Occurrence Of Ventricular Fibrillation Research Articles

Part 7: The Era of Reperfusion

Part 7: The Era of Reperfusion

4-aminopyridine inhibits the occurrence of ventricular fibrillation but not ventricular tachycardia in the reperfused, P6olated rat heart.

The 4-aminopyridine (4-AP)-sensitive transient outward current (Ito) has been reported to play an important role in the ischemia- or high [Ca2+]o-induced reentrant ventricular arrhythmias. However, the role of 4-AP sensitive Ito in reperfusion arrhythmia remains unknown. Rat hearts were perfused with Tyrode solution (control), and treated with 0.5 micromol/L verapamil, 1 micromol/L glibenclamide, 10 micromol/L E-4031 or 2 mmol/L 4-AP. After a 10-min perfusion, hearts were subjected to 30-min global ischemia followed by 10-min reperfusion. The effects of the ion-channel blockers on the incidence of ventricular tachycardia (VT), torsades de pointes (Tdp) and ventricular fibrillation (VF) during the reperfusion period were investigated. Verapamil and 4-AP abolished VF and Tdp. The incidence of VT was also attenuated by verapamil, but not by 4-AP. Glibenclamide and E-4031 (a blocker of a rapidly activating component of delayed rectifier K+ current) did not affect the incidence of those tachyarrhythmias. Accordingly, (1) the underlying mechanism of VF or Tdp is different from that of VT, and (2) 4-AP sensitive Ito is required for the occurrence of reperfusion Tdp or VF in the present model.

Experimental study of the effects of multi-site sequential ventricular pacing on the prophylaxis of ventricular fibrillation.

Previous studies report a significant prophylactic effect on the occurrence of atrial fibrillation by simultaneous multi-site atrial pacing. We investigated the effects of multi-site sequential ventricular pacing (MSVP), which may be preferable to simultaneous multi-site pacing in terms of the prophylaxis of the occurrence of ventricular fibrillation (VF). Needle electrodes were inserted at ten different epicardial sites on both ventricles for MSVP in 12 adult beagle dogs. Four premature ventricular extrastimuli (PVE) were introduced to provoke VF reproducibly from a separate electrode in the left ventricle. The 4 PVE were applied to try to provoke VF during MSVP in a comparable fashion to the activation sequence during sinus rhythm. We compared the prophylactic effects of MSVP on the inducibility of VF by changing the number of stimulation sites to either 1, 3, 5, or 10 epicardial sites. We performed a total of 363 trials of induction and suppression of VF. The occurrence rates of VF by the 4 PVE for the various number of epicardial stimulation sites of MSVP, i.e., at 1, 3, 5, and 10 sites, were 0.8263, 0.4286, 0.4450, and 0.2857, respectively (p < 0.05). There was a significant prophylactic effect of MSVP on the inducibility of VF, and this effect became stronger as the number of MSVP sites was increased from 3 to 10. The hemodynamic state was relatively stable during MSVP. MSVP seems to be a promising method with which to reduce the occurrence of VF, and a larger number of stimulation sites would be more effective in terms of the prophylaxis of VF.

The effect of Xin’an capsule"Equation missing" on ventricular arrthythmia in animals) on ventricular arrthythmia in animals

Objective: To observe the effects of Xin’an capsule (XAC) on experimental ventricular arrhythmia (EVA) in animals and to explore the possible mechanism.Methods: Three types of animal arrhythmic model (ventricular arrythmia in guinea pigs induced by Ouabin, in rats caused by reperfusion after ligation of descending anterior branch of coronary artery and by CaCl2) were used to study the effects of XAC on ventricular arrhythmia (VA).Results: After XAC treatment, the dosage of Ouabin needed for inducing ventricular premature beat (VPB), ventricular tachycardia (VT) and ventricular fibrillation (VF) increased in guinea pigs. The sustaining time of reperfusion induced VT and total occurrence of ventricular arrhythmias decreased. XAC also showed an effect in increasing CaCl2 dosage needed to cause VA, and decreased the occurrence of VF and death in rats

Relation between activation sequence fluctuation and arrhythmogenicity in sodium-channel blockades.

