cardiovascular-agents and Seizures

The management of severe head injuries in general and that of high intracranial pressure (ICP) in particular are among the most challenging tasks in neurocritical care. One of the difficulties still faced by clinicians is that of reducing variability among centers when implementing management protocols. The purpose of this paper is to propose a standardized protocol for the management of high ICP after severe head injury, consistent with recently published clinical practice guidelines and other clinical evidence such as that provided by the systematic reviews of the Cochrane Collaboration. Despite significant advances in neuromonitoring, deeper insight into the physiopathology of severe brain trauma and the many therapeutic options available, standardized protocols are still lacking. Recently published guidelines provide sketchy recommendations without details on how and when to apply different therapies. Consequently, great variability exists in daily clinical practice even though different centers apply the same evidence-based recommendations. In this paper we suggest a structured protocol in which each step is justified and integrated into an overall strategy for the management of severe head injuries. The most recent data from both the preliminary and definitive results of randomized clinical trials as well as from other sources are discussed. The main goal of this article is to provide neurotraumatology intensive care units with a unified protocol that can be easily modified as new evidence becomes available. This will reduce variation among centers when applying the same therapeutic measures. This goal will facilitate comparisons in outcomes among different centers and will also enable the implementation of more consistent clinical practice in centers involved in multicenter clinical trials.

Topics: Adrenal Cortex Hormones; Analgesics; Anticonvulsants; Brain Edema; Brain Injuries; Calcium Channel Blockers; Cardiovascular Agents; Case Management; Combined Modality Therapy; Craniocerebral Trauma; Critical Care; Electrophysiology; Evidence-Based Medicine; Fluid Therapy; Hemodynamics; Humans; Hypnotics and Sedatives; Intracranial Hypertension; Monitoring, Physiologic; Neuromuscular Nondepolarizing Agents; Practice Guidelines as Topic; Seizures

Electroconvulsive therapy (ECT) is often associated with acute hyperdynamic responses, and we hypothesize that diltiazem can blunt this response. We measured the effect of a 10-mg dose of diltiazem on heart rate and mean arterial pressure during ECT. Furthermore, we assessed seizure duration by using both the cuff method and two-lead electroencephalogram. We studied 18 patients with a randomized, double-blinded, placebo-controlled cross-over study design. Diltiazem significantly reduced heart rate and mean arterial pressure just after medication, and it also significantly reduced the increases in these variables after ECT, as compared with the placebo. The use of diltiazem was, however, associated with a shortened seizure duration, possibly making ECT less effective. Because of the reduction in seizure duration, the routine administration of diltiazem may not be advisable because it can possibly interfere with the psychotherapeutic efficacy of ECT. However, diltiazem medication for ECT is potentially useful for reducing tachycardia and hypertension in high-risk patients.. Diltiazem can blunt acute hyperdynamic responses after electroconvulsive therapy, but seizure duration is also significantly reduced, possibly making this therapy less effective.

Topics: Adult; Aged; Blood Pressure; Cardiovascular Agents; Cross-Over Studies; Diltiazem; Double-Blind Method; Electroconvulsive Therapy; Electroencephalography; Female; Heart Rate; Hemodynamics; Humans; Hypertension; Male; Middle Aged; Seizures; Tachycardia

Neurological complications including seizures have been reported with ranolazine. We sought to quantify the risk of seizure-related hospitalizations or emergency department events following ranolazine exposure in the Sentinel System (2006-2015).. Eligibility criteria were new use of ranolazine after 183 days washout period and absence of seizure diagnoses, anti-epileptic drugs, or seizure-related disorders during the baseline period.. Among 52,155 ranolazine users, we identified 28 seizures in the 1-32 days after new ranolazine dispensing: 12 occurring in days 1-10 (high-risk window), 11 in days 11-20 (moderate-risk window) and 5 in the control window (days 21-32). Assuming an equal likelihood of seizure events across the 32-day observation window, we estimate an attributable risk of 0.9 excess cases per 10,000 exposed users. Using a self-controlled risk interval design with exact logistic regression, seizures were elevated in the high-risk window (relative risk [RR] 2.88 (95% confidence interval [CI] 1.01-8.33) compared with the control window. No significant increased risk was observed in the moderate window. Half of the seizure cases had a diagnosis of renal disease, although seizure risk was not significant (RR 3.20 [CI 0.82-14.01]). A majority of patients in both risk windows were 75 years or older.. Our study suggests risk among younger ranolazine patients is rare. Given the imprecision of the risk estimates, we interpret the elevated seizure risk following ranolazine exposure with caution. Further analysis in a larger elderly population is warranted.

