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PubMed1982

[Mobile coronary unit of Florence: early care of arrhythmias not due to acute coronary insufficiency].

The aim of Mobile Coronary Care Units (M.C.C.U.) is to reduce the delay in delivering intensive care to patients with a heart attack. In the city of Florence a M.C.C.U. has been available since November 1979. During the first year the staff of the M.C.C.U. has treated 158 cases of serious cardiac arrhythmias which occurred among 486 interventions. In 94 patients cardiac arrhythmias followed an acute coronary attack. In 64 patients coronary heart disease could not be demonstrated. This study concerns the latter group of patients. The mean age was 65.2 years and 39 patients (61%) were women. The mean time from the onset of the symptoms to the arrival of the M.C.C.U. team was 3h and 2 min, whereas the mean time from the call to the arrival was 14 min. Sixty patients had atrial arrhythmias (29 atrial fibrillation, 2 atrial flutter, 22 atrial tachycardia, 7 premature atrial contractions) and 4 patients had ventricular arrhythmias (1 ventricular tachycardia, 1 ventricular flutter, 2 premature ventricular contractions). In thirty-nine patients (61%) the cardiac arrhythmia was abolished by the staff of the M.C.C.U.. Of the remaining 28 patients, 10 were brought to the hospital and 18 were left at home. None of these needed later admission to the hospital. So the treatment at home of cardiac arrhythmias has been successful in the majority of patients. Bunaftine was the antiarrhythmic drug more frequently used (23 cases, 34%) with a high percentage of success (87%). In planning medical emergency services to the community, one can envisage the use of the M.C.C.U. facilities to treat at home those arrhythmias that are not associated with an acute coronary attack.

Adult↗

PubMed1994

Systolic arterial pressure recovery after ventricular fibrillation/flutter in humans.

Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 +/- 2, and the mean drop in systolic pressure was 84 +/- 16 mmHg. The mean recovery time for systolic pressure was 10 +/- 6 seconds, the average systolic pressure recovery rate was 13 +/- 14 mmHg/sec, and the mean percent systolic pressure recovery was 94% +/- 9%. A negative logarithmic relation was found to exist between the rate of systolic arterial pressure recovery and the duration of ventricular fibrillation or flutter with a correlation coefficient of 0.68 to 0.97 (P < 0.05) in five of the seven patients. A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.

Adult↗

PubMedDate not supplied

Arrhythmia during mitral commissurotomy.

The authors studied in detail arrhythmias recorded during 110 operations of mitral commissurotomy. In all cases supraventricular and ventricular arrhythmias developed and their type, as well as frequency, depended on the stage of operation. Life-endangering ventricular arrhythmias (ventricular flutter or fibrillation) were never observed and ventricular tachycardia occurring when the orifice was being dilated always regressed spontaneously when a Dubost dilator was removed. Rapid differential diagnosis of arrhythmias is facilitated greatly by additional ECG recording from oesophageal lead. Indications for pharmacological treatment are discussed. This treatment was used, however, in several cases only.

Adolescent↗

PubMed1996

Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients.

