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

Helsinki, a city of 500,000 inhabitants, is served by a two-tiered emergency medical system with basic emergency medical technicians in ordinary ambulances and one physician-staffed prehospital emergency care unit. All 266 patients with prehospital cardiopulmonary resuscitation during 1987 were studied. Two hundred twelve patients with presumed heart disease and a witnessed arrest were analyzed further. Their response times for basic life support and advanced life support were 5.5 and 10.7 minutes, respectively. The initial cardiac rhythm in 144 patients (68%) was ventricular fibrillation. In 79 of these patients, cardiopulmonary resuscitation was successful, and 39 patients (27%) were discharged from hospital. The patients who survived had shorter response times for basic life support and their arrest locations was more often outside home, compared with the nonsurvivors. The results seem comparable with emergency medical systems in the United States, but a need to reduce response times is identified.
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PMID:Prehospital resuscitation in Helsinki, Finland. 236 61

In the young patient resuscitated from sudden cardiac arrest, the risks of recurrence are uncertain and so are the criteria defining therapeutic efficacy for the presumed cause of the initial event. In this study, we analyzed the outcome of 15 consecutive young patients, who were resuscitated from pulseless ventricular tachycardia or ventricular fibrillation and who were evaluated by comprehensive hemodynamic and electrophysiological testing. Patients were 11.2 +/- 2.7 (mean +/- SD) years old at the time of their event, and each was known to have some form of heart disease before sudden cardiac arrest. Ventricular tachycardia or fibrillation was inducible by programmed electrical stimulation in eight patients. Accessory atrioventricular connections, with antegrade effective refractory periods less than 220 msec, were identified in three patients. Sustained atrial flutter was the only arrhythmia inducible in two patients, and no arrhythmias were inducible in two other patients. Surgical or electrophysiological-guided medical therapy resulted in noninducibility of the ventricular arrhythmias in six patients. Surgical division of the accessory atrioventricular connections was performed in three patients, and arrhythmias were not inducible after operation. The four patients with atrial flutter or without defined arrhythmia were treated with an empiric therapy. During 37 +/- 14 months of follow-up, the nine patients with documented noninducibility of a defined cause of sudden cardiac arrest were free of recurrent events. In contrast, during 18 +/- 10 months of follow-up, two of the six patients with empiric therapy or persistent inducibility of ventricular tachycardia died suddenly, and three others had recurrence of ventricular tachycardia or fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment and follow-up of pediatric survivors of sudden cardiac death. 219 20

We investigated 303 (men: women = 2:1) cases who suffered sudden heart arrest in Yamagata city since 1984 to 1987. The incidence rate was 41.0/100,000/year, and increased markedly with increasing age. There was a tendency for sudden death to occur in the winter season, evening and early morning. Two major causes were cardiac disease (especially ischemic heart disease) (46.4%) and intracranial hemorrhages (18.6%). 20% of all the heart-arrest cases were able to be saved, but, depending on the kind of heart disease the survival rate varied greatly (18.8% in acute myocardial infarction and 71.4% in vasospastic angina), (40.0% in ventricular fibrillation and 13.3% in the bradycardic arrhythmias). Survival rate was also effected by the time interval from the onset till the beginning of cardio-pulmonary resuscitation. About one half of the cases had histories of cardiac disease. Premonitory symptoms were observed in at least one third of the cases.
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PMID:[Sudden cardiac death in the emergency hospital]. 240 68

In order to eliminate the need for epicardial electrodes, two large transvenous catheter electrodes or one catheter and one extrathoracic patch electrode have been proposed as alternative electrode configurations for defibrillation and ventricular tachycardia cardioversion by implantable cardioverter/defibrillators. We compared the efficacy and safety of endocardial shocks delivered through these two electrode systems in man in a prospective randomized crossover study. Twelve patients with sustained ventricular tachycardia and heart disease undergoing electrophysiologic study were evaluated. A transvenous tripolar cardioversion electrode catheter with a large distal defibrillation electrode (surface area, 400 mm2) and proximal defibrillation electrode (surface area, 800 mm2) was positioned in the right ventricular apex with a cutaneous patch electrode placed on the cardiac apex. Sustained ventricular tachycardia was induced at electrophysiologic study. Shocks were delivered using two catheter electrodes only (right ventricular cathode and right atrial anode = method I), and one catheter electrode and cutaneous patch (right ventricular cathode and cutaneous apical patch anode = method II). Synchronized monophasic shocks were delivered using three preselected protocols based on ventricular tachycardia cycle length and morphology. Initial shock energies were 25 joules for polymorphic ventricular tachycardia and ventricular fibrillation, 15 joules for monomorphic rapid ventricular tachycardia (cycle length less than or equal to 300 msec), and 5 joules for monomorphic slow ventricular tachycardia (cycle length greater than 300 msec). Ventricular tachycardia was reinduced and shock energies titrated until cardioversion threshold was obtained. Identical ventricular tachycardia episodes were treated with both methods at each energy level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical efficacy of dual electrode systems for endocardial cardioversion of ventricular tachycardia: a prospective randomized crossover trial. 240 86

