piperidines and Heart-Arrest

To compare two protocols for sedation and analgesia during therapeutic hypothermia: midazolam and fentanyl versus propofol and remifentanil. The primary outcome was the time from discontinuation of infusions to extubation or decision not to extubate (offset time). Secondary outcomes were blood pressure, heart rate, use of vasopressors and inotropic drugs, pneumonia and neurological outcome.. This was an open, randomised, controlled trial on 59 patients treated with therapeutic hypothermia (33-34 °C for 24 h) after cardiac arrest in two Norwegian university hospitals between April 2008 and May 2009. The intervention was random allocation to sedation and analgesia with propofol/remifentanil or midazolam/fentanyl.. Twenty-nine patients received propofol and remifentanil, and 30 midazolam and fentanyl. Baseline characteristics were similar. Sedation and analgesia were stopped in 35 patients, and extubation was performed in 17 of these. Sedation had to be continued for 24 patients. Time to offset was significantly lower in patients given propofol and remifentanil [mean (95 % confidence intervals) 13.2 (2.3-24) vs. 36.8 (28.5-45.1) h, respectively, p < 0.001]. Patients given propofol and remifentanil needed norepinephrine infusions twice as often (23 vs. 12 patients, p = 0.003). Incidence of pneumonia and 3-month neurological outcome were similar in the two groups.. Time to offset was significantly shorter in patients treated with propofol and remifentanil. However, the clinical course in 40 % of patients prevented discontinuation of sedation and potential benefits from a faster recovery. The propofol and remifentanil group required norepinephrine twice as often, but both protocols were tolerated in most patients.

Topics: Aged; Anesthetics, Intravenous; Deep Sedation; Drug Therapy, Combination; Female; Fentanyl; Heart Arrest; Humans; Hypothermia, Induced; Male; Midazolam; Middle Aged; Norway; Piperidines; Propofol; Remifentanil

To establish the maximum tolerated dose of lonafarnib, a novel farnesyltransferase inhibitor, in combination with paclitaxel in patients with solid tumors and to characterize the safety, tolerability, dose-limiting toxicity, and pharmacokinetics of this combination regimen.. In a Phase I trial, lonafarnib was administered p.o., twice daily (b.i.d.) on continuously scheduled doses of 100 mg, 125 mg, and 150 mg in combination with i.v. paclitaxel at doses of 135 mg/m(2) or 175 mg/m(2) administered over 3 h on day 8 of every 21-day cycle. Plasma paclitaxel and lonafarnib concentrations were collected at selected time points from each patient.. Twenty-four patients were enrolled; 21 patients were evaluable. The principal grade 3/4 toxicity was diarrhea (5 of 21 patients), which was most likely due to lonafarnib. dose-limiting toxicities included grade 3 hyperbilirubinemia at dose level 3 (100 mg b.i.d. lonafarnib and 175 mg/m(2) paclitaxel); grade 4 diarrhea and grade 3 peripheral neuropathy at dose level 3A (125 mg b.i.d. lonafarnib and 175 mg/m(2) paclitaxel); and grade 4 neutropenia with fever and grade 4 diarrhea at level 4 (150 mg b.i.d. lonafarnib and 175 mg/m(2) paclitaxel). The maximum tolerated dose established by the continual reassessment method was lonafarnib 100 mg b.i.d. and paclitaxel 175 mg/m(2). Paclitaxel appeared to have no effect on the pharmacokinetics of lonafarnib. The median duration of therapy was eight cycles, including seven cycles with paclitaxel. Six of 15 previously treated patients had a durable partial response, including 3 patients who had previous taxane therapy. Notably, two of five patients with taxane-resistant metastatic non-small cell lung cancer had partial responses.. When combined with paclitaxel, the recommended dose of lonafarnib for Phase II trials is 100 mg p.o. twice daily with 175 mg/m(2) of paclitaxel i.v. every 3 weeks. Additional studies of lonafarnib in combination regimens appear warranted, particularly in patients with non-small cell lung cancer.