Topics: Aged; Anticonvulsants; Cardiovascular Agents; Cohort Studies; Humans; Kidney Diseases; Logistic Models; Ranolazine; Risk Assessment; Seizures; United States; United States Food and Drug Administration

Topics: Acoustic Stimulation; Adrenergic Uptake Inhibitors; Animals; Anticonvulsants; Atomoxetine Hydrochloride; Blood Pressure; Brugada Syndrome; Cardiovascular Agents; Disease Models, Animal; Epilepsy; Female; Heart Rate; Male; Mice, Inbred DBA; Respiration; Respiratory System Agents; Seizures

Ranolazine is a new anti-anginal medication that was approved by the US Food and Drug Administration (FDA) in 2006 for patients with symptomatic chronic angina despite optimized therapy. This paper presents a case report of a fifteen year old male patient admitted to the pediatric intensive care unit after ranolazine overdose ingestion. He had recurrent new onset seizures that are most likely due to ranolazine overdose. Seizures have never been reported with ranolazine use or abuse.

Topics: Adolescent; Cardiovascular Agents; Drug Overdose; Glasgow Coma Scale; Humans; Male; Ranolazine; Seizures; Suicide, Attempted

Hypertension and heart failure belong to common comorbid conditions with epilepsy so drug interactions between antiepileptics and cardiovascular drugs are possible in clinical practice. The aim of this study was to evaluate the effects of angiotensin AT1 receptor antagonists (losartan potassium and candesartan cilexetil), angiotensin-converting enzyme (ACE) inhibitors (captopril and perindopril arginine) and diuretics (hydrochlorothiazide and ethacrynic acid) on the anticonvulsant activity of levetiracetam (LEV) in mice.. The protective action of LEV was examined in the maximal electroshock seizure threshold test. Drugs were administered intraperitoneally (ip). Additionally, combinations of cardiovascular drugs with LEV were tested for adverse effects in the passive avoidance task and the chimney test.. Losartan potassium (50mg/kg), candesartan cilexetil (8mg/kg), captopril (50mg/kg), hydrochlorothiazide (100mg/kg) and ethacrynic acid (100mg/kg) did not affect the anticonvulsant activity of LEV. Perindopril arginine (10mg/kg) raised the convulsive threshold for LEV administered at doses of 100, 300 and 500mg/kg. This interaction could be pharmacodynamic in nature because the brain concentration of LEV remained unchanged by perindopril. The adverse effects of the combined treatment with LEV and cardiovascular drugs were not observed in the passive avoidance task or the chimney test.. Although experimental data can be hardly extrapolated to clinical practice, it is suggested that perindopril arginine may positively influence the anticonvulsant action of LEV in epileptic patients. The use of losartan potassium, candesartan cilexetil, captopril, hydrochlorothiazide or ethacrynic acid in patients treated with LEV seems neutral regarding its anticonvulsant activity.

Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Anticonvulsants; Avoidance Learning; Cardiovascular Agents; Disease Models, Animal; Diuretics; Dose-Response Relationship, Drug; Drug Interactions; Electroshock; Injections, Intraperitoneal; Levetiracetam; Mice; Piracetam; Seizures

Since the advent of cardiopulmonary resuscitation more than 40 years ago, we have achieved a return to spontaneous circulation in a growing proportion of patients with cardiac arrest. Nevertheless, most of these patients die in the first few days after admission to the intensive care unit (ICU), and this situation has not improved over the years. Mortality in these patients is mainly associated to brain damage. Perhaps recognizing that cardiopulmonary resuscitation does not end with the return of spontaneous circulation but rather with the return of normal brain function and total stabilization of the patient would help improve the therapeutic management of these patients in the ICU. In this sense, the term cardiocerebral resuscitation proposed by some authors might be more appropriate. The International Liaison Committee on Resuscitation recently published a consensus document on the "Post-Cardiac Arrest Syndrome" and diverse authors have proposed that post-arrest care be integrated as the fifth link in the survival chain, after early warning, early cardiopulmonary resuscitation by witnesses, early defibrillation, and early advanced life support. The therapeutic management of patients that recover spontaneous circulation after cardiopulmonary resuscitation maneuvers based on life support measures and a series of improvised actions based on "clinical judgment" might not be the best way to treat patients with post-cardiac arrest syndrome. Recent studies indicate that using goal-guided protocols to manage these patients including therapeutic measures of proven efficacy, such as inducing mild therapeutic hypothermia and early revascularization, when indicated, can improve the prognosis considerably in these patients. Given that there is no current protocol based on universally accepted evidence, the Steering Committee of the National Cardiopulmonary Resuscitation Plan of the Spanish Society of Intensive Medicine and Cardiac Units has elaborated this document after a thorough review of the literature and an online discussion involving all the members of the committee and a consensus meeting with the aim of providing a platform for the development of local protocols in different ICSs in our country to fit their own means and characteristics.

