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PubMed1995

Predictors of mortality in patients with sustained ventricular tachycardias or ventricular fibrillation and depressed left ventricular function: importance of beta-blockade.

To study prognostic factors in patients with sustained ventricular tachycardias (VT) or ventricular fibrillation (VF) complicated by left ventricular dysfunction, we evaluated the predictive value of demographic, clinical, and hemodynamic parameters for cardiac mortality and sudden cardiac death in 85 patients with VT or VF and left ventricular ejection fraction < 0.45 (mean 0.27 +/- 0.10). Patients underwent serial drug testing and received appropriate antiarrhythmic treatment, with amiodarone given as last-resort therapy. During a follow-up of 24 +/- 13 months, 23 patients died of cardiac causes, and 18 of them died suddenly. Left ventricular ejection fraction < or = 0.27 and amiodarone treatment were related to greater cardiac mortality and increased risk of sudden cardiac death, whereas beta-blockade was associated with improved survival. In the multivariate model cardiac mortality was best predicted by a left ventricular ejection fraction < or = 0.27, and absence of beta-blockade and severe left ventricular dysfunction were the strongest predictors of sudden cardiac death. We conclude that severe left ventricular dysfunction predicts increased cardiac mortality and high risk of sudden cardiac death. Moreover, beta-blocking treatment is associated with lower cardiac mortality and a reduced risk of sudden cardiac death in patients with sustained VT or VF and depressed left ventricular function. beta-Blocking agents may therefore be an important addition to conventional antiarrhythmic treatment in patients with VT or VF and left ventricular dysfunction.

Adrenergic beta-Antagonists↗
PubMed1999

Idiopathic verapamil-sensitive left ventricular tachycardia complicated by right ventricular outflow tract ventricular tachycardia and ventricular fibrillation.

Idiopathic ventricular tachycardias (VTs) are generally divided into those arising from the right ventricle and those arising from the left ventricle. There has been few reports of two morphologically distinct VT occurring in patients with no apparent structural heart disease. We report a patient with verapamil-sensitive left VT with a right bundle branch block pattern that spontaneously changed to VT with a left bundle branch block pattern. Ventricular fibrillation was induced by the application of programmed stimulation. Although it is unclear if our patient with pleomorphic VT has ventricular vulnerability, it is necessary to investigate further and follow him carefully.

Adult↗
PubMed2002

Precountershock cardiopulmonary resuscitation improves ventricular fibrillation median frequency and myocardial readiness for successful defibrillation from prolonged ventricular fibrillation: a randomized, controlled swine study.

STUDY OBJECTIVE: After prolonged ventricular fibrillation (VF), precountershock cardiopulmonary resuscitation (CPR) will improve myocardial "readiness" for defibrillation compared with immediate defibrillation. METHODS: After 10 minutes of untreated VF, 32 swine (27+/-1 kg) were randomly assigned to receive immediate countershocks (DEFIB), CPR for 3 minutes followed by countershocks (CPR), or CPR for 3 minutes plus intravenous epinephrine followed by countershocks (CPR+EPI). VF waveform was evaluated by fast Fourier transformation. RESULTS: VF amplitude and median frequency by fast Fourier transformation decreased during the untreated VF interval in all groups, and the median frequency subsequently increased during each minute of precountershock CPR. Although the VF median frequency in the 3 groups did not differ after 10 minutes of untreated VF (8.9+/-0.8 Hz versus 8.4+/-0.5 Hz versus 7.3+/-0.5 Hz, respectively), immediately before the first shock the VF median frequency was much lower in the DEFIB group than in either the CPR or CPR+EPI groups (8.9+/-0.8 Hz versus 13.1+/-0.8 Hz versus 13.8+/-0.9 Hz, respectively; P <.01). None of the 10 animals in the DEFIB group attained return of spontaneous circulation after the first set of shocks versus 5 of 10 animals in the CPR group and 6 of 12 animals in the CPR+EPI group (DEFIB versus each CPR group; P <.05). Cardiac output 1 hour after resuscitation was substantially worse in the DEFIB group than in the CPR or CPR+EPI groups (74+/-7 mL/kg per minute versus 119+/-7 mL/kg per minute versus 104+/-15 mL/kg per minute; P <.05). CONCLUSION: Precountershock CPR can result in substantial physiologic benefits compared with immediate defibrillation in the setting of prolonged VF. Moreover, these benefits can be attained with or without the addition of intravenous epinephrine.

