Ventricular Fibrillation Group Research Articles

Electrophysiologic characteristics andimplications of induced ventricular fibrillationin symptomatic patients with brugada syndrome

ObjectivesThe study examined the electrocardiographic and electrophysiologic characteristics in relation to programmed ventricular stimulation (PVS)-induced ventricular fibrillation (VF), as well as the implications of PVS-induced VF on the recurrence of cardiac events in symptomatic Brugada syndrome. BackgroundBrugada syndrome is characterized by ST-segment elevation in the right precordial leads (V1–V3) and an episode of VF. MethodsThirty-four symptomatic patients with Brugada syndrome (33 men and 1 woman; 44 ± 12 years old) were classified into two groups according to the inducibility of VF with PVS: 22 patients with induced VF requiring direct cardioversion for termination (Induced VF group) and 12 patients without induced VF (Noninduced VF group). ResultsThe induced VF group showed a longer QRS duration, a higher incidence of right bundle branch block and late potentials detected on the signal-averaged electrocardiogram, longer His-ventricular intervals and a longer conduction time from the RVOT to the left ventricle at extrastimulation than those in the non-induced VF group. However, there was no significant difference in the recurrence of cardiac events (VF documented by an implantable cardioverter-defibrillator and sudden cardiac death) between the two groups (8 [36%] of 22 patients vs. 7 [58%] of 12 patients) during long-term follow-up (range 1 to 149 months; mean 38). ConclusionsOur data suggest that induction of VF by PVS depends on the severity of depolarization abnormalities but does not predict the recurrence of cardiac events in symptomatic Brugada syndrome, indicating that both depolarization and repolarization abnormalities are important in the development of VF.

Adenoviral gene transfer to the heart during cardiopulmonary bypass: effect of myocardial protection technique on transgene expression.

Adenoviral gene transfer to the arrested heart during cardiopulmonary bypass (CPB) is a novel method of allowing prolonged vector contact with the myocardium. In this model we investigated the importance of temperature, duration of arrest and cardioplegia on transgene expression. First-generation adenoviral vector (1 x 10(12) total viral particles) containing the transgene for the human beta2-adrenoceptor (Adeno-beta(2)AR) or beta-galactosidase (Adeno-beta(gal)) was delivered to neonatal piglets via the proximal aorta, during simulated cardiac surgery, and allowed to dwell for the cross-clamp duration. Four treatment groups received Adeno-beta(2)AR. Groups A (n=4) and B (n=6) underwent cold crystalloid cardioplegia arrest for 10 and 30 min, respectively, Group C (n=5) underwent warm crystalloid cardioplegia arrest for 10 min, and Group D (n=5) underwent warm fibrillatory arrest for 10 min. Group E (n=6) received Adeno-beta(gal) and underwent cold crystalloid cardioplegia arrest (30 min). Animals were weaned off CPB and recovered for 2 days. Receptor density was assessed in membrane fractions using radioligand binding and compared using the Mann-Whitney U-test. Left ventricular transgene overexpression, as evidenced by elevated betaAR density, following Adeno-beta(2)AR treatment was greatest with cold cardioplegia (Group A 588+/-288.8 fmol/mg; P=0.002 and Group B 520+/-250.9 fmol/mg; P=0.01) versus control (Group E 109+/-8.4 fmol/mg). Overexpression also occurred with warm cardioplegia (Group C 274+/-69.5 fmol/mg; P=0.05) and ventricular fibrillation (Group D 215+/-48.4 fmol/mg; P=0.02) versus control. Comparison of the combined cold cardioplegia groups versus those treated with warm conditions showed a trend towards increased expression with cold conditions (P=0.1). Receptor density was also significantly increased in the right ventricle of animals in Group B (165+/-18.1 fmol/mg; P=0.03) and Group D (181+/-23.4 fmol/mg; P=0.02) versus control (Group E 118+/-5.8 fmol/mg). Cold crystalloid cardioplegia is not detrimental to gene transfer in vivo. In fact, there was a trend towards increased left ventricular transgene expression when the adenoviral vector was delivered following cold versus warm cardioplegia. Shorter periods of contact with the vector may reduce transgene overexpression. Therefore, gene transfer is possible during cardiac surgery with clinically used myocardial protection techniques.