To examine the correlation between activation sequence fluctuation and arrhythmogenicity, we investigated temporal changes in the activation sequence by measuring activation times [negative first derivative of voltage over time (-dV/dt) in QRS] from the entire heart in 18 dogs. The heart was paced by constant atrial stimulation. The character of the activation sequence fluctuation was established by a principal component analysis, in which the first principal component was defined as a stable component of the sequence and the second or third component as a fluctuated component. Steady state contained 2.2 +/- 0.6% (percent total principal component, mean +/- SD) of fluctuated components, which appeared in a beat-by-beat manner (activation sequence alternans). Activation sequence alternans was observed only during flecainide administration and not during lidocaine or disopyramide administration. Fluctuated components at a high dose of flecainide significantly increased (3.3 +/- 0.8%). Ventricular fibrillation ensued in all dogs (n = 6) exposed to flecainide after an increase in activation sequence alternans. In conclusion, flecainide evoked local activation sequence alternans. This phenomenon correlated with the occurrence of ventricular fibrillation.

Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio cordis).

Sudden death due to relatively innocent chest-wall impact has been described in young individuals (commotio cordis). In our previously reported swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mph baseball impacts to the precordium. Because activation of the K(+)(ATP) channel has been implicated in the pathogenesis of ST elevation and ventricular fibrillation in myocardial ischemia, we hypothesized that this channel could be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis. In the initial experiment, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K(+)(ATP) channel, and chest impact was given on the QRS. The results of these strikes were compared with animals in which no glibenclamide was given. In the second phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fashion), with chest impact delivered just before the T-wave peak. With QRS impacts, the maximal ST elevation was significantly less in those animals given glibenclamide (0.16+/-0.10 mV) than in controls (0.35+/-0.20 mV; P=0.004). With T-wave impacts, the animals that received glibenclamide had significantly fewer occurrences of ventricular fibrillation (1 episode in 27 impacts; 4%) than controls (6 episodes in 18 impacts; 33%; P=0.01). In this experimental model of commotio cordis, blockade of the K(+)(ATP) channel reduced the incidence of ventricular fibrillation and the magnitude of ST-segment elevation. Therefore, selective K(+)(ATP) channel activation may be a pivotal mechanism in sudden death resulting from low-energy chest-wall trauma in young people during sporting activities.

Heme oxygenase and cardiac function in ischemic/reperfused rat hearts

We investigated whether the expression of heme oxygenase (HO) isozymes was related to the occurrence of ventricular fibrillation (VF) induced by ischemia/reperfusion in nondiabetic and diabetic myocardium. To study the role of HO-1 and HO-2 mRNA expression in VF, isolated hearts obtained from nondiabetic and 8-week diabetic rats were subjected to 30 min of ischemia followed by 2 h of reperfusion. Expression of HO-1 and HO-2 mRNA was studied in fibrillated and nonfibrillated myocardium using Northern blotting and reverse transcription polymerase chain reaction (RT-PCR). The effect of zinc protoporphyrin IX (Zn-PPIX), a potent inhibitor of HO activity, on HO activity was also studied in ischemic/reperfused hearts. Upon reperfusion, an expression of HO-1 was observed in nonfibrillated myocardium. HO-1 mRNA expression was significantly reduced in hearts showed VF. Zn-PPIX (5 μM) treatment reduced HO activity from its control values of 398 ± 27 (in nondiabetics) and 370 ± 20 pmol bilirubin/h (in diabetics) to 69 ± 14 (in nondiabetics, p < .05) and 60 ± 11 pmol bilirubin/h (in diabetics, p < .05), respectively, and all hearts, upon reperfusion, showed VF in both nondiabetic and diabetic subjects. HO-2 expression was unchanged in nonfibrillated and fibrillated myocardium. Postischemic function showed no correlation with the expression of these genes. Our data show that the mechanism(s) of ischemia/reperfusion-induced VF involves the downregulation of HO-1 mRNA and a reduction in HO activity. Furthermore, the mechanism(s) of VF at molecular level involving HO isozymes does not show a significant difference between nondiabetics and diabetics.

