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PubMed2000

Effects of [K(+)](o) on electrical restitution and activation dynamics during ventricular fibrillation.

To test whether hyperkalemia suppresses ventricular fibrillation (VF) by reducing the slope of the action potential duration (APD) restitution relation, we determined the effects of the extracellular K(+) concentration ([K(+)](o)) ([KCl] = 2.7-12 mM) on the restitution of APD and maximum upstroke velocity (V(max)) the magnitude of APD alternans and spatiotemporal organization during VF in isolated canine ventricle. As [KCl] was increased incrementally from 2.7 to 12 mM, V(max) was reduced progressively. Increasing [KCl] from 2.7 to 10 mM decreased the slope of the APD restitution relation at long, but not short, diastolic intervals (DI), decreased the range of DI over which the slope was >/=1, and reduced the maximum amplitude of APD alternans. At [KCl] = 12 mM, the range of DI over which the APD restitution slope was >/=1 increased, and the maximum amplitude of APD alternans increased. For [KCl] = 4-8 mM, the persistence of APD alternans at short DI was associated with maintenance of VF. For [KCl] = 10-12 mM, the spontaneous frequency during VF was reduced, and activation occurred predominantly at longer DI. The lack of APD alternans at longer DI was associated with conversion of VF to a periodic rhythm. These results provide additional evidence for the importance of APD restitution kinetics in the development of VF.

Action Potentials↗

PubMed1999

Endogenous adenosine reduces the occurrence of ischemia-induced ventricular fibrillation in rat heart.

The aim of this study was to determine whether endogenous adenosine has antiarrhythmic effects on ischemia-induced ventricular tachyarrhythmias. We therefore modulated the effect of endogenous adenosine in isolated rat hearts using four different approaches. First, interstitial adenosine was elevated by metabolic inhibition with either EHNA (erythro-9-(2-hydroxy-3-nonly)adenine) or acadesine [5-amino-1-beta-D-imidazole-4-carboxamide). Second, cardiac effects of A1 adenosine receptors were allosterically enhanced with PD81,723 (2-amino-4,5-dimethyl-3-thienyl)[3-(trifluoromethyl)phenyl]-methanone . Third, endogenous adenosine release was suppressed with NBMPR (S-(4-nitrobenzyl)-6-thioinosine), and fourth, adenosine receptor subtypes were blocked with antagonists of different selectivity. Regional ischemia, induced by coronary artery ligation, caused ventricular fibrillation of a reproducible kind in about 20% of untreated hearts with a low calcium concentration in the perfusion medium (0.80 mmol/l CaCl2) and in about 75% with high calcium (1.85 mmol/l) within an observation period of 30 min. At high calcium, EHNA (1 and 10 micromol/l) and acadesine (500 micromol/l) suppressed the occurrence of ventricular fibrillation from 68% (controls) to 47%, 33% and 38%, respectively. Conversely, PD81,723 (10 micromol/l) did not influence the occurrence of ventricular fibrillation. At low calcium, NBMPR (0.1 and 1 micromol/l) resulted in a concentration-dependent rise of ventricular fibrillation from 13% (controls) to 40% and 57%, respectively. The adenosine receptor antagonists theophylline (100 micromol/l), XAC (Xanthine Amine Congener; 1 micromol/l) and 8-PT (8-phenyltheophylline; 1 micromol/l) caused a rise in the occurrence of ventricular fibrillation from 25%, 15% and 18% (controls) to 57%, 39% and 44%, respectively, and the selective A2a receptors antagonist CSC (8-(3-chlorostyryl)caffeine; 5 micromol/l) from 20% to 56%. Conversely, the selective A1 receptor blocker DPCPX (8-cyclopentyl-1,3-dipropyl-xanthine; 1 micromol/l) was ineffective. NBMPR or EHNA concentration-dependent suppressed or increased ischemia-induced adenosine overflow, respectively, in a concentration-dependent manner, whereas the adenosine receptor antagonists did not influence adenosine overflow. We conclude that endogenous adenosine is an antiarrhythmic mediator accumulating in acute ischemic myocardium to a level which effectively decreases the occurrence of ventricular fibrillation by an A2 adenosine receptor activation in the isolated rat heart.

Adenine↗

PubMed2005

Myofiberbreak-up: a marker of ventricular fibrillation in sudden cardiac death.

