aconitine and Tachycardia--Ventricular

The effects of antiarrhythmic agents, including Classes I and IV and 3-10 mM Mg2+ on aconitine-induced arrhythmias were examined using a conventional microelectrode and patch clamp method in Langendorff-perfused rabbit hearts and isolated guinea-pig ventricular myocytes. Intracoronary application of 0.1 microM aconitine induced polymorphic ventricular tachycardia (PVT) which continued for more than 60 minutes. Application of aconitine to ventricular myocytes caused a prolonged action potential duration (APD) and the appearance of early afterdepolarization (EAD) together with the occurrence of an inward hump of the I-V curve around -60 to -40 mV and increased outward current at positive voltages. Application of 10 microM TTX and 5 mM or higher Mg2+ restored aconitine-induced PVT to sinus rhythm in Langendorff-perfused preparations and also shortened the prolonged APD, demonstrating the abolishment of EAD by aconitine in ventricular myocytes. However, antiarrhythmic agents did not exert such effects. In conclusion, the antiarrhythmic actions of Mg2+ and TTX in aconitine-induced arrhythmia are to abolish EAD and shorten the prolonged APD by suppression of the inward Na+ current around -60 to -40 mV.

Topics: Aconitine; Action Potentials; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Guinea Pigs; In Vitro Techniques; Magnesium; Membrane Potentials; Myocardium; Patch-Clamp Techniques; Rabbits; Tachycardia, Ventricular; Tetrodotoxin

A rare case of aconitine poisoning accompanied by bidirectional ventricular tachycardia was reported. A 67-year-old male ate several leaves of a wild plant which had been collected in Fukushima Prefecture, Japan. About 90 minutes later, he felt numbness and weakness of the limbs and vomiting took place, and he was admitted to our hospital. The blood pressure was 80/60mmHg, and the electrocardiogram showed multiple premature ventricular contractions and bidirectional ventricular tachycardia. After bolus injection of lidocaine, continuous administration of the drug was started. Immediately after starting the treatment, the arrhythmia disappeared and hemodynamic changes improved. Thereafter the wild plant was ascertained to be a species of Aconitium. Diagnosis of aconitine poisoning was made. According to the fact that aconitine acts as a agonist of Na-channel receptor, antiarrhythmic agents which belong to Vaughan-Williams' classification I might be the first choice for the therapy of aconitine induced arrhythmias.

Topics: Aconitine; Aged; Humans; Lidocaine; Male; Tachycardia, Ventricular

Lethal ventricular tachyarrhythmias (LVTA)-related sudden cardiac death (SCD) is one of the major causes of death worldwide. However, the mechanisms underlying LVTA induced by myocardial ion channel diseases (MICDs) are not yet fully understood. Here, we produced an LVTA rat model induced by aconitine, to mimic MICDs-elicited LVTA, and constructed a global pathway network via integrating proteomic and lipidomic data, and our previously published metabolomic data. Results showed that both proteome and lipidome were disturbed during the LVTA process. Most of the differentially expressed proteins and lipid species were correlated. Proteomic data indicated disturbance of energy metabolism (e.g. fatty acid β-oxidation and the tricarboxylic acid cycle) and activation of the protein kinase C and nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase pathway; these alterations led to lowered ATP and elevated ROS, respectively. Altered levels of the Ca

Topics: Aconitine; Animals; Lipidomics; Metabolic Networks and Pathways; Metabolomics; Proteomics; Rats; Tachycardia, Ventricular

Topics: Aconitine; Cardiac Electrophysiology; Cardiopulmonary Resuscitation; Drugs, Chinese Herbal; Electrocardiography; Extracorporeal Membrane Oxygenation; Female; Humans; Middle Aged; Multiple Organ Failure; Tachycardia, Ventricular; Treatment Outcome; Voltage-Gated Sodium Channel Agonists

Patients who overdose on aconite can present with life-threatening ventricular arrhythmia. Aconite must be prepared and used with caution to avoid cardiotoxic effects that can be fatal. We herein describe a case of a patient who had an accidental aconite overdose but survived with no lasting effects. The patient had prepared Chinese herbal medication to treat his pain, which resulted in an accidental overdose of aconite with cardiotoxic and neurotoxic effects. The patient had ventricular tachycardia, bidirectional ventricular tachycardia and ventricular fibrillation. Following treatment with anti-arrhythmic medications, defibrillation and cardiopulmonary resuscitation, he made an uneventful recovery, with no further cardiac arrhythmias reported.