Mitral valve surgery under perfused ventricular fibrillation with moderate hypothermia.

The safety and myocardial protective effect of perfused ventricular fibrillation (VF) under moderate hypothermia were investigated. Through a midline sternotomy and opening the left atrium from the right side, isolated mitral valve surgery was performed under aortic cross-clamping (ACC) and cardioplegic arrest using Bretschneider HTK solution in 96 patients, and under perfused VF in 20 patients (VF Group). Patient characteristics, clinical outcomes, and perioperative variables were compared. A satisfactory surgical view was obtained in all VF Group patients. Patient characteristics in the 2 groups were similar, and both groups had comparable results for mortality and morbidity, operation time, cardiopulmonary bypass time, peak levels of creatine kinase (CK) and its myocardial fraction, hours of mechanical ventilation, intensive care unit stay, and postoperative left ventricular ejection fraction. Even in VF Group patients with preoperative critical hemodynamic compromise, inotropes could be discontinued within 3 days. Thus, no detrimental effect of perfused VF was observed. On the other hand, in patients who underwent ACC and cardioplegic arrest of 120min or longer, peak levels of CK and its myocardial fraction were significantly higher than those of the rest of C group patients and VF Group patients. Perfused VF under moderate hypothermia can be a good alternative myocardial protection strategy during mitral valve surgery, particularly in patients in whom ACC is unsuitable or the duration of ACC is expected to be long.

Electrical induction of ventricular fibrillation for resuscitation from postcountershock pulseless and asystolic cardiac arrests.

There is increasing evidence that defibrillation from prolonged ventricular fibrillation (VF) before CPR decreases survival. It remains unclear, however, whether harmful effects are due primarily to initial countershock of ischemic myocardium or to resultant postdefibrillation rhythms (ie, pulseless electrical activity [PEA] or asystole). We induced 15 dogs into 12 minutes of VF and randomized them to 3 groups. Group 1 was defibrillated at 12 minutes and then administered advanced cardiac life support (ACLS); group 2 was allowed to remain in VF and was subsequently defibrillated after 4 minutes of ACLS; group 3 was defibrillated at 12 minutes, electrically refibrillated, and then defibrillated after 4 minutes of ACLS. All group 1 and 3 animals were defibrillated into PEA/asystole at 12 minutes. After 4 minutes of ACLS, group 2 and 3 animals were effectively defibrillated into sinus rhythm. The extension of VF in group 2 and 3 subjects paradoxically resulted in shorter mean resuscitation times (251+/-15 and 245+/-7 seconds, respectively, versus 459+/-66 seconds for group 1; P<0.05) and improved 1-hour survival (10 of 10 group 2 and 3 dogs versus 1 of 5 group 1 dogs; Fisher's exact, P<0.005) compared with more conservatively managed group 1 subjects. Precountershock CPR during VF appears more conducive to resuscitation than CPR during postcountershock PEA or asystole. The intentional induction of VF may prove useful in the management of PEA and asystolic arrests.

Interlead Difference in QT Interval Rate Adaptation During Exercise in Coronary Artery Disease Patients Susceptible to Ventricular Fibrillation

Background: Nonhomogeneity in ventricular repolarization predisposes to ventricular tachyarrhythmias. Rate adaptation of the QT interval parallels rate adaptation of the action potential, both of which reflect the repolarization phase in ventricular myocardium. The aim of this study was to examine in patients with coronary artery disease (CAD) the relation of interlead differences in QT interval rate-adaptation to arrhythmia vulnerability. Methods: We studied 29 CAD patients with a history of ventricular fibrillation (VF) not associated with acute myocardial infarction (VF group), and their 29 individually matched CAD controls without arrhythmic events (controls). Rate adaptation of the QT intervals in the 12 leads of the electrocardiogram were determined from QT intervals measured at rest and at the end of each 3 minute load step during exercise test. The relation between heart rate (HR) and QT interval (QT/HR slope) was calculated separately in each lead by the linear regression equation. The slopes of these equations were used to characterize spatial QT interval rate adaptation. Results: The steepest QTapex/ HR slopes in any lead were (mean ±mD SD) −2.45 ± 0.63 in the VF group and -1.97 ± 0.45 in controls (P = 0.008), whereas the smallest slopes showed no difference (P = NS). The standard deviations of QTapex/ HR slopes were 0.48 ± 0.23 in the VF group and 0.33 ± 0.12 in controls (P = 0.012). Conclusions: Rate adaptation of the QTapex interval is locally exaggerated, resulting in nonhomogenous exercise response of the QTapex intervals in CAD patients susceptible to life-threatening ventricular arrhythmias. A.N.E. 2000;5(4):346–353

