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PubMed2006

Ventricular fibrillation waveform characteristics are different in ischemic heart failure compared with structurally normal hearts.

BACKGROUND: For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration. METHODS: Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency). RESULTS: All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF (p=0.02), a broader bandwidth (p=0.001) and different frequency characteristics over time (p<0.001). CONCLUSIONS: VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.

Animals↗
PubMed1989

Isolated episode of exercise-related ventricular fibrillation in a healthy athlete.

A 19-year-old man had a documented ventricular fibrillation during a football match. He was a top-level athlete, and after successful resuscitation, he was extensively studied. Electrolytic disturbances, long QT syndrome and nervous mechanisms were all ruled out. Right and left ventriculography, coronary angiograms, electrophysiologic study and endomyocardial biopsy all proved normal. A beta-blocker was empirically given in the absence of any reliable test to guide therapy more scientifically.

Adult↗
PubMed2002

Modified moving average analysis of T-wave alternans to predict ventricular fibrillation with high accuracy.

T-wave alternans is a marker of cardiac electrical instability with the potential for arrhythmia risk stratification. The modified moving average method was developed to measure alternans in settings with artifacts, noise, and nonstationary data. Algorithms were developed and performance characteristics were validated with simulated electrocardiograms (ECGs). Experimental laboratory ECGs with dynamically changing alternans values were analyzed. Alternans values estimated by modified moving average analysis correlated strongly with input alternans values (r(2) = 0.9999). Rapidly changing alternans levels and phase reversals did not perturb the measurement. When heart rate was increased from 60 to 180 beats/min, with T-wave alternans apex moving from 237 to 103 ms after the R wave, the measured alternans peak varied <5% from input value. Simulated 50- to 1,000-microV motion artifact spikes typical of treadmill ECGs produced inaccuracies <2%. Alternans values in experimental laboratory study using standard electrodes tracked vulnerability to myocardial ischemia-induced ventricular fibrillation with 100% sensitivity and specificity at a cut point of 0.75 mV. Modified moving average analysis is a robust method that precisely measures T-wave alternans in settings with artifacts, noise, and nonstationary data typical of clinical ECGs and yields an accurate estimate of risk for ventricular fibrillation.

Algorithms↗
PubMed1997

Age-related mortality, clinical heart failure, and ventricular fibrillation in 4259 Danish patients after acute myocardial infarction.

AIMS: To evaluate the prognosis of patients > or = 80 years old, we analysed a large, community-based population with acute myocardial infarction who received intensive observation and similar pharmacotherapy regardless of age. METHODS AND RESULTS: In a 12-year period, before the introduction of thrombolysis, 4259 consecutive patients hospitalized with acute myocardial infarction from the same hospital in Denmark were prospectively registered. Their complications and mortality in hospital, and 1 and 5 years after discharge were analysed retrospectively. Overall, in-hospital mortality was 11% for patients less than < 50 years old, 22% for patients 60-69 years old and 43% for patients > or = 80 years old. Two thirds of patients > or = 80 years old had heart failure, and cardiogenic shock was twice as common in this age group than in patients 60-69 years. Heart failure was a strong independent risk, factor for post-discharge mortality, particularly in the oldest age groups. Four out of eight patients > or = 80 years survived one year if discharged alive after experiencing in-hospital ventricular fibrillation. CONCLUSION: The life-saving potential of preventing or treating heart failure seems considerable even in the oldest patient groups. Patients > or = 80 years old who survive in-hospital ventricular fibrillation have an acceptable prognosis 1 year post-discharge.

Aged↗
PubMed2005

Adrenal adenoma presenting with ventricular fibrillation.

We report the case of a 58-year-old man who presented with ventricular fibrillation. The serum potassium level was 1.8 mEq/L after successful cardioversion. Coronary angiography showed a normal heart with no structural defects, but 12-lead electrocardiography showed indications of left ventricular hypertrophy, which was confirmed by echocardiography. Laboratory examinations showed a suppressed renin level and an elevated serum aldosterone level. Computed tomography then revealed a right adrenal mass. The patient was treated with surgical resection of the adenoma. This case emphasizes the importance of meticulous search for secondary causes of hypertension, before the occurrence of serious complications.

Adenoma↗
PubMed1995

Bupivacaine hastens the ischemia-induced decrease of the electrical ventricular fibrillation threshold.