Topics: Adult; Aged; Alkyl and Aryl Transferases; Anemia; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Dose-Response Relationship, Drug; Farnesyltranstransferase; Fatigue; Female; Heart Arrest; Humans; Leukopenia; Male; Middle Aged; Neoplasms; Neutropenia; Paclitaxel; Piperidines; Pyridines; Treatment Outcome

Cardiac arrest (CA) is the most common cause of acute neurologic insult in children. Many survivors have significant neurocognitive deficits at 1 year of recovery. Epoxyeicosatrienoic acids (EETs) are multifunctional endogenous lipid signaling molecules that are involved in brain pathobiology and may be therapeutically relevant. However, EETs are rapidly metabolized to less active dihydroxyeicosatrienoic acids by soluble epoxide hydrolase (sEH), limiting their bioavailability. We hypothesized that sEH inhibition would improve outcomes after CA in an infant swine model. Male piglets (3-4 kg, 2 weeks old) underwent hypoxic-asphyxic CA. After resuscitation, they were randomized to intravenous treatment with an sEH inhibitor (TPPU, 1 mg/kg; n = 8) or vehicle (10% poly(ethylene glycol); n = 9) administered at 30 min and 24 h after return of spontaneous circulation. Two sham-operated groups received either TPPU (n = 9) or vehicle (n = 8). Neurons were counted in hematoxylin- and eosin-stained sections from putamen and motor cortex in 4-day survivors.. Piglets in the CA + vehicle groups had fewer neurons than sham animals in both putamen and motor cortex. However, the number of neurons after CA did not differ between vehicle- and TPPU-treated groups in either anatomic area. Further, 20% of putamen neurons in the Sham + TPPU group had abnormal morphology, with cell body attrition and nuclear condensation. TPPU treatment also did not reduce neurologic deficits.. Treatment with an sEH inhibitor at 30 min and 24 h after resuscitation from asphyxic CA does not protect neurons or improve acute neurologic outcomes in piglets.

Topics: Animals; Asphyxia; Cell Death; Endoplasmic Reticulum Stress; Enzyme Inhibitors; Epoxide Hydrolases; Heart Arrest; Male; Motor Cortex; Nervous System Diseases; Neurons; Phenylurea Compounds; Piperidines; Putamen; Swine; Treatment Outcome

Motor deficits are present in cardiac arrest survivors and injury to cerebellar Purkinje cells (PCs) likely contribute to impairments in motor coordination and post-hypoxic myoclonus. N-Methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity is a well-established mechanism of cell death in several brain regions, but the role of NMDA receptors in PC injury remains understudied. Emerging data in cortical and hippocampal neurons indicate that the GluN2A-containing NMDA receptors signal to improve cell survival and GluN2B-containing receptors contribute to neuronal injury. This study compared neuronal injury in the hippocampal CA1 region to that in PCs and investigated the role of NMDA receptors in PC injury in our mouse model of cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Analysis of cell density demonstrated a 24% loss of PCs within 24 h after 8 min CA/CPR and injury stabilized to 33% by 7 days. The subunit promiscuous NMDA receptor antagonist MK-801 protected both CA1 neurons and PCs from ischemic injury following CA/CPR, demonstrating a role for NMDA receptor activation in injury to both brain regions. In contrast, the GluN2B antagonist, Co 101244, had no effect on PC loss while protecting against injury in the CA1 region. These data indicate that ischemic injury to cerebellar PCs progresses via different cell death mechanisms compared to hippocampal CA1 neurons.

Topics: Animals; Brain Ischemia; CA1 Region, Hippocampal; Calbindins; Cardiopulmonary Resuscitation; Cell Death; Disease Models, Animal; Dizocilpine Maleate; Excitatory Amino Acid Antagonists; Heart Arrest; Male; Mice, Inbred C57BL; Nerve Tissue Proteins; Neurons; Neuroprotective Agents; Piperidines; Purkinje Cells; Receptors, N-Methyl-D-Aspartate; Tissue Culture Techniques

The clearance of sedatives and analgesics may be reduced by therapeutic hypothermia. However, little is known about the concentrations of such drugs during rewarming. The aim of this study was to describe the serum concentrations of sedatives and analgesics during rewarming from therapeutic hypothermia.. Blood samples were collected for quantification of drug concentrations in 22 patients given analgesia/sedation with either remifentanil/propofol or fentanyl/midazolam during rewarming from therapeutic hypothermia (33-34°C) after cardiac arrest. Samples for were drawn before (-2 h) and during rewarming (0-8 h). Linear mixed effects models were used to describe serum concentrations and adjust for rates of infusion during rewarming from therapeutic hypothermia.. Subjects with samples analyzed were remifentanil (n = 8), propofol (n = 14), fentanyl (n = 8), and midazolam (n = 8). Age, body mass index, and simplified acute physiology score II [mean (standard deviation)] were 64 (14.2) years, 27.3 (3.7) kg/m(2), and 69 (13.2), respectively. While the concentration of fentanyl was not significantly affected by temperature, concentrations of remifentanil, propofol, and midazolam decreased with core temperature by 16%, 12%, and 11% (mean values) from 33°C to 37°C after adjusting for rates of infusion, respectively.. Concentrations of remifentanil, propofol, and midazolam decreased during rewarming from therapeutic hypothermia when adjusting for rates of infusion. No changes were demonstrated for fentanyl.

