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Ventricular fibrillation occurred in an apparently healthy 19 year old man. The results of non-invasive and invasive studies suggested right ventricular dysplasia. Electrophysiological studies showed atrial paralysis, hypoexcitability of multiple areas of the right ventricle, and inducible poorly tolerated ventricular tachycardia.
The effect of chronic angiotensin converting enzyme (ACE) inhibition on the incidence of fatal ventricular fibrillation during regional myocardial ischaemia and reperfusion is not known. A reduction in cardiac angiotensin II and/or a vagomimetic response may result in antiarrhythmic activity. Pigs pre-treated with the ACE inhibitor trandolapril 0.3 mg.kg-1 or placebo orally for 10 days were subjected to thoracotomy. The left anterior descending coronary artery was ligated (CAL) for 20 min and reperfused for 45 min. Trandolapril decreased cardiac ACE activity and prevented the fall in the ventricular fibrillation threshold (VFT) during ischaemia: after 5 min of ischaemia the VFT in the trandolapril group was 25.5 +/- 4.6 mA (mean +/- SEM) vs 13.1 +/- 2.2 mA in the placebo group (P < 0.05). Trandolapril also decreased the incidence of spontaneous ventricular fibrillation during reperfusion to 1/6 vs 6/7 in the placebo group (P < 0.05). Heart rate in the trandolapril group fell. During ischaemia, trandolapril increased blood flow in the non-ischaemic zone, but decreased blood flow in the central ischaemic zone of the left ventricle. Similarly it decreased tissue levels of phosphocreatine in this zone. During reperfusion trandolapril increased blood flow both in non-ischaemic and central ischaemic zones. Chronic oral pre-treatment with trandolapril resulted in marked antifibrillatory effects which were associated with inhibition of cardiac ACE activity and a decreased heart rate.
The objective of this study is to evaluate the correlation between the absolute ventricular fibrillation voltage (AVFV) computed from electrocardiogram (ECG) and the outcome of defibrillation shocks. Orthogonal ECG (sagittal, x; transverse, y; and longitudinal, z) was recorded from 11 dogs during 10 seconds of electrically induced ventricular fibrillation followed by defibrillation shocks with 50% probability of success. The transvenous two-leads defibrillation system was used to deliver defibrillation shocks. The envelope voltage was estimated by using the Hilbert transform. The comparison of the envelope voltages between 236 successful trials and 249 unsuccessful trials did not show any consistent and statistically significant differences. In contrast with the previously reported correlation, the moving average of AVFV was not higher in the successful trials. In the Z direction, the successful trials had lower voltage than did the unsuccessful trials (P < 0.05). These results suggest that the absolute voltage of ECG during ventricular fibrillation is not robustly correlated with the outcome of defibrillation shocks.
The objective of the present study was to examine the susceptibility of diabetic rats with cardiomyopathy to hypokalemia-induced ventricular fibrillation and to localize gap junction protein connexin-43 as well as subcellular changes that may be involved in the development of severe arrhythmia. Our results showed a significantly higher incidence of sustained ventricular fibrillation in diabetic hearts as compared with control hearts, 80% vs 20%, respectively. Diabetic cardiomyopathy itself was accompanied by a distinct decrease in connexin-43-immunopositive gap junctions. Moreover, interstitial fibrosis and subcellular alterations to various degrees were observed in diabetic hearts, and a further deterioration of the ultrastructure and impairment of intercellular junctions, and a stronger local decrease in connexin-43 levels due to hypokalemia were found. These changes were heterogeneously distributed throughout the myocardium and occurred earlier and were more pronounced in diabetic hearts than control hearts. In conclusion, our results indicate that diabetic cardiomyopathy is associated with down-regulation of gap junction proteins and may account for the higher vulnerability of diabetic rats to ventricular fibrillation in combination with impairment of intercellular communication due to hypokalemia.