Topics: Aconitine; Adult; Anti-Arrhythmia Agents; Cardiopulmonary Resuscitation; Cardiotoxicity; Drug Overdose; Drugs, Chinese Herbal; Electric Countershock; Electrocardiography; Humans; Male; Tachycardia; Tachycardia, Ventricular; Treatment Outcome; Ventricular Fibrillation

Enhanced late inward Na current (INa-L) modulates action potential duration (APD) and plays a key role in the genesis of early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) and triggered activity.. The purpose of this study was to define the influence of selective block of INa-L on EAD- and DAD-mediated triggered ventricular tachycardia (VT) and ventricular fibrillation (VF) in intact hearts using (GS967), a selective and potent (IC50 = 0.13 ± 0.01 μM) blocker of INa-L.. VT/VF were induced either by local aconitine injection (50 μg) in the left ventricular muscle of adult (3-4 months) male rats (N = 21) or by arterial perfusion of 0.1 mM hydrogen peroxide (H2O2) in aged male rats (24-26 months, N = 16). The left ventricular epicardial surface of the isolated-perfused hearts was optically mapped using fluorescent voltage-sensitive dye, and microelectrode recordings of action potentials were made adjacent to the aconitine injection site. The suppressive and preventive effects of GS967 (1 μM) against EAD/DAD-mediated VT/VF were then determined.. Aconitine induced VT in all 13 hearts studied. Activation map (N = 6) showed that the VT was initiated by a focal activity arising from the aconitine injection site (cycle length [CL] 84 ± 12) that degenerated to VF (CL 52 ± 8 ms) within a few seconds. VF was maintained by multifocal activity with occasional incomplete reentrant wavefronts. Administration of GS967 suppressed the VT/VF in 10 of 13 hearts (P < .001). Preexposure to GS967 for 15 minutes before aconitine injection prevented initiation of VT/VF in 5 of 8 additional hearts (P < .02). VF reoccurred within 10 minutes on washout of GS967. Microelectrode recordings (N = 7) showed that VT/VF was initiated by EAD- and DAD-mediated triggered activity at CL of 86 ± 14 ms (NS from VT CL) that preceded the VF. GS967 shortened APD, flattened the slope of the dynamic APD restitution curve, and reduced APD dispersion from 42 ± 12 ms to 8 ± 3 ms (P < .01). H2O2 perfusion in eight fibrotic aged hearts promoted EAD-mediated focal VT/VF, which was suppressed by GS967 in five hearts (P < .02).. The selective INa-L blocker GS967 effectively suppresses and prevents aconitine and oxidative stress-induced EADs, DADs, and focal VT/VF. Suppression of EADs, DADs, and reduction of APD dispersion make GS967 a potentially useful antiarrhythmic drug in conditions of enhanced INa-L.

Topics: Aconitine; Action Potentials; Animals; Anti-Arrhythmia Agents; Disease Models, Animal; Male; Pyridines; Rats; Rats, Inbred F344; Tachycardia, Ventricular; Triazoles; Ventricular Fibrillation