BACKGROUND: Electrophysiologically, ventricular fibrillation is defined as a "chaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge". To this point its morphological equivalent has not been defined. MATERIAL AND METHOD: Several groups of different diseases and types of accidental death in normal subjects were studied. A complete autopsy was performed and the hearts were examined in 432 cases. A total of 16 myocardial samples per heart were processed for histological examination and sections were stained by haematoxylin and eosin or by specific stains. The frequency, location and extent of myocellular segmentation (stretching and/or rupture) of intercalated discs and associated changes of myocardial bundles and single myocells were investigated. A quantitative analysis was performed and the data were processed for statistical evaluation. RESULTS: The frequency of MFB was maximal in coronary (88%) and Chagas (76%) groups followed by the intracranial brain haemorrhage group (52%). The extent of myofiberbreak-up was maximal in coronary/Chagas groups followed by intracranial haemorrhage and transplant groups. CONCLUSIONS: No correlation was seen between gender, age, heart weight, degree of coronary atherosclerosis, myocardial fibrosis, survival and MFB. If our postulate is correct, finding MFB in the myocardium might allow the diagnosis of a malignant arrhythmia followed by cardiac arrest due to ventricular fibrillation even in the absence of clinical information (sudden death out-of-hospital).

Adult↗

PubMed1992

Control of ventricular fibrillation after coronary artery occlusion via intracerebroventricular injections.

The central nervous system (CNS) may play a larger role than previously thought in the development of ventricular fibrillation after coronary artery occlusion. The probability of ventricular fibrillation after complete, permanent occlusion of the left anterior descending coronary artery was 52% in conscious control pigs. After the administration into the lateral cerebral ventricle of tyrosine, the amino acid precursor of the catecholamine neurotransmitters, 100% of the animals developed ventricular fibrillation. After tyrosine plus propranolol, a beta-adrenoceptor antagonist, only 9% of pigs developed ventricular fibrillation. Treatment with propranolol alone did not affect the outcome. Catecholamine synthesis in the CNS may be associated with the development of ventricular fibrillation after coronary artery occlusion.

Animals↗

PubMed2003

Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model.

UNLABELLED: Refractory ventricular fibrillation (VF) is a complication of severe hypothermia. Despite mixed experimental data, some authors view bretylium as the drug of choice in hypothermic VF. Bretylium was removed from Advanced Cardiac Life Support guidelines, and, to date, efficacy of amiodarone in hypothermia is unknown. OBJECTIVES: To compare defibrillation rates from hypothermic VF after drug therapy with amiodarone, bretylium, and placebo. METHODS: This was a randomized, blinded, and placebo-controlled laboratory experiment. Thirty anesthetized dogs were mechanically ventilated and instrumented to monitor coronary perfusion pressure (CPP), rectal core temperature, and electrocardiogram (ECG). Animals were cooled to 22 degrees C or the onset of spontaneous VF. Ventricular fibrillation was induced as needed with a transthoracic AC current. Cardiopulmonary resuscitation (CPR) was initiated and animals were randomized (n = 10 each group) to receive amiodarone 10 mg/kg (A), bretylium 5 mg/kg (B), or placebo (P) intravenously. CPR was continued while monitoring for chemical defibrillation. Rewarming was limited to removal from the cold environment. After 10 minutes, up to three escalating defibrillatory shocks were administered. Hemodynamic monitoring continued after resuscitation. Return of spontaneous circulation (ROSC) was defined as a sustainable ECG rhythm generating a corresponding arterial pressure tracing lasting a minimum of 15 minutes. Sample size permitted 80% power to detect a 60% difference in conversion rate between groups. RESULTS: CPR was adequate based on CPP > 15 mm Hg in all animals. Mean (+/-SD) CPP was 35.3 +/- 18.8 mm Hg with an overall lower trend in the amiodarone group (p = 0.06). Baseline variables were similar between groups. No instance of chemical defibrillation was noted. There was no significant difference in ROSC rates between groups. Resuscitation rates were: amiodarone = 1/10, bretylium = 4/10, and placebo = 3/10 (p = 0.45). CONCLUSIONS: In this model of severe hypothermic VF, neither amiodarone nor bretylium was significantly better than placebo in improving the resuscitation rate.

Amiodarone↗

PubMed1994

Effect of interventions that increase cyclic AMP levels on susceptibility to ventricular fibrillation in unanesthetized dogs.