Predictive Factors of Ventricular Fibrillation Triggered by Pause-Dependent Torsades de Pointes Associated with Acquired Long QT Interval:.

Death due to acquired torsades de pointes usually is caused by ventricular fibrillation (VF), but the contributing factors to VF triggered by pause-dependent torsades de pointes are not understood. We evaluated 91 patients who fulfilled four criteria: (1) pause-dependent torsades de pointes; (2) prolonged QT interval and/or corrected QT (QTc) (>0.44 sec); (3) long-short initiation sequence; and (4) conditions known to induce pause-dependent torsades de pointes. There were 38 patients with a documented VF (group I) and 53 without VF (group II). Absolute and relative dispersions of QT and QTc were calculated based on the 12-lead standard ECG. Group I differed from group II with regard to myocardial infarction history (32% vs 13%; P = 0.035), left ventricular ejection fraction (44% +/- 14% vs 65% +/- 9%; P < 0.0001), presence of structural heart disease (100% vs 20.8%; P < 0.0001), QT mean (591 +/- 73 msec vs 514 +/- 78 msec; P < 0.0001), QTc mean (563 +/- 76 msec vs 508 +/- 90 msec; P = 0.002), absolute QT dispersion (166 +/- 56 msec vs 84 +/- 49 msec; P < 0.0001), relative QT dispersion (9.9% +/- 3.5% vs 6.3% +/- 3.2%; P < 0.0001), absolute QTc dispersion (158 +/- 57 msec vs 81 +/- 44 msec; P < 0.0001), and relative QTc dispersion (9.9% +/- 3.6% vs 6.2% +/- 3%; P < 0.0001). Multiple regression analysis showed that ejection fraction (P = 0.0001), presence of structural heart disease (P < 0.0001), and relative QTc dispersion (P = 0.038) were the only independent predictors of VF. Left ventricular function, presence of structural heart disease, and QTc relative dispersion should be evaluated carefully in patients with conditions susceptible to inducing torsades de pointes.

Investigating the dual nature of endothelin-1: Ischemia or direct arrhythmogenic effect?

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide, which may also elicit severe ventricular arrhythmias. The aims of our study were to compare the effects of total left anterior descending coronary artery (LAD) occlusion to intracoronary (ic.) ET-1 administration and to investigate the pathomechanism of ET-1 induced arrhythmias in 3 groups of anesthetized, open-chest mongrel dogs. In group A (n = 10) a total LAD occlusion was carried out for 30 min, followed by a 60 min reperfusion period. In groups B and C ET-1 was administered into LAD for 30 min at a rate of 30 pmol/min ( n = 6) and 60 pmol/min ( n = 8). Epi- and endocardial monophasic action potential (MAP) recordings were performed to detect electrophysiologic changes and ischemia. Blood samples for lactate measurements were collected from the coronary sinus (CS) and from the femoral artery. Infrared imaging was applied to follow epimyocardial heat emission changes. At the end of the ET-1 infusion period coronary blood flow (CBF) was reduced significantly in groups B and C {(Δ CBF 30 MIN B : 21 ± 2%, p < 0.05; C : 35 ± 2%, p < 0.05)} , paralleled by a significant epimyocardial temperature decrease in group C (ΔT 30MIN: −0.65 ± 0.29 °C, p < 0.05). Two dogs died of ventricular fibrillation (VF) in the reperfusion period in group A . Ventricular premature contractions and non-sustained ventricular tachycardic episodes appeared in group B , whereas six dogs died of VF in group C . Significant CS lactate level elevation indicating ischemia was observed only in group A from the 30 th min occlusion throughout the reperfusion period (control vs. 30 min: 1.3 ± 0.29 vs. 2.2 ± 0.37 mmol/l, p < 0.05). Epi- and endocardial MAP durations (MAPD 90) and left ventricular epicardial (LV EPI) upstroke velocity decreased significantly in group A in the occlusion period. ET-1 infusion significantly increased LV EPI MAPD 90 in group B and both MAPD 90-s in group C . In conclusion, ischemic MAP and CS lactate changes were observed only in group A . Although ET-1 reduced CBF significantly in groups B and C , neither MAP nor lactate indicated ischemic alterations. ET-1 induced major ventricular arrhythmias appeared before signs of myocardial ischemia developed, though reduced CBF presumably contributed to sustaining the arrhythmias.

