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PubMed1989

A prospective, randomized evaluation of effect of ventricular fibrillation duration on defibrillation thresholds in humans.

The effect of ventricular fibrillation duration in humans on defibrillation efficacy as it pertains to the time of intervention of an automatic implantable defibrillator is unknown. If a difference in defibrillation efficacy exists in the early period after ventricular fibrillation onset, it may affect algorithms used by antiarrhythmic devices for arrhythmia detection and therapy. Therefore, a prospective, randomized evaluation was performed of the effect of ventricular fibrillation durations of 10 s and 20 s on defibrillation thresholds in 10 survivors of sudden cardiac arrest undergoing implantation of an automatic cardioverter defibrillator. The initial duration of ventricular fibrillation was chosen randomly. Subsequently, each patient served as his or her own control for the alternate duration of ventricular fibrillation to that chosen initially. The mean leading edge defibrillation threshold voltage was 411 +/- 114 V when ventricular fibrillation persisted for 10 s and 419 +/- 125 V when it persisted for 20 s (p = 0.73). The mean defibrillation threshold current was 11.4 +/- 2.8 A when ventricular fibrillation persisted for 10 s and 11.4 +/- 3.2 A when it persisted for 20 s (p = 0.97). The delivered energy defibrillation threshold was 11.5 +/- 5.9 J when ventricular fibrillation persisted for 10 s and 12.0 +/- 6.9 J when it persisted for 20 s (p = 0.67). These findings show that the defibrillation threshold does not change between 10 and 20 s of ventricular fibrillation in out-of-hospital survivors of cardiac arrest at the time of surgical implantation of an automatic defibrillator. The data may have influence on the programming of defibrillator detection algorithms.

Algorithms↗

PubMed1990

Promotion of ventricular tachycardia induction by procainamide in dogs with inducible ventricular fibrillation late after myocardial infarction.

UNLABELLED: The influence of procainamide on inducible ventricular tachyarrhythmias was evaluated in 35 dogs with experimental myocardial infarction, and 9 normal dogs. Programmed stimulation was performed from the right ventricular apex via a percutaneously positioned electrode catheter, using up to five extrastimuli before and after intravenous administration of procainamide (15 mg/kg). Procainamide levels in postinfarct dogs were 8.5 +/- 0.7 micrograms/mL (range 5.3-13.6 micrograms/mL). Procainamide exerted its greatest effect in postinfarct dogs with reproducible baseline ventricular fibrillation. Six of nine dogs (P less than 0.05) with ventricular fibrillation had sustained monomorphic ventricular tachycardia (cycle length: 147 +/- 4 msec) induced after procainamide administration. This ventricular tachycardia required significantly more extrastimuli than baseline ventricular fibrillation (3 +/- 0.3 extrastimuli before vs 4 +/- 0.3 extrastimuli after procainamide). Procainamide never converted ventricular fibrillation to ventricular tachycardia in normal dogs. Procainamide had minimal effect on inducible ventricular tachycardia after myocardial infarction. Ventricular tachycardia induction was abolished in only 2 of 17 dogs despite significant prolongation of electrophysiological parameters. Ventricular tachycardia cycle length, and the number of extrastimuli required were unchanged by procainamide in this subgroup. CONCLUSION: Ventricular tachycardia is insensitive to the antiarrhythmic properties of procainamide in this model. In contrast, procainamide is able to convert postinfarction ventricular fibrillation to ventricular tachycardia, presumably by promoting sustained, organized reentry. This previously undescribed action is an unusual form of proarrhythmic effect, and suggests that this drug should be used cautiously in patients after myocardial infarction.

Animals↗

PubMed1983

Electrophysiologic observations during the spontaneous initiation of ischemia-induced ventricular fibrillation.