To examine the impact of hypokalemia on cardiac electrical stability, the thresholds for repetitive extrasystole and ventricular fibrillation were determined before and after potassium depletion in 15 chloralose-anesthetized dogs. A reduction in serum potassium concentration from 3.6 to 2.1 mEq/L induced by hemodialysis decreased the repetitive extrasystole threshold by 30% and the ventricular fibrillation threshold by 25% (p less than 0.01). The increase in ventricular vulnerability following acute coronary occlusion was markedly augmented by concomitant potassium depletion. Thus, hypokalemia enhances the propensity for ventricular fibrillation in the normal as well as in the ischemic canine heart. These findings shed light on clinical observations of enhanced susceptibility to life-threatening arrhythmias during acute myocardial ischemia in hypokalemic patients.
Recent evidence suggests that the dominant frequencies during ventricular fibrillation (VF) may be used as indicators of dispersion in repolarization and in activation patterns. In the present study, we quantified dominant frequencies from multiple epicardial electrodes to investigate if there are differences in the averaged frequencies within the electrograms recorded from the left and the right ventricles. Further, we quantified whether the difference in average frequency between the two ventricles changed during 30 seconds of VF. Results from eighteen trials in two pigs showed that during the entire duration of VF the average dominant frequencies of all electrodes over the left ventricle were higher than those over the right ventricle (p < 0.005). The dominant frequencies are reciprocal of cycle periods or activation intervals during VF. Our results show that on average, activations in the left ventricle occurred at a faster rate than those in the right ventricle. Activation intervals at any site are determined by the refractory period at that site and the arrival time of next activation. Although differences in cellular properties may have contributed to the observed differences in activation intervals between the ventricles, it is possible that activation arrival times may be different as well. It is possible that the increased tissue mass of the left ventricle may increase the probability that any site will get excited at a faster rate after it is recovered from previous activation.
BACKGROUND: A number of factors have previously been shown to be predictive of survival from out-of-hospital ventricular fibrillation. These include witnessed collapse, prompt initiation of cardiopulmonary resuscitation, early application of defibrillation, and younger age. Arrests occurring away from home are also associated with improved survival. Additionally, hospital mortality after successful resuscitation has been related to a history of congestive heart failure as well as to some of the factors noted above. An association of prearrest comorbidity with outcome has not been systematically evaluated. METHODS AND RESULTS: We define here a comorbidity index, which is constructed from histories of chronic conditions as well as a number of recent symptoms in 282 victims of out-of-hospital VF. This indicator of comorbidity is strongly associated with outcome (P = .004). However, when analyzing a comprehensive set of predictors of survival after out-of-hospital ventricular fibrillation, including the index of comorbidity, we could identify overall only about one fourth of the variation that one might hope to account for. CONCLUSIONS: Comorbidity appears to be an important (but usually overlooked) predictor of survival from out-of-hospital ventricular fibrillation. However, most of the statistical variability in predicting survival remains unexplained when we consider comorbidity in conjunction with previously identified predictors of survival.
BACKGROUND: Programmed electrical stimulation of the heart as a method to induce tachyarrhythmias has been described since the 1960s. To date, no study has examined optimal drive cycle length in the induction of ventricular fibrillation (VF) during defibrillation threshold testing after implantable cardioverter-defibrillator placement. We hypothesized that longer drive cycle length, by means of the longer action potential duration, would promote intramyocardial phase 2 reentry and facilitate induction of VF. METHODS: Fifty consecutive implants were randomized in a prospective crossover format for this study. The group consisted of 40 men and 10 women, with each patient receiving either a 400 or 600 ms initial drive train prior to 1.2 J internal shock on the T wave with a goal to induce ventricular fibrillation. The timing of the T wave shock was determined by measuring the interval from the beginning of the QRS to the apex of the T wave in lead II. Successful inductions were defibrillated via the cardioverter defibrillator. Patients were then crossed over and the protocol repeated. RESULTS: Twenty of 23 (87%) patients were successfully induced into VF in the initial 400 ms drive train arm whereas 22 of 27 (81%) were successfully induced in the 600 ms arm. Thus, a total of 44 (88%) patients were successfully induced at 400 ms, 41 (82%) patients were successfully induced at 600 ms, and 2 (4%) patients were not inducible at either cycle length, but were inducible with 50 Hz ventricular stimulation. However, no significant difference was noted between the two groups. CONCLUSION: No investigation to date has questioned whether a relationship exists between drive cycle length and initiation of ventricular fibrillation. Our study addresses this question, though negative for difference between 400 and 600 ms drive trains. Further research into optimal strategies for inducing ventricular fibrillation will minimize patient sedation time and discomfort while undergoing defibrillator threshold testing.