Although the autonomic nervous system has been implicated in the formation of ventricular fibrillation, the precise mechanism by which this is mediated remains undetermined. In particular, the role of second messengers, generated by beta-adrenoceptor activation, has been postulated to mediate the pro-arrhythmic effects of the sympathetic nervous system. Thus, a 2 min occlusion of the left circumflex coronary artery was initiated during the last minute of exercise in canines with healed myocardial infarctions (produced by ligation of left anterior descending artery). Fifteen dogs were found to be susceptible to the formation of ventricular fibrillation while 17 animals were resistant. Nine resistant dogs were treated with the phosphodiesterase inhibitor isobutylmethyl xanthine (IBMX, 1 mg/kg) in combination with an infusion of 8-bromo-cAMP (100-150 micrograms/kg/min beginning 45 min prior to exercise). Heart rate and left ventricular dP/dtmax significantly increased, but failed to elicit, arrhythmias during the exercise and ischemia test. Nine resistant animals were also treated with the adenylate cyclase activator forskolin, (100 micrograms/kg), which provoked the same hemodynamic changes as the cyclic AMP infusion but also failed to induce ventricular fibrillation. Both forskolin (n = 3) and IBMX (n = 3) induced large increases in myocardial cAMP levels (control 5.2 +/- 0.5, forskolin 8.1 +/- 0.8 pmol/mg non-collagen protein; control 5.0 +/- 0.8, IBMX 6.8 +/- 0.3 pmol/mg non-collagen protein). Ten resistant animals were treated with the beta-adrenoceptor agonist isoproterenol (1-10 micrograms/kg/min), which failed to cause ventricular fibrillation despite significant increases in the hemodynamic parameters described above. Finally, experiments were repeated after 8-bromo-cAMP infusion and IBMX pretreatment in 8 susceptible animals with pharmacologic denervation (atropine+propranolol+prazosin). In spite of hemodynamic increases indicative of an increase in myocardial cyclic AMP levels, arrhythmias were not re-introduced. These data suggest that changes in cAMP may not be responsible for ventricular fibrillation in this model of sudden cardiac death.

1-Methyl-3-isobutylxanthine↗

PubMed1992

The effect of hexane on the ventricular fibrillation threshold of the isolated perfused rat heart.

This investigation was conducted to determine the influence of hexane on the ventricular fibrillation threshold of the isolated perfused rat heart and myocardial electrolyte levels. Ventricular fibrillation threshold was measured using the Langendorff perfusion apparatus. Heart rate was measured by a universal digital counter and the cardiac flow by collecting the outflow of the heating chamber below the heart into a graduated measuring cylinder. Magnesium and zinc were measured by atomic absorption spectrophotometry and potassium by flame photometry. Two groups of rats were studied; those in the experimental group were given 0.2 ml of hexane and the control group 0.2 ml olive oil subcutaneously for 90 days. Their hearts were removed under anaesthesia. Half of the experimental and control hearts were mounted on the Langendorff perfusion apparatus and the heart rate, coronary flow and ventricular fibrillation threshold were measured. The hearts of the other half were used to measure myocardial electrolyte levels. In the experimental group the ventricular fibrillation threshold decreased (4.72 (S.D. +/- 1.87) vs 9.48 (S.D. +/- 2.98); P less than 0.001). There was no change in the coronary flow and heart rate in between the groups. The mean myocardial potassium levels (2586 (S.D. +/- 162) vs 2968 (S.D. +/- 218) micrograms/g; P less than 0.001), magnesium levels (164 (S.D. +/- 28) vs 208 (S.D. +/- 18) micrograms/g; P less than 0.001) and zinc levels (19.6 (S.D. +/- 4) vs 33.8 (S.D. +/- 6.8) micrograms/g; P less than 0.001) were significantly lower in the hexane-treated group compared to controls. Hexane, a constituent of glue and benzine, is cardiotoxic; marked derangement in myocardial electrolytes and a reduced ventricular fibrillation threshold, indicating an increased myocardial vulnerability to arrhythmias, was noted in the experimental animals.

Animals↗

PubMed1976

Beneficial effect of lidocaine on ventricular electrical stability and spontaneous ventricular fibrillation during experimental myocardial infarction.