Recurrencia de la arritmia en pacientes con infarto de miocardio antiguo tratados con desfibrilador implantable: análisis según la presentación clínica inicial

The importance of the clinical presentation in the frequency and type of recurrences of ventricular arrhythmias in patients that received an automatic implantable defibrillator is not well known. The purpose of this study was to analyze the frequency and type of recurrences in patients with an old myocardial infarction that received an automatic implantable defibrillator with electrogram recording. We analyzed 100 patients classified in 3 groups according to their clinical presentation: Sustained Monomorphic Ventricular Tachycardia (VT Group n = 65), Cardiac Arrest (CA Group = 19), and Syncope (Syncope Group n = 16). There were no significant differences in the clinical variables among the different groups, nor in the inducibility of arrhythmia at the electrophysiologic study. In a follow-up 27 +/- 14 months, 54% of patients presented at last one episode of sustained ventricular arrhythmia. All recurrences except one were as sustained monomorphic ventricular tachycardia (776 episodes). 81% of episodes of sustained monomorphic ventricular tachycardia (630) were treated with antitachycardia pacing with an effectiveness of 89%. There were no differences in the probability of arrhythmic recurrence among groups but death probability was higher in the ventricular fibrillation group at 36 follow-up months (38% vs 7% and 12% in the sustained monomorphic ventricular tachycardia and syncope groups respectively, p = 0.0113). In the patients with an old myocardial infarction and malignant ventricular arrhythmias, most of recurrences are due to sustained monomorphic ventricular tachycardia independently of the clinical presentation. The antitachycardia pacing is not only effective in patients with documented sustained monomorphic ventricular tachycardia but also in those that are presented as cardiac arrest or syncope.

The transthoracic impedance cardiogram is a potential haemodynamic sensor for an automated external defibrillator.

The American Heart Association has endorsed the concept of Public Access Defibrillation. However, there have been reports of inappropriate direct current shocks from automatic external defibrillators. The specificity of automatic external defibrillators for shockable rhythms may be improved by the incorporation of a haemodynamic sensor. This study examined the use of four parameters extracted from the impedance cardiogram i.e. Peak dz/dt (the peak of the impedance cardiogram measured from the line dz/dt=0 ohms(-1)), Peak-trough (the peak-to-trough measurement of the impedance cardiogram ohms(-1)), Area 1 (the area under the C wave of the impedance cardiogram above the line dz/dt=0 mohm) and Area 2 (the area under the impedance cardiogram 50 ms on either side of the Peak and above the line dz/dt=0 mohm) as predictors of cardiac output. At 116 cardiac arrest calls the ECG and impedance cardiogram were recorded through two ECG/defibrillator pads placed in an antero-apical position. Nine recordings were rejected for artefact. The rhythm recorded in the remaining 107 calls was asystole (19), ventricular fibrillation (14), agonal rhythm (20), electromechanical dissociation (22), ventricular tachycardia (27) and sinus rhythm (5). These rhythms were divided into those associated with haemodynamic collapse i.e. no pulse -- asystole, ventricular fibrillation, agonal rhythm, electromechanical dissociation and shockable ventricular tachycardia (associated with loss of consciousness, pulselessness or a systolic blood pressure of <80 mmHg) (Group 1) and those associated with a satisfactory cardiac output i.e. non-shockable ventricular tachycardia (conscious with a pulse) and sinus rhythm (Group 2). On univariate analysis each of the four impedance cardiogram parameters were significantly greater in Group 2 than Group 1 (P<0.001). On multivariate analysis the parameters which best differentiated the two groups were Area 1 and Peak-trough. Thus the impedance cardiogram is a potential haemodynamic sensor for an automatic external defibrillator.