The incidence of sudden death in the Wolff-Parkinson-White (WPW) syndrome is not well documented and probably underestimated. This retrospective study concerned 28 consecutive patients presenting with ventricular fibrillation either spontaneously (20) or during electrophysiological investigation (8) but whose characteristics allowed them to be assimilated into a single group. Their clinical and electrophysiological characteristics were compared with those of 60 consecutive patients with the WPW syndrome who had documented atrial fibrillation (and even reciprocating tachycardia) but never ventricular fibrillation. There were no significant differences between the two groups with respect to the following clinical parameters: sex, duration of symptoms, the type of tachycardia previously recorded, history of syncope and presence of underlying cardiac disease. With respect to the electrophysiological data, there were no differences in the point of anterograde block, the effective anterograde refractory period of the accessory pathway, the effective and functional refractory periods of the right atrium and atrial vulnerability. On the other hand, a significant difference was observed in the age of patients with ventricular fibrillation (29 +/- 13 years vs 36 +/- 12 years; p < 0.02), the prevalence of multiple accessory pathways (25% vs 7%; p < 0.04) with a dominant localisation in the postero-septal region (75% vs 47%, p < 0.026), preexcitation during exercise stress testing and under antiarrhythmic therapy (95% vs 68%, p < 0.037). The most discriminating parameter was the shorter RR interval during atrial fibrillation (172 +/- 23 ms vs 230 +/- 50 ms, p < 0.008). Multivariate analysis only showed one independent predictive factor: the minimum preexcited RR interval.(ABSTRACT TRUNCATED AT 250 WORDS)
This study was designed to assess myocardial vulnerability by measuring ventricular pacing threshold (VPT), multiple extrasystoles threshold (MET), ventricular tachycardia threshold (VTT) and ventricular fibrillation threshold (VFT) by means of the pulse train stimulating method. The results showed that: (1) VFT is a quantitative index of myocardial vulnerability: (2) MET, positively correlated with VFT, might become a substitute for VFT as an index of vulnerability to ventricular fibrillation: (3) atenolol, both in normal and ischemic myocardium, is able to make a significant elevation of VFT, which is considered as an antifibrillation effect: (4) nitrendipine exerted no apparent effects on all the parameters.
During ICD-implantation it is necessary to induce ventricular fibrillation several times to determine the defibrillation threshold. In third generation ICDs there are several options to induce ventricular fibrillation. We want to present a new method, called T-wave-shock, which is first available in the PCD Jewel 7219 (Medtronic). The T-wave-shock is the delivery of a low-energy-shock into the vulnerable period after ventricular stimulation with a basic cycle-length. We applied the T-wave-shock in 46 consecutive ICD-recipients intraoperatively and at the pre-hospital-discharge test. The method is highly effective when applying the shock into the ascending part of the T-wave (98% of the patients were inducible), and the duration of cardial and cerebral ischemia during induction is short (between 3.1 and 3.8 s). This raises defibrillation efficacy.
Ventricular fibrillation (VF) and ventricular tachycardia (VT) are common phenomena during reperfusion. In experimental research many hearts have to be excluded from haemodynamic evaluation because of severe arrhythmias. Theoretically, electroconversion or mechanical conversion (MC) might be used to convert VF or VT. MC induces a physical shock analogous to a chest thump. The aim of this study was to investigate the efficacy of MC in isolated, perfused rat hearts, and to see whether MC itself induced myocardial cell injury and functional impairment. Langendorff-perfused rat hearts (n = 89) from several experimental series subjected to 30 min of global ischaemia and 60 min of reperfusion were retrospectively analysed. Left ventricular systolic (LVSP), end-diastolic (LVEDP), and developed (LVDP) pressures, coronary flow (CF), and heart rate (HR) were measured. If VF or VT continued for 1 min during reperfusion, MC was attempted by a flick of the forefinger to the right ventricle. If VF or VT still occurred, MC was repeated. Hearts that did not have regular beating after 20 min of reperfusion were excluded. Release of cardiac troponin T (cTnT) was measured before ischaemia and after 20 min of reperfusion. Forty-four out of 89 hearts had VF or VT during reperfusion. Thirty-five hearts were converted, 18 of which were converted by one or two MCs only. The higher the total number of MCs employed, the more cTnT was released. After 20 min of reperfusion, LVEDP, LVDP and CF were better in hearts with a higher number of MCs and with increased release of cTnT. After 60 min of reperfusion, LVEDP was still improved in hearts with more cTnT release, whereas LVSP was lower, and LVDP and CF were independent of the number of MCs. There was no consistent correlation between release of cTnT and heart dysfunction. In conclusion, MC effectively converted VF or VT. MCs increased post-ischaemic myocardial cell damage, as judged from increased cTnT release. Post-ischaemic dysfunction was partly attenuated in hearts with multiple MCs, and did not correlate with release of cTnT. We feel that MCs should not be used in isolated, perfused hearts.