A few studies have indicated that adenosine terminated triggered-activity idiopathic ventricular tachycardia, but all involved a small number of cases. The effects of adenosine triphosphate (ATP) on wide QRS tachycardia have thus not yet been completely clarified. This retrospective study was performed to evaluate the therapeutic and diagnostic utility of ATP in wide QRS tachycardia. A total of 18 patients with wide QRS tachycardia (QRS width > 120 msec, rate > or = 150 beats/min) were evaluated. ATP, 20-40 mg, was administered intravenously. An electrophysiological study and treadmill stress test were performed in all patients to elucidate the mechanism of the tachycardia. ATP terminated tachycardia or induced atrio-ventricular block in all 6 patients who had supraventricular tachycardia, but it had no effect on preexcited atrial fibrillation or pre-excited atrial flutter. Ventricular tachycardia was terminated by ATP in 5 of the 10 patients. In 4 of these 5 patients, the focus of the tachycardia was the right ventricular outflow tract. No entrainment phenomenon was demonstrated by electrophysiological study with induction of the tachycardia by stress test or isoproterenol infusion, suggesting the contribution of triggered activity to the tachycardia. In the remaining patient with complete right bundle branch block type tachycardia with right axis deviation, the mechanism of ventricular tachycardia could not be determined. In the 5 patients in whom ATP failed to terminate ventricular tachycardia, the reentry mechanism was suggested by the presence of entrainment phenomenon depicted on electrophysiological study. In summary, this study suggests that ATP terminates supraventricular wide QRS tachycardia and ventricular tachycardia due to triggered-activity, but that it has no effect on pre-excited atrial fibrillation or flutter or on ventricular tachycardia due to a reentry mechanism. These findings add to the mounting evidence regarding the therapeutic and diagnostic utility of ATP in wide QRS tachycardia.

Adenosine Triphosphate↗

PubMed1997

Malignant ventricular dysrhythmia in broiler chickens dying of sudden death syndrome.

A flock of broiler chickens was monitored intensively for overt signs indicative of sudden death. Electrocardiographic tracing of terminal cardiac activity was obtained from six broilers succumbing to sudden death syndrome and from six control chickens which were killed by cervical dislocation. Normal sinus rhythm, heart rate and electrocardiogram (ECG) pattern with P, QRS, and T deflections were observed for two to three minutes in the control chickens. The ECG tracing from birds dying of sudden death syndrome showed no identifiable P, QRS, or T waveforms. Initial more regular oscillatory waves resembling ventricular flutter, changed to irregular, undulating waves characteristic of ventricular fibrillation. A straight line, indicating cessation of heart activity, appeared within four to six minutes of the onset of clinical signs. It was concluded that the sudden death syndrome is associated with an acute cardiovascular failure caused by a lethal cardiac dysrhythmia, ventricular fibrillation.

Animals↗

PubMedDate not supplied

Subarachnoid hemorrhage: frequency and severity of cardiac arrhythmias. A survey of 70 cases studied in the acute phase.

The frequency and severity of cardiac arrhythmias were studied in 70 patients with spontaneous subarachnoid hemorrhage investigated prospectively with 24-hour Holter monitoring. Patients were less than 70 years old and without clinical and/or ECG signs of previous heart disease; Holter monitoring was initiated within 48 hours of subarachnoid hemorrhage. Arrhythmias were detected in 64 of the 70 patients (91%). Twenty-nine of the 70 patients (41%) showed serious cardiac arrhythmias; malignant ventricular arrhythmias, i.e., torsade de pointe and ventricular flutter or fibrillation, occurred in 3 cases. Serious ventricular arrhythmias were associated with QTc prolongation and hypokalemia. No correlation was found between the frequency and severity of cardiac arrhythmias and the neurologic condition, the site and extent of intracranial blood on computed tomography scan, or the location of ruptured malformation. The extremely high incidence of cardiac arrhythmias, sometimes serious, in the acute period after subarachnoid hemorrhage and the absence of clinical and radiologic predictors make systematic continuous ECG monitoring compulsory to improve the overall results of subarachnoid hemorrhage, irrespective of early or delayed surgical treatment.

Acute Disease↗

PubMed2003

[Treatment of ventricular arrhythmias].