Topics: Advanced Cardiac Life Support; Algorithms; Cardiopulmonary Resuscitation; Cardiovascular Agents; Combined Modality Therapy; Critical Care; Diuretics; Glasgow Outcome Scale; Heart Arrest; Hemodynamics; Humans; Hypnotics and Sedatives; Hypothermia, Induced; Hypoxia, Brain; Intensive Care Units; Life Support Systems; Monitoring, Physiologic; Myocardial Revascularization; Neuromuscular Blockade; Seizures; Syndrome

Patients with unrepaired abdominal aortic aneurysm (AAA) may have depression and other psychiatric disorders for which electroconvulsive therapy (ECT) may be recommended. It is unclear whether ECT, which transiently, yet markedly, increases blood pressure and heart rate, can be safely performed in patients with AAA. We investigated the safety of ECT in patients with unrepaired AAA.. A retrospective review was conducted of the medical records of all patients with unrepaired AAA who underwent ECT for severe depressive syndromes at Mayo Clinic, Rochester, Minn, between January 1, 1995, and June 30, 2007.. Eight patients (5 men and 3 women) with unrepaired AAA who underwent ECT were identified. Median age was 78.5 years (range, 67-83 years). All patients had AAA (median diameter, 3.95 cm [range, 3.0-5.2 cm]). The median number of treatments was 8.5 (range, 4-48). None of the patients died during the periprocedural period or experienced symptoms or signs suggestive of AAA expansion or rupture. Follow-up imaging data were available for 6 patients whose median post-ECT AAA diameter was 4.65 cm (range, 3.3-5.3 cm). Expansion of AAA ranged from 0.1 cm (for 11 and 13 months in 2 patients) to 1.0 cm (for 29 months in 1 patient), which is less than the expected mean expansion rates for AAAs of these diameters.. Electroconvulsive therapy was safe for 8 patients with unrepaired AAA treated at our institution. Our findings may be informative to clinicians who manage the care of patients with unrepaired AAA who are undergoing ECT.

Topics: Aged; Aged, 80 and over; Anesthesia; Aortic Aneurysm, Abdominal; Blood Pressure; Cardiovascular Agents; Depressive Disorder; Electroconvulsive Therapy; Female; Heart Rate; Humans; Male; Retrospective Studies; Safety; Seizures

Under both pathological and experimental conditions, area CA3 of the adult or juvenile hippocampus generates periodic population discharges known as interictal bursts. Whereas the ionic and synaptic basis of individual bursts has been comprehensively studied experimentally and computationally, the pacemaker mechanisms underlying interictal rhythmicity remain conjectural. We showed previously that rhythmic population discharges resembling interictal bursts can be induced in hippocampal slices from first postnatal week mice, in Mg2+-free solution with GABA(A) receptor-mediated inhibition blocked. Here we show that these neonatal bursts occurred with high temporal precision and that their frequency and regularity were greatly reduced by the bradycardic agent ZD-7288 when applied at concentrations and durations that selectively block the hyperpolarization-activated, cationic current I(h). Augmenting I(h) by elevating intracellular cAMP dramatically increased burst frequency in a protein kinase A-independent manner. Burst amplitudes were strongly correlated with the preceding, but not the following, interburst intervals. The experimentally observed distribution of interburst intervals was modeled by assuming that a burst was triggered whenever the instantaneous rate of spontaneous EPSPs (sEPSPs) exceeded a threshold and that the mean sEPSP rate was minimal immediately after a burst and then relaxed exponentially to a steady-state level. The effect of blocking I(h) in any given slice could be modeled by decreasing only the steady-state sEPSP rate, suggesting that the instantaneous rate of sEPSPs is governed by the level of I(h) activation and raising the novel possibility that interburst intervals reflected the slow activation kinetics of I(h) in the neonatal CA3.