The threshold for electrically induced ventricular fibrillation was determined in anesthetized open-chest dogs, before and after blockade of atrioventricular (A-V) conduction. Without exception, the threshold was significantly elevated after creation of the block. The precise mechanism of this effect is not known at this time. However, it is apparent that when ventricular fibrillation thresholds are being determined, the functional status of A-V conduction should be established and maintained throughout the study.
Patients with symptomatic ventricular tachycardia, ventricular fibrillation, or aborted sudden cardiac death remain at high risk for arrhythmia recurrence. In recent years, strategies to treat these patients have changed. Concerns about the proarrhythmia risk and uncertain efficacy of class I agents have resulted in a shift in interest to non-class I antiarrhythmic drugs such as sotalol and amiodarone. Both drugs have class III antiarrhythmic properties (i.e., both lengthen repolarization and refractoriness); however, each also has its own additional electrophysiologic effects. Prospectively designed, randomized studies have shown that both sotalol and amiodarone have more potent antiarrhythmic actions than class I agents. However, even as the advantages of sotalol and amiodarone have been recognized, enthusiasm for nonpharmacologic modes of treatment, particularly the implantable cardioverter-defibrillator (ICD), has also markedly increased. The ICD has been shown to decrease dramatically the incidence of sudden death, which may lead to the reduction of total mortality. Whether patients with life-threatening ventricular tachyarrhythmias should be treated first with antiarrhythmic agents or with an ICD is an important question. The results of recent studies suggest that treatment with an ICD is more effective than electrophysiologically guided treatment with class I agents. However, results of prospectively designed randomized studies comparing the efficacy of the ICD with that of sotalol and amiodarone must become available before definitive recommendations can be made concerning the use of the ICD as first-line therapy in patients with ventricular tachycardia/ventricular fibrillation or aborted sudden cardiac death. In addition, there may be a significant role for the use of antiarrhythmic drugs in conjunction with ICDs.
A 51 year old woman sustained ventricular fibrillation while receiving perphenazine and protriptyline. After successful resuscitation and clinical stabilization, cardiac electrophysiologic studies were performed before and after the administration of each of these medications. Perphenazine widened the ventricular echo zone and facilitated induction of short salvoes of ventricular tachycardia (repetitive ventricular response). Protriptyline also widened the ventricular echo zone and allowed easy induction of long runs of ventricular tachycardia. Both psychotropic agents increased the incidence of ventricular dysrhythmias in this patient. The electrophysiologic study is a useful technique in determining the interaction between psychotropic drugs and life-threatening arrhythmias; it may provide a means of identifying the patients with cardiac disease in whom administration of these agents may be fatal.
