.8% (3/79), and both right and left 3.8% (3/79). With increasing experience, the success rate (cure of tachycardia) improved from 85% in the first 40 patients to 95% in the last 40 patients. One surgical death (1.3%) occurred secondary to a paradoxical air embolus. Atrial ectopic tachycardia was treated by cryoablation (nine), excision (one), combined excision and cryoablation (six), and atrial disconnection (two). The ectopic focus was located on the right atrial wall in 13 patients (72.2%) and cardiopulmonary bypass was required in eight (44.4%). The operation was successful in 89%; two patients with multiple ectopic foci continued to have uncontrolled tachycardia after the operation. Ventricular tachycardia presenting in the first 2 years of life was due to gross tumor in three cases (rhabdomyoma two, fibroma one) or microscopic hamartomatous change (Purkinje tumor) in five cases and was treated by excision alone or with adjuvant cryoablation. In four cases no tumor was found but the area of ectopic focus was successfully cryoablated. One child with diffuse endocardial tumor died of low cardiac output after the operation. Ventricular tachycardia in older children was localized to outflow patch aneurysms or other areas in the right ventricle following tetralogy of Fallot repair (three patients, treated by excision or cryoablation) and arrhythmogenic right ventricular dysplasia (two patients, treated by right ventricular disconnection). We conclude that mapping and operation for supraventricular tachycardia resulting from accessory pathways are predictable and curative in a high percentage of patients. Atrial ectopic tachycardias are more difficult to precisely localize but can be cured by a combination of excisional and cryoablative techniques. Ventricular tachycardia in infants is lethal and is commonly due to ectopic foci or microscopic tumors that may not be apparent on preoperative angiography or echocardiography. Electrophysiologically directed operations in these patients can be lifesaving.
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PMID:Definitive operation for refractory cardiac tachyarrhythmias in children. 405 40

Continuous 24 hour electrocardiography (Holter method) was carried out during work time in 64 workers. They were divided into two groups: the first group comprised 34 subjects with either organic heart disease (coronary artery disease, valvular heart disease, operated coarctation, hypertrophic cardiomyopathy) or a documented arrhythmia without proven underlying cardiac disease; the second group comprised 30 subjects without known cardiac disease but complaining of symptoms suspected to be of cardiac origin or with isolated electrocardiographic abnormalities. At the end of the study we concluded that Holter monitoring is possible in subjects performing physical occupations even in difficult conditions. The trends of heart rate, especially mean heart rate calculated over 10 minute periods, confirmed the relationship between heart rate and the intensity of the physical activity. Atrial extrasystoles and episodes of supraventricular tachycardia were as common in the first as in the second group (20% and 18% respectively). This did not apply to ventricular extrasystoles: they were observed in both groups but were significantly more common in the first group (55% compared to 33%); ventricular extrasystoles, usually of a single configuration and isolated, were more common in the first group, especially amongst the coronary patients. Sinus node dysfunction was only observed in the second group (12.5%), in young subjects, and this occurred with only one exception at night. These findings support previous reports in the literature. However, the interpretation of these results is difficult because of the absence of well established normal values.
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PMID:[Continuous electrocardiographic registration in occupational medicine]. 642 4

A 58 year old man who died of metastatic carcinoma had undergone electrophysiological investigation 4 years previously for a Wolff-Parkinson-White syndrome (Rosenbaum Type A, Frank and Boineau Type IV) associated with supraventricular tachycardia (SVT) at 180/mn, atrial fibrillation and flutter and slow junctional (or low atrial) rhythm at 70-80/mn. Atrial extrasystoles or appropriate atrial stimulation not only induced and terminated the SVT but also the junctional rhythm and allowed passage from one arrhythmia to another. These studies showed the presence of a left lateral Kent bundle responsible for orthodromic SVT with retrograde conduction through the accessory pathway, and suggested that the junctional rhythm might be due to longitudinal dissociation of the AV node. Autopsy findings confirmed the presence of the left posterolateral Kent bundle in an almost horizontal position, parallel to the mitral annulus (it might therefore have escaped eventual surgical section) and the longitudinal dissociation of the AV node.
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PMID:[Wolff-Parkinson-White syndrome and longitudinal dissociation of the atrioventricular node. Anatomical and electrophysiological correlates]. 679 2

Atrial premature beats are caused by premature and abnormal depolarization of the atria, responsible for an anticipated QRS complex. Usually, the shape of this complex is identical to that of sinus beats. The diagnosis is made by electrocardiography, but it may meet with problems due to lack of recognition of premature P waves (and the more so as these may not give a ventricular response) or to the deformation of the QRS complex by a bundle branch block mimicking a ventricular premature beat. As in all instances, premature atrial beats are generally followed by a pause. Atrial premature beats, isolated in most cases, may trigger off supraventricular tachycardia episodes of varying duration. The clinical expression of atrial premature beats ranges from perceptible palpitations to complete latency. The decision to treat is determined by the functional repercussions of the disorder. Supplementary data are always useful to evaluate the significance of the disorder. Using the Holter recording system makes it possible to count the premature beats over a 24 h period, to find out whether they are preponderant in day time (suggesting an adrenergic factor) or at night (suggesting vagotonic disorders), and to identify bouts of atrial fibrillation that would have not been felt. Investigations for an underlying heart disease are mandatory. Any one of the cardiopathies of adulthood, and notably mitral valve lesions, may be encountered, as well as congenital heart diseases such as interatrial communication. The frequency of atrial premature beats tends to increase as cardiac failure develops, and its course can be made worse by some drugs (such as digitalis compounds) or by metabolic disorders (e.g. hypokaliaemia). However, there are many cases where no cardiopathy is detected. Within the group of isolated atrial premature beats, disorders found in athletes (in theory manifestations of hypervagotonia) can be individualized. In practice, therapeutic abstention is the rule, especially when premature beats are latent. In cases with poor functional tolerance, nervous sedatives of beta-blockers may be useful. Antiarrhythmic drugs are rarely necessary, but they may be prescribed if episodes of paroxysmal atrial fibrillation are present.
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PMID:[What is a practical approach to atrial extrasystole?]. 769 54


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