Several studies have questioned the efficacy of lidocaine in reducing the incidence of ventricular fibrillation shortly after acute myocardial infarction when arrhythmogenic mechanisms may be different from those operative several hours later. To determine whether lidocaine inhibits the occurrence of early ventricular fibrillation, the left anterior descending and septal coronary arteries were occluded at their origins in open chest anesthetized dogs. Fourteen of 16 control dogs died with ventricular fibrillation. Fifteen dogs received two different dose regimens of lidocaine before coronary occlusion. Of the 11 treated dogs maintaining lidocaine bl), 6 survived (P less than 0.05). Five dogs received the larger dose; all died, four having blood levels of 6.3 mug/ml or greater at the time of death. Ventricular fibrillation threshold also increased in six of eight dogs when lidocaine was administered after coronary occlusion. It is concluded that lidocaine at blood levels of 1.2 to 5.5 mug/ml significantly reduces the incidence of ventricular fibrillation early after coronary occlusion. Administration of this agent therefore may be of particular value in the early phase of acute myocardial infarction.

Animals↗

PubMed1988

Contrast media-induced ventricular fibrillation. A comparison of Hypaque-76, Hexabrix, and Omnipaque.

Contrast media occasionally produce ventricular fibrillation during coronary angiography. We compared the fibrillatory propensity of the conventional ionic contrast medium, Hypaque-76 (H76) to the low osmolar ionic dimer Hexabrix (HB) and to the nonionic agent Omnipaque (OM) in 20 open chest anesthetized dogs. Intracoronary injection of 6 mL of contrast medium produced spontaneous ventricular fibrillation in four of ten dogs with H76, compared with two of ten with HB, and zero of ten with OM (P = .07). The induction of two premature beats by programmed stimulation of the myocardium during injection of 4 mL of contrast medium produced ventricular fibrillation in ten of ten dogs with H76, compared with three of ten with HB, and zero of ten with OM (P less than .001). Both H76 and HB produced ventricular fibrillation in ten of ten dogs when three premature beats were induced, compared with two of ten dogs with OM (P less than .001). Four mL H76 produced a 109 +/- 18 msec increase in the QT interval, compared with an 82 +/- 17 msec increase with HB, and a 45 +/- 12 msec increase with OM. We conclude that both low osmolar HB and OM are less fibrillatory than the conventional ionic medium H76, and that the nonionic medium OM is less fibrillatory than the ionic dimer contrast medium HB.

Angiography↗

PubMed2004

The effect of bupivacaine on myocardial tissue hypoxia and acidosis during ventricular fibrillation.

UNLABELLED: Previously we observed that during bupivacaine-induced circulatory collapse, myocardial tissue pH declined more slowly than expected. Here we evaluated the effect of bupivacaine on myocardial acidosis induced by ventricular fibrillation. Sixteen dogs were anesthetized with 1.5% end-tidal isoflurane, the chest was opened, and a probe that measured oxygen pressure (PmO(2)), carbon dioxide pressure, pH, and temperature was inserted into myocardial tissue. After baseline measures, each dog received either 10 mg/kg bupivacaine (n = 8) or a sham saline treatment (n = 8). Three minutes later ventricular fibrillation was initiated electrically, and the rate of change in PmO(2) and pH during ventricular fibrillation was measured. Baseline physiological measures were similar in the two groups of dogs. During ventricular fibrillation there was a rapid decrease in PmO(2), and the rate of decrease was not different between sham- and bupivacaine-treated dogs. Tissue pH decreased during ventricular fibrillation, and the rate of decrease was 4 times faster in sham- compared with bupivacaine-treated dogs (P < 0.05). These results show that bupivacaine attenuated myocardial tissue acidosis during ventricular fibrillation. This potentially beneficial effect may be a result of bupivacaine's ability to inhibit myocardial lactate and carbon dioxide production. This suggests a potential clinical application of bupivacaine for myocardial preservation. IMPLICATIONS: In this animal study pretreatment with bupivacaine attenuated the progression of myocardial acidosis during ventricular fibrillation. The dogs regained normal hemodynamic variables after lipid infusion. The findings suggest such that bupivacaine may protect the heart against ischemic acidosis.

Acidosis↗

PubMed1985

Observations on 100 patients with continuous intraoperative monitoring of intramyocardial pH. The adverse effects of ventricular fibrillation and reperfusion.