Increased frequency of thorax injuries with ACD-CPR

A prospective, randomised out-of-hospital study in a two-tiered system with active compression–decompression (ACD) cardiopulmonary resuscitation (CPR) versus standard (STD) CPR in patients following non-traumatic cardiac arrest was planned to test the hypothesis that ACD-CPR by the first tier may increase the occurrence of ventricular fibrillation as compared with STD-CPR. Furthermore, in a later phase of the study, sternal and rib fractures induced by both CPR methods were determined by extensive autopsy. After enrolling 90 patients the study was terminated because of a high frequency of chest injuries found at autopsy. Forty-two patients received STD-CPR from the first tier and ACD-CPR from the second tier. Thirty-three patients received ACD-CPR only by the first and the second tier, while 15 patients received STD-CPR only from the first and second tiers. In order to obtain a sufficiently large control group for autopsy findings after STD-CPR, STD-CPR was performed in an additional 33 patients within a second period of 4 months. There was no improvement in the number of patients found in ventricular fibrillation after ACD-CPR as compared to STD-CPR performed by the first tier. In patients undergoing autopsy ( n=35) there were significantly more sternal fractures with ACD-CPR versus STD-CPR (14/15 vs. 6/20; P<0.005) and rib fractures (13/15 vs. 11/20; P<0.05) In conclusion, ACD-CPR appears to cause more CPR-related injuries than does standard CPR, but as a result of a number of limitations on this study, this fact cannot be proven beyond doubt.

Intracoronary flecainide induces ST alternans and reentrant arrhythmia on intact canine heart: A role of 4-aminopyridine-sensitive current.

The electrical alternans shown on an ST segment, ST alternans, is known as one of the most important predictors of ventricular fibrillation (VF). It has also been reported that sodium channel inhibition changes action potential configuration, especially on the repolarization phase. Thus, the sodium channel blocker may produce ST alternans and trigger reentrant arrhythmia. A sodium channel blocker (disopyramide, lidocaine, or flecainide) was infused selectively into the left anterior descending coronary artery in anesthetized, open-chest dogs. Sixty unipolar electrograms were simultaneously recorded from the entire cardiac surface of the heart. The amplitude of ST alternans (STa) was determined as the difference in the ST-segment magnitude between 2 consecutive electrograms. We accepted the greatest STa among 60 leads for evaluation. High-dose flecainide (100 microg. kg-1. min-1) increased STa and evoked a spontaneous VF. The STa in high-dose flecainide loading (8.7+/-3.4 mV; mean+/-SEM) was significantly greater than that in disopyramide or lidocaine (0. 9+/-0.4 and 0.8+/-0.2 mV, P<0.05). Treatment of 4-aminopyridine (4-AP) suppressed the increase in STa and the occurrence of VF evoked by flecainide, while E4031 or verapamil did not inhibit those. Flecainide caused the ST alternans that was closely correlated to the occurrence of VF. Because the ST alternans was suppressed by 4-AP treatment, a 4-AP-sensitive current such as Ito or Isus may play an important role on this phenomenon.

"Brugada" syndrome: clinical data and suggested pathophysiological mechanism.