Terfenadine is a second generation histamine receptor antagonist which is widely used as a non‑sedating antihistamine to relieve allergic responses. However, terfenadine has been associated with a number of side effects on cardiac electrical activities through blocking multiple ion channels in the heart, particularly K+ channels. Previous studies have also implied that terfenadine may have a potential antiarrhythmic effect; however, the electrophysiological influence by which terfenadine exerts its antiarrhythmic action remains elusive. Based on evidence from previous studies, it was hypothesized that the antiarrhythmic effect of terfenadine may be similar to that of amiodarone. The present study aimed to examine the effect of terfenadine on the QTc interval and on experimental ventricular arrhythmia in rats by comparing with that of amiodarone. The effect of terfenadine and amiodarone on the QTc interval was evaluated by comparison of multiple electrocardiograms. Barium chloride/aconitine was intraperitoneally injected to induce ventricular arrhythmias. Normal saline was administered to control rats. In comparison with normal saline, terfenadine and amiodarone similarly dose‑dependently prolonged the QTc interval in rats. In the barium chloride/aconitine-induced ventricular arrhythmia model, terfenadine and amiodarone did not only similarly delay the onset time of arrhythmias induced by barium chloride (all P<0.05), but also increased the cumulative dosage of aconitine required to induce various arrhythmias (all P<0.05). Furthermore, the two drugs equivalently caused a significant decrease in the duration of ventricular tachycardia in comparison with the normal saline controls (all P<0.05). The present study suggested that terfenadine prolonged the QTc interval and decreased ventricular tachycardia duration. The potential protective effect of terfenadine in ventricular arrhythmia may be similar to that of amiodarone.

Topics: Aconitine; Amiodarone; Animals; Anti-Arrhythmia Agents; Barium Compounds; Chlorides; Electrocardiography; Protective Agents; Rats; Rats, Sprague-Dawley; Tachycardia, Ventricular; Terfenadine

According to some reports regarding the increase of cardiac events following sleep deprivation, our study was conducted to clarify the effects of rapid eye movement (REM) sleep deprivation on susceptibility to lethal ventricular arrhythmias in rat.. The animal groups included the control group; the sham 48 and sham 72 groups (without sleep deprivation); and the test 48 and test 72 groups, who experienced REM sleep deprivation for 48h and 72h, respectively. For induction of cardiac arrhythmia, aconitine was infused via the tail vein of the animals.. After 72h of REM sleep deprivation, the blood pressure (BP) levels and the QTc interval of the electrocardiogram (ECG) were significantly increased (P<.05 and P<.01, respectively). However, the sleep deprivation had no significant effect on the heart rate (HR), myocardial oxygen consumption index, and plasma corticosterone level. Furthermore, sleep deprivation increased the latency times of premature ventricular contraction (PVC), ventricular tachycardia (VT), and also the PVC number; however, it did not increase the number, duration, and severity of VT and ventricular fibrillation (VF).. Our findings suggest that 72h of REM sleep deprivation is associated with increased risk for hypertension and QT interval prolongation under nonstressful conditions; however, it does not increase the susceptibility to lethal ventricular arrhythmia in rat.

Topics: Aconitine; Animals; Blood Pressure; Corticosterone; Disease Models, Animal; Electrocardiography; Heart Rate; Humans; Male; Oxygen Consumption; Rats; Rats, Wistar; Risk Factors; Sleep Deprivation; Sleep, REM; Tachycardia, Ventricular; Ventricular Fibrillation; Voltage-Gated Sodium Channel Agonists

Two people out of three who accidentally ate boiled aconite leaves died in 2012. This was a typical case of aconite poisoning in Japan: Aconite (Aconitum spp.) was mistakenly collected instead of Anemone flaccida, an edible wild plant. The leaves of these plants are quite similar to each other. Chemical analyses of the aconite plant left at the scene suggested intake of a fatal amount of aconitine alkaloids by each person. The collector, who died, had missed the botanical differences between the two plants, even though he owned a wild plant guidebook. A. flaccida should be collected with its flowers in order to aid positive indentification and avoid aconite poisoning.