Cold blood cardioplegia or intermittent cross-clamping in coronary artery bypass grafting?

Background. We determined that cold blood cardioplegia and intermittent ventricular fibrillation with ischemia were associated with similar enzyme and myocardial protein leakage in a randomized, prospective study of 40 patients. We have continued to use both methods in our unit, according to surgeons’ preference. Methods. In our database we have reviewed 1,923 patients who have undergone first-time elective or urgent coronary artery bypass grafting from January 1992 to May 1997. Results. Five hundred seventy-eight patients underwent coronary artery bypass grafting with cold blood cardioplegia and 1,345 had ventricular fibrillation and aortic cross-clamping. The preoperative factors were virtually identical. Intraoperative differences were only those inherent to the two techniques: temperature and cross-clamp time. Mortality was 2.5% for ventricular fibrillation and aortic cross-clamping arrest and 2.1% for cardioplegia ( p = 0.55 by χ 2 test). There was a higher use of the intraaortic balloon pump in the ventricular fibrillation and aortic cross-clamping group (2.4% versus 1.0%; p = 0.04), but no other differences in outcome were detected. Conclusions. A truly randomized trial to demonstrate which technique is superior is impractical at this level of difference because it would require 37,000 patients to avoid a beta error. We have to base our practice on the retrospective data available. Each technique has its merits in practice, which are discussed.

Autonomic modulation of qt intervals in post-myocardial infarction patients with and without ventricular fibrillation

The autonomic nervous system plays an important role in the genesis of sudden cardiac death. The aim of this study was to evaluate spatial autonomic QT interval modulation at the myocardial level. Circadian patterns of QT intervals and heart rate variability (HRV) components and their hourly linear correlations were determined by Holter recordings in 15 healthy subjects (controls), in 15 post-myocardial infarction (MI) patients resuscitated from ventricular fibrillation (VF) (VF group), and in 15 matched infarction patients without a history of arrhythmia events (MI group). QT intervals were measured in modified leads V 1 and V 5 individually at same stable heart rates during each hour and related to hourly measures of HRV. Controls had highly significant correlations between QT intervals and the high-frequency component of HRV (parasympathetic modulation), and between QT intervals and low- to high-frequency ratio (sympathetic modulation) uniformly in both leads (r from 0.62 to 0.81, p <0.001). The MI group had impaired sympathetic modulation in V 5 (r = 0.34, p = NS), but had uniform and exaggerated sensitivity to parasympathetic modulation. In the VF group the QT difference between V 1 and V 5 leads correlated with parasympathetic modulation (r = 0.401, p <0.05) and sympathetic modulation (r = 0.446, p <0.05). Thus, normal subjects exhibit spatially uniform autonomic QT modulation. Myocardial damage can result in abolished, exaggerated, or regionally discordant QT modulation, and this may generate arrhythmic vulnerability.

Dispersions of the QT Interval in Postmyocardial Infarction Patients Presenting With Ventricular Tachycardia or With Ventricular Fibrillation

Increased QT interval dispersion is associated with ventricular arrhythmias. The aim of this study was to examine if in postmyocardial infarction patients with impaired left ventricular function, increased QT dispersion is associated with ventricular tachycardia (VT) and ventricular fibrillation (VF). Measures of QT dispersion, calculated as maximum–minimum (D) and standard deviation (SD) of QT end, QT apex, JT end, JT apex, and T end intervals in the 12-lead electrocardiogram, were compared in patients who late after myocardial infarction experienced sustained VT (VT group) only, VF (VF group) only, or had no ventricular arrhythmias (controls). The 25 patients in each group were individually matched for age, gender, number of diseased coronary vessels, location of the previous myocardial infarction, and left ventricular ejection fraction. Dispersion measures of QT end, QT apex, and JT apex intervals separated VT group from controls, but none of the measures separated the VF group from controls. QT endD was 49 ± 18 ms in controls, 57 ± 18 ms in the VF group (controls vs VF group, p = NS), and 65 ± 29 ms in the VT group (controls vs VT group, p <0.05). VT group had increased QT apexSD, JT apexSD, and JT apexD compared with the VF group. The cycle length of induced sustained monomorphic VT, present in 19 VT and 19 VF patients, correlated with several dispersion indexes in the VT group, but not with those in the VF group. Thus, in postmyocardial infarction patients with a severely damaged left ventricle, increased QT dispersion is associated with susceptibility to sustained VT, but not to VF.