Intramyocardial pH and temperature data recorded in 100 patients undergoing cardiac operations were analyzed to elucidate the effects of ventricular fibrillation and reflow. All patients underwent a single period of aortic clamping. Systemic hypothermia (25 degrees C) and intermittent cold crystalloid K+ cardioplegia were employed for myocardial protection. Baseline myocardial pH was 6.88 +/- 0.03 at a temperature of 36.5 degrees +/- 0.2 degree C. During the period of hypothermic ventricular fibrillation prior to aortic clamping, ventricular fibrillation did not affect myocardial pH in 45 patients (Group 1). In 21 patients (Group 2), it caused a significant drop in intramyocardial pH despite cooling. Group 2 patients had a higher incidence of valvular heart disease and left ventricular hypertrophy. They also exhibited low intramyocardial pH values during the subsequent periods of aortic clamping and reflow, indicating inadequate myocardial protection. During the period of reflow, reperfusion acidosis (pH less than 6.8 at 32 degrees C) was encountered in 39 patients (Group B) as opposed to 37 patients (Group A) whose pH remained well above 6.8 during that period. Group B patients had a higher incidence of valvular heart disease and left ventricular hypertrophy, tended to have more ischemic anterior walls prior to cardiopulmonary bypass, sustained longer periods of aortic clamping, had intramyocardial pH evidence of suboptimal protection during aortic clamping, were affected more adversely by ventricular fibrillation during reflow, and tended to have a higher operative mortality. Thus: Depending on the underlying myocardial disease, the adequacy of protection during aortic clamping, and the conditions of reflow, intramyocardial pH in man can fall significantly during ventricular fibrillation and reflow. The metabolic correlate of injury with reflow is a reperfusion acidosis that can reach as low as pH 5.98. When encountered, reperfusion acidosis can be minimized by prompt defibrillation.

Adult↗

PubMed1989

Effect of calcium channel antagonists on susceptibility to sudden cardiac death: protection from ventricular fibrillation.

The effects of calcium channel antagonists and an agonist on susceptibility to ventricular fibrillation were investigated using chronically instrumented dogs with a healed anterior wall myocardial infarction. Three to 4 weeks after the infarction, a 2-min coronary occlusion was initiated during the last minute of exercise and continued for 1 min after cessation of exercise. Twenty-two dogs developed ventricular fibrillation (susceptible) whereas the remaining 14 animals did not (resistant) during this exercise plus ischemia test. The exercise plus ischemia test was repeated in the susceptible dogs after the following treatments: verapamil (n = 17, 250 micrograms/kg), nifedipine (n = 9, 10 and 100 micrograms/kg) and magnesium sulfate (n = 9, 100 mg/kg). Verapamil prevented ventricular fibrillation in all dogs whereas the high dose of nifedipine protected eight of nine animals; the low dose of nifedipine protected one of nine animals and magnesium sulfate protected seven of nine dogs. Finally, the calcium channel agonist Bay K8644 (n = 9, 30 micrograms/kg) was given to resistant animals. All resistant dogs developed ventricular fibrillation when the exercise plus ischemia test was repeated after Bay K8644. These data suggest that calcium entry may play a critical role in the development of arrhythmias during ischemia, with increased calcium entry provoking arrhythmias and calcium entry blockade preventing the lethal events.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1992

Cellular automaton model of ventricular fibrillation.

A theoretical analysis of ventricular fibrillation and the requirements for fibrillation are performed using a discrete element neighborhood (cellular automaton) model of ventricular conduction. The model is configured as a 2500 element rectangular grid on the surface of a cylinder. It is shown that vulnerability to fibrillation is strongly influenced by excited state duration which primarily determines the nature of the underlying reentry activity. As excited state duration is increased fibrillation changes from "coarse" macroreentrant activity to the more chaotic "fine" fibrillation sustained by multiple wavelets of microreentry. In general, defibrillation is achieved by a stimulus strong enough to depolarize the majority of relative refractory elements. The threshold for defibrillation is increased for the more irregular microreentrant fibrillation.

Computer Simulation↗

PubMed2005

Pediatric defibrillation doses often fail to terminate prolonged out-of-hospital ventricular fibrillation in children.