Topics: Animals; Animals, Newborn; Biological Clocks; Cardiovascular Agents; Cations; Colforsin; Computer Simulation; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Enzyme Inhibitors; Excitatory Postsynaptic Potentials; GABA Antagonists; GABA-A Receptor Antagonists; Hippocampus; In Vitro Techniques; Mice; Models, Neurological; Periodicity; Potassium Channel Blockers; Pyrimidines; Receptors, GABA-A; Seizures; Synaptic Transmission

The anticonvulsant (AC drug)- or ethanol (EtOH)-modified effects of cardiovascular (CV) drugs against cocaine (COCA)-induced toxicity were examined in male ICR mice. Nontoxic doses of the CV drugs nimodipine (NIMO), prazosin (PRA), phentolamine (PHEN), propranolol (PRO), and enalapril (ENA) were used with or without the AC drugs diazepam (DZP), phenobarbital (PHB), phenytoin (PHY), and EtOH. Each CV drug combined with or without each AC drug was administered intraperitoneally (IP) 5 min before an IP injection of COCA 75 mg/kg. Of the CV drugs examined, PRA 5 mg/kg and PHEN 5 mg/kg protected against COCA-induced seizures, but only the alpha1-adrenergic blocking agent PRA protected against COCA-induced deaths. Of the AC drugs examined, DZP 5 mg/kg and PHB 50 mg/kg, as well as EtOH 3 g/kg, attenuated the severity of the COCA-induced seizures, but only PHB protected against COCA-induced deaths. The total mortality rate was significantly, often synergistically, decreased compared to the COCA-only group when the appropriate CV drugs were combined with the AC drugs: PRA 5 mg/kg in the EtOH-cotreated groups, PRA 5 mg/kg, PHEN 5 mg/kg or ENA 10 mg/kg in the DZP-cotreated groups, and NIMO 5 mg/kg, PRA 5 mg/kg, PHEN 5 mg/kg, or PRO 10 mg/kg in the PHB-cotreated groups. The decrease in the COCA concentration in the blood and/or brain was not always accompanied by an attenuation of the mortality rate. However, the attenuation of severe seizures by a single PRA, PHEN, DZP, or PHB cotreatment was accompanied by a decrease in the brain COCA concentration.

Topics: Animals; Anticonvulsants; Cardiovascular Agents; Cocaine; Diazepam; Enalapril; Ethanol; Male; Mice; Mice, Inbred ICR; Phenobarbital; Phentolamine; Propranolol; Seizures

Topics: Cardiovascular Agents; Humans; Muscle Relaxants, Central; Poisoning; Seizures; Strychnine; Suicidal Ideation; Suicide; Toxicology

Topics: Animals; Anticonvulsants; Cardiovascular Agents; Mice; Muscle Relaxants, Central; Neuromuscular Agents; Seizures; Strychnine

Topics: Anesthetics, Local; Antipsychotic Agents; Cardiovascular Agents; Seizures; Tranquilizing Agents

Topics: Atropine; Cardiovascular Agents; Child; Drug-Related Side Effects and Adverse Reactions; Fever; Humans; Infant; Muscle Relaxants, Central; Seizures

Topics: Animals; Cardiovascular Agents; Curare; Muscle Relaxants, Central; Rabbits; Seizures

Topics: Anesthesia; Anesthesiology; Cardiovascular Agents; Muscle Relaxants, Central; Seizures

Topics: Cardiovascular Agents; Convulsive Therapy; Muscle Relaxants, Central; Seizures; Ventilators, Mechanical

Topics: Cardiovascular Agents; Death; Dehydration; Ergot Alkaloids; Hypoglycemia; Hypoglycemic Agents; Seizures

Topics: Cardiovascular Agents; Convulsive Therapy; Electroconvulsive Therapy; Humans; Muscle Relaxants, Central; Seizures

Topics: Cardiovascular Agents; Hypersensitivity; Muscle Relaxants, Central; Seizures; Succinylcholine

Topics: Cardiovascular Agents; Convulsive Therapy; Electricity; Muscle Relaxants, Central; Seizures

Topics: Cardiovascular Agents; Ergot Alkaloids; Oxytocics; Seizures

Topics: Anticonvulsants; Blood-Brain Barrier; Cardiovascular Agents; Ergot Alkaloids; Ergotamine; Muscle Relaxants, Central; Seizures; Sympatholytics

Topics: Brain; Cardiovascular Agents; Cardiovascular Diseases; Cardiovascular System; Ergot Alkaloids; Seizures; Sympatholytics

Topics: Cardiovascular Agents; Hydantoins; Phenytoin; Seizures