The term ventricular arrhythmia denotes various disorder in the cardiac rhythm--from isolated monomorphic ventricular extrasystoles to ventricular flutter and fibrillation. The choice of therapy of ventricular arrhythmias is primarily based on prognostic aspects. Ventricular tachycardias represent the main cause of sudden cardiac death, which is responsible for more than 60% of all deaths for cardial causes. In the industrially advanced countries the ventricular tachyarrhythmias represent more than 90% of cases based on coronary disease. The prevention of sudden death is directed particularly to prevention and therapy of ischaemic heart disease. The prognostic classification divides ventricular tachycardias into benign, potentially malignant and malignant ones, respectively. The benign arrhythmias do not require therapy. In the malignant (i.e. potentially lethal) ventricular tachyarrhythmias the implantation of cardioverter-defibrillator represents the most efficient treatment. In the largest group of patients with potentially malignant ventricular arrhythmias the present risk-oriented stratification enables a partial identification of persons with markedly increased risk of sudden death. They may be considered for preventive implantation of cardioverter-defibrillator. In some patients the therapeutic effect is reached by application of various therapeutic methods including a combination of pharmacological and non-pharmacological therapy, which also includes catheterization or surgical ablation of the arrhythmogenic substrate. A corresponding attention should be devoted to the basal cardial disease.

Death, Sudden, Cardiac↗

PubMed1985

The yield of programmed ventricular stimulation in mitral valve prolapse patients with ventricular arrhythmias.

A high-risk subset of patients with mitral valve prolapse (MVP) and a predisposition to sudden cardiac death (SCD) has been proposed. We analyzed the results of programmed ventricular stimulation (PVS) in 20 patients with MVP and ventricular arrhythmias (ventricular premature depolarization in 6, ventricular couplets in 2, nonsustained ventricular tachycardia [VT] in 7, ventricular fibrillation [VF] in 5) and in 12 "normal" control subjects. With the use of an identical stimulation protocol from the right ventricular apex (twice diastolic threshold, three extrastimuli), 9 of 20 MVP patients and 1 of 12 normal subjects had inducible ventricular arrhythmias (p less than 0.05). When more aggressive attempts at ventricular stimulation were used, an additional five MVP patients had positive responses to PVS while no normal subjects did. In the MVP group, the following arrhythmias were induced: nonsustained polymorphic VT in 10, VF in three, and ventricular flutter in one. In all but two patients, triple ventricular extrastimuli were required to elicit this response. Two of the 10 MVP patients undergoing electropharmacologic testing had a successful antiarrhythmic regimen identified, while 13 patients were discharged on empiric antiarrhythmic therapy. At a follow-up of 19.8 +/- 13.1 months, all 19 MVP patients who could be contacted were alive. Five patients had symptomatic recurrences at follow-up including two SCD survivors (VT in one and VF in one). In conclusion, it was found that the majority of MVP patients with ventricular arrhythmias have inducible ventricular tachyarrhythmias during PVS and are more susceptible to this than patients without structural heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2006

Prevalence of arrhythmias and their risk factors mid- and long-term after the arterial switch operation.

Early results of the arterial switch operation (ASO) for transposition of the great arteries (TGA) are good, but there are few mid- and long-term data on postoperative arrhythmias, especially in Japan. In this study, clinical data on 624 1-year survivors who had an ASO between 1976 and 1995 were collected from six institutes in Japan up to October 2002. Sixty (9.6%) 1-year survivors had significant arrhythmias. Bradycardia occurred in 22 patients, including complete atrioventricular block (CAVB) in 12, sick sinus syndrome (SSS) in 6, and second-degree atrioventricular block in 4. Syncope developed in 2 with CAVB and 2 with SSS. Ten patients with bradycardia underwent permanent pacemaker implantation. Supraveutricular tachycardia (SVT) was seen in 25 patients, including paroxysmal supraventricular tachycardia in 16, atrial flutter in 7, and atrial fibrillation in 2. Six patients with SVT received antiarrhythmic medication. SVT was transient in 20 and persistent in 5. Ventricular arrhythmias occurred in 13 patients, including nonsustained ventricular tachycardia in 5, paroxysmal ventricular contractions with couplets in 5, ventricular flutter in 2, and sustained ventricular tachycardia in 1. Four patients with ventricular arrhythmias received antiarrhythmic medication. Of the study patients, 8 died 1 year or more after ASO. Death was directly related to arrhythmia in 1 patient and was due to nonsustained ventricular tachycardia with severe congestive heart failure. The presence of a ventricular septal defect (VSD) was a risk factor for postoperative arrhythmia. Patients with TGA and VSD had more arrhythmias than those with TGA and an intact ventricular septum (13.7 vs 8.7%, p < 0.05), and this was especially true for CAVB (3.9% vs 1.0%, p < 0.05). In 36 patients clearly documented time onset of postoperative arrhythmia arrhythmia developed in 18 (50%) after less than 1 year and in 15 (42%) after more than 5 years. In summary serious arrhythmias after ASO were uncommon, but postoperative arrhythmias, such as unpaced CAVB, SSS, and VT, were related to morbidity and mortality. VSD was a risk factor for postoperative arrhythmia, especially CAVB. Approximately half of the arrhythmias developed late. Lifelong monitoring with respect to arrhythmia is needed for patients after ASO.