The occurrence of ventricular fibrillation (VF) in the absence of any structural heart disease is classified as “primary electrical disease” or (in the absence of any relevant findings) “idiopathic VF.” This diagnosis implies that the arrhythmogenic substrate is inherent to the excitable and conducting properties of the heart. With the exception of a positive family history, demographic variables are, as a rule, not very helpful in establishing the diagnosis of primary electrical disease.1 The paradigm of primary electrical disease is the long-QT syndrome (LQTS), in which altered ionic channel function secondary to mutations in genes encoding ion channels has been shown to underlie QT-interval prolongation.2 3 In 1992, Brugada and Brugada4 described 8 patients with a history of aborted sudden death and a distinct ECG pattern, consisting of right bundle-branch block (RBBB) with ST-segment elevation in the right precordial leads (V1, V2, and V3, Figure 1⇓) and normal QT interval in the absence of any structural heart disease (as determined by routine clinical, biochemical, echocardiographic, and angiographic examinations). In 4 of the reported patients, a family history was suspected. Figure 1. ECG tracings of 1 patient originally described by Brugada and Brugada.4 Tracings show RBBB with ST-segment elevation in right precordial leads. There is marked left axis deviation, suggesting presence of left anterior hemiblock. In presence of RBBB, QTc is prolonged (482 ms). Patients with these unique ECG abnormalities have been recognized as a distinct subgroup in male Thai patients presenting with cardiac arrest due to VF.5 In northeastern Thailand, sudden unexpected death, typically occurring during sleep, is a leading cause of death in young men, and 40% of these patients have a family history of sudden death.6 The suspected inherited occurrence of the entity strongly suggested possible involvement …

Endogenous Adenosine Reduces the Occurrence of Ischemia-induced Ventricular Fibrillation in Rat Heart

The aim of this study was to determine whether endogenous adenosine has antiarrhythmic effects on ischemia-induced ventricular tachyarrhythmias. We therefore modulated the effect of endogenous adenosine in isolated rat hearts using four different approaches. First, interstitial adenosine was elevated by metabolic inhibition with either EHNA (erythro-9-(2-hydroxy-3-nonly)adenine) or acadesine [5-amino-1-β-D-imidazole-4-carboxamide). Second, cardiac effects of A1adenosine receptors were allosterically enhanced with PD81,723 (2-amino-4,5-dimethyl-3-thienyl)[3-(trifluoromethyl)phenyl]-methanone. Third, endogenous adenosine release was suppressed with NBMPR (S-(4-nitrobenzyl)-6-thioinosine), and fourth, adenosine receptor subtypes were blocked with antagonists of different selectivity. Regional ischemia, induced by coronary artery ligation, caused ventricular fibrillation of a reproducible kind in about 20% of untreated hearts with a low calcium concentration in the perfusion medium (0.80 mmol/l CaCl2) and in about 75% with high calcium (1.85 mmol/l) within an observation period of 30 min. At high calcium, EHNA (1 and 10μmol/l) and acadesine (500μmol/l) suppressed the occurrence of ventricular fibrillation from 68% (controls) to 47%, 33% and 38%, respectively. Conversely, PD81,723 (10μmol/l) did not influence the occurrence of ventricular fibrillation. At low calcium, NBMPR (0.1 and 1μmol/l) resulted in a concentration-dependent rise of ventricular fibrillation from 13% (controls) to 40% and 57%, respectively. The adenosine receptor antagonists theophylline (100μmol/l), XAC (Xanthine Amine Congener; 1μmol/l) and 8-PT (8-phenyltheophylline; 1μmol/l) caused a rise in the occurrence of ventricular fibrillation from 25%, 15% and 18% (controls) to 57%, 39% and 44%, respectively, and the selective A2areceptors antagonist CSC (8-(3-chlorostyryl)caffeine; 5μmol/l) from 20% to 56%. Conversely, the selective A1receptor blocker DPCPX (8-cyclopentyl-1,3-dipropyl-xanthine; 1μmol/l) was ineffective. NBMPR or EHNA concentration-dependent suppressed or increased ischemia-induced adenosine overflow, respectively, in a concentration-dependent manner, whereas the adenosine receptor antagonists did not influence adenosine overflow. We conclude that endogenous adenosine is an antiarrhythmic mediator accumulating in acute ischemic myocardium to a level which effectively decreases the occurrence of ventricular fibrillation by an A2adenosine receptor activation in the isolated rat heart.

Ventricular fibrillation and shortening, alternans and after-depolarizations of epicardial monophasic action potentials during coronary occlusion and reperfusion: effect of repetition of ischemia.

