Episodes Of Ventricular Arrhythmias Research Articles

Role of vagotony in sinus node dysfunction in children with symptomatic congenital long QT syndrome

The present study examined chronotropic dysfunction and the role of vagotony in congenital long QT syndrome, sinus node function and the effects of parasympathetic blockade. Six patients with congenital long QT syndrome were studied. The four males and two females, aged 1-15 years, had episodes of syncope and malignant ventricular arrhythmias. Congenital long QT syndrome was defined as a corrected QT interval greater than 0.45 s, T wave alternans and the age at diagnosis. The sinus heart rate measured from a 24 h electrocardiograph was abnormally low (< 50 min) in three patients (1, 4 and 5 years old) and did not increase sufficiently with the administration of atropine in five of the six patients with congenital long QT syndrome. From intracardiac electrophysiological studies, the corrected sinus node recovery time was prolonged in three patients and the total sinoatrial conduction time was prolonged in two patients. In most patients who had an abnormally long sinoatrial conduction time and corrected sinus node recovery time, these values returned to normal following atropine administration. In one patient, the corrected sinus node recovery time was prolonged paradoxically by atropine. Sinus node dysfunction in congenital long QT syndrome was affected by vagotony associated with a right sympathetic nerve system abnormality.

The rabbit dual coronary perfusion model: a new method for assessing the pathological relevance of individual products of the ischaemic milieu: role of potassium in arrhythmogenesis

The aim was to develop a new model for determining which factors associated with ischaemia and reperfusion are sufficient for arrhythmogenesis, and to use the model for examining regional hyperkalaemia and K+ washout. DESIGN AND EXPERIMENTAL MATERIAL: Rabbit hearts (n = 150) were perfused with a buffered solution containing K+ in the normal range (2,3,4, or 5 mM). The circumflex coronary artery was perfused independently with a similar solution at a similar rate. A regional increase in K+ concentration was produced, followed by restoration of control K+ to mimic regional changes in K+ during ischaemia and reperfusion. Regional hyperkalaemia (K+ = 9, 12, 15, or 18 mM) mimicked (concentration dependently) the known effects of regional ischaemia on the ECG in three important respects, producing ventricular arrhythmias, regional changes in ECG configuration, and regional alternans. The relationship between arrhythmias and K+ was bell shaped with a peak in susceptibility at 15 mM K+. Arrhythmia susceptibility was reduced and onset delayed by raising the K+ concentration delivered to the adjacent coronary bed. Arrhythmogenesis could be replicated in five or more successive runs in a single heart, indicating a lack of preconditioning. Readmission of control K+ (washout of high K+) mimicked the effects of reperfusion by rapidly causing new episodes of ventricular arrhythmias. The concentration dependence of this effect was exponential, not bell shaped, with washout of 18 mM K+ most arrhythmogenic. There was no preconditioning phenomenon. Regional hyperkalaemia and K+ washout are factors sufficient to account for arrhythmogenesis during ischaemia and reperfusion, respectively. The new model is suitable for assessment of whether these factors are also necessary for arrhythmogenesis (by equivalent evaluation of other putative arrhythmogens).

Prophylaxis of atrial fibrillation with magnesium sulfate after coronary artery bypass grafting

Ninety-nine consecutive consenting patients were prospectively entered into a randomized, double-blind, placebo-controlled trial to determine the efficacy of postoperative magnesium therapy on the incidence of cardiac arrhythmias after elective coronary artery bypass grafting. No patient had documented or suspected arrhythmias preoperatively. Forty-nine patients received 178 mEq of magnesium given over the first 4 postoperative days, and 50 patients received only placebo. The clinical characteristics of both groups were similar. The preoperative mean serum magnesium concentration was similar in both study (1.90 mEq/L) and placebo (1.90 mEq/L) groups. The mean postoperative serum magnesium concentration in study patients was significantly elevated over postoperative days 1 through 4 when compared with preoperative levels ( p < 0.001). The postoperative mean serum magnesium concentration in control patients declined and remained significantly depressed through postoperative day 3 ( p < 0.001), but increased to preoperative levels by postoperative day 4. The mean serum magnesium concentration was significantly greater in the study patients as compared with the control patients over postoperative days 1 through 4 ( p < 0.001). Although there was no significant difference between groups with respect to episodes of ventricular arrhythmias, there was a significant decrease in the number of episodes of atrial fibrillation in the group receiving magnesium therapy ( p < 0.02). There were no recognized adverse effects of magnesium therapy. Prophylactic magnesium administration seems to lessen the incidence and severity of atrial fibrillation after coronary artery bypass grafting.