Electrophysiologic features of spontaneous, ischemia-induced ventricular fibrillation were studied in 17 dogs using multiple endocardial bipoles positioned in normal and ischemic zones and at the border of ischemic myocardium. All dogs showed ventricular tachyarrhythmias prior to the initiation of ventricular fibrillation. The heart rate prior to the fatal arrhythmia in the ventricular fibrillation dogs was significantly faster than that of nonventricular fibrillation dogs. There was no difference in the coupling intervals of the initial premature complex between episodic and sustained ventricular arrhythmia in most dogs. However, shorter coupling intervals initiated sustained arrhythmia in some dogs. Sites of initiation of arrhythmia were mostly in the ischemic zone. Furthermore, diastolic electrical activity was consistently observed in the ischemic zone during fatal arrhythmia in dogs showing diastolic activity. Cycle length during the fatal arrhythmia prior to ventricular fibrillation gradually shortened, whereas cycle length of episodic ventricular tachycardia remained approximately 200 msec followed by lengthening prior to restoration of sinus rhythm. The disparity of local activation (time differences between the earliest and latest onset of the activation in the five recording sites) increased during the fatal arrhythmia. Examples of progressive intraventricular block (Wenckebach-like) between the border and the center of ischemic myocardium leading to ventricular fibrillation are resynchronization of this disparity leading to the termination of ventricular tachycardia are shown. The recording of continuous electrical activity using bipolar electrodes with an interelectrode distance of 1 mm suggests a smaller reentrant pathway during fatal arrhythmia. Our observations confirm the importance of endocardial recordings within ischemic myocardium, and adds new insight into the events leading to both episodic and sustained ventricular tachycardia.

Animals↗

PubMed1982

[Clinical-electrophysiological findings in patients following ventricular fibrillation].

30 patients, successfully resuscitated from ventricular fibrillation outside acute myocardial infarction, were studied by programmed right-ventricular stimulation. The stimulation studies were carried out one week up to 1.5 years after the event (median two months). Mean age of the patients was 50.2 +/- 8.8 years, 27 were male. The majority of patients had coronary heart disease and/or localized or diffuse ventricular contraction abnormalities. In 26 patients the stimulation protocol included the application of premature single and double ventricular stimuli during sinus rhythm and a paced ventricular rhythm at cycle lengths of 500, 430, 370 and 330 msec until ventricular tachycardia, ventricular flutter or ventricular fibrillation were induced. 4 patients were studied only at a cycle length of 500 msec. Using this stimulation protocol, in 7 patients (26.9%) sustained ventricular tachycardia, in 5 patients (19.2%) ventricular flutter and in 7 patients (26.9%) ventricular fibrillation were induced. These arrhythmias were induced at a basic cycle length of 500 ms in 10 patients, at 430 ms in 3 patients, at 370 ms in 4 patients and at 330 ms in 2 patients. In the remaining patients, only ventricular echo beats (one to six) of the intra-ventricular reentry type were induced. Thus these results show a persistent increase in ventricular vulnerability in a high percentage of patients (73%), provided that appropriate stimulation techniques are used. These observations may have great importance for the management of these patients.

Arrhythmias, Cardiac↗

PubMed1988

Prevention of ventricular fibrillation after aortic declamping during cardiac surgery.

Ventricular fibrillation is common after aortic declamping during cardiac surgery, and the metabolic demands of such fibrillation, or its treatment by means of countershock, may contribute to myocardial injury. To determine the effects of administering intravenous lidocaine just before aortic declamping, we randomly divided 194 cardiac surgery patients into 2 groups. One hundred patients (group A) received lidocaine, 200 mg intravenously, 3 minutes before aortic declamping; and 94 patients (group B) received no medication before declamping. Multiple baseline variables, including clamp times, medications, electrolyte values, ventricular function, and the extent and type of surgery, were similar for both groups. After aortic declamping, 31 of the 100 patients in group A had ventricular fibrillation, as did 57 of the 94 patients in group B (p < 0.001). Of those who fibrillated, the group-A patients required a mean of 1.76 countershocks, whereas the group-B patients required a mean of 2.68 countershocks (p < 0.05). Serum potassium level also affected the incidence of ventricular fibrillation, independently of lidocaine. Elevated serum potassium levels were associated with a lower incidence of ventricular fibrillation. Although lidocaine was independently protective at all potassium levels, the combination of lidocaine and a high serum potassium level had the greatest effect in preventing fibrillation. In patients who had potassium levels higher than 5.1 mEq/l and who were also given lidocaine, the incidence of ventricular fibrillation was lower than 15%.

Journal Article↗

PubMed1994

The effects of lidocaine on the vulnerable period during ventricular fibrillation.