Animals↗
PubMed1978

Contrast agents lower ventricular fibrillation threshold.

Ventricular fibrillation thresholds were measured in anesthetized, closed-chest dogs during the injection of Renografin 76 or Conray 400 into the left coronary artery. Both agents significantly lowered fibrillation threshold--Renografin to 58 +/- 7%; Conray to 20 +/- 5% of control, respectively. The experimental method estimates fibrillatory potential of contrast media more precisely than previous methods. The initial results parallel relative toxicities observed in clinical usage.

Animals↗
PubMed2002

Inhibition of angiotensin-converting enzyme reduces susceptibility of hypertrophied rat myocardium to ventricular fibrillation.

Left ventricular (LV) hypertrophy increases susceptibility to reperfusion arrhythmias and the angiotensin-converting enzyme inhibitor, ramipril, may reduce that susceptibility via regression of LV hypertrophy. Rats (n=12 per group) were subjected to abdominal aortic constriction (AC) or sham-operation (SH) and from 3 to 6 weeks after surgery, 3 AC groups received ramipril (0.01, 0.1, or 1 mg/kg per day p.o.) while the SH and 1 AC group received vehicle. Six weeks after surgery (ie after 3 weeks of treatment), the hearts were excised and subjected to independent Langendorf perfusion of left and right coronary beds. The left coronary bed was then subjected to ischemia (7 min) and reperfusion (5 min). Hypertrophied hearts from the vehicle AC group showed a significant increase in the incidence of reperfusion-induced ventricular fibrillation (VF) compared with control hearts from the SH group (92%* vs 33%: *p<0.05); this difference was abolished by ramipril (42%, 50%, and 42%, at 0.01, 0.1, or 1 mg/kg per day, respectively). The LV weight/body weight ratio was significantly increased in all AC groups (regardless of ramipril treatment) relative to the SH group. At the cellular level, myocyte length was significantly increased in the vehicle AC group, but was normalized by ramipril treatment (1 mg/kg per day). At the molecular level, atrial natriuretic factor (ANF) mRNA expression was also significantly increased in the vehicle AC group, but was again normalized by ramipril treatment (1 mg/kg per day). In conclusion, short-term treatment with ramipril reduced susceptibility to severe ventricular arrhythmias in hypertrophied rat hearts. This protection was achieved in the absence of a significant reduction in LV weight, but was accompanied by regression of myocyte hypertrophy, as reflected by reductions in cell size and ANF expression.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Can catheter ablation in cardiac arrest survivors prevent ventricular fibrillation recurrence?

Ventricular tachyarrhythmias are the most common cause for sudden cardiac death. The success of catheter ablation for supraventricular tachycardias led to the supposition that ablation could also be used in the treatment of ventricular tachycardias. Despite the promising results in bundle branch reentry and some forms of idiopathic ventricular tachycardia, the success rate in patients with coronary artery disease is still low. There is hope that new approaches to reliably localize the critical region of the tachycardia and new ablation techniques to create larger areas of injury may lead to a wider application of ablation therapy in the treatment of ventricular tachycardia. Survivors of cardiac arrest typically have more rapid and unstable arrhythmias than patients with sustained ventricular tachycardia, and these rapid arrhythmias frequently degenerate into ventricular fibrillation. The instability of the arrhythmia makes it impossible to localize the arrhythmia origin with current mapping techniques. Experimental and clinical data, however, suggest that these arrhythmias also frequently start from a localized area of electrical activation. With developments in mapping techniques and energy delivery, catheter ablation may soon become a feasible therapeutic approach in some patients with unstable arrhythmias. The article discusses the prerequisites for this approach and suggests the patients who may be appropriate candidates for this technique.

Arrhythmias, Cardiac↗
PubMed2003

Abnormal cardiac innervation in patients with idiopathic ventricular fibrillation.