Between September 1980 and June 1984 we assessed the specificity of induction of ventricular tachycardia (VT) with one or two ventricular extrastimuli in a consecutive series of 148 patients undergoing electrophysiological assessment for the Wolff-Parkinson-White (WPW) syndrome by standard electrophysiological techniques. Fifteen patients (10%) had six or more beats of VT induced by one ventricular extrastimulus after a ventricular drive (9 patients), two ventricular extrastimuli during reciprocating tachycardia (6 patients), and during a single atrial extrastimulus (1 patient). None of the six men and nine women, aged 16-61 years, had apparent heart disease. VT lasted for 20 +/- 14 (mean +/- standard deviation) cycles with a cycle length of 235 ms +/- 27 and was generally polymorphic. One patient had ventricular fibrillation. These patients were compared to 15 age- and sex-matched patients studied in the same time period. There was no difference in anterograde effective refractory period of the accessory pathway (316 +/- 92 vs 319 +/- 68 ms), ventricular effective refractory period (218 +/- 12 vs 227 +/- 23), shortest pacing cycle length maintaining 1:1 anterograde conduction over the accessory pathway (306 +/- 132 vs 320 +/- 67) or minimum R-R interval between preexcited beats during atrial fibrillation (280 +/- 68 vs 294 +/- 105). All patients are alive and well over a follow-up interval of 20 +/- 11 months on no antiarrhythmic therapy (13 patients) or on propranolol (2 patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonclinical ventricular tachycardia in the Wolff-Parkinson-White syndrome. 241 49

Strong experimental evidence links ventricular fibrillation to an increased temporal dispersion of the recovery of excitability. The effect of an overall prolongation of repolarization and an increased basic dispersion of repolarization on premature dispersion was studied on ventricular surface in 10 dogs. Our observations reveal the operation of several fundamental electrophysiologic mechanisms controlling the conduction and the refractoriness in the ventricular myocardium in vivo. Action potential (AP) duration was influenced by the heart rate, the duration of the preceding AP and the proximity to the repolarization of the preceding AP. These effects can both slow, or enhance ventricular conduction, during propagation of premature impulses. This model may be applicable to several clinical situations where APs are prolonged (hypothermia, drug effects, changes in electrolytes) or when dispersion of refractoriness is increased (long QT-time syndrome, neural imbalance of the heart with and without heart disease.
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PMID:Effect of uniformly prolonged, and increased basic dispersion of repolarization on premature dispersion on ventricular surface in dogs: role of action potential duration and activation time differences. 241 50

Neural mechanisms have important influences on ventricular repolarization. The normal gradients of repolarization such as that from long to short duration on the endocardial-epicardial axis are probably not the result of nonuniform neural effects. The ventricular distributions of individual cardiac sympathetic nerves is, however, localized and provides a possible basis for nonuniform effects on repolarization in various disease states. Such localized sympathetic effects are the probable mechanism of electrocardiographic waveform abnormalities associated with neurologic disease and a possible mechanism of the idiopathic prolonged QT interval syndromes. The medical significance of nonuniform neural influences on ventricular repolarization includes the evaluation of neurogenic electrocardiographic waveform abnormalities that may be erroneously attributed to intrinsic heart disease. Of greater importance, nonuniform repolarization has established relations to cardiac arrhythmias including ventricular fibrillation and nonuniform sympathetic effects on repolarization may be a significant factor in the occurrence and persistence of these disorders. Parasympathetic influences on ventricular repolarization are slight compared to sympathetic effects and may operate by opposing adrenergic effects.
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PMID:Neural mechanisms involved in the regulation of ventricular repolarization. 241 52