Usefulness of right ventricular pulse pressure as a potential sensor for hemodynamically unstable ventricular tachycardia

The automatic implantabte cardioverter defibrillator has had a major impact on the management of patients with ventricular tachyarrhythmias. Future devices will offer tiered therapy for ventricular arrhythmias, based on a sensor capable of discriminating hemodynamically stable from unstable ventricular tachycardia (VT). We studied 27 patients with sustained VT/ventricular fibrillation during 70 episodes of sustained ventricular arrhythmias (>30 seconds or requiring cardioversion). In this study, phasic arterial pressure (mm Hg), VT cycle length (ms) and right ventricular (RV) pulse pressure (mm Hg) were measured before, during the first 30 beats and after each episode of VT. During the first 10 beats of 23 episodes of unstable VT, the mean (± standard error of the mean) decrease in RV pulse pressure from baseline was 22 ± 1.8 mm Hg; it was 13.8 ± 2A mm Hg during the first 10 beats of 47 episodes of stable VT, (p = 0.01, stable vs unstable). For the next 20 beats of VT, RV pulse pressure decreased from baseline by 22 ± 2.5 mm Hg during unstable and by 12.0 ± 2.5 mm Hg during stable VT (p = 0.0001, stable vs unstable). The percent decrease of RV pulse pressure correlated well with the percent decrease in mean arterial pressure and percent decrease in systolic arterial pressure (r = 0.70; r = 0.69, respectively; p < 0.001) during VT, but poorly with the VT cycle length (r = 0.27, p < 0.05). The percent decrease in RV pulse pressure is a useful hemodynamic sensor for discriminating between stable and unstable VT.

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation.

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.

Intravenous amiodarone for the rapid treatment of life-threatening ventricular arrhythmias in critically ill patients with coronary artery disease

This study examined the effectiveness of intravenous amiodarone for rapid control and prevention of recurrent life-threatening ventricular tachyarrhythmias associated with cardiovascular collapse. In 22 critically ill patients with coronary artery disease (mean ejection fraction 27 ± 13%), recurrent ventricular tachyarrhythmias proved refractory to 3.7 ± 1.1 (mean ± standard deviation) conventional antiarrhythmic drugs. In the 24-hour period before intravenous amiodarone treatment, patients experienced 2.4 ± 2.3 (range 1 to 9) episodes of lifethreatening ventricular tachycardia, ventricular fibrillation or both, requiring 4.0 ± 3.9 direct current cardioversions. Within the 24 hours after initiation of intravenous amiodarone therapy (900 to 1,600 mg/day), 20 of 22 patients remained alive and had 1.1 ± 1.6 episodes of life-threatening ventricular arrhythmias, requiring 1.9 ± 3.1 direct current cardioversions. In the second 24-hour period, there were 19 survivors and life-threatening arrhythmias were reduced to 0.4 ± 0.7 episode/ patient requiring 0.4 ± 0.9 direct current cardioversion. Overall, arrhythmias were controlled in 11 of 22 (50%) patients within the first 24 hours, and in 14 of 22 (64%) in the second 24 hours. Intravenous amiodarone therapy was well tolerated. Twelve patients were discharged from the hospital and 8 remained alive at a mean follow-up of 22 ± 14 months. Thus, in critically ill patients, intravenous amiodarone may be useful for rapid control of spontaneous, refractory, life-threatening ventricular tachyarrhythmias.

The value of the clinical history to assess prognosis of patients with ventricular tachycardia or ventricular fibrillation after myocardial infarction.