INTRODUCTION: It was postulated that a subthreshold defibrillation shock failed to halt ventricular fibrillation because the shock itself reinitiated ventricular fibrillation by falling into the vulnerable period of the wavefronts. Whether or not the timing of the vulnerable period is determined by the ventricular fibrillation cycle length is unknown. METHODS AND RESULTS: We determined the patterns of epicardial activation in ten dogs by computerized mapping techniques during unsuccessful defibrillation. Lidocaine was then given to prolong the ventricular fibrillation cycle length, and the computerized mapping studies were repeated. The results showed that lidocaine increased the ventricular fibrillation cycle length from 110 +/- 13 msec to 156 +/- 5 msec (P < 0.001). Among 55 episodes of unsuccessful defibrillation, the site of the earliest postshock activation occurred in the center of the mapped tissue 12 times at baseline and 14 times during lidocaine infusion. At electrodes that registered as postshock early sites, the preshock intervals clustered within a narrow range both before (58 +/- 14 msec) and during (101 +/- 18 msec, P < 0.001) lidocaine infusion. The correlation between the preshock intervals and the ventricular fibrillation cycle length was significant for these 26 sites (r = 0.87, P < 0.001). CONCLUSION: We conclude that a vulnerable period is present during ventricular fibrillation, and the timing of the vulnerable period is determined by the ventricular fibrillation cycle length.

Animals↗

PubMed1977

The effects of heart rate, myocardial ischemia and vagal stimulation on the threshold for ventricular fibrillation.

The minimum current required to cause ventricular fibrillation was determined by electrical stimulation of the normal or ischemic canine left ventricle. The threshold for ventricular fibrillation in the normal heart decreased when the heart rate was rapid. Strong vagal stimulation did not affect the ventricular fibrillation threshold when the heart rate was fixed. The fall in the ventricular fibrillation threshold in the presence of acute myocardial ischemia was greater and more prolonged when the heart rate was rapid. These findings indicate the importance of the immediate correction of tachycardia in patients suffering from acute myocardial infarction.

Animals↗

PubMed1976

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Arrhythmias, Cardiac↗

PubMed1986

Relation between ventricular arrhythmia and sudden cardiac death in patients with acute myocardial infarction: the predictors of ventricular fibrillation.

Continuous electrocardiographic monitoring was recorded in 102 patients during the first 48 hours after the onset of myocardial infarction. One hundred forty-eight episodes of ventricular tachycardia having an ectopic rate of 180/min or more and without a background of treatment with antiarrhythmic drugs were analyzed; these included 125 cases of ventricular tachycardia that terminated spontaneously and 23 cases that deteriorated to ventricular fibrillation. Episodes of ventricular tachycardia with a polymorphic configuration were more frequent in the group with than in the group without ventricular fibrillation (30.4 and 8%, respectively). The incidence of ventricular tachycardia continuing for more than 100 QRS complexes was 20 times greater in the group with ventricular fibrillation, and ventricular tachycardia initiated by and R on T ventricular premature beat was recorded three times more often in this group. The 10 minute pretachycardia interval in both groups showed no significant difference in the incidence, complexity, intensity or dynamic pattern of ventricular premature contractions. The data provide reason to doubt the significance of ventricular premature beats as harbingers of sudden death from ventricular fibrillation. Rather, ventricular tachycardia with an ectopic rate of 180/min or more, a polymorphic configuration and persistence for more than 100 QRS complexes (or initiated by an R on T ventricular premature beat) is a more reliable predictor of the occurrence of ventricular fibrillation.

Adult↗

PubMed1982

Initiation of ventricular fibrillation outside hospital in patients with acute ischaemic heart disease.

Factors which may predispose to ventricular fibrillation were assessed in 48 consecutive patients who developed ventricular fibrillation outside hospital after the arrival of a mobile coronary care team. Before the initiation of ventricular fibrillation, late cycle ventricular extrasystoles were recorded in 38 patients (79%) and R on T extrasystoles in 27 patients (56%). R on T extrasystoles were relatively infrequent--an average of three occurred during a mean monitoring time of 27 minutes. Multifocal extrasystoles occurred in only three patients (6%), consecutive extrasystoles in 14 (29%), and self-terminating ventricular tachycardia in three (6%). Ventricular extrasystoles occurring at more than five a minute were uncommon during this phase. The time from "warning arrhythmias" to the development of ventricular fibrillation in many patients was short, thus limiting the administration of antiarrhythmic agents. There was a significant increase in the heart rates recorded immediately before ventricular fibrillation when compared with those documented initially. Thus, an increase in heart rate appeared to be a predisposing factor in the initiation of ventricular fibrillation. An R on T extrasystole was the most important factor in the initiation of ventricular fibrillation: it occurred in 33 patients (69%). In nine (19%) ventricular tachycardia and in six (12%) a late cycle extrasystole or idioventricular rhythm initiated ventricular fibrillation.

Adult↗

PubMed1995

Alteration of ventricular fibrillation by propranolol and isoproterenol detected by epicardial mapping with 506 electrodes.