Topics: Aconitine; Aconitum; Adult; Aged; Chromatography, High Pressure Liquid; Fatal Outcome; Female; Heart Arrest; Humans; Male; Middle Aged; Plant Leaves; Shock, Cardiogenic; Tachycardia, Ventricular; Tandem Mass Spectrometry

Modulation of the inward rectifier K current (IK1) has profound effect on cardiac excitability and underlies new antiarrhythmic strategies. However, IK1-specific pharmacological tools, especially the selective IK1 agonists, are still lacking in the market. Zacopride, a gastrointestinal prokinetic drug, was found to be a selective IK1 channel agonist. By using the whole-cell patch clamp technique, it was found that zacopride (0.1-10 μmole/L) dose dependently enhanced the IK1 current in isolated rat cardiomyocytes, had no effects on other ion channels, transporters, or pumps. At the same dosage range, zacopride hyperpolarized the resting potential and shortened the action potential duration. When applied at the optimal dose of 1.0 μmole/L, zacopride could prevent or eliminate aconitine induced after depolarization and triggered activity in isolated cardiomyocytes. In a rat model of aconitine-induced arrhythmias both ex vivo and in vivo, zacopride (1.0 μmole/L or 25 μg/kg, respectively) treatment apparently protected the heart from ventricular tachyarrhythmias, which compares favorably with 7.5 mg/kg of lidocaine, a classical aconitine antidote. In conclusion, zacopride was found to be a selective IK1 agonist, and agonizing IK1 could prevent or eliminate aconitine-induced arrhythmias in the rat.

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Benzamides; Bridged Bicyclo Compounds, Heterocyclic; Cells, Cultured; Disease Models, Animal; Dose-Response Relationship, Drug; Electrocardiography; Guinea Pigs; Male; Membrane Potentials; Myocytes, Cardiac; Patch-Clamp Techniques; Potassium Channels, Inwardly Rectifying; Rats; Rats, Sprague-Dawley; Tachycardia, Ventricular

Many studies have shown that the relationship between alcohol consumption and most cardiovascular diseases is U-shaped, with nondrinkers and heavier drinkers having higher risks than moderate drinkers. However, the association between cardiac arrhythmias and acute alcohol consumption is not well understood. We set up several experimental arrhythmia animal models to examine the effects of acute administration of ethanol on arrhythmia. The results showed 0.4, 0.8 and 1.6 g/kg ethanol consumption obviously delayed the onset time of atrial fibrillation (AF) (P < 0.05 or P < 0.01) and increased the survival rates on acetylcholine-CaCl₂-induced AF in mice. Ethanol (0.4, 0.8 and 1.6 g/kg) consumption significantly delayed the onset time of ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA) (P < 0.01), and 0.4 and 0.8 g/kg ethanol consumption increased the survival rates on CaCl₂-induced arrhythmia in rats. Ethanol (0.4 g/kg) essentially increased the cumulative dosage of aconitine required to CA (P < 0.05), and 0.8 g/kg, 1.6 g/kg ethanol reduced the cumulative aconitine dosage to induce VT, VF and CA (P < 0.05 or P < 0.01) on aconitine-induced arrhythmia in rats. Ethanol (0.4, 0.8 and 1.6 g/kg) consumption remarkably increased the cumulative dosage of deslanoside to induce ventricualr premature contraction (P < 0.01) on deslanoside-induced arrhythmia in guinea pigs. Collectively, our results indicate that low concentrations of ethanol had anti-arrhythmic effect on experimental arrhythmia, and high concentrations of ethanol may aggravated the occurrence of experimental arrhythmia.

Topics: Acetylcholine; Aconitine; Animals; Arrhythmias, Cardiac; Atrial Fibrillation; Calcium Chloride; Cardiotonic Agents; Central Nervous System Depressants; Cholinergic Agonists; Deslanoside; Disease Models, Animal; Drug Interactions; Ethanol; Guinea Pigs; Heart Arrest; Male; Mice; Mice, Inbred ICR; Rats; Rats, Sprague-Dawley; Risk Factors; Tachycardia, Ventricular; Ventricular Fibrillation; Voltage-Gated Sodium Channel Agonists