Multivariate analysis using 70 variables in 200 patients who suffered from ventricular tachycardia or ventricular fibrillation after myocardial infarction detected eleven variables that were associated with an increased risk of sudden arrhythmic death and cardiac death during a mean follow-up period of 2 years. Four of the 11 variables came from the patient's clinical history: (1) cardiac arrest at the time of the first spontaneous episode of arrhythmia, (2) New York Heart Association functional class for dyspnoea = III, (3) ventricular tachycardia or ventricular fibrillation occurring early (after 3 days and within 2 months) after myocardial infarction, (4) multiple myocardial infarctions before the first episode of ventricular tachyarrhythmia. Total mortality, incidence of sudden arrhythmic death and of non-sudden cardiac death increased with an increasing number (zero, one, two, three, four) of variables seen in individual patients. Patients with zero or one variable had an incidence of sudden death of 2.8% and a 4.2% incidence of non-sudden cardiac death at 26 months, while patients with more than two variables had a 13.5% and a 20.3% incidence respectively of sudden and non-sudden cardiac death. The strongest predictor of sudden death was the occurrence of cardiac arrest during the first spontaneous episode of ventricular arrhythmia. The strongest predictor of non-sudden cardiac death was the New York Heart Association functional class. The use of the four variables to stratify risk revealed seven subgroups of patients with incidences of sudden death ranging from 0 to 28%.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemoperfusion for N-Acetylprocainamide Intoxication

Letters and Corrections1 December 1986Hemoperfusion for N-Acetylprocainamide IntoxicationSTEVEN C. BORKAN, M.D.STEVEN C. BORKAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-6-965 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The data presented by Braden, and coworkers (1) do not show the clear superiority of hemoperfusion over hemodialysis for treatment of severeN-acetylprocainamide intoxication. The evidence is circumstantial that a markedly elevated level of this metabolite was responsible for precipitating thetorsade de pointesbecause two separate episodes of ventricular arrhythmia occurred before any procainamide was administered, because thetorsade de pointesoccurred 3 days after intravenous procainamide therapy was discontinued, and because theN-acetylprocainamide level had already fallen from 56 to 49.5 /µg/mL. Although hemoperfusion produced an impressive 38% decrement in the plasma 7V-acetylprocainamide level (to...

Verapamil Potassium Cardioplegia and Cardiac Conduction

This clinical study analyzes the effect of potassium cardioplegic solution containing verapamil hydrochloride (1 mg/L) on cardiac conduction after release of the aortic cross-clamp and throughout recovery. Fifty consecutive patients undergoing open-heart operation were studied as a unit for postoperative conduction abnormalities. They were also analyzed in groups based on spontaneous ventricular conversion to regular rhythm (54%) and the need for single DC cardioversion (32%), or multiple DC cardioversions (14%). Results showed that spontaneous ventricular conversion had no relationship to aortic cross-clamp time and that DC cardioversion using 10 Ws had no detrimental effects on the myocardium or incidence of conduction abnormalities. The need for transient intraoperative pacing was lowest with spontaneous ventricular conversion, but not statistically different from single or multiple DC cardioversions. Only 3 patients (6%) required pacing in the intensive care unit. The incidence of postoperative atrial and ventricular arrhythmias was similar in all groups, and no deaths or episodes of malignant ventricular arrhythmias occurred. This study concludes that verapamil potassium cardioplegia is associated with excellent myocardial protection and a high incidence of transient intraoperative dysfunction of the atrioventricular node (70%) but a low incidence of postoperative pacing. Benign postoperative arrhythmias occur, but at hospital discharge, few conduction abnormalities (10%) persist.

Automatic defibrillation in man: The initial surgical experience

The automatic implantable defibrillator is an electronic device designed to detect and promptly correct malignant ventricular arrhythmias. Nineteen patients, all survivors of multiple cardiac arrests because of ventricular arrhythmias unresponsive to therapy, have undergone implantation of the automatic defibrillator. In seven patients who had had a previous cardiac operation, implantation was performed through a left lateral thoracotomy. A median sternotomy was used in five patients without a previous operation. In six patients cardiac procedures were performed concomitantly with defibrillator implantation. There were no operative deaths. The average follow-up is 6 months, the longest being 14 months. Following implantation, 47 episodes of malignant ventricular arrhythmias were documented. Twenty-six occurred spontaneously (17 of them outside the hospital); all were corrected with a single 25 joule pulse. Seventeen of 21 arrhythmias induced postoperatively were terminated. Although further validation is required, this study demonstrates that the automatic defibrillator is capable of diagnosing and terminating potentially lethal ventricular arrhythmias. Finally, implantation can be safely accomplished in an exceedingly high risk population.