Topics: Aged; Aged, 80 and over; Analgesics; Body Mass Index; Body Temperature; Combined Modality Therapy; Female; Fentanyl; Heart Arrest; Humans; Hypnotics and Sedatives; Hypothermia, Induced; Male; Metabolic Clearance Rate; Midazolam; Middle Aged; Models, Biological; Piperidines; Propofol; Randomized Controlled Trials as Topic; Remifentanil; Rewarming

We report a patient with concealed sick sinus syndrome who developed intraoperative bradycardia and asystole. An 81-year-old man was scheduled to undergo total gastrectomy under general and epidural anesthesia. There was no history of syncope, and preoperative 12-lead ECG showed normal sinus rhythm. Anesthesia was induced with propofol and remifentanil, maintained with sevoflurane, remifentanil and thoracic epidural infusion of lidocaine, fentanyl and levobupivacaine. Bradycardia was detected on ECG 110 minutes after the start of surgery. Intravenous atropine (0.5 mg, repeated up to a total dose of 1.5 mg) was ineffective in restoring a normal heart rhythm. Ten minutes later, the ECG changed to asystole lasting for about 15 seconds. Regular chest compression and intravenous administration of dopamine (5 microg x kg(-1) x min(-1)) resulted in successful recovery of sinus rhythm. Postoperative ECG showed sinus rhythm. The final diagnosis by a cardiologist was concealed sick sinus syndrome. Many anesthetic agents have some effects on the cardiac conduction system. Remifentanil may have played a role in the development of asystole in this patient. The existence of concealed sick sinus syndrome should be kept in mind even in patients who show no clinical abnormalities on preoperative assessment.

Topics: Aged, 80 and over; Anesthesia, Epidural; Anesthesia, General; Atropine; Bradycardia; Dopamine; Electrocardiography; Gastrectomy; Heart Arrest; Humans; Infusions, Intravenous; Intraoperative Complications; Male; Piperidines; Remifentanil; Sick Sinus Syndrome; Stomach Neoplasms

Topics: Analgesia, Obstetrical; Analgesia, Patient-Controlled; Analgesics, Opioid; Female; Heart Arrest; Humans; Labor, Induced; Piperidines; Pregnancy

Topics: Analgesia, Obstetrical; Analgesics, Opioid; Female; Heart Arrest; Humans; Piperidines; Pregnancy

Topics: Analgesia, Obstetrical; Analgesics, Opioid; Female; Heart Arrest; Humans; Piperidines; Pregnancy

Topics: Analgesia, Obstetrical; Analgesia, Patient-Controlled; Analgesics, Opioid; Female; Fetal Heart; Heart Arrest; Humans; Labor Pain; Labor, Induced; Maternal-Fetal Exchange; Piperidines; Pregnancy

This case report describes the management of a patient, diagnosed with an intrauterine death at 31 weeks' gestation, who suffered a cardiorespiratory arrest during her induced labour while using a remifentanil PCA. She made a full recovery from resuscitation which included a peri-mortem caesarean section.

Topics: Adult; Analgesia, Obstetrical; Analgesia, Patient-Controlled; Analgesics, Opioid; Cardiopulmonary Resuscitation; Cesarean Section; Codeine; Female; Fetal Death; Heart Arrest; Heroin; Humans; Labor, Induced; Piperidines; Pregnancy; Remifentanil; Young Adult

Topics: Analgesia, Obstetrical; Analgesia, Patient-Controlled; Analgesics, Opioid; Female; Heart Arrest; Humans; Infusions, Intravenous; Piperidines; Pregnancy; Remifentanil; Treatment Outcome; United Kingdom

Topics: Analgesia, Obstetrical; Analgesia, Patient-Controlled; Analgesics, Opioid; Female; Heart Arrest; Humans; Medical Audit; Midwifery; Piperidines; Pregnancy; Remifentanil

Moderate therapeutic hypothermia is often used in aneurysm surgery and is therefore a technique anesthesiologists are familiar with. We report the case of a patient who had entered into a coma after cardiac arrest in the postanesthetic recovery unit during central venous catheterization; the patient required 35 minutes of advanced cardiopulmonary resuscitation before heart rhythm and tissue perfusion were restored. The protocol for treating post-cardiac arrest syndrome included therapeutic hypothermia, which was maintained for 12 hours. The patient was extubated after 2 days, with no neurologic deficit. Post-cardiac arrest syndrome is associated with multiple biochemical reactions which are attenuated by hypothermia. Currently available evidence does not allow definitive recommendations regarding the different techniques for inducing therapeutic hypothermia, the ideal temperature to maintain, the duration, or the rewarming process. Further studies are required.