Adolescent↗

PubMed1986

Diagnosis of fetal arrhythmias using echocardiographic and Doppler techniques.

Fetal echocardiography is the most practical method for diagnosing prenatal arrhythmias. Because some prenatal tachyarrhythmias have been shown to respond to antiarrhythmic drugs, correctly diagnosing fetal arrhythmias has assumed new importance. With the aid of two-dimensional echocardiographic imaging, an M-mode cursor can be aligned to record atrial and ventricular wall motion--either independently or simultaneously. A consistent feature in the fetus is prominent atrial wall contractions that can be readily recorded on the M-mode tracing. By matching atrial and ventricular wall contractions with assumed P waves and QRS complexes, the fetal electrocardiogram can be reconstructed. In 57 fetuses studied, recurrent atrial and ventricular ectopic beats were the most common prenatal arrhythmias. However, atrial flutter, ventricular tachycardia, atrial and ventricular bigeminy and atrial and ventricular bradyarrhythmias have been correctly identified and in some instances appropriately treated. Marked fetal bradycardia in the midtrimester of pregnancy is shown for the first time to be caused by transducer pressure on the maternal abdominal wall.

Arrhythmias, Cardiac↗

PubMed1987

Sudden death during ambulatory Holter monitoring.

Four cases of sudden cardiac death during ambulatory Holter monitoring are described. All had coronary arterial disease. Two patients were on antiarrhythmic drug therapy and both had a prolonged QTc-interval on their resting electrocardiogram. The predominant rhythm was sinus rhythm in all. In one patient, severe bradycardia terminated in asystole. In the remaining 3 patients, ventricular flutter (which was initiated in 2 instances by a short run of polymorphous ventricular tachycardia) degenerated into ventricular fibrillation. The lethal event was triggered once by an early cycle ventricular premature beat and twice by late cycle ventricular premature beats. There was no specific pattern of warning arrhythmias preceding sudden cardiac death. Signs of ischemia/sympathetic overactivity preceding sudden cardiac death were found in 3 patients. Autopsy studies were performed in 2 patients and revealed acute ischemic myocardial damage.

Aged↗

PubMed1989

Flecainide-induced ventricular tachycardia and fibrillation in patients treated for atrial fibrillation.

Flecainide acetate has a recognized proarrhythmic effect in patients treated for ventricular tachycardia. Three patients developed severe ventricular arrhythmias while taking flecainide for atrial fibrillation. Patient 1 had normal ventricular function and idiopathic atrial fibrillation. Treadmill exercise tests during digoxin therapy showed no ventricular arrhythmia; however, during flecainide therapy the patient developed ventricular flutter at his peak exercise level that required cardioversion. Patient 2 had normal ventricular function and a prosthetic mitral valve. During therapy with flecainide, 150 mg twice daily, he had an episode of sustained ventricular tachycardia, also at his peak exercise level. Patient 3 had paroxysmal atrial fibrillation and hypertrophic cardiomyopathy but no previous ventricular arrhythmia. She died suddenly within 10 days of starting flecainide therapy. Judged from previous findings none of these patients was considered at high risk for proarrhythmia. These cases suggest a possible relation between vigorous exercise, atrial fibrillation, and the proarrhythmic properties of flecainide and indicate the limitations of classifying patients as "high-risk" or "low-risk" for proarrhythmic complications of anti-arrhythmic therapy.