Myocardial ischemia sensitizes the cardiotoxic effects of bupivacaine, especially the propensity to ventricular fibrillation. To investigate this sensitization and to elucidate its mechanism, the influence of bupivacaine alone, or associated with ischemia, was studied on electrical fibrillation threshold in anesthetized, open chest pigs. Determination of fibrillation threshold was performed with impulses of 100 ms duration at the rate of 180 bpm, in the absence of ischemia and at the end of increasing periods of ischemia (30, 60, 120, 180 s) obtained by complete occlusion of the left anterior descending coronary artery close to its origin. The effect of bupivacaine (1.00 mg/kg initial dose plus 0.04 mg.kg-1.min-1 over 25 min) was compared to the control in the same animals. This effect corresponded to 1.4-1.8 micrograms/mL plasma concentrations likely to be observed in humans after regional anesthesia. Bupivacaine significantly increased the fibrillation threshold before coronary occlusion from approximately 7.0 to 9.5 mA. In contrast, during ischemia the fibrillation threshold was shifted to the left and down, with a hastening of spontaneous fibrillation. Recording of monophasic action potentials in the ischemic area revealed that conduction time was prolonged by more than 100% under the combined influence of ischemia and bupivacaine, whereas the major enhancement of excitability due to ischemia was not attenuated by bupivacine. Therefore, bupivacaine should be used with caution in the condition of ischemia, especially if heart rate is rapid. In the present experiments, tachycardia is another factor in the enhancement of bupivacaine effects on conduction.

Action Potentials↗
PubMed1989

Time-series analysis of heart rate variability during submaximal exercise. Evidence for reduced cardiac vagal tone in animals susceptible to ventricular fibrillation.

Periodic fluctuations in the R-R interval have been used as noninvasive measures of cardiac autonomic tone. For example, a reduced heart rate variability has been shown to correlate with an increased mortality in patients recovering from myocardial infarction. The effects that physiologic perturbations such as exercise have on this heart rate variability have not been investigated. Therefore, heart rate variability was measured throughout a submaximal exercise test in 36 mongrel dogs with healed anterior myocardial infarctions. The amplitude of the respiratory component (0.24-1.04 Hz) was determined by time-series analysis techniques and was used as an index of cardiac vagal tone. On a subsequent day, a 2-minute coronary occlusion was initiated during the last minute of exercise. Twenty-two animals developed ventricular fibrillation (susceptible), whereas 14 animals did not (resistant). Exercise elicited a significantly greater increase in heart rate (resistant, 205.4 +/- 7.1; susceptible, 227.0 +/- 5.4 beats/min) in susceptible animals, which was accompanied by a greater reduction in the cardiac vagal tone index (resistant, 2.7 +/- 0.3; susceptible, 1.1 +/- 0.2 ln msec2) as compared with resistant animals. Conversely, atropine sulfate (50 micrograms/kg) given during exercise elicited a greater heart rate increase in the resistant dogs (heart rate change: resistant, 54.2 +/- 7.0; susceptible, 18.7 +/- 4.4 beats/min). Taken together, these data suggest that exercise elicited a greater reduction in cardiac vagal tone in animals known to be susceptible to ventricular fibrillation.

Adrenergic beta-Antagonists↗
PubMed1994

Comparison of adrenergic agonists for the treatment of ventricular fibrillation and pulseless electrical activity.

The primary role of epinephrine for the treatment of ventricular fibrillation (VF) and pulseless electrical activity (PEA) is to increase blood flow to the myocardium and central nervous system and ultimately improve survival. However, despite the administration of epinephrine, survival following VF or PEA is low. In an attempt to improve outcome from VF and PEA, alternative adrenergic agonists (methoxamine, phenylephrine, norepinephrine) which have different pharmacological properties than epinephrine have been evaluated. In order to determine the role of alternative adrenergic agonists for the treatment of VF and PEA this paper will compare the pharmacological properties and pharmacodynamic effects of these drugs to epinephrine. Specifically, receptor physiology along with the effects of adrenergic agonists on coronary perfusion pressure, survival, myocardial oxygen demand, and cerebral blood flow will be discussed.

Adrenergic Agonists↗
PubMed2001

Implantation of cardioverter defibrillators without induction of ventricular fibrillation.