Topics: Aged; Anesthesia, General; Anesthetics, Intravenous; Decision Trees; Heart Arrest; Humans; Hypothermia, Induced; Male; Piperidines; Remifentanil; Syndrome

Three patients undergoing surgery for cerebello-pontine angle meningioma suffered transient episodes of asystole. All patients exhibited return to the previous heart rate with cessation of surgical manipulations and administration of anticholinergic agents. These reactions were apparently elicited by activation of the trigeminocardiac reflex (TCR) by direct stimulation of the trigeminal nerve or branches in the dura mater or cerebellar tentorium. Remifentanil was used in all three cases as an anesthetic agent, so may be a cause of the TCR. The possibility of activation of the TCR should be considered during surgical manipulation around the trigeminal nerve or the distribution of the trigeminal nerve branches. Transient bradycardia, hypotension, or asystole can occur regardless of whether there is pressure on the brainstem during posterior fossa meningioma surgery.

Topics: Adult; Anesthetics, Intravenous; Cerebellopontine Angle; Dura Mater; Female; Heart Arrest; Humans; Infratentorial Neoplasms; Intraoperative Complications; Meningioma; Middle Aged; Neurosurgical Procedures; Piperidines; Reflex; Remifentanil; Trigeminal Nerve

The Tako-Tsubo syndrome (or transient left ventricular apical balloning) is a new clinical entity, very similar to acute myocardial infarction, but different by its excellent short-term prognosis. It has been reported after a physical or an emotional stress, and it is diagnosed by a coronary angiogram and a left ventriculography. We report here a case of Tako-Tsubo syndrome related to an anaphylactic shock caused by succinylcholine during general anaesthesia of a female patient, wearing an unadjustable gastric band.

Topics: Anaphylaxis; Anesthesia, General; Anesthesia, Intravenous; Diabetes Mellitus, Type 2; Female; Gastroplasty; Heart Arrest; Humans; Intraoperative Complications; Laparoscopy; Middle Aged; Neuromuscular Depolarizing Agents; Obesity; Pelvic Floor; Piperidines; Postoperative Complications; Propofol; Pulmonary Edema; Remifentanil; Succinylcholine; Takotsubo Cardiomyopathy; Ventricular Fibrillation

A 45-year-old man was scheduled for laparoscopic cholecystectomy. He had hypertension controlled with beta-adrenergic, calcium channel and angiotensin II receptor blocking agents. Because he had complications of symptomatic cervical spondylosis and sleep apnea syndrome, we performed awake fiberoptic intubation with remifentanil at a dose of 0.05 microg x kg(-1) min(-1). After intubation and following administration of propofol and vecuronium, ECG unexpectedly changed to asystole. We administered atropine 1.5 mg and performed chest compressions, which successfully restored sinus rhythm within 10 seconds. However, no cardiac disease was detected by a cardiologist. The operation was scheduled a week later again. Anti-hypertensive agents were discontinued. A temporary pacing wire was inserted before surgery, and atropine 0.5 mg was administered before anesthetic induction with remifentanil. No cardiac event was noticed through the perioperative period. We suggest that even a low dose of remifentanil may cause asystole in patients taking beta-adrenergic and calcium channel blocking agents, and preemptive administration of atropine may be effective.

Topics: Anesthetics, Intravenous; Atropine; Cholecystectomy, Laparoscopic; Heart Arrest; Humans; Male; Middle Aged; Piperidines; Remifentanil

Topics: Bendroflumethiazide; Butyrophenones; Cisapride; Diuretics; Electrocardiography; Female; Furosemide; Gastrointestinal Agents; Heart Arrest; Histamine H1 Antagonists; Humans; Middle Aged; Piperidines; Potassium Chloride; Sodium Chloride Symporter Inhibitors; Torsades de Pointes