BACKGROUND: The recommended dose for pediatric defibrillation is 2 J/kg, based on animal studies of brief duration ventricular fibrillation (VF) and a single pediatric study of short duration in-hospital VF. In a piglet model of out-of-hospital (prolonged) cardiac arrest, this recommended dose was usually ineffective at terminating VF. We, therefore, hypothesized that pediatric dose defibrillation may be less effective for prolonged out-of-hospital pediatric VF. METHODS: We evaluated retrospectively all cardiac arrests in children less than 13 years old in Tucson from November 1998 to April 2003, with special attention to all children in ventricular fibrillation. We determined the rate of ventricular fibrillation termination after pediatric dose shocks in this cohort, and compared this rate with a published historical pediatric in-hospital defibrillation control group. A pediatric dose shock was defined as 2 J/kg (+/-10 J). All shocks in both groups were provided as monophasic damped sinusoidal waveforms. RESULTS: Thirteen of 151 (9%) children with out-of-hospital cardiac arrest had documented VF. Eleven children received a total of 14 pediatric dose shocks. The median minimum untreated dispatch-to-shock time in unwitnessed arrest or collapse-to-shock in witnessed arrest for those 11 children was 11 min (interquartile range 25-75%; 9-15.5 min). Seven of the 14 pediatric dose shocks terminated the VF (six to asystole, one to pulseless electrical activity). Nine children (68%) died in the emergency department and four (31%) in the pediatric intensive care unit; none survived to hospital discharge. Failure to terminate VF after a pediatric dose shock in this study group with prolonged out-of-hospital ventricular fibrillation was substantially more common than the previously reported in-hospital data (7/14 versus 5/57; OR 10.4; 95% CI 2.6-42; P=0.001). CONCLUSIONS: Termination of VF after a pediatric defibrillation dose is substantially worse for prolonged pediatric out-of-hospital VF cardiac arrest compared with in-hospital (short duration) ventricular fibrillation. The optimal pediatric defibrillation dose for prolonged VF is not known.

Adolescent↗

PubMed2004

Cardioverter defibrillator implantation in a child with isolated noncompaction of the ventricular myocardium and ventricular fibrillation.

Isolated noncompaction of the ventricular myocardium is a rare unclassified cardiomyopathy and is thought to be due to arrest of myocardial morphogenesis. In fetal life, it is characterized by an excessively prominent trabecular meshwork and deep intratrabecular recesses, and occurs in the left ventricle in the absence of structural heart disease. Echocardiography provides evidence for the diagnosis. The noncompacted ventricular myocardium may be accompanied by depressed ventricular function, systemic embolism, Wolff-Parkinson-White syndrome, left bundle branch block, and ventricular arrhythmia. Although onset of symptoms is frequently delayed until adulthood, symptomatic children have a poor prognosis. In this report, we describe a case of 6-year-old girl who had a history of recurrent syncope. Transthoracic echocardiographic examination showed a localized prominent trabeculation and deep intratrabecular recesses at the inferoapical region of the left ventricle. She had several episodes of ventricular fibrillation which was refractory to pharmacological treatment. An implantable cardioverter defibrillator (ICD) was successfully operated three times during follow-up.

Cardiomyopathies↗

PubMed1994

[Value of searching ventricular late potentials in patients recovering from ventricular fibrillation].

The prognostic value of ventricular late potentials (VLP) was studied in 38 survivors of ventricular fibrillation (VF) resuscitated after cardiac arrest. Thirty-seven patients had coronary artery disease, 24 within one month of myocardial infarction, and one patient had valvular heart disease. There were 7 deaths within 2 years, including 5 sudden deaths, the average follow-up in the remaining patients being 46 +/- 30 months. Bad prognostic factors included low left ventricular ejection fraction, anterior myocardial infarction, VF occurring after the first 24 hours of myocardial infarction and the presence of VLP. The 2 year mortality rate was 35% in patients with VLP compared with only 5% when they were absent (p < 0.05). The subgroup with the highest risk of death was that of anterior myocardial infarcts with VLP (45% 2 year mortality). The clinical circumstances surrounding VF were important; patients with clinical and electrical signs of ischaemia at the time of VF tended to have a better prognosis than the others, especially in the absence of VLP: in this subgroup of 12 "ischaemic" VFs without VLP the mortality at 2 years was nil, whereas the other 26 patients had a 27% death rate (0.05 < p < 0.10). Programmed ventricular stimulation was only carried out in 14 cases: it showed that the long-term mortality was very high (60%) in patients with VLP and inducible ventricular tachycardia (VT). Therefore, the implantation of an automatic defibrillator device would seem to be justified in patients resuscitated from VF who have both VLP and inducible VT, but of no value in cases of "ischaemic" VF without VLP.