INTRODUCTION: We hypothesized that drugs which alter ventricular refractoriness or excitability produce quantifiable changes in ventricular fibrillation. METHODS AND RESULTS: We used a 528-channel mapping system to quantify the effects of the beta-antagonist, propranolol, and the beta-agonist, isoproterenol, on activation patterns in ventricular fibrillation. A plaque of 506 (22 x 23) electrodes spaced 1.12 mm apart and covering about 5% of the ventricular epicardium was sewn to the anterior right ventricle in 18 pigs (30 kg). Propranolol (0.25 to 0.4 mg/kg) increased the refractory period at a right ventricular epicardial site while isoproterenol (3 to 5 micrograms/min) shortened it. Ventricular fibrillation was induced by programmed stimulation, and unipolar electrograms were recorded from the 506 plaque electrodes for 2 seconds beginning 1, 15, and 30 seconds after the onset of fibrillation. Active epicardial recording sites were identified from the first derivative of the unipolar potentials (dV/dt) detected at each electrode. Then, neighboring active sites were grouped into activation fronts by computer analysis. In six pigs the effect of repeated inductions of ventricular fibrillation was assessed by comparing ventricular fibrillation after saline with a preceding control episode of fibrillation. Each activation front excited 40% +/- 46% of the mapped region before blocking. No changes were observed with saline and multiple inductions of fibrillation. In another six pigs, ventricular fibrillation after propranolol was compared with a preceding control episode of fibrillation. Ventricular fibrillation after propranolol exhibited a decreased activation rate per epicardial recording site and fewer activation fronts per second. There was no change in the amount of tissue excited by each activation front or the number of reentry cycles per activation front compared with control. In addition, there was no change in the maximum negative dV/dt detected per activation at an epicardial site. In six pigs ventricular fibrillation during isoproterenol was compared with control episodes of ventricular fibrillation before and 45 minutes after washout of the drug. The control episodes of fibrillation were not different from each other. Compared with control, ventricular fibrillation during isoproterenol exhibited an increased activation rate per epicardial site, an increased amount of tissue excited by each activation front, and an increased maximum negative dV/dt for each activation. There was no change in the number of activation fronts per second or the number of reentry cycles per activation front compared with control. CONCLUSION: Quantitative analysis revealed that propranolol and isoproterenol do not have symmetrically opposite effects on ventricular fibrillation. Propranolol decreased the number of activation fronts while isoproterenol increased the amount of tissue excited by each activation front. Thus, drugs that alter ventricular refractoriness or excitability alter ventricular fibrillation.

Animals↗

PubMed1999

Cerebral blood flow velocity during repeatedly induced ventricular fibrillation.

STUDY OBJECTIVE: To investigate the effect of induced ventricular fibrillation and defibrillation on cerebral blood flow (CBF) was investigated using a transcranial Doppler. DESIGN: Prospective clinical study. SETTING: University hospital. PATIENTS: 12 ASA physical status III and IV patients who underwent implantable cardioverter defibrillator placement during general anesthesia. INTERVENTIONS: Cerebral blood flow velocity was measured repeatedly during induced ventricular fibrillation and subsequent defibrillation. MEASUREMENTS AND MAIN RESULTS: The mean flow velocity in the middle cerebral artery was measured using a transcranial Doppler. The mean flow velocities decreased significantly immediately after ventricular fibrillation was induced, but they returned to preventricular fibrillation levels immediately after successful defibrillation. Repeatedly induced ventricular fibrillations have no cumulative detrimental effect on the CBF velocity. CONCLUSIONS: Repetitively induced ventricular fibrillation and defibrillation during the insertion of implantable cardioverter defibrillator did not show any detrimental changes in CBF. Transcranial Doppler may be a more sensitive device than other currently available cerebral monitors to detect changes in cerebral circulation during a brief episode of ventricular fibrillation and defibrillation.

Blood Flow Velocity↗

PubMed1998

Electrocardiographic measures of ventricular repolarisation dispersion in patients with coronary artery disease susceptible to ventricular fibrillation.