Ifenprodil, a NMDA receptor polyamine site antagonist, reduces experimental cardiac arrest (CA)-elicited brain edema, which is associated with an up-regulation of aquaporin 4 (AQP4), a brain water-selective channel. However, the interacting roles of NMDA receptors and AQP4 in CA-elicited brain edema are unknown. The objective of this study was to test our hypothesis that ifenprodil treatment is associated with a down-regulation of brain AQP4.. Twenty-five rats were assigned to normal controls (group 1, n = 6) or subjected to eight minutes of asphyxial CA treated with placebo (group 2, n = 9) or ifenprodil (group 3, n = 10). Ifenprodil at 10 mg/kg or normal saline of equal volume was given intraperitoneally, 5 minutes before CA. The density of AQP4 protein and actin bands was scanned and expressed as the ratios of the optical density of AQP4 relative to that of actin. The ANOVA analysis was used to compare the group differences.. The ratios of the optical density of AQP4 to that of actin were 0.88 +/- 0.06 in group 1, 1.11 +/- 0.08 in group 2 (p < 0.05 vs. group 1), and 0.78 +/- 0.04 in group 3 (p < 0.01 vs. group 2; NS vs. group 1).. Ifenprodil given before CA is associated with a downregulation of brain AQP4 in rats.

Topics: Animals; Brain; Brain Edema; Down-Regulation; Heart Arrest; Phosphorylation; Piperidines; Rats; Rats, Sprague-Dawley; Treatment Outcome; Vasodilator Agents

Topics: Adult; Anesthetics, Intravenous; Electric Stimulation Therapy; Epilepsy; Female; Heart Arrest; Humans; Intraoperative Complications; Piperidines; Remifentanil; Vagus Nerve

A 47-year-old woman with Cushing's syndrome suffered a severe anaphylactic reaction on induction of anaesthesia, resulting in circulatory arrest. A spontaneous cardiac output appeared after 25 minutes of chest compression and she regained consciousness three hours later, with no neurological deficit. A Bispectral Index monitor demonstrated values greater than 40 throughout the whole period of resuscitation. Possible implications for this observation are discussed.

Topics: Anaphylaxis; Cardiopulmonary Resuscitation; Electroencephalography; Female; Heart Arrest; Humans; Middle Aged; Monitoring, Intraoperative; Piperidines; Propofol; Remifentanil; Vecuronium Bromide

Topics: Aged; Anesthetics, Combined; Anesthetics, Inhalation; Anesthetics, Intravenous; Heart Arrest; Humans; Male; Methyl Ethers; Piperidines; Remifentanil; Sevoflurane

Topics: Animals; Endothelin-1; Graft Survival; Heart Arrest; Liver Transplantation; Peptides, Cyclic; Piperidines; Platelet Activating Factor; Pyridinium Compounds; Swine; Tacrolimus; Time Factors; Tissue and Organ Harvesting; Transplantation, Homologous

Topics: Anesthetics, Intravenous; Female; Heart Arrest; Humans; Laryngoscopy; Middle Aged; Piperidines; Propofol

Topics: Adenosine; Allopurinol; Animals; Aspartate Aminotransferases; Cold Temperature; Endothelin Receptor Antagonists; Glutathione; Graft Survival; Heart Arrest; Hyaluronic Acid; Insulin; L-Lactate Dehydrogenase; Liver; Liver Transplantation; Organ Preservation; Organ Preservation Solutions; Peptides, Cyclic; Perfusion; Piperidines; Platelet Activating Factor; Pyridinium Compounds; Raffinose; Swine; Transplantation, Homologous

Topics: Aged; Analgesics, Opioid; Anesthetics, Inhalation; Heart Arrest; Humans; Male; Methyl Ethers; Piperidines; Remifentanil; Sevoflurane

Anoxic depolarization (AD) and failure of ion homeostasis play an important role in ischemia-induced neuronal injury. In the present study, different drugs with known ion-channel-modulating properties were examined for their ability to interfere with cardiac-arrest-elicited AD and with the changes in the extracellular ion activity in rat brain. Our results indicate that only drugs primarily blocking membrane Na+ permeability (NBQX, R56865, and flunarizine) delayed the occurrence of AD, while compounds affecting cellular Ca2+ load (MK-801 and nimodipine) did not influence the latency time. The ischemia-induced [Na+]e reduction was attenuated by R56865. Blockade of the ATP-sensitive K+ channels with glibenclamide reduced the [K+]e increase upon ischemia, indicating an involvement of the KATP channels in ischemia-induced K+ efflux. The KATP channel opener cromakalim did not affect the AD or the [K+]e concentration. The ischemia-induced rapid decline of extracellular calcium was attenuated by receptor-operated Ca2+ channel blockers MK-801 and NBQX, but not by the voltage-operated Ca2+ channel blocker nimodipine, R56865, and flunarizine.