The relationship between the occurrence of ventricular fibrillation (VF) and repolarization abnormalities of the ischemic and reperfused myocardium is poorly understood. The present study examined the temporal relationship between ischemia- and reperfusion-induced changes in monophasic action potential (MAP) configurations and the occurrence of VF, and assessed the effects of repetition of ischemia. The left anterior descending coronary artery of 32 anesthetized dogs was occluded twice for 5 min, 30 min apart, during constant atrial pacing while recording MAPs from the epicardial ischemic zone. During the first occlusion, shortening of the MAP duration at 90% repolarization (APD90) and an increase in MAP alternans, defined as the maximal difference in APD90 between 2 consecutive beats, were observed. Afterdepolarizations also occurred transiently in 35% of the animals during occlusion and in 29% upon reperfusion. VF occurred in 28% (9/32 of the dogs) during the first sequence, and the incidence was higher in the subgroups with maximal alternans > or =20 ms (p<0.05), maximal shortening rate > or =30%, and afterdepolarizations. During the second sequence, the incidence of VF was reduced to 9% (3/32, p<0.05), associated with a significant reduction in the MAP changes. Thus, repolarization abnormalities of the ischemic and reperfused myocardium appear to be related to the occurrence of VF. The amelioration of the repolarization abnormalities by repetition of ischemia may be involved in its antifibrillatory effect.

Implication of sympathetic innervation of the heart in antiarrhythmic action of intra-atrial laser irradiation

The role of sympathetic nervous system in the antiarrhythmic effect of intra-atrial laser irradiation (λ=632.8 nm) during myocardial ischemia was studied in acute experiments on Nembutal-anesthetized cats. Laser irradiation applied after bilateral, dextral, or sinistral transection of cardiac branches of stellate ganglia increased the number of ischemic rhythm disturbances that developed after occlusion of the circumflex branch of the left coronary artery. The maximum increase in the number of arrhythmias was observed after dextral transection, the occurrence of ventricular fibrillation being 100%. Bilateral transection provoked a larger number of ischemic rhythm disturbances than the sinistral transection. It is probable that the development of the antiarrhythmic effect of laser irradiation requires sustained sympathetic activity targeted at the nonischemic regions in the myocardium that could play a stabilizing role during local ischemic damage to the heart.

Effect of Chronic Severe Diabetes on Myocardial Stunning in the Dog

In this study, we examined whether chronic severe diabetes may affect ischaemic and post-ischaemic regional myocardial dysfunctionin vivoin the dog. Diabetes was chemically induced in randomized animals and major metabolic alterations were observed confirming the severity and chronicity of the diabetes. After 70 days, halothane-anaesthetized dogs underwent a 20-min coronary occlusion, followed by reperfusion. During ischaemia, global left ventricle function (dP/dtmax) was more altered (P<0.005) in diabetics (n=10) than in controls (n=10), whereas area-at-risk (29±2.5% of the left ventricle in diabeticsv32.4±1.9% in controls) and ischaemic subendocardial myocardial blood flow (radioactive microsphere technique, 0.11±0.02v0.10±0.03 ml/min/g) were similar. During reperfusion, both groups developed significant (P<0.05) regional myocardial dysfunction (somomicrometry, 41±14% of baseline in controls and 66±8% in diabetics), whereas the difference between groups was not significant. No dog of either group developed myocardial cell necrosis on tissue histology. Multivariate analyses, including the severity of prior ischaemia and the occurrence of ventricular fibrillation as covariables, confirmed that myocardial stunning was not increased in diabetics, although ischaemia was clearly less-well-tolerated in diabetic dogs as global (dP/dtmax) as well as regional myocardial function were significantly (P<0.05) more altered in diabetics during ischaemia. Whilst alteration of arachidonate and cholesterol metabolism may partly explain this apparent paradox, further studies are required to resolve this issue.

Endogenous adenosine suppresses norepinephrine-induced ventricular arrhythmias in rat heart.