Topics: Aconitine; Aconitum; Aged, 80 and over; Emergency Service, Hospital; Heart Arrest; Humans; Male; Tachycardia, Ventricular

The therapeutic usefulness of doxorubicin (Dox), an anthracycline antibiotic used as an anticancer agent, is limited by its cardiotoxicity. Dox-induced cardiotoxicity is mainly attributed to accumulation of reactive oxygen species and interaction of Dox with cellular iron metabolism. The present study investigated the effects of the iron chelator deferiprone (Def) against Dox-induced cardiotoxicity in rats. Dox (15 mg/kg) was injected intraperitoneally as a single dose, and Def (10 mg/kg) was administered orally for 10 days. Dox showed cardiotoxicity as evidenced by increased heart rate, elevated ST segment, prolonged QTc interval, and increased T wave amplitude. In addition, Dox enhanced aconitine cardiotoxicity by decreasing its dose, producing ventricular tachycardia. Administration of Def significantly attenuated Dox-induced electrocardiographic changes. Cardiotoxicity of Dox was confirmed biochemically by a significant elevation in serum creatine kinase-MB and lactate dehydrogenase activities as well as by myocardial malondialdehyde and reduced glutathione contents. Moreover, Dox caused a significant decrease in myocardial superoxide dismutase activity. Administration of Def significantly attenuated the biochemical changes. These results suggest that Def might be a potential cardioprotective agent against Dox-induced cardiotoxicity.

Topics: Aconitine; Animals; Antibiotics, Antineoplastic; Creatine Kinase, MB Form; Deferiprone; Doxorubicin; Drug Interactions; Electrocardiography; Glutathione; Heart; Heart Diseases; Heart Rate; Iron; Iron Chelating Agents; L-Lactate Dehydrogenase; Male; Malondialdehyde; Myocardium; Pyridones; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Superoxide Dismutase; Tachycardia, Ventricular

Aconite poisoning was examined in five patients (four males and one female) aged 49 to 78 years old. The electrocardiogram findings were as follows: ventricular tachycardia and ventricular fibrillation in case 1, premature ventricular contraction and accelerated idioventricular rhythm in case 2, AIVR in case 3, and nonsustained ventricular tachycardia in cases 4 and 5. The patient in case 1 was given percutaneous cardiopulmonary support because of unstable hemodynamics, whereas the other patients were treated with fluid replacement and antiarrhythmic agents. The main aconitine alkaloid in each patient had a half-life that ranged from 5.8 to 15.4 h over the five cases, and other detected alkaloids had half-lives similar to the half-life of the main alkaloid in each case. The half-life of the main alkaloid in case 1 was about twice as long as the half-lives in the other cases, and high values for the area under the blood concentration-time curve and the mean residence time were only observed in case 1. These results suggest that alkaloid toxicokinetics parameters may reflect the severity of toxic symptoms in aconite poisoning.

Topics: Accelerated Idioventricular Rhythm; Aconitine; Aconitum; Aged; Area Under Curve; Arrhythmias, Cardiac; Biotransformation; Chromatography, High Pressure Liquid; Drugs, Chinese Herbal; Electrocardiography; Female; Half-Life; Humans; Male; Middle Aged; Severity of Illness Index; Tachycardia, Ventricular; Tandem Mass Spectrometry; Toxicology; Ventricular Fibrillation; Ventricular Premature Complexes

We define the potential sources, clinical manifestations, and treatment of aconitine poisoning.. The database of the National Poison Center in Taiwan was retrospectively searched for the diagnosis of aconitine poisoning for 1990 to 1999. The reasons for taking the aconite roots, the clinical features, management, and possible predisposing factors were noted.. A total of 17 cases occurred and consisted of 9 men and 8 women aged 30 to 70 years. Thirteen patients ingested aconite roots as treatment for rheumatism and wounds. Two patients volunteered to test the effects of aconite roots in a drug study. Two patients accidentally ingested the aconite roots. After a latent period of 10 to 90 minutes, patients developed a combination of neurologic (n=17), cardiovascular (n=14), gastrointestinal (n=9), and other (n=5) features typical of aconitine poisoning. Four patients developed ventricular tachycardia. All patients received supportive treatment. Patients with ventricular tachycardia were also treated with charcoal hemoperfusion. All patients made a complete recovery.. Life-threatening ventricular tachycardia can occur after the consumption of aconite roots. The risk is higher with inadequately processed aconite roots, large doses, or tincture preparations. With increasing popularity of herbal medicines, herb-induced aconitine poisoning may also be seen in Western countries.