Frequency and complexity of ventricular arrhythmias increases with age and increasing severity of heart disease. However, fatal ventricular fibrillation occurs frequently in the absence of symptomatic warning arrhythmias. Several classifications of ventricular arrhythmias are discussed. The morphology of ventricular premature complexes (VPC), their frequency and complexity at rest, during ordinary activity, or after exercise do not influence life expectancy of subjects without heart disease, nor in those with coronary artery disease with no history of myocardial infarction. In the survivors of myocardial infarction, the frequency and "complexity" of ventricular arrhythmias appears to be an independent risk factor for sudden and nonsudden cardiac death. However, the low specificity and predictive value of ventricular arrhythmias makes their assessment difficult for practical purposes. The prognosis of most patients with ventricular arrhythmias is determined predominantly by the condition of the heart. "Complex" arrhythmias at rest and during exercise do not appear to worsen prognosis and life expectancy in individuals without heart disease. Ambulatory electrocardiographic monitoring has serious limitations as a guide for clinical decision making. Ventricular tachycardias in patients with coronary artery disease are not strictly related to the frequency and "complexity" of ventricular premature complex, but correlate with the presence of ventricular aneurysms, poor ventricular function and late potentials in the signal-averaged high frequency electrocardiogram. Recording of such late potentials is a new and promising noninvasive technique for identification of patients with serious arrhythmias but the sensitivity and specificity of this method remains to be established.
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PMID:Noninvasive assessment of ventricular arrhythmias in clinical practice: prognostic implications. 242 48

The proarrhythmic effects of class IA antiarrhythmic drugs were prospectively evaluated during programmed ventricular stimulation in 24 consecutive patients with frequent ventricular premature beats whose baseline study, performed while no antiarrhythmic drugs were being taken, showed no inducible sustained ventricular arrhythmias. No patient had nonsustained (greater than 5 beats) or sustained ventricular tachycardia by history or baseline 24 hour ambulatory electrocardiographic monitoring. Sequential stimulation studies using up to three extra-stimuli were performed after administration of procainamide, quinidine and disopyramide on different days. Proarrhythmic response was defined as induction of one or more of the following: sustained monomorphic ventricular tachycardia; sustained polymorphic ventricular tachycardia; ventricular fibrillation; reproducibly inducible nonsustained monomorphic ventricular tachycardia. During 55 antiarrhythmic drug trials (24 of procainamide, 21 of quinidine, 10 of disopyramide) in the 24 patients, 6 patients had a proarrhythmic response: sustained monomorphic ventricular tachycardia in 3, ventricular fibrillation in 2, nonsustained monomorphic ventricular tachycardia in 1. Thus, 11% of drug trials resulted in a proarrhythmic response and 25% of patients had a proarrhythmic response to one of the drugs tested. A proarrhythmic response to one drug did not predict a similar response to another drug of the same class. The 6 patients with a proarrhythmic response did not differ significantly from the other 18 patients with regard to underlying heart disease, electrocardiographic or baseline 24 hour ambulatory electrocardiographic characteristics; however, they did have a higher incidence of digoxin usage (p less than 0.02), a shorter baseline right ventricular effective refractory period (p less than 0.01) and a smaller increment in effective refractory period during antiarrhythmic drug testing (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proarrhythmic effects of antiarrhythmic drugs during programmed ventricular stimulation in patients without ventricular tachycardia. 243 19

Aggravation of arrhythmia by antiarrhythmic drugs is a potentially serious complication. In over 1,287 noninvasive drug studies involving 11 antiarrhythmic drugs, arrhythmia aggravation occurred in 117 tests (9%). During 248 electrophysiologic tests, 45 cases (18%) of aggravation occurred. In an attempt to define predictors of this complication, 51 patients with aggravated arrhythmia were compared with 102 patients without this complication. Arrhythmia aggravation was not associated with age, sex, type or extent of heart disease, baseline electrocardiogram, drug-induced changes on electrocardiogram or density of baseline arrhythmia on monitoring or exercise testing. Aggravation with 1 drug did not predict occurrence with another drug of the same class. The only statistically important relation was the type of presenting arrhythmia. Patients with a history of a sustained tachyarrhythmia (ventricular tachycardia or ventricular fibrillation) had a risk of this complication that was 2.5 times greater than that of patients presenting with only nonsustained ventricular tachycardia or ventricular premature beats (p = 0.01). There was also a relation to the presence of left ventricular dysfunction (p = 0.04). For the most part, however, aggravation of arrhythmia is not predictable, and cautious use of antiarrhythmic drugs is essential.
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PMID:Aggravation of arrhythmia by antiarrhythmic drugs--incidence and predictors. 243 88


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