Efficacy of intravenous disopyramide in acute cardiac arrhythmias.

The efficacy of intravenous disopyramide was studied during 200 episodes of supraventricular and ventricular arrhythmias in 160 patients, mainly presenting with acute myocardial infarction or cardiac failure. Disopyramide 50 mg was administered in a few seconds and any remaining dose within 2 to 5 min. The overall success rate was 80.5%. Intravenous disopyramide was more effective in patients with ventricular arrhythmias (85%) than in those with supraventricular arrhythmias (76%). Dose dependent prolongation of the PR interval, QRS time and the QT interval occurred in 16.32 and 20% of the cases, respectively. The adverse effects were aggravation of the arrhythmias, decrease of blood pressure and anticholinergic activity.

Resistant Ventricular Arrhythmias Treated with Lorcainide, a New Antiarrhythmic Drug

A 68-year-old patient developed increasingly frequent episodes of ventricular and supraventricular arrhythmias over the past five years. During the last 12 months, he was admitted to the hospital on several occasions with complex arrhythmias including multifocal PVCs, bigeminy, trigeminy, ventricular tachycardia, and atrial flutter and fibrillation. Large and frequent doses of quinidine, procainamide, disopyramide, propranolol, and digoxin failed to suppress his arrhythmias. He had no previous history of myocardial infarction or other heart diseases. Coronary arteriography revealed no obstruction of any major arteries or their branches. A new antiarrhythmic drug, lorcainide, was given intravenously and it suppressed all PVCs, including bigeminy and ventricular tachycardia. All his arrhythmias have been completely suppressed by oral regimens of lorcainide, 100 mg four times daily, for the past four months. This is the first case of oral treatment of ventricular arrhythmias with lorcainide in this country.

The use of disopyramide in resistant cardiac arrhythmias due to acute ischaemic heart disease.

Disopyramide, a new anti-arrhythmic drug, has been assessed in twenty-one episodes of cardiac arrhythmia secondary to acute ischaemic heart disease which failed to respond to more conventional suppressive therapy with lignocaine and other standard drugs. The intravenous administration of 100 mg of disopyramide resulted in suppression of two out of seven episodes of supraventricular arrhythmia, and eleven out of fourteen episodes of ventricular arrhythmias. Successful suppression correlated with blood levels of disopyramide in most cases of ventricular arrhythmias but not in the supraventricular arrhythmias. There were no adverse effects on blood pressure or cardiac function. There were minimal effects on conduction in the electrocardiogram. It is concluded that disopyramide, which probably acts by direct depression of myocardial irritability, is a useful new anti-arrhythmic drug in acute myocardial infarction, especially in those patients with ventricular arrhythmias resistant to more conventional anti-arrhythmic therapy.

Life-threatening arrhythmias in the mitral valve prolapse syndrome

This study describes seven patients with the mitral valve prolapse or click-murmur syndrome who have survived one or more episodes of life-threatening ventricular arrhythmias. These arrhythmias include cardiac arrest due to ventricular fibrillation, recurrent ventricular tachycardia causing syncope or sustained ventricular tachycardia requiring electroversion. These patients were seen over a two-year period in a single medical center. Five of the seven had repolarization abnormalities in the resting electrocardiogram. Premature ventricular contractions were present in the routine resting electrocardiograms of six of the seven patients and were frequent during treadmill testing and ambulatory electrocardiographic monitoring in all six tested. There were electrolyte abnormalities or changes in medications known to affect myocardial repolarization during the week before the episode in three of the four patients with cardiac arrest. The diagnosis of mitral valve prolapse click-murmur syndrome was made prior to the episode of life-threatening arrhythmia in only two of the seven patients. Varying forms of antiarrhythmic therapy were given to these patients during follow-up periods of five to 26 months. Although the incidence of fatal arrhythmias in the mitral prolapse syndrome is probably small, we suggest that such arrhythmias may not be extremely rare, particularly among those patients who have repolarization abnormalities in the resting electrocardiogram and frequent premature beats. Patients with unexplained ventricular arrhythmias should be screened for mitral valve prolapse.