BACKGROUND: The upper limit of vulnerability (ULV) is the weakest shock at which ventricular fibrillation (VF) is not induced by a T-wave shock. This study tested the hypothesis that a vulnerability safety margin based on the ULV can be used as an implantable cardioverter-defibrillator implantation criterion. METHODS AND RESULTS: Implantable cardioverter-defibrillators were implanted in 80 patients if T-wave shocks did not induce VF and the baseline-rhythm R wave was >/=7 mV. The T-wave shock was 10 J in the first 45 patients (group A) and 15 J in the last 35 patients (group B). After inductionless implantations, the first VF shock was programmed to the T-wave shock plus 5 J. If T-wave shocks induced VF, the ULV was measured and the first shock was programmed to the ULV+5 J. Inductionless implantations were performed in 58 patients (72%), 28 in group A (62%) and 30 in group B (86%; P=0.04). If T-wave scanning had been done at 15 J in group A patients, inductionless implantations could have been performed in 84% of them. At 3 months, VF was induced twice during electrophysiological study in 75 patients (94%). All VFs were detected in </=4.7 s and were terminated by the first shock. During follow-up, 197 of 198 appropriate first shocks for rapid ventricular tachycardia or VF (99%) were successful in patients who had inductionless implantations (95% confidence intervals, 97% to 100%). CONCLUSION: Inductionless implantations can be performed in >80% of implantable cardioverter-defibrillator recipients using a vulnerability safety margin based on a T-wave scan at 15.

Aged↗
PubMed2000

Control of idiopathic ventricular fibrillation by implantable cardioverter-defibrillator in a child who survived sudden death.

Idiopathic ventricular fibrillation (VF) is extremely rare in children who have not previously undergone cardiac surgery. Patients resuscitated from idiopathic VF remain at risk for recurrence. The use of an implantable cardioverter-defibrillator (ICD) effectively prevents such recurrences. We report the case of a 12-year-old girl who had a history of recurrent syncope and had survived an episode of VF. Serial studies after prolonged but successful resuscitation, including echocardiography, an electrocardiogram (ECG), and coronary angiography failed to reveal abnormal cardiac structures responsible for VF. No abnormal conduction pathways or abnormal early or late after depolarization were found on electrophysiologic study. The ST segments of the 12-lead ECG remained normal after procainamide challenge. The patient underwent ICD implantation 2 weeks after admission and syncope did not recur during a follow-up of 14 months. This report emphasizes that idiopathic VF may be responsible for syncope in children. ICD therapy prevents the recurrence of idiopathic VF and the associated risk of sudden death.

Child↗
PubMed1992

Postpausal ventricular fibrillation analyzed by Holter-ECG: a case report.

A 70-year-old male patient with a myocardial infarction, 3 months previously, happened to be wearing a Holter monitor at cardiac arrest during micturition. The patient had ventricular fibrillation (VF) and was successfully resuscitated by means of defibrillation. Analysis of the Holter tape revealed atrial fibrillation and secondary ventricular premature beats (VPB), i.e., VPBs dependent upon a relatively long interval between the two preceding heartbeats. The VF was preceded by an especially long R-R interval (1.45 sec) following a run of especially short R-R intervals implying the sharpest deceleration of the ventricular rate during 1 hour Holter recording preceding the cardiac arrest. A peculiar large alteration of the T wave configuration was also found to precede the VF.

Aged↗
PubMed1992

Prognosis of ventricular fibrillation in hospital.

In a retrospective study of 520 patients with in-hospital ventricular fibrillation 421 (81%) had acute myocardial infarction (MI), 66 (13%) had ischaemic heart disease (IHD) without MI, 33 (6%) had no signs of IHD. The in-hospital mortality of these three groups was 51%, 52%, and 27%, respectively (P = 0.01). Logistic regression analysis demonstrated that heart failure and cardiogenic shock were significant risk factors for in-hospital death among patients with IHD. Among discharged patients 1 and 5 years survival was 78% and 51% for patients with MI, 63% and 25% for patients with IHD, 67% and 54% for patients without IHD. A proportional hazard model demonstrated old age, heart failure and cardiogenic shock as risk factors for long-term prognosis, while MI was associated with a reduced relative risk ratio = 0.58 of long-term mortality among patients with IHD. In conclusion, patients with known IHD suffering in-hospital VF without AMI have a very poor short- and long-term prognosis. These patients need extensive cardiac examination.

Aged↗
PubMed1997

Can a class III antiarrhythmic drug improve electrical defibrillation efficacy during ventricular fibrillation?