Idiopathic ventricular fibrillation (VF) is diagnosed in up to nearly 10% of survivors of out-of-hospital cardiac arrest. The arrhythmogenic substrate is unknown. This study examined the role of cardiac innervation as a possible contributor to this arrhythmia. Eight patients with idiopathic VF were compared with eight normal subjects (controls) by [123] I metaiodobenzylguanidine SPECT (MIBG), measuring peak uptake, late uptake, and clearance of the nuclear tracer. The left ventricle was divided in 13 segments in the bull's-eye target plot. Peak and late MIBG uptake was increased in the anterolateral segments (2,3,7,8) compared to the inferoposterior and septal segments, in controls and in patients. No difference was observed between controls and patients in the inferoposterior and septal segments. In contrast, a significantly higher MIBG uptake was observed in patients compared to controls in the anterolateral segments (94 +/- 4% vs 81 +/- 11%, P < 0.03 for peak uptake; 94 +/- 5% vs 79 +/- 12%, P < 0.01 for late uptake). No difference was observed in MIBG clearance in any segment in either study group. Cardiac sympathetic innervation is highly heterogeneous, though predominant in anterolateral segments in normal subjects. Patients with idiopathic VF exhibit the same distribution, though have a significantly greater density of sympathetic terminals in the anterolateral segments than controls, which may promote ventricular arrhythmias.

3-Iodobenzylguanidine↗
PubMed2001

Accelerated inactivation in a mutant Na(+) channel associated with idiopathic ventricular fibrillation.

Idiopathic ventricular fibrillation (IVF) can cause sudden death in both adults and children. One form of IVF (Brugada syndrome), characterized by S-T segment elevation (STE) in the electrocardiogram, has been linked to mutations of SCN5A, the gene encoding the voltage-gated cardiac Na(+) channel. A missense mutation of SCN5A that substitutes glutamine for leucine at codon 567 (L567Q, in the cytoplasmic linker between domains I and II) is identified with sudden infant death and Brugada syndrome in one family. However, neither the functional effect of the L567Q mutation nor the molecular mechanism underlying the pathogenicity of the mutation is known. Patch-clamp analysis of L567Q channels expressed in human embryonic kidney cells revealed a marked acceleration and a negative shift in the voltage dependence of inactivation. Unlike other Brugada mutations, this phenotype was expressed independently of temperature or auxiliary beta(1)-subunits. These results support a proposed linkage between Brugada syndrome and some instances of sudden infant death and the hypothesis that reduced Na(+) conductance is the primary cause of IVF with STE.

Cell Line↗
PubMed1993

Autoregressive modeling of epicardial electrograms during ventricular fibrillation.

During ventricular fibrillation (VF), electrograms from bipolar epicardial electrodes generally appear to have little organization or structure. We sought to identify any well defined organization or structure in these signals by determining if they could be modeled as an autoregressive stochastic process with a white noise excitation during the short time period (6.5-8 s) typically used by automatic implantable defibrillators. The autoregressive model is then used to synthesize VF signals using a white noise excitation with the same probability distribution function as the estimated excitation determined from the autoregressive model for that particular true VF episode. Both the original and ten synthesized VF signals for each patient are then compared using root mean square (rms) amplitude, the number of zero crossings per second, the amplitude distribution of the signals, the rate, and percent variation of rate. The results of examining the synthesized VF waveforms indicate that the rms amplitudes are similar to the true VF waveforms. While the synthesized VF signals had higher rate, more regular RR intervals, more zero crossings per second, and spent less time at baseline than the VF signal from which they were generated, these differences are generally not significant (p > or = 0.05). The use of such synthesized VF signals may allow more thorough testing of VF detection algorithms than is possible with the present limited libraries of human VF recordings.

Defibrillators, Implantable↗
PubMed2004

Angular velocity: a new method to improve prediction of ventricular fibrillation duration.

Ventricular fibrillation (VF) is a leading cause of sudden death. Electrical defibrillation is the primary modality of treatment, but evidence is accumulating that its use in the late stage of VF prior to providing ventilation, chest compressions and the administration of appropriate medication is detrimental. In VF of <5 min duration a 'shock first' strategy is effective. In VF of 5> min duration a 'perfuse first' approach is more effective. Because of the difficulty in determining the duration of VF in the clinical setting we have sought to develop method which analyze 5 s intervals of VF waveform and quickly provide an estimate of duration. Such methods would be useful in directing clinical interventions. Using methods of nonlinear dynamics and fractal geometry we have previously derived a quantitative measure of VF duration, namely the scaling exponent (ScE). In this study we report on a novel method also based on nonlinear dynamics, the angular velocity (AV). By constructing a flat, circular disk-shaped structure in a three-dimensional phase space and measuring the velocity of rotation of the position vector over time, a statistic is developed which rises from 58 rad/s at 1 min to 79 rad/s at 4 min and then decreases in a linear manner to 32 rad/s at 12.5 min. Using ScE and AV probability density estimated, VF of <5 min duration can be identified with 90% sensitivity on the basis of a single 5 s recording of the waveform. The combination of ScE and AV can be used in developing strategies for the treatment of VF during the different clinical phases of VF.