Topics: Aconitine; Aconitum; Adult; Aged; Bradycardia; Electrocardiography; Female; Humans; Male; Middle Aged; Phytotherapy; Retrospective Studies; Rheumatic Diseases; Tachycardia, Ventricular; Ventricular Premature Complexes; Wounds and Injuries

The present study was designed to test a hypothesis that nonfatal ventricular arrhythmia such as ventricular premature beats (VPB) is a contributing factor in the elevation of blood pressure variability (BPV).. Blood pressure (BP) and electrocardiogram were continuously recorded. The relation between VPB and BPV was observed under conscious state in chronic myocardial infarction (MI) rats one month after ligation of the left coronary artery, and further verified under anesthetized state in rat model of ventricular arrhythmia produced by acute intravenous infusion of aconitine.. MI rats exhibited a big difference in the count and pattern of VPB, and were divided into no VPB, occasional VPB, and frequent VPB groups. Among the three groups, there were no differences in BP, heart period (HP), and MI size. However, BPV was markedly higher in frequent not occasional VPB rats, and HP variability (HPV) was larger in both frequent and occasional VPB rats, when compared with no VPB rats. In the whole population of MI rats, BPV was positively correlated with VPB and HPV, not with BP, HP and MI size. Infusion of aconitine had no effect on BP, HP, BPV, and HPV during the period without VPB. Frequent VPB after several minutes of aconitine infusion induced significant increase in BPV and HPV with no change in BP and HP. BPV was also positively correlated with VPB and HPV, not with BP and HP. Hemodynamics in aconitine-evoked ventricular tachycardia was characterized as lower BP, higher BPV, and higher HPV.. High BPV can be caused by frequent not occasional VPB in rats.

Topics: Aconitine; Animals; Blood Pressure; Heart Rate; Hypertension; Male; Myocardial Infarction; Myocardium; Rats; Rats, Sprague-Dawley; Tachycardia, Ventricular; Ventricular Premature Complexes

The focal source hypothesis of ventricular fibrillation (VF) posits that rapid activation from a focal source, rather than action potential duration (APD) restitution properties, is responsible for the maintenance of VF. We injected aconitine (100 microg) into normal isolated perfused swine right ventricles (RVs) stained with 4-[beta-[2-(di-n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) for optical mapping studies. Within 97 +/- 163 s, aconitine induced ventricular tachycardia (VT) with a mean cycle length 268 +/- 37 ms, which accelerated before converting to VF. Drugs that flatten the APD restitution slope, including diacetyl monoxime (10-20 mM, n = 6), bretylium (10-20 microg/ml, n = 3), and verapamil (2-4 microg/ml, n = 3), reversibly converted VF to VT in all cases. In two RVs, VF persisted despite of the excision of the aconitine site. Simulations in two-dimensional cardiac tissue showed that once VF was initiated, it remained sustained even after the "aconitine" site was eliminated. In this model of focal source VF, the VT-to-VF transition occurred due to a wave break outside the aconitine site, and drugs that flattened the APD restitution slope converted VF to VT despite continuous activation from aconitine site.