Action Potentials↗

PubMed1995

Nonexocytotic noradrenaline release and ventricular fibrillation in ischemic rat hearts.

In myocardial ischemia, nonexocytotic noradrenaline release has been identified as underlying mechanism of ischemia-evoked noradrenaline release. Nonexocytotic noradrenaline release can be suppressed by inhibitors of the neuronal noradrenaline carrier (uptake), such as desipramine. Utilizing this pharmacological intervention the role of local noradrenaline release in the genesis of ischemia-induced ventricular arrhythmias was studied. Regional ischemia was induced in rat isolated perfused hearts by ligature of the left anterior descending coronary artery, and the venous effluent obtained during the first 2 min of reperfusion was used to measure the release of endogenous noradrenaline by high-performance liquid chromatography methods. Coronary occlusion caused ventricular fibrillation in a well reproducible manner with an incidence of 70 to 80% during a 30 min observation period. Blockage of uptake1 by desipramine decreased the occurrence of ischemia-induced ventricular fibrillation to 60% (0.01 mumol/l) or 20% (0.1 mumol/l), and ventricular fibrillation was completely suppressed by 1 mumol/l desipramine. Likewise, desipramine (0.01-1 mumol/l) concentration-dependently reduced endogenous noradrenaline release during 30 min of regional myocardial ischemia. Nisoxetine, a structurally unrelated inhibitor of uptake1, also suppressed ischemia-evoked ventricular fibrillation. In contrast to its antifibrillatory effect during regional myocardial ischemia, desipramine precipitated arrhythmias when ventricular fibrillation was induced by perfusing normoxic hearts with exogenous noradrenaline. Combination of desipramine (0.1 mumol/l) with exogenous noradrenaline (0.01 to 1 mumol/l) increased the incidence of ventricular fibrillation compared to noradrenaline perfusion alone. Under these conditions, uptake1-blockade is known to increase the extracellular concentration of the perfused noradrenaline. Finally, in the isolated, spontaneously beating papillary muscle of the left rat heart, desipramine (0.1 and 1.0 mumol/l) had no effect on the upstroke velocity of action potentials, the action potential duration and the effective refractory period. In conclusion, the findings demonstrate that nonexocytotic noradrenaline release is an important mediator of ischemia-induced ventricular fibrillation in isolated hearts of the rat. It is also documented that uptake1 inhibitors such as desipramine reveal their effects on ventricular fibrillation secondary to their action on transmembrane noradrenaline transport.

Adrenergic Uptake Inhibitors↗

PubMed2004

Mother rotors and the mechanisms of D600-induced type 2 ventricular fibrillation.

BACKGROUND: Two types of ventricular fibrillation (VF) have been demonstrated in isolated rabbit hearts during D600 infusion. Type 1 VF is characterized by the presence of multiple, wandering wavelets, whereas type 2 VF shows local spatiotemporal periodicity. We hypothesized that a single mother rotor underlies type 2 VF. METHODS AND RESULTS: One (protocol I) or 2 (protocol II) cameras were used to map the epicardial ventricular activations in Langendorff-perfused rabbit hearts. Multiple episodes of type 2 VF were induced in 22 hearts by high-concentration (> or =2.5 mg/L) D600 (protocol I). During type 2 VF, a single spiral wave (n=19) and/or an epicardial breakthrough pattern (n=11) was present in 14 hearts. These spiral waves either slowly drifted or intermittently anchored on the papillary muscle (PM) of the left ventricle. Dominant-frequency (DF) analyses showed that the highest local DF was near the PM (12.5+/-1.1 Hz). There was an excellent correlation between the highest local DF of these spiral waves and breakthroughs (11.8+/-1.7 Hz) and the DF of simultaneously obtained global pseudo-ECG (11.2+/-1.8 Hz, r=0.97, P<0.0001) during type 2 VF. We also successfully reproduced the major features of type 2 VF by using the Luo-Rudy action-potential model in a simulated, 3-dimensional tissue slab, under conditions of reduced excitability and flat action-potential duration restitution. CONCLUSIONS: Either a stationary or a slowly drifting mother rotor can result in type 2 VF. Colocalization of the stationary mother rotors with the PM suggests the importance of underlying anatomic structures in mother rotor formation.

Action Potentials↗