Algorithms↗
PubMed2002

A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation.

BACKGROUND: Ventricular fibrillation (VF) remains the most salvageable rhythm in patients suffering a cardiopulmonary arrest (CA). However, outcome remains poor if there is no response to initial defibrillation. Some evidence suggests that intravenous magnesium may prove to be an effective antiarrhythmic agent in such circumstances. STUDY HYPOTHESIS: Intravenous magnesium sulphate given early in the resuscitation phase for patients in refractory VF (VF after 3 DC shocks) or recurring VF will significantly improve their outcome, defined as a return of spontaneous circulation (ROSC) and discharge from hospital alive. DESIGN: A randomised, double blind, placebo controlled trial. Pre-defined primary and secondary endpoints were ROSC at the scene or in accident and emergency (A&E) and discharge from hospital alive respectively. SETTING, PARTICIPANTS, AND INTERVENTION: Patients in CA with refractory or recurrent VF treated in the prehospital phase by the county emergency medical services and/or in the A&E department. One hundred and five patients with refractory VF were recruited over a 15 month period and randomised to receive either 2-4 g of magnesium sulphate or placebo intravenously. RESULTS: Fifty two patients received magnesium treatment and 53 received placebo. The two groups were matched for most parameters including sex, response time for arrival at scene and airway interventions. There were no significant differences between magnesium and placebo for ROSC at the scene or A&E (17% v 13%). The 4% difference had 95% confidence intervals (CI) ranging from -10% to +18%. For patients being alive to discharge from hospital (4% v 2%) the difference was 2% (95% CI -7% to +11%). After adjustment for potential confounding variables (age, witnessed arrest, bystander cardiopulmonary resuscitation and system response time), the odds ratio (95% CI) for ROSC in patients treated with magnesium as compared with placebo was 1.69 (0.54 to 5.30). CONCLUSION: Intravenous magnesium given early in patients suffering CA with refractory or recurrent VF did not significantly improve the proportion with a ROSC or who were discharged from hospital alive.

Aged↗
PubMed2000

Is all ventricular fibrillation the same? Influence of mode of induction on characteristics of ventricular fibrillation.

INTRODUCTION: Little information is available on the relationship between the mode of induction of ventricular fibrillation (VF) to VF characteristics. METHODS AND RESULTS: VF was induced from the anterior left ventricle by programmed electrical stimulation, burst pacing, alternating current (AC), high current S2 at a site remote from S1, T wave shock, and intersecting wavefronts in seven normal dogs and seven dogs with chronic myocardial infarction. Using two electrode arrays, 112 electrograms were recorded from the anterior and lateral wall. Cycle lengths were analyzed and activation vectors were created by summing orthogonally recorded bipolar electrograms. The magnitude of the vector loops was integrated over time to produce an "ensemble vector" index (EVI) whose magnitude is high when beat-to-beat activation direction is consistent and low when activation direction is variable. T wave shock-induced VF had a significantly longer cycle length 1 to 5 seconds after VF onset than other modes of induction (P < 0.05). The frequency-corrected EVI was significantly larger for AC current and T wave shock-induced VF as opposed to all other modes of VF induction in early VF (P < 0.0001). After 10 seconds of VF, these differences persisted only on the anterior wall. CONCLUSION: VF induced in animals by T wave shock and AC current had different characteristics than VF induced by other methods. These findings may have implications for our understanding of VF pathophysiology.

Animals↗
PubMed1998

Fast Fourier transform analysis of ventricular fibrillation intervals to predict ventricular refractoriness and its spatial dispersion.