Effect of sotalol on clinical arrhythmias

Sotalol (MJ 1999) was administered to 20 patients for the treatment of 22 episodes of supraventricular and 6 episodes of ventricular arrhythmias. The dose range was 9 to 50 mg intravenously and 20 to 80 mg orally given every 6 hours. In 4 of 6 patients supraventricular tachycardia was converted to normal sinus rhythm. In 4 with episodic supraventricular tachycardia, Sotalol prevented further recurrences in all. In 1 patient atrial flutter was converted to normal sinus rhythm. In 3 others with atrial flutter, and in 3 with atrial fibrillation, Sotalol slowed the ventricular response from an average rate of 125 to 72 beats/min. In 1 patient with episodic atrial fibrillation and another with episodic ventricular tachycardia, Sotalol prevented further recurrences. In 1 of 2 patients Sotalol decreased the frequency of premature atrial contractions; in 5 patients with premature ventricular contractions, it abolished them in 2 and reduced their frequency in the other 3. Side effects included transient hypotension in 3 patients and bradycardia sufficient to require reducing the dose of Sotalol in 4. It is concluded that Sotalol is a moderately effective antiarrhythmic drug which may be preferable to other beta adrenergic blocking agents because of its lack of substantial myocardial depressant effects.

Urinary excretion of catecholamines and their main metabolites after myocardial infarction; relationahip to the clinical syndrome.

Abstract Serial measurements of the urinary excretion of noradrenaline (NA), adrenaline (A), normetanephrine + meta‐nephrine (NMN) and vanillylmandelic acid (VMA) have been made in 18 patients with acute myocardial infarction and in 2 patients with severe and recurrent episodes of angina pectoris. The urinary excretion of these 4 compounds was significantly elevated in the patients with myocardial infarction whereas it was within the normal range in the 2 patients with angina pectoris. — NA+A / NMN+VMA ratio was calculated in the 18 patients with myocardial infarction. This ratio was significantly higher in the patients (during the first 4 days after the onset of the infarction) than in the controls. This may indicate that the rate of enzymatic inactivation of NA and A is relatively decreased after myocardial infarction.— The excretion of catecholamines and metabolites was found to be higher in patients with hypotension (systolic blood pressure &lt; 90 mm Hg) and heart failure, than in patients without these complications. Frequent and. severe ventricular arrhythmias were observed in the 6 patients with the highest urinary excretion of catecholamines and metabolites. Among the 12 patients who had a less marked increase in excretion of these compounds, 2 had episodes of ventricular arrhythmias, 5 had supraventricular arrhythmia and 5 had no complications. — Our results suggest that in most cases of myocardial infarction, the marked release of catecholamines is accompanied by a decreased rate of inactivation of these amines. This must lead to high levels of circulating catecholamines which could be related to the development of arrhythmias.

Heritable Q-T prolongation without deafness.

The family, reported on, have a syndrome of prolonged Q-T interval, potentially fatal episodes of ventricular arrhythmias, and normal hearing. The direct familial transmission demonstrated in this pedigree is consistent with an autosomal dominant mode of inheritance. To protect other members of the family from the consequences of ventricular arrhythmia experienced by the irreversibly brain-damaged index patient, a series of physiologic investigations was undertaken on this patient in a search for a suitable prophylactic medical regimen. The attacks of ventricular arrhythmia were found to be precipitated by increase in systemic pressure, sinus tachycardia, and extrasystoles occurring in the supernormal phase of repolarization (R in T syndrome). Propranolol was demonstrated to be an effective agent in preventing the ventricular arrhythmia in the index case and in other family members. Since administration of the beta-adrenergic stimulator isoproterenol did not produce ventricular fibrillation, it is assumed that the action of propranolol in preventing ventricular arrhythmia is not mediated through beta-adrenergic blockade, but through its direct antiarrhythmic properties. The subject experienced no ill effect from the series of investigations.