Single-beat analysis of ventricular late potentials in the surface electrocardiogram using the spectrotemporal pattern recognition algorithm in patients with coronary artery disease.

Post-infarction risk stratification can be ascertained from beat-to-beat variations in ventricular late potentials. However, gaining such information by conventional late potential analysis using signal averaging is still not possible. We therefore developed the spectrotemporal pattern recognition algorithm in order to detect beat-to-beat variations in late potentials. Based on the spectrotemporal pattern recognition algorithm two-dimensional correlation function, the typical spectral pattern of late potentials can be identified in spectrotemporal maps of single beats, even in the presence of noise. Surface electrocardiograms of 385 patients after myocardial infarction (85 with documented sustained ventricular tachycardia (group 1), 100 with fast, polymorphic ventricular tachycardia (> 270 cycles.min-1) or primary ventricular fibrillation (group 2), 200 without ventricular arrhythmias (group 3) and 45 healthy volunteers (group 4), were analysed. The spectrotemporal pattern recognition algorithm detected late potentials in single beats in 89% of group 1 patients, in 79% of group 2, in 22% of group 3 and in 4% of normals. The spectrotemporal pattern recognition algorithm measured late potential frequency and extension of late potentials into the ST segment, which was significantly different between groups 1 and 2. Beat-to-beat variations in late potentials, with respect to frequency and extension into the ST segment, were markedly higher in patients with a history of primary ventricular fibrillation. Single-beat analysis using the spectrotemporal pattern recognition algorithm may improve risk stratification of patients after myocardial infarction, and provides information on patients prone to ventricular fibrillation.

T wave spectral variance: A new method to determine inhomogeneous repolarization by T wave beat-to-beat variability in patients prone to ventricular arrhythmias

Inhomogeneous repolarization is considered to be associated with increased risk of ventricular arrhythmias, but exact determination of the end of the T wave is difficult, and a single measurement of the QTc interval may be insufficient for risk stratification. A new algorithm was therefore developed to determine the beat-to-beat variability of the T wave in Holter electrocardiographic recordings. This algorithm, termed T Wave Spectral Variance (TWSV) uses the two-dimensional fast Fourier transform to determine the beat-to-beat variability of the T wave in Holter ECG recordings. The two-dimensional fast Fourier transform was calculated by use of a data matrix with 1,024 consecutive single beats (first dimension) and a 200-ms segment centered on the T wave (second dimension). The power spectra of the 2D-FFT revealed the frequency content of the T wave in the first dimension and the periodicity of these frequencies in cycles per beat in the second dimension. A TWSV index of periodicity was calculated by dividing total spectral energy by spectral energy at 0 cycles per beat. A TWSV index of 0 means a constant T wave from beat to beat; a TWSV index of 1 means a completely irregular T wave. Of the 200 patients investigated, all of whom had had myocardial infarctions, 50 had documented sustained ventricular tachycardia (VT) (<230 beats/min) (group 1), 50 had ventricular fibrillation (VF) (group 2), and 100 were without VT or VF (group 3); 10 normal subjects were also investigated. The visually determined QTc was 442 ± 62 ms in group 1, 402 ± 13 ms in group 2, 411 ± 26 ms in group 3, and 398 ± 43 ms in normal subjects (differences not significant). The TWSV index was 0.95 ± 0.14 in group 1, 0.90 ± 0.16 in group 2, and 0.64 ± 0.24 in group 3; it showed a highly constant T wave in normal subjects (0.52 ± 0.23). Differences between patients with VT and VF as against patients without VT or VF were significant ( P < .05), whereas no statistical differences between patients with VT and VF could be found. Thus, TWSV, a new method to assess beat-to-beat variability of the T wave, revealed increased heterogeneity of repolarization in patients prone to both VT and VF after myocardial infarction, whereas a single QTc interval measurement showed no significant differences.