Topics: Aconitine; Action Potentials; Animals; Anti-Arrhythmia Agents; Bretylium Compounds; Computer Simulation; Diacetyl; Electrocardiography; Female; Male; Swine; Tachycardia, Ventricular; Ventricular Fibrillation; Verapamil

"Torikabuto" is a kind of plant which contains deadly poison. Its ingredient is aconitine alkaloids. We report a case of aconitine poisoning with fatal arrhythmia and acute pulmonary edema who was saved with cardio pulmonary bypass. A 41-year-old male ate to mistake "Torikabuto" for wild plant. He developed symptoms of dysarthria and admitted to our hospital. He developed ventricular tachycardia and fibrillation soon after his admission. Then he developed cardiogenic shock. He was resuscitated and supported with a percutaneous cardio pulmonary bypass. Ventricular tachycardia disappeared 24 hours after admittion. About 1 week later, cardio pulmonary bypass was terminated and about 3 months later, he discharged from our hospital.

Topics: Aconitine; Acute Disease; Adult; Cardiopulmonary Bypass; Humans; Male; Plant Poisoning; Plants, Toxic; Pulmonary Edema; Tachycardia, Ventricular; Treatment Outcome

With the increasing trend of cross mixing of populations, aconitine induced poisoning and its related arrhythmias may be more frequently encountered worldwide. However, the clinical experience is often too limited to draw any conclusion on the optimal treatment for tachycardia induced by aconitine intoxication. The clinical presentation, serial electrocardiographic changes, and responses to antiarrhythmic agents are reported in a patient with aconitine induced life threatening ventricular tachyarrhythmia. Amiodarone was effective in suppressing polymorphic ventricular tachycardia, which might provide an example of successful pharmacological intervention in aconitine induced ventricular tachyarrhythmia.

Topics: Aconitine; Adjuvants, Immunologic; Amiodarone; Anti-Arrhythmia Agents; Electrocardiography; Humans; Male; Middle Aged; Tachycardia, Ventricular

To determine the effect of verapamil in ventricular tachycardias, we performed an experimental and clinical study. Experimental ventricular tachycardias (VT) were produced in dog hearts with minute aconitine crystals introduced into the periphery of a left ventricular area, damaged by intramural injection of 1.0-1.5 ml phenol. The response of these tachycardias to 0.2 mg/kg verapamil was analyzed. Verapamil was infused into the superior vena cava over 15-20 min. Leads II, aVL, intraventricular right and left unipolar records, as well as one of the superior vena cava, were registered under control conditions, in the presence of VT, and after application of verapamil. Recordings were obtained at constant intervals, waiting for the recovery of sinus rhythm (SR) and the posterior reappearance of tachycardia. Experiments were performed for 6 to 8 h under continuous infusion of Hartmann's solution. Throughout these periods, variations in systemic systolic pressure were recorded. From 75 animals submitted to this treatment, 30 (40%) recovered transiently the SR, whereas the drug exerted no antiarrhythmic effect in 19 (25%), and arterial systolic pressure fell importantly in 10 (13%) animals. In two more groups, of 15 dogs each, the VT response to verapamil was compared with the response to lidocaine and flecainide. Endovenous verapamil (5-10 mg) was administered to 10 patients, coursing with VT and having a structurally normal heart, after this arrhythmia was induced by electrical stimulation. The response to verapamil was satisfactory in nine patients (90%), in which VT originated in the septal and apical regions of the left ventricle. Verapamil seems to be effective in experimental and clinical ventricular tachycardias related to calcium-dependent potentials, in which the sustaining mechanism could either be triggered activity or reentry.

Topics: Aconitine; Adult; Animals; Anti-Arrhythmia Agents; Cardiac Pacing, Artificial; Dogs; Electrocardiography; Flecainide; Humans; Lidocaine; Tachycardia, Ventricular; Verapamil