OBJECTIVES: We tested whether a new class III drug (MS-551) administered during ventricular fibrillation (VF) could decrease the defibrillation threshold (DFT) in anesthetized canine hearts. BACKGROUND: Pretreatment with class III antiarrhythmic agents is known to enhance electrical defibrillation efficacy. METHODS: In a preliminary study (n = 10), we ascertained the validity of DFT determination by a sequence of incremental defibrillation shocks in a single fibrillation/defibrillation episode. We then compared the DFTs after 130 s of VF with and without administration of MS-551 (2 mg/kg body weight) at 10 s after the onset of VF in 12 open chest dogs and 8 closed chest dogs. RESULTS: MS-551 decreased the DFT in both experimental models (open chest [mean +/- SD]: from 416 +/- 106 to 318 +/- 92 V, p < 0.05; closed chest: from 714 +/- 75 to 615 +/- 112 V, p < 0.05). The change (delta) in DFT in each heart was inversely correlated with the drug-induced prolongation of VF cycle length before the defibrillation attempt (delta DFT vs. delta VF cycle length 10 s before the first discharge: r = -0.58 and -0.81, p < 0.05). CONCLUSIONS: MS-551 given after the induction of VF improved defibrillation efficacy. Class III antiarrhythmic agents deserve consideration when VF is resistant to electrical defibrillation during cardiopulmonary resuscitation.

Action Potentials↗
PubMedDate not supplied

A quantitative framework for analyzing epicardial activation patterns during ventricular fibrillation.

Few techniques have been developed for deriving quantitative measures of activation patterns during ventricular fibrillation (VF). Such measures have many potential applications, for example, assessing the effects of time, drugs, or electrical interventions. We have developed a new framework for quantifying VF patterns as mapped from an array of approximately 500 unipolar electrodes. Individual activation wavefronts are isolated from one another using an algorithm that groups together adjacent active electrogram samples (dV/dt < -0.5 V/sec). Contacts between wavefronts are detected: these include fractionations, in which a single wavefront breaks into multiple wavefronts, and collisions, in which multiple wavefronts coalesce to form a new wavefront. The timing and contact relationships between wavefronts are summarized as a directed graph. From this model of the VF episode, we derive several parameters: number of wavefronts, number of fractionations, number of collisions, mean wavefront size, mean area swept out, and mean duration. As an example of this analysis, we computed these parameters in six open-chest pigs at 5, 10, 15, and 20 sec after electrical induction of VF. The number of wavefronts and the number of collisions decreased, whereas the mean wavefront size and mean area swept out increased during this period. These results are consistent with previous studies showing a recovery of organization during the first minute of VF.

Algorithms↗
PubMed2000

Atrial function during cardiac arrest caused by ventricular fibrillation.

OBJECTIVES: To report observations on preserved regular atrial electrical and mechanical systole during ventricular fibrillation (VF) and to quantitate blood flow generated by atrial contractions in this setting. METHODS: In 10 rats, right atrial pressure pulses were continuously recorded before and for an interval of 8 min after inducing VF. In 3 isolated, perfused rat hearts, epicardial right atrial electrograms were recorded after inducing VF. In 15 pigs, transesophageal echo-Doppler measurements were obtained with pulsed and color-Doppler visualization of flow across the mitral valve after onset of VF. RESULTS: In each rat, regular right atrial pressure pulses were documented during VF. These persisted over an average interval of 7.5 min. In isolated, perfused hearts, right atrial contractions were accompanied by regular atrial depolarizations. In pigs, regular atrial contractions generated atrial stroke volumes of approximately 12 mL, or 25% of prearrest values during the first minute after onset of VF, but those declined to approximately 6 mL after 10 min of untreated cardiac arrest. Blood flow from the left atrium into the left ventricle failed to advance significantly into the systemic circuit. During atrial diastole, we observed reversal of flow into the left atrium. CONCLUSIONS: Atrial contractions are preserved during the initial 8 min or more after cardiac arrest due to VF. Substantial forward flow into the left ventricle failed to advance through the outflow tract but regurgitated into the atrium during atrial diastole.

Animals↗
PubMed1996

Reentrant wave fronts in Wiggers' stage II ventricular fibrillation. Characteristics and mechanisms of termination and spontaneous regeneration.