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.

Association Between Hemodynamic Parameters and the Degeneration of Sustained Ventricular Tachycardias into Ventricular Fibrillation in Rats

Sustained ventricular tachycardias (VT) often degenerate into ventricular fibrillation (VF). In the present study, the impact of VT on mean arterial blood pressure (MAP), myocardial blood flow (MBF), and myocardial oxygen consumption (MVO2) was assessed. In addition, the degeneration of sustained VT into VF was analysed with respect to MAP. MBF was measured in 48 anesthetized rats with colored microspheres; arterial catecholamine levels were measured by HPLC in 16 additional rats during control conditions and VT. MBF (4.66±1.29 ml/g/min; mean±s.d.) did not change with the onset of VT (5.37±1.92 ml/g/min,n.s.). Epinephrine (0.22±0.13 ng/ml) and norepinephrine (0.37±0.12 ng/ml) increased during VT (3.55±2.68 ng/ml,P<0.01; 0.88±0.44 ng/ml,P<0.05), respectively. VF was more frequent when MAP remained normal (MAP>80 mmHg: 26%) than with hypotension (MAP<80 mmHg: 2%,P<0.05). Mechanical failure was observed in 10% of rats with severe hypotension (MAP<60 mmHg), and 2% with moderate hypotension (MAP 60–80 mmHg). The endo-epicardial MBF ratio in the VF group was significantly lower than that in the non-VF group (0.94±0.17v1.11±0.24,P<0.05). Conclusions: severe hypotension predisposes to the occurrence of acute mechanical failure during VT; moderate hypotension during VT, however, serves as a protective mechanism against VF in structurally normal hearts. Subendocardial hypoperfusion in the presence of an increased energy demand during VT is suggested to be responsible for the initiation of VF.

Effects of lidocaine and diltiazem on recovery of electrophysiologic activity during partial reperfusion following severe myocardial ischemia in canine hearts

The effects of lidocaine and diltiazem on recovery of electrophysiologic activity during partial reperfusion following severe myocardial ischemia were investigated in 28 dogs. The left anterior descending artery was ligated, and the distal end was connected to the carotid artery. Myocardial ischemia was induced by retrograde blood flow for 10 minutes, after which flow-limited reperfusion (30–60% of the coronary flow before ischemia) was performed. The dogs were divided according to the agent administered before ischemia into the following three groups: saline (group S, n = 11); lidocaine (group L, n = 8, 0.07 mg/kg/min by intravenous drip infusion following 2 mg/kg intravenous injection); and diltiazem (group D, n = 9, 0.02 mg/kg/min by intravenous drip infusion. There were no significant differences among the three groups in the incidence of ventricular tachyarrhythmia, which occurred as ventricular tachycardia (VT) or ventricular fibrillation (VF). In each group, the occurrence of VT was frequently preceded by delayed potential which was initiated after reperfusion, with depressed conduction in the epicardium, suggesting reentry (82%, 96%, and 87%, not significant). The determining factors for VT with degeneration into VF were long duration of VT in groups S and L (VT with degeneration into VF vs VT without, 1.2 ± 0.2 seconds vs 0.6 ± 0.1 seconds, P < .05, in group S and 11.6 ± 2.5 seconds vs 2.2 ± 0.4 seconds, P < .05, in group L), and decrease in average R-R interval during VT in groups L and D (195 ± 8 ms vs 313 ± 17 ms, P < .01, in group L and 201 ± 11 ms vs 327 ± 28 ms, P < 0.01, in group D). In addition, occurrence of epicardial electrophysiologic activity with reduced time from onset of the QRS complex in the surface electrocardiogram to the onset of the activity during VT preceded VF in group L (VT with degeneration into VF vs VT without, 130.0 ± 15.1 ms vs 185.8 ± 21.4 ms, P < .05), while that with prolongation of the time had this effect in group D (116.0 ± 15.7 ms vs 69.0 ± 10.7 ms, P < .05). It is concluded that, even when partial reperfusion is applied, neither lidocaine nor diltiazem suppresses VT because neither drug decreases delayed potential acting as a triggering factor or suppresses VF, since the alteration of the epicardial conductivity during VT can change the VT circuit to a smaller one.