A technique of fast Fourier transform analysis has been used to derive mean ventricular fibrillation (VF) intervals, and to confirm that these VF intervals predict ventricular refractory periods. Twenty episodes of VF were induced by a rapid ventricular pacing in 12 sheep. VF activations in a 10-second period were simultaneously acquired from 64 epicardial sites with an electrode sock. The VF electrograms were analyzed by a fast Fourier transform analysis. The dominant peak frequency of the VF spectrum in each epicardial site was converted into milliseconds and served as a mean VF interval. The dominant peak frequency of VF electrograms ranged from 8.1 to 11.5 Hz, and the corresponding mean VF intervals were 87 to 124 ms. In five sheep, the mean VF intervals and the effective refractory periods were determined by the extrastimulus technique obtained from 29 epicardial sites. There was a very good correlation between the two parameters when the effective refractory periods were determined at a basic cycle length of 300 ms (r = 0.89, P < 0.001) and 400 ms (r = 0.87, P < 0.001), respectively. VF was induced twice in eight sheep. The maximum difference in the mean VF intervals between the two VF episodes in the same sheep was 3 ms (P > 0.05). In conclusion, mean VF intervals determined by the fast Fourier transform analysis have a good reproducibility and a good correlation with ventricular refractory periods measured by the classic extrastimulus technique. The mean VF intervals could serve as an index of ventricular refractoriness.

Animals↗
PubMed2004

A simulation study of the effects of cardiac anatomy in ventricular fibrillation.

In ventricular fibrillation (VF), the principal cause of sudden cardiac death, waves of electrical excitation break up into turbulent and incoherent fragments. The causes of this breakup have been intensely debated. Breakup can be caused by fixed anatomical properties of the tissue, such as the biventricular geometry and the inherent anisotropy of cardiac conduction. However, wavebreak can also be caused purely by instabilities in wave conduction that arise from ion channel dynamics, which represent potential targets for drug action. To study the interaction between these two wave-breaking mechanisms, we used a physiologically based mathematical model of the ventricular cell, together with a realistic three-dimensional computer model of cardiac anatomy, including the distribution of fiber angles throughout the myocardium. We find that dynamical instabilities remain a major cause of the wavebreak that drives VF, even in an anatomically realistic heart. With cell physiology in its usual operating regime, dynamics and anatomical features interact to promote wavebreak and VF. However, if dynamical instability is reduced, for example by modeling of certain pharmacologic interventions, electrical waves do not break up into fibrillation, despite anatomical complexity. Thus, interventions that promote dynamical wave stability show promise as an antifibrillatory strategy in this more realistic setting.

Animals↗
PubMed1993

Electrophysiologic variables characterizing the induction of ventricular tachycardia versus ventricular fibrillation after myocardial infarction: relation between ventricular late potentials and coupling intervals for the induction of sustained ventricular tachyarrhythmias.

OBJECTIVES: The aim of this study was to analyze the relations between the presence of ventricular conduction delay and the necessary coupling intervals for the induction of sustained ventricular tachyarrhythmias. METHODS: The electrophysiologic and signal-averaged electrocardiographic (ECG) data from 83 patients with previous myocardial infarction and inducible sustained monomorphic ventricular tachycardia (n = 71) and ventricular fibrillation (n = 12) were analyzed. RESULTS: The sum of the coupling intervals needed for inducing ventricular tachycardia and ventricular fibrillation was 485 +/- 59 ms and 387 +/- 36 ms, respectively (p < 0.001). The mean difference between the effective refractory period and the second coupling interval for the induction of ventricular tachycardia and ventricular fibrillation was -3 +/- 40 ms and 24 +/- 29 ms, respectively (p < 0.02). QRS duration and duration of terminal low amplitude signals of the QRS complex (p < 0.004) were longer in patients with inducible ventricular tachycardia than in patients with inducible ventricular fibrillation. The root mean square of the voltage during the last 40 ms of QRS complex was lower in patients with inducible ventricular tachycardia than in patients with inducible ventricular fibrillation (p < 0.007). Patients with inducible ventricular tachycardia presented with a greater prevalence of ventricular late potentials than that of patients with inducible ventricular fibrillation (p < 0.007). For arrhythmia induction, significantly shorter coupling intervals were necessary in patients without than in patients with ventricular late potentials. A positive correlation was found between the cycle length of the induced ventricular tachycardia and the filtered QRS duration as well as with the sum of the coupling intervals. CONCLUSIONS: Induction of ventricular fibrillation requires shorter coupling intervals than does induction of ventricular tachycardia. The presence of ventricular conduction delay seems to be a marker of facilitated induction of sustained monomorphic ventricular tachycardia rather than of ventricular fibrillation. The coupling intervals required to induce ventricular tachycardia or fibrillation are longer in patients with than in those without an abnormal signal-averaged ECG.