The mechanisms of Wiggers' stage II ventricular fibrillation (VF) are poorly understood. Using computerized mapping techniques, we studied the patterns of activation during Wiggers' stage II VF in 13 open-chest dogs. In 7 of the 13 dogs, the right ventricular Purkinje fibers and adjacent subendocardial myocytes were ablated with Lugol solution. VF was induced electrically, and 3 to 5 seconds of data were obtained beginning approximately 2.5 seconds after the onset of VF. Dynamic displays of the activation patterns and isochronal maps revealed the presence of reentrant wave fronts in 17 of 33 runs of VF in ablated ventricles and in 12 of 45 runs of VF in intact ventricles. The incidence of reentry was not different between the subendocardium-ablated group versus the nonablated group (1.7 +/- 1.6 versus 1.2 +/- 1.6 rotations per episode of VF, P = .19). There were no differences in the core size (25 +/- 19 versus 29 +/- 18 mm2), life span (3.4 +/- 1.1 versus 3.2 +/- 1.2 rotations), or cycle length (111 +/- 12 versus 107 +/- 8 ms) in ablated ventricles versus intact ventricles, respectively. The core was unstable as it meandered within the mapped area displacing the entire reentrant wave front. In all episodes, the reentrant wave fronts were spontaneously initiated by an interaction between two propagating wave fronts roughly perpendicular to each other. The second wave front met the tail of the first wave front 69 +/- 11 ms (range, 40 to 90 ms) after its latest activation, indicating that the interaction occurred during a vulnerable period. The reentrant wave fronts terminated spontaneously (n = 7), as the result of interference by an invading wave front (n = 19 or meandered off the mapped region (n = 3). We conclude the following: (1) Reentrant activities with short life spans and meandering cores are present during Wiggers' stage II VF in dogs. (2) New reentrant wave fronts are generated when one wave front interacts with another wave front during its vulnerable period. (3) The reentrant wave fronts terminate spontaneously or as the result of interference. (4) Chemical subendocardial ablation does not affect the incidence, life span, cycle length, or core size of the reentrant wave fronts.

Animals↗
PubMed2005

Organization of myocardial activation during ventricular fibrillation after myocardial infarction: evidence for sustained high-frequency sources.

BACKGROUND: Studies of ventricular fibrillation (VF) in small mammals have revealed localized sustained stationary reentry. However, studies in large mammals with surface mapping techniques have demonstrated only relatively short-lived rotors. The purpose of this study was to identify whether sustained high-frequency activation with low beat-to-beat variability was present at intramural sites in a postinfarct ovine model of VF. METHODS AND RESULTS: VF was induced in 12 sheep 77+/-40 days after anterior myocardial infarction. Electrical activation was recorded with 20 multielectrode transmural plunge needles. Unipolar electrogram frequency content and local cycle duration variability were studied in 30-second recordings beginning 5 seconds after the onset of VF. Higher mean beat frequency was associated with lower SD of the cycle duration intervals (r=-0.91, P<0.001). The mean beat frequency and the SD of cycle duration intervals of the highest-frequency electrode were 8.8+/-2.0 Hz and 17+/-11 ms. In 3 cases, a region with regular activation throughout the recording was identified (SD of the cycle duration interval, 6.0+/-0.7 ms). Two of these sites and 67% of all sites with low local cycle duration variability were intramural. They occurred within regions with a high dominant frequency as determined by fast Fourier transform of the unipolar electrogram. CONCLUSIONS: Regions with the highest frequency of activation during VF were always associated with a low local cycle duration variability and usually intramural in this chronic infarct model. In a minority of cases, a region of stable, rapid, and very regular activation could be identified. These findings support the hypothesis that relatively stable periodic sources form a component of the mechanism of VF in this model.

Animals↗
PubMed1997

Idiopathic ventricular fibrillation induced with vagal activity in patients without obvious heart disease.

BACKGROUND: Recently, idiopathic ventricular fibrillation (VF) has gained much attention. Although several subgroups have been described, its pathogenesis, mechanism, treatment, and prognosis remain unknown. METHODS AND RESULTS: We studied six cases of idiopathic VF with transient late r' waves and ST elevation (late r'/ST elevation) in leads V1 through V3. Late r'/ST elevation was augmented before and after VF episodes. Signal-averaged ECGs showed late potentials even when no late r'/ST elevation occurred. During late r', a conduction delay was observed by use of body-surface maps at the anterior wall and outflow tract of the right ventricle without inhomogeneity of the repolarization phase. There was a decrease or total disappearance of late r'/ST elevation with isoproterenol, atropine, and exercise stress testing and induction or exacerbation with propranolol, edrophonium, and hyperventilation. VF was induced by programmed electrical stimulation in all cases but two, in which it was induced only after edrophonium injection. In two cases, VF was exacerbated by propranolol, and in all cases, it was uninducible with isoproterenol. Heart rate spectral analysis just before VF episodes showed a sudden rise in vagal activity in two cases. As the VF mechanism, a conduction delay exists at the anterior wall and outflow tract of the right ventricle that is possibly exacerbated by an abrupt rise in vagal activity, inducing random reentry that results in VF. Class I antiarrhythmic agents and beta-blockers were ineffective for this VF. All subjects required implantable cardioverter-defibrillators. CONCLUSIONS: We propose this VF associated with late r'/ST elevation in the precordial leads and influenced by vagal activity as a new possible mechanism of idiopathic VF.

Adult↗