Fluxo coronário desregulado durante reperfusão pós cardioplegia

Metabolic coronary blood flow recruitment and distribution were studied in the setting of ventricular fibrillation (VF) during post-cardioplegia reperfusion. Fifteen pigs were placed on cardiopulmonary bypass and subjected to one hour of intermittent cold blood antegrade cardioplegia, followed by controlled myocardial reperfusion. According to the electromechanical status during the first ten minutes of reperfusion, the animals were allocated into 3 groups (n=5). Whereas Group 1 remained asystolic, the other two groups developed short (Group 2) or long duration VF (Group 3). Myocardial oxygen consumption (MVO2), in m/O2 /min/g (mean ± standard error) during reperfusion was 1.325 ± 0.144 (Group 1); 2.472 ± 0.208 (Group 2) and, 2.469 ± 0.228 (Group 3). MVO2 difference between asystolic and both short and long duration VF hearts was significant (p<0.001). Groups 1.2 and 3 endo-epi ratio and global coronary blood flow rate (169.3 ± 11.7; 185.0 ± 15.7 and 179.9 ± 13.2 ml/min/100g; respectively) were similar. These results demonstrate that coronary blood flow autoregulation was impaired because there was no increase in myocardial perfusion in response to the increase oxygen consumption imposed by VF during the first ten minutes of post cryocardioplegia reperfusion. This finding is of great clinical importance because it suggests that VF can potentially aggravate reperfusion lesions in formerly compromised hearts, i.e., those with coronary artery obstruction, ventricular distension or ventricular hypertrophy.

Plasma norepinephrine increased during coronary occlusion in hypertensive pigs that developed ventricular fibrillation

Although hypertension is associated with increased risk of sudden cardiac death, the mechanisms involved remain enigmatic. Little is known about hemodynamic and plasma catecholamine concentration changes during coronary artery occlusion in hypertensive subjects. To study this, 30 pigs were implanted with catheters in the aorta and a silk snare around the left anterior descending coronary artery that could later be pulled to permanently occlude the artery. Perinephritic hypertension was induced in 14 of the animals over 3 weeks by wrapping one kidney in silk followed by contralateral nephrectomy. Coronary artery occlusion (CAO) was carried out in all pigs in the conscious resting state. Ventricular fibrillation (VF) developed in 50% of each group within 15 min after coronary artery occlusion. The hypertensive VF group showed an increase in norepinephrine concentration of 112 ± 46%; a significantly greater increase than the intact VF group, which showed a 29 ± 7% increase in norepinephrine concentration 5 min after coronary artery occlusion ( p < 0.05).

Aborted sudden death in the Wolff-Parkinson-White syndrome

In a population of 690 patients with Wolff-Parkinson-White (WPW) syndrome referred to our hospital from January 1979 to February 1995, 15 patients (2.2%) had an aborted sudden death out of the hospital. This retrospective study examines their clinical and electrophysiologic characteristics. Gender, accessory pathway localization, and presence of multiple accessory pathways were compared between patients with and without spontaneous ventricular fibrillation (VF). Whereas gender and the presence of multiple accessory pathways did not significantly differ between both groups, septally located pathways occurred significantly more often in the VF group. In patients with aborted sudden death, spontaneous VF was found significantly more often in men (13 of 15). VF was the first manifestation of the WPW syndrome in 8 patients. The remaining 7 patients had documented episodes of atrial fibrillation, circus movement tachycardia, or both (n = 2). Ten of the 15 patients were exercising or under emotional stress at the time of aborted sudden death. Only 1 patient had 2 accessory pathways. The location of the accessory pathway was septal (midseptal or posteroseptal) in 11 patients, left lateral in 4, and right lateral in 1.