Adult↗
PubMed1998

The effects of ventricular fibrillation duration and site of initiation on the defibrillation threshold during early ventricular fibrillation.

OBJECTIVES: The purpose of this study was to determine if the defibrillation threshold (DFT) is lower during the first few cycles of ventricular fibrillation (VF) than after 10 s of VF and, if so, if the effect is caused by local or global factors. BACKGROUND: The DFT may be low very early during VF because: (1) for the first few cycles VF arises from a localized region close to a defibrillation electrode where the shock field is strong (local factors), or (2) during early VF the effects of ischemia and sympathetic discharge have not yet fully developed and the heart has not yet completely dilated (global factors). METHODS: Protocol 1 included seven pigs in which a defibrillation electrode and a pacing catheter were both placed in the right ventricular apex. VF was induced by delivering a high current premature stimulus from the pacing catheter that should have caused reentry confined to the right ventricular apex for the first few cycles of VF. A bipolar electrogram was recorded from the tip of the defibrillation catheter. Using a three reversal up-down protocol, the DFT was determined for biphasic shocks delivered after 1, 2, 3, 4, 5, 7, 10, 15, 20 and 25 activations in this electrogram and after 10 s (control). Protocol 2 included seven pigs undergoing the same procedure as in protocol 1 except that an additional pacing catheter was placed in the left ventricle. Defibrillation thresholds were determined after 1, 2, 3, 4 and 5 VF activations following VF induction from the right ventricle (RV) or the left ventricle (LV) and after 10 s (control). RESULTS: In protocol 1, the mean +/- SD DFrs were lower during the first three cycles than after 10 s of VF (3.0 +/- 4.1 J for the first VF cycle vs 15.8 +/- 6.6 J after 10 s of VF, p < 0.05). In protocol 2, the DFF for the first few cycles of VF induced away from the defibrillation electrode in the LV (6.9 +/- 1.4 J for the first VF cycle) was significantly lower than that after 10 s of VF (16.0 +/- 2.2 J), whereas the DFF for the first few cycles induced near the defibrillation electrode in the right ventricular apex was significantly lower (2.3 +/- 2.7 J for the first VF cycle) than that induced from the LV. CONCLUSIONS: This study demonstrates that the DFT is significantly lower during the first few VF cycles of VF than after 10 s of VF and that this decrease may be caused by both local factors and global factors. These results provide an impetus for exploring earlier shock delivery in implantable devices.

Animals↗
PubMed1991

Ventricular fibrillation threshold is influenced by left ventricular stretch and mass in the absence of ischaemia.

STUDY OBJECTIVE: Ischaemic heart disease is known to contribute to the development of ventricular arrhythmias. However, the role of non-ischaemic variables has been less well defined. We therefore studied the effect of myocardial stretch and ventricular mass on the vulnerability of the rat heart to ventricular fibrillation. DESIGN AND EXPERIMENTAL MATERIAL: Two groups of rat hearts were studied in an isolated buffer perfused apparatus: group I, mature female animals with an average dry left ventricular weight of 73 mg and group II, a group of retired breeders with an average left ventricular weight of 122 mg. Hearts performed isovolumetric work at either low (0 mm Hg) or high (20 mm Hg) left ventricular end diastolic pressures. MEASUREMENTS AND MAIN RESULTS: Ventricular fibrillation was provoked by trains of ventricular extrastimuli delivered at increasing current until development of the arrhythmia. The current required to provoke ventricular fibrillation decreased in both groups at the high left ventricular end diastolic pressure and the larger hearts in group II were more vulnerable to ventricular fibrillation than those in group I. The decrease in ventricular fibrillation threshold occurred in the absence of an increase in myocardial lactate production or a decrease in endocardial to epicardial flow ratios. CONCLUSIONS: This study thus identified two variables, myocardial stretch and ventricular mass, which influence the development of ventricular fibrillation and which are independent of myocardial ischaemia in this animal model. These observations may be relevant to an understanding of the increased incidence of lethal arrhythmias which occur in patients with dilated cardiomyopathies.

Animals↗