The effect of injecting ethanol directly into the myocardium to control aconitine-induced ventricular tachycardia (VT) was evaluated in anesthetized dogs. In 17 dogs, VT was induced by injecting aconitine (1.0 microgram, median dose) directly into the epicardium. After inducing persistent VT for up to 3 min, 0.6 ml (median volume) of 96% ethanol was injected into the same epicardial region. Regular sinus rhythm reappeared in 15 dogs with no change in systolic blood pressure; the other 2 dogs died of ventricular fibrillation (VF). In another 13 dogs, VT was induced by injecting aconitine directly into the endocardium using a Variocath needle catheter. After persistent VT for up to 3 min, a regular sinus rhythm was restored in 7 dogs by injecting 2.0 ml (median volume) of 96% ethanol; the remaining 6 dogs died of VF. Histology showed no transmural necrosis and the subendocardial necrotic areas were essentially the same in the dogs that recovered from VT as in those that died. There was no statistically significant relationship between doses of ethanol and VT duration. These preliminary results suggest that the injection of ethanol into the myocardium may efficiently terminate VT when other techniques fail.

Topics: Aconitine; Animals; Dogs; Electrocardiography, Ambulatory; Endocardium; Ethanol; Female; Injections; Male; Myocardium; Necrosis; Tachycardia, Ventricular

We examined the effects of Mg2+ on aconitine-induced polymorphic ventricular tachycardias (PVT) in excised rabbit hearts under Langendorff perfusion and in Purkinje-muscle preparations. Local electrograms using bipolar electrodes and transmembrane potentials with the microelectrode technique were recorded from Langendorff hearts and Purkinje-muscle preparations, respectively. In Langendorff preparations, intracoronary application of 0.1 microM aconitine induced PVT 28.8 +/- 3.4 min after development of regular monomorphic ventricular tachycardias (MVT) in all 18 preparations. Application of 5 and 10 mM Mg2+ restored aconitine-induced PVT to sinus rhythm after 26.8 +/- 3.4 min (n = 9), but < 3 mM Mg2+ was not effective in restoring of sinus rhythm. Increased Mg2+ concentrations < or = 5 mM in the coronary perfusate prevented development of PVT by aconitine. Intracoronary application of 10 microM tetrodotoxin (TTX) also restored aconitine-induced PVT to sinus rhythm after 3.2 +/- 0.8 min (n = 4). Although applications of 50 microM lidocaine, 10 microM flecainide, or 1 microM verapamil could change PVT to MVT, they were not effective in restoring sinus rhythm. In Purkinje-muscle preparations, spontaneous action potentials (AP) from slow diastolic depolarization appeared after aconitine at the maximum diastolic potential of -75.0 +/- 3.7 mV in Purkinje fibers and were conducted to ventricular muscles (n = 5). Spontaneous activity gradually increased in rate and then developed triggered activity arising from early after depolarization (EAD). EAD induced by aconitine always appeared first in Purkinje fibers and later in muscle fibers. Once triggered activities started from EAD, rate, rhythm and amplitudes of APs became fast and variable.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aconitine; Animals; Anti-Arrhythmia Agents; Electrophysiology; Heart; Heart Ventricles; In Vitro Techniques; Magnesium; Microelectrodes; Purkinje Fibers; Rabbits; Tachycardia, Ventricular; Tetrodotoxin

The antiarrhythmic effect of Jiawei Zhigancao Tang injection (JZTI) was studied in experimental arrhythmia induced by aconitine or by CaCl2 in anesthetized rats. The prophylactic dose of JZTI (5g/kg, i.v.) reduced the incidence rate of premature ventricular complexes, ventricular tachycardia (P < 0.01), delayed the onset time of arrhythmia induced by CaCl2 (P < 0.01), and the recovery time of sinus rhythm occurred earlier than that of control group (P < 0.01). The therapeutic dose of JZTI (10g/kg, i.v.) raised the rate of aconitine-induced arrhythmia to sinus rhythm conversion (P < 0.05). The results showed that JZTI could significantly antagonize arrhythmia induced by aconitine or by Cacl2 in rats.

Topics: Aconitine; Animals; Arrhythmias, Cardiac; Calcium Chloride; Drugs, Chinese Herbal; Rats; Tachycardia, Ventricular

Topics: Aconitine; Arrhythmias, Cardiac; Cardiovascular Diseases; Humans; Phenethylamines; Procainamide; Tachycardia, Ventricular