Topics: Adenosine Triphosphate; Animals; Benzothiazoles; Calcium; Dizocilpine Maleate; Flunarizine; Glyburide; Heart Arrest; Hypoxia; Ion Channels; Male; Nimodipine; Piperidines; Potassium; Potassium Channels; Quinoxalines; Rats; Rats, Wistar; Sodium; Thiazoles

Thirty-eight patients with prior history of cardiac arrest underwent programmed electrical stimulation (PES) studies and serial drug testing. Lorcainide was tested acutely in all 38 patients and prevented ventricular tachycardia (VT) or ventricular fibrillation (VF) induction in 14 patients and failed in 24 (efficacy rate 37%). Procainamide had failed clinically (cardiac arrest or breakthrough VT) in 16 patients, seven patients had previously severe adverse side effects, and thus only 15 were tested on procainamide at PES testing with seven protected. Following initial studies, 14 patients were started on lorcainide oral therapy and 24 on other therapy determined effective at PES testing (N-acetylprocainamide-two, flecainide-nine, bethanidine-three, slow-release procainamide hydrochloride-three, quinidine-two, cibenzoline-one, amiodarone-four). After 29 +/- 7 months follow-up, three are alive on lorcainide therapy, five discontinued therapy due to side effects; six died--three sudden deaths (33%) and two cardiac deaths (both myocardial infarctions). Twenty out of 24 patients are alive who were started on PES predicted effective therapy other than lorcainide; four died--three sudden deaths (13%) and one cardiac nonsudden death. Antiarrhythmic therapy guided by PES studies gives overall encouraging results in a cardiac arrest group of patients. Lorcainide, however, is not tolerated well and affords less protection against a sudden death recurrence than is noted in a population on other antiarrhythmic therapy predicted effective at PES testing.

Topics: Arrhythmias, Cardiac; Benzeneacetamides; Blood Pressure; Cardiac Pacing, Artificial; Electrocardiography; Female; Heart Arrest; Humans; Male; Middle Aged; Piperidines; Procainamide; Recurrence

Twenty-six patients (19 men and 7 women) with symptomatic ventricular tachycardia (VT) were studied using invasive and noninvasive techniques to induce VT. Of the study population, 12% had syncope and VT on Holter monitoring, 30% had cardiac arrest and 58% had symptomatic VT. All patients had antiarrhythmic agents stopped 5 half-lives before evaluation and then had autonomic profile (upright tilt, cold pressor test, exercise testing and hand grip) as well as programmed electrical stimulation studies performed. Autonomic profile testing induced VT in 5 of 26 patients (19%) and in only 1 patient was the arrhythmia reproducibly induced. All 26 patients had VT induced on electrophysiologic testing; 9 patients had nonsustained and 17 had sustained VT. Lorcainide administered intravenously prevented VT induction in 20 of 26 patients tested, whereas procainamide was effective in 11 of 24 patients. Ten of the 13 not protected by procainamide were protected by lorcainide. Twenty patients were started on long-term lorcainide therapy and followed up for 29 +/- 3.4 months. Five patients have discontinued therapy, 2 because of breakthrough arrhythmias, 2 because of severe sleep-wake disturbances and 1 because of private physician preference. An additional 3 patients died during therapy because of myocardial infarction in 1, progressive myopathy in 1 and sudden death in 1. Sixty percent of patients started on lorcainide therapy have continued. In this patient population, noninvasive induction of VT is not a sensitive or reproducible technique in assessing antiarrhythmic therapy. Furthermore, when selected on the basis of electrophysiologic testing, lorcainide is a well-tolerated and effective antiarrhythmic agent.

Topics: Aged; Anti-Arrhythmia Agents; Benzeneacetamides; Dose-Response Relationship, Drug; Drug Evaluation; Electric Stimulation; Electrophysiology; Exercise Test; Female; Heart Arrest; Hemodynamics; Humans; Male; Middle Aged; Piperidines; Procainamide; Syncope; Tachycardia

Topics: Adult; Amides; Clopamide; Diuretics; Female; Heart Arrest; Humans; Male; Middle Aged; Nephrotic Syndrome; Piperidines

Topics: Biological Phenomena; Heart Arrest; Histamine; Histamine Antagonists; Humans; Pheniramine; Piperidines