Adult↗

PubMedDate not supplied

[Auricular fibrillation and flutter with slow ventricular frequency. Clinical and electrophysiological study].

We have studied atrio-ventricular conduction in 9 patients with atrial fibrillation and flutter and ventricular response below 90 per minute, by means of His bundle electrograms. Despite the finding of intraventricular conduction defects in 6 cases, the block of the atrial impulses occurred at the high atrio-ventricular junction in every case. In four patients the arrhythmia was an incidental finding and there were no other signs of cardiac disease. Several patients tolerated low ventricular rates for years without symptoms, but in two cases it was necessary to insert a pacemaker to treat cerebral ischemic symptoms. The problems of interpretation of the His bundle electrogram, in the presence of atrial fibrillation, are discussed in detail.

Aged↗

PubMedDate not supplied

Antagonists of PAF and histamine inhibit ouabain-induced cardiac arrhythmias in sensitized guinea-pigs.

Platelet-activating factor (PAF) seems to be involved in different pathophysiological conditions, including cardiac arrhythmia. The arrhythmogenic potency of PAF has been shown experimentally by different methods. PAF antagonists inhibit the PAF-induced enhanced arrhythmogenicity. The present paper demonstrates that the threshold dose of ouabain-induced arrhythmia is decreased in sensitized guinea-pigs. Antagonists of PAF (BN 52021, WEB 2086, WEB 2170) and histamine antagonist clemastine can increase the threshold dose of ouabain-induced arrhythmia. A combination of WEB 2170 and clemastine, each of the drug is a low dose which is without effect when applying one of them only, shows a highly significant antiarrhythmic effect in this method. The threshold dose of ouabain necessary to induce ventricular flutter was increased from 89 micrograms/kg to 129 micrograms/kg and the threshold dose of ventricular fibrillation was enhanced from 101 micrograms/kg to 137 micrograms/kg. In dependence on the pathophysiological conditions, different mediators seem to be involved in the occurrence of cardiac arrhythmia. Therapeutically influencing these mediators could be a real chance to optimise the treatment of such kind of cardiac arrhythmias.

Anaphylaxis↗

PubMed1990

Torsade de pointes and syncopal attacks in a 26-year old woman with congenital complete heart block and prolonged QT interval.

A 26-year old woman with congenital complete heart block and prolonged QT interval presented for the first time with syncopal attacks associated with torsade de pointes in adulthood. Cardioversion followed by overdrive pacing was needed to finally control the unstable rhythm. During episodes of non-capture, paraoxysms of torsade de pointes leading to ventricular flutter were recorded by a 24-hour ambulatory electrocardiographic monitoring. Beta-blockade and permanent ventricular pacing finally abolished both the syncopal attacks and the torsade phenomena. The prognosis of congenital complete heart block associated with QT prolongation resembles that of the Romano-Ward syndrome. Recognition of this variant would facilitate earlier treatment of this rare but potentially lethal disorder.

Adult↗

PubMed1988

Prediction of successful suppression of sustained ventricular tachyarrhythmias by serial drug testing from data derived at the initial electrophysiologic study.