OBJECTIVE: To study electrocardiographic measures of ventricular repolarisation dispersion in patients prone to ventricular fibrillation compared with controls matched for the extent of coronary heart disease and the use of beta blockers. DESIGN: A case-control study. SETTING: Cardiovascular laboratory of a tertiary referral centre. PATIENTS: Fifty patients with documented ventricular fibrillation not associated with acute myocardial infarction, and their controls matched for sex, age, number of diseased coronary vessels, left ventricular ejection fraction, previous myocardial infarction and its location, and the use of beta blockers. MAIN OUTCOME MEASURES: Electrocardiographic measures of QT, JT, and Tend interval dispersions in a 12 lead electrocardiogram. RESULTS: The ventricular fibrillation patients compared to controls showed increased mean (SD) QTapex dispersion (53 (18) ms v 44 (18) ms, respectively; p < 0.01) and mean (SD) Tend dispersion (46 (17) ms v 38 (15) ms, respectively; p < 0.05). CONCLUSIONS: Increased QTapex and Tend dispersions are associated with a susceptibility to ventricular fibrillation even when the extent of the coronary heart disease and use of beta blockers are taken into consideration. However, because of a considerable overlap between the groups, measures of QT dispersion assessed from a 12 lead electrocardiogram do not provide clinically useful information for identification of patients at risk of sudden cardiac death.

Case-Control Studies↗

PubMed1989

The protective effect of vagus nerve stimulation on catecholamine-halothane-induced ventricular fibrillation in dogs.

Parasympathetic neural activity modulates some ventricular arrhythmias in man. Therefore, a canine model of arrhythmias produced by the interaction of halothane and catecholamines was used to study the effects of vagal stimulation on the induction of ventricular fibrillation. The dose of catecholamine required to induce ventricular fibrillation was determined during a constant heart rate. Vagal stimulation reversibly raised the norepinephrine dose that produced ventricular fibrillation from 16.4 +/- 2.4 to 30.0 +/- 3.8 micrograms (p less than 0.001, n = 10), and the epinephrine dose from 15.5 +/- 2.0 to 22.5 +/- 2.6 micrograms (p less than 0.001, n = 5). Following atropine, vagal stimulation failed to raise the threshold dose of norepinephrine (16.8 +/- 2.4 vs. 18.3 +/- 3.3 micrograms, nonsignificant, n = 6) or epinephrine (15.5 +/- 2.0 vs. 16.0 +/- 2.3 micrograms, nonsignificant, n = 5). Ligation of the cervical vagus nerves did not affect the epinephrine threshold dose (16.3 +/- 3.3 vs. 17.5 +/- 2.7 micrograms, nonsignificant, n = 5). Following elevation of basal vagal tone by morphine premedication, the norepinephrine threshold of 53.0 +/- 9.2 micrograms declined by a nonsignificant amount to 46.5 +/- 11.5 micrograms after vagotomy (nonsignificant, n = 5). Thus resting vagal tone does not prevent catecholamine-halothane-induced ventricular fibrillation, whereas increasing vagal tone by electrical stimulation substantially protects against this arrhythmia. The protection is mediated through a muscarinic cholinergic receptor.

Animals↗

PubMed1992

Metabolic consequences and predictability of ventricular fibrillation in hypoxia. A 31P- and 23Na-nuclear magnetic resonance study of the isolated rat heart.

BACKGROUND: Ventricular fibrillation has deleterious metabolic and functional consequences for the heart. This study had two purposes: first, to define the effects of ventricular fibrillation during hypoxia on energy metabolism and accumulation of intracellular Na+ and, second, to test whether the occurrence of ventricular fibrillation can be predicted from functional or metabolic parameters. METHODS AND RESULTS: Isolated isovolumic rat hearts were perfused with oxygenated Krebs-Henseleit buffer at 37 degrees C. After a prehypoxic period, hearts were subjected to hypoxic perfusion (95% N2-5% CO2) for 30 minutes. High-energy phosphates and intracellular pH were determined by 31P-nuclear magnetic resonance (NMR) spectroscopy, and intracellular Na+ accumulation was followed by 23Na-NMR spectroscopy in combination with the shift reagent dysprosium triethylenetetraminehexa-acetate. Five of 10 (31P-NMR) and four of 10 (23Na-NMR) hearts developed spontaneous ventricular fibrillation at 19 +/- 2 minutes (31P-NMR) and 18 +/- 3 minutes (23Na-NMR) of hypoxia (ventricular fibrillation group), whereas other hearts (non-ventricular fibrillation group) remained beating throughout hypoxia. Cardiac function and high-energy phosphate content declined during hypoxia, and ventricular fibrillation exacerbated this decline significantly. Similarly, ventricular fibrillation exacerbated the accumulation of intracellular Na+ occurring during hypoxia. Statistical analysis showed that the event of ventricular fibrillation could be predicted from changes of end-diastolic pressure, rate-pressure product, and creatine phosphate content before ventricular fibrillation. However, the strongest predictor of ventricular fibrillation was intracellular Na+ accumulation, which occurred in ventricular fibrillation hearts throughout the hypoxic period long before ventricular fibrillation was initiated. CONCLUSIONS: Loss of systolic and diastolic functions, creatine phosphate depletion, and, in particular, intracellular Na+ accumulation may be causally related to induction of ventricular fibrillation during hypoxia, all of which are most likely linked to concomitant intracellular Ca2+ accumulation.

