Ajmaline: An alkaloid found in the root of RAUWOLFIA SERPENTINA, among other plant sources. It is a class Ia antiarrhythmic agent that apparently acts by changing the shape and threshold of cardiac action potentials.Rauwolfia: A plant genus of the APOCYNACEAE or dogbane family. Alkaloids from plants in this genus have been used as tranquilizers and antihypertensive agents. RESERPINE is derived from R. serpentina.Brugada Syndrome: An autosomal dominant defect of cardiac conduction that is characterized by an abnormal ST-segment in leads V1-V3 on the ELECTROCARDIOGRAM resembling a right BUNDLE-BRANCH BLOCK; high risk of VENTRICULAR TACHYCARDIA; or VENTRICULAR FIBRILLATION; SYNCOPAL EPISODE; and possible sudden death. This syndrome is linked to mutations of gene encoding the cardiac SODIUM CHANNEL alpha subunit.Secologanin Tryptamine Alkaloids: Compounds formed by condensation of secologanin with tryptamine resulting in a tetrahydro-beta-carboline which is processed further to a number of bioactive compounds. These are especially found in plants of the APOCYNACEAE; LOGANIACEAE; and RUBIACEAE families.Anti-Arrhythmia Agents: Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.Electrocardiography: Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.Bundle-Branch Block: A form of heart block in which the electrical stimulation of HEART VENTRICLES is interrupted at either one of the branches of BUNDLE OF HIS thus preventing the simultaneous depolarization of the two ventricles.Fonofos: An organothiophosphorus cholinesterase inhibitor that is used as an insecticide.Chemical Industry: The aggregate enterprise of manufacturing and technically producing chemicals. (From Random House Unabridged Dictionary, 2d ed)Environmental Pollutants: Substances or energies, for example heat or light, which when introduced into the air, water, or land threaten life or health of individuals or ECOSYSTEMS.Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation.Directories as Topic: Lists of persons or organizations