This study investigated whether data available after the initial electrophysiologic study in patients with sustained ventricular tachyarrhythmia could identify those patients in whom serial drug testing is likely to be efficacious. One hundred six patients with inducible sustained ventricular tachyarrhythmia, whose initial study included short-term drug testing with intravenous procainamide, were evaluated. The baseline arrhythmia induced (in the absence of all antiarrhythmic drugs) was monomorphic tachycardia with a cycle length greater than 200 ms in 81 patients and ventricular flutter or fibrillation in the remaining 25 patients. After intravenous infusion of procainamide (1,250 +/- 300 mg), a ventricular tachyarrhythmia could still be induced in 80 patients during testing with up to three extrastimuli. Serial drug testing with one to four trials of oral conventional and investigational agents was then undertaken. Evaluation of 15 clinical, hemodynamic and electrophysiologic variables by stepwise logistic regression identified two independent predictors of successful response to oral antiarrhythmic drugs: 1) noninducibility of ventricular tachycardia after intravenous procainamide (p less than 0.001), and 2) left ventricular ejection fraction greater than or equal to 40% (p less than 0.05). Subgroup analysis combining each of these variables identified patients with a high, intermediate or low probability of finding a successful oral drug regimen. Patients whose arrhythmia was suppressed by intravenous procainamide had a 100% likelihood (if left ventricular ejection fraction was greater than or equal to 40%) or an 87% likelihood (if ejection fraction was less than 40%) of responding to an oral regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2001

Antiarrhythmic effects of adenosine on ischemia-induced ventricular fibrillation.

PURPOSE: The antiarrhythmic efficacy of adenosine during states of AV-nodal reentrant tachycardias is well known and clinically established. Adenosine is also able to reduce ventricular arrhythmias when applied before coronary ligation in rats. Hypoxia or ischemia leads to an increased production of adenosine by cardiac myocytes. The purpose of this study was to evaluate if adenosine also has a direct antiarrhythmic effect on ischemia-induced ventricular fibrillation. MATERIALS AND METHODS: In this study, the antiarrhythmic effects of adenosine on ventricular fibrillation during global (low flow) ischemia were evaluated in isolated guinea pig hearts perfused by the method of Langendorff. RESULTS: Adenosine showed a dose-dependent prolongation of the peak to peak interval of the ventricular ECG signal during ventricular fibrillation until ventricular flutter or tachycardia occurred at a concentration of 2 mmol/L. At a concentration of 20 mmol/L, adenosine converted ventricular fibrillation into ventricular tachycardia with intermittent periods of asystole. This conversion of ventricular fibrillation to asystole was antagonised by 200 micromol/L theophylline. CONCLUSION: Adenosine appears to have an antiarrhythmogenic effect both in supraventricular and ventricular rhythm disturbances. During myocardial infarction, where huge amounts of adenosine are present in ischemic regions, asystole may respond to adenosine antagonists.

Adenosine↗

PubMed1984

Effects of atrial pacing, isoprenaline and lignocaine on experimental polymorphous ventricular tachycardia.

In 22 anaesthetised dogs, iv, administration of quinidine sulphate (30 mg X kg-1) over 5 min produced bradycardia and marked prolongation of the QT interval. Right ventricular extrastimulations, four times diastolic threshold, provoked polymorphous ventricular tachycardia in 18 dogs, and typical torsade de pointes was observed in four of these 18 dogs. Ventricular flutter was induced in another four dogs. In one of these 22 dogs, double stimuli were required to induce ventricular tachyarrhythmias, in 19 dogs triple stimuli, and in two dogs quadruple stimuli. Using this experimental model, effects of interventions including atrial pacing, isoprenaline, and lignocaine on the QT interval and induction of polymorphous ventricular tachycardia by extrastimuli were studied. Atrial pacing shortened QT interval only slightly and did not prevent induction of polymorphous ventricular tachycardia in nine dogs studied. Isoprenaline infusion definitely shortened QT interval, and in four out of nine dogs triple stimuli could not elicit polymorphous ventricular tachycardia. By contrast, although the QT interval was not shortened, lignocaine was effective in preventing induction of polymorphous ventricular tachycardia by triple stimuli in three out of nine dogs. These results indicate atrial pacing is an ineffective means of preventing induction of polymorphous ventricular tachycardia by extrastimuli in dogs with a long QT interval, but that isoprenaline and lignocaine are effective in some dogs.

Animals↗