Adenosine Triphosphate↗

PubMed1971

Bretylium tosylate in the management of refractory ventricular fibrillation.

Nine patients who had recurrent ventricular fibrillation following acute myocardial infarction or angina were given bretylium tosylate in a dose of 5 mg./kg. intramuscularly every eight hours after other measures had proved ineffective. Provided the patients were not in shock or in heart failure, there was a considerable reduction in the episodes of ventricular fibrillation.A second group of nine patients who developed recurrent ventricular fibrillation following open heart surgery were given bretylium intravenously, which controlled the arrhythmia in every instance.Bretylium did not completely abolish ventricular premature beats but the latter did not initiate ventricular fibrillation even when they occurred on the T wave.

Adult↗

PubMed1994

Prognosis of early versus late ventricular fibrillation complicating acute myocardial infarction.

Earlier studies have suggested that patients exhibiting late (> 24 h) ventricular fibrillation during acute myocardial infarction had a poorer outcome in comparison to myocardial infarction patients with early (< 24 h) ventricular fibrillation. Between August 1981 and July 1983, 5839 consecutive patients with acute myocardial infarction were hospitalized in 13 out of 21 operating coronary care units in Israel. Demographic and medical data were collected from hospitalization charts and during 1 year of follow-up. Mortality assessment was done for 99% of hospital survivors up to mid-1988 (mean, 5.5 years). The incidence of ventricular fibrillation in the SPRINT Registry was 6% (371/5839). Patients with ventricular fibrillation in the setting of cardiogenic shock (n = 107) were excluded from analysis. Patients with late ventricular fibrillation (n = 109; 41%) were older and had a more complicated hospital course than patients with early ventricular fibrillation (n = 155; 59%). In-hospital and 1-year post-discharge mortality were significantly higher in patients with late ventricular fibrillation (63% and 17%) as compared to patients with early ventricular fibrillation (26% and 4%, respectively; P < 0.05 for each). This difference vanished 5 years after hospital discharge. After multiple logistic regression analysis late occurrence of ventricular fibrillation emerged as an independent predictor of increased in-hospital mortality (Odds ratio, 4.29; 95% confidence interval, 2.11-8.74) but not for subsequent death. Patients with late ventricular fibrillation during the hospital course of acute myocardial infarction had a poorer immediate and subsequent outcome in comparison to patients with early ventricular fibrillation.

Aged↗

PubMed1981

Clinical, electrocardiographic and follow-up observations in patients having ventricular fibrillation during Holter monitoring. Role of quinidine therapy.

Ventricular fibrillation occurred during Holter electrocardiographic monitoring in 5 of 3,307 consecutive patients. All five patients had Holter studies for evaluation of antiarrhythmic drug therapy; their ages ranged from 51 to 65 years. No patient had acute myocardial infarction; all had congestive heart failure and severe left ventricular dysfunction. One patient had ischemic and four had nonischemic cardiomyopathy. All patients had recently begun treatment with oral quinidine and had plasma quinidine levels of 1.24 to 5.18 microgram/ml. The Holter monitoring revealed that all had a long Q-T interval and that ventricular fibrillation began during frequent ventricular premature beats and was immediately preceded by ventricular tachycardia of the torsade de pointes type. The coupling interval of the ventricular premature beats initiating torsade de pointes was late (440 to 720 ms) and followed long preceding cycles (840 to 1920 ms). Ventricular fibrillation resolved spontaneously in two patients, but two of the remaining three patients died despite attempted cardiopulmonary resuscitation. It is concluded that (1) left ventricular dysfunction, chronic ventricular arrhythmias and initiation of quinidine therapy were the common findings in these patients; (2) a long Q-T interval, late coupled ventricular premature beats and long preceding cycles facilitate initiation of ventricular fibrillation in quinidine-treated patients; and (3) direct on-line monitoring should be utilized in the management of these patients.

Aged↗