Adenosine is an antiarrhythmic substance particularly effective in catecholamine-dependent tachycardias. Although endogenous adenosine substantially accumulates in catecholamine-stimulated hearts, little is known about the antiarrhythmic potency of endogenous adenosine in this condition. Therefore, we sought to demonstrate a potential antifibrillatory effect of endogenous adenosine either by blockade of adenosine receptors with 8-phenyltheophylline (8-PT) or by suppression of endogenous adenosine release with nitrobenzyl-6-thioinosine (NBTI). The study was performed in spontaneously beating Langendorff-perfused rat hearts. Adenosine release into the effluent was determined by HPLC methods. Catecholamine stimulation was induced by perfusing the hearts with norepinephrine (1 mumol/l) for 30 min, which caused ventricular tachycardia (VT) in 31% and ventricular fibrillation (VF) in 25% of control hearts (n = 35). When 8-PT (10 mumol/l) was added to the perfusion buffer prior to norepinephrine, the incidence of VT and VF increased to 79 and 68%, respectively. The addition of 8-PT did not affect the catecholamine-dependent formation of adenosine. Perfusion of the hearts with NBTI (10 mumol/l) prior to norepinephrine reduced adenosine release and increased the occurrence of both VT (65%) and VF (40%). In summary, the results indicate that adenosine is an endogenous antiarrhythmic substance, which accumulates in catecholamine-stimulated myocardium to a level, which effectively suppresses the occurrence of ventricular arrhythmias.

Incidence and prognosis of early primary ventricular fibrillation in acute myocardial infarction—results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI-2) database

Primary ventricular fibrillation (VF) complicating acute myocardial infarction (MI) predicts short-term mortality.The broad category of patients with primary VF might include subgroups with different outcomes. It is still not certain whether early-onset (≤4 hours) primary VF is a risk predictor, and information on correlates of these early fibrillations is scarce. This study sought to prospectively analyze the incidence and prognosis of early, as opposed to late (time window >4 to 48 hours) primary VF and retrospectively identify predisposing factors for early-onset primary VF. We analyzed the incidence and recurrence rate of early and late primary VF in 9,720 patients with a first acute MI, treated with thrombolytics, enrolled in the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-2 trial. The independent prognostic significance of early and late primary VF was assessed by logistic regression analysis. The incidence rates of early and late primary VF were 3.1% and 0.6%, respectively; recurrence rates were 11% and 15%, respectively. The 2 variables most closely related to early primary VF were hypokalemia and systolic blood pressure <120 mm Hg on admission. Patients with early primary VF had a more complicated in-hospital course than matched controls. Both early (odds ratio [OR] 2.47, 95% confidence interval [CI] 1.48 to 4.13) and late primary VF (OR 3.97, 95% CI 1.51 to 10.48) were independent predictors of in-hospital mortality. Postdischarge to 6-month death rates were similar for both primary VF subgroups and controls. Primary VF, irrespective of its timing, was an independent predictor of in-hospital mortality. Postdischarge to 6-month prognosis was unaffected by the occurrence of either early or late primary VF.

Discordant S-T alternans contributes to formation of reentry: a possible mechanism of reperfusion arrhythmia.

Although a relationship between S-T alternans and life-threatening arrhythmia has been recognized, the mechanism is poorly understood. We examine the role of S-T alternans in the occurrence of ventricular fibrillation (VF) after reperfusion. The left anterior descending coronary artery was occluded for 20 min and then abruptly reperfused in 12 intravenously anesthetized open-chest dogs. Sixty unipolar epicardial electrograms were recorded during the control state, at the end of occlusion, and after reperfusion. The largest magnitude of S-T alternans among 60 leads was defined as the maximum S-T alternans. Isochronal maps of activation time in paced beat and spontaneous ventricular premature contractions (VPC) were analyzed. After reperfusion, VF ensued in six dogs. The maximum S-T alternans augmented progressively with time after reperfusion until VF occurred. In three dogs with VF, when activation of VPC resulted in conduction block and formed reentry, VF ensued. The conduction block was located between sites of discordant S-T alternans (S-T alternans at adjacent leads was out of phase). These data indicate that discordant S-T alternans relates to VF by facilitating the formation of a reentrant circuit.