Since 1977, six patients (five males and one female), aged 14 to 35 years, resuscitated from ventricular fibrillation, were referred to our department for detailed evaluation, after exclusion of major cardiac pathologic conditions. Four patients had a family history of heart disease. Basic ECGs showed sinus rhythm in all of them. PR interval was prolonged in one. Two patients had complete and one had incomplete right bundle branch block. One patient had inverted t waves in V1-3 and late potentials. Three had an upsloping ST-T segment elevation in V1-2. The cardiothoracic index was less than 0.5 in five and 0.50 in one. In one of the five patients studied, the clinical episode of ventricular fibrillation was reproduced by stimulation of the right ventricular outflow tract during electrophysiologic study. Results of cross-sectional echocardiography and angiography showed predominantly structural and wall motion abnormalities of the right ventricle in five patients and slight wall motion abnormalities of the left ventricle in two. Two patients also had mitral and tricuspid valve prolapse. Coronary arteries were normal in all five patients examined. Results of endomyocardial biopsy showed no abnormalities in one patient, fibrosis in two, and fibrolipomatosis in one. Two patients died during follow-up: autopsy was performed in one and results showed right ventricular cardiomyopathy. Thus in five of these selected patients with apparent idiopathic ventricular fibrillation, some abnormalities, predominantly of the right ventricle, were documented only after detailed investigation; however, clinical history and some nonspecific ECG abnormalities were factors in the diagnostic procedure.
The effect of a critical coronary artery stenosis on myocardial blood flow and metabolism in the fibrillating heart was assessed by placing 10 dogs on cardiopulmonary bypass, venting the ventricle, inducing ventricular fibrillation, and applying critical stenosis to the left anterior descending coronary artery (LAD). Endocardial and epicardial blood flows were measured by the radioactive microsphere technique prior to the application of the stenosis and after one hour and 2 hours of fibrillation. Intramyocardial oxygen tension (PO2) and carbon dioxide tension (PCO2) were continuously monitored in the LAD-supplied myocardium by a mass spectrometer probe inserted at midmyocardial depth. Selective arterial-coronary venous lactate differences were determined at control, one hour, and 2 hours. At the end of the 2 hour period, vital dye injection defined the distribution of the LAD. Endocardial flow to the myocardium of the stenosed LAD was reduced by 50 per cent after one hour and by 70 per cent after 2 hours (p less than 0.05). Epicardial flow fell 40 per cent after one hour and 50 per cent after 2 hours (p less than 0.05). Endocardial and epicardial flow in the distribution of the unstenosed circumflex coronary artery remained unchanged. Changes in myocardial PO2 and PCO2 in the LAD-supplied myocardium indicated the development of severe ischemia in all 10 dogs and suggested myocardial infarction in 5. There was a conversion from lactate extraction to lactate production during the 2 hour period of ventricular fibrillation. From this study, it is concluded that the myocardium distal to a critical stenosis suffers a progressive reduction in flow during ventricular fibrillation which does not occur in regions supplied by unstenosed coronary arteries. Thus prolonged fibrillation in the presence of a flow-limiting coronary stenosis may play a role in the pathogenesis of myocardial infarction during coronary bypass surgery.
INTRODUCTION: The sensing performance of transvenous lead systems may be adversely affected by the delivery of high-energy shocks. This may be due to the proximity of the sensing and energy-delivery electrodes on transvenous leads. METHODS AND RESULTS: The time required for detection of ventricular fibrillation and redetection after a failed first shock was compared in 93 patients with five different lead system-pulse generator combinations: Cadence--Endotak 60 series, Ventak P--Endotak 60 series, Jewel--Transvene, Cadence--TVL, and Cadence--Transvene. A total of 418 successful and 204 failed first shocks were delivered during induced ventricular fibrillation. Redetection times (RED) were consistently shorter than detection times (DET) in the Jewel-Transvene (RED minus DET: -1.9 +/- 0.8 sec, P < 0.0001), the Cadence-TVL (-1.6 +/- 1.0 sec, P < 0.0001), and the Cadence-Transvene combinations (-2.0 +/- 0.9 sec, P < 0.0004). Redetection times were not significantly different than detection times in the Cadence-Endotak combination (0.9 +/- 3.1 sec; P = 0.09). Redetection times were significantly longer than detection times in the Ventak-Endotak combination (1.2 +/- 2.3 sec; P = 0.034). Prolonged individual redetection episodes (> 8.2 sec) were observed in the Cadence-Endotak (7 [10%] of 73 episodes) and the Ventak-Endotak (4 [10%] of 39 episodes), but not in the Jewel-Transvene, the Cadence-TVL, and the Cadence-Transvene combinations. CONCLUSIONS: Redetection of ventricular fibrillation may be delayed in some transvenous lead-pulse generator combinations. Successful redetection of ventricular fibrillation following a failed first shock should be demonstrated prior to hospital discharge of patients with implantable defibrillators.