Experimental studies of electroacupuncture on ventricular fibrillation threshold in rats with acute ischemic myocardium.

By ligating the proximate left anterior descend (LAD) of coronary artery and inducing the ventricular fibrillation with electrical stimulation, the preventive effects of electroacupuncture (EA) on ventricular fibrillation were observed. The results showed that the ventricular fibrillation threshold (VFT) of rats with acute ischemic myocardium was raised after acupuncturing some acupoints, which could prevent the occurrence of ventricular fibrillation. Furthermore, the combination of EA and propranolol could enhance the VFT effectively, and they showed a good synergistic effect.

Electrocardiographic identification of abnormal ventricular depolarization and repolarization in patients with idiopathic ventricular fibrillation.

We sought to gain more insight into the arrhythmogenic etiology of idiopathic ventricular fibrillation (VF) by assessing ventricular depolarization and repolarization properties by means of various electrocardiographic (ECG) techniques. Idiopathic VF occurs in the absence of demonstrable structural heart disease. Abnormalities in ventricular depolarization or repolarization have been related to increased vulnerability to VF in various cardiac disorders and are possibly also present in patients with idiopathic VF. In 17 patients with a first episode of idiopathic VF, 62-lead body surface QRST integral maps, QT dispersion on the 12-lead ECG and XYZ-lead signal-averaged ECGs were computed. All subjects of a healthy control group had a normal dipolar QRST integral map. In patients with idiopathic VF, either a normal dipolar map (29%,), a dipolar map with an abnormally large negative area on the right side of the thorax (24%) or a nondipolar map (47%) were recorded. Only four patients (24%) had increased QT dispersion on the 12-lead ECG and late potentials could be recorded in 6 (38%) of 16 patients. During a median follow-up duration of 56 months (range 9 to 136), a recurrent arrhythmic event occurred in 7 patients (41%), all of whom had an abnormal QRST integral map. Five of these patients had late potentials, and three showed increased QT dispersion on the 12-lead ECG. In patients with idiopathic VF, ventricular areas of slow conduction, regionally delayed repolarization or dispersion in repolarization can be identified. Therefore, various electrophysiologic conditions, alone or in combination, may be responsible for the occurrence of idiopathic VF. Body surface QRST integral mapping may be a promising method to identify those patients who do not show a recurrent episode of VF.

QT prolongation and dispersion in myocardial ischemia and infarction

The ability of QT interval dispersion to predict the occurrence of ventricular fibrillation (VF) after acute myocardial infarction treated with thrombolytic therapy is controversial. Continuous 12-lead electrocardiographic (ECG) monitoring for 48 hours or longer provides an opportunity to detect transient changes of QT dispersion and correlate such changes with the clinical outcome. In 543 consecutive patients enrolled in the TAMI-9 and GUSTO I studies, serial changes of the QT dispersion were analyzed in an attempt to predict the occurrence of VF with a system that monitored continuously the 12-lead ECG and stored it at least every 20 minutes. Measurements of QT dispersion were made at a median time of 2.37 hours after the onset of chest pain and at 24- and 48-hour intervals. A total of 43 patients experienced VF during the acute phase of myocardial infarction; of these patients, 33 (77%) had anterior infarcts. However, despite the higher preponderance of anterior myocardial infarcts in the VF group, patients with anterior infarcts did not have longer QT dispersion than those with other infarct locations. Similarly, no significant differences in the QT dispersion were observed at any time between the group with VF and that without. Women had increased QT dispersion in the initial and 24-hour ECG as compared with men ( P = .005). However, this normalized at the 48-hour measurements. Despite this difference, there was no higher incidence of VF in female patients. In conclusion, the data suggest that QT dispersion alone is not sufficient to explain the occurrence of VF in the acute phase of myocardial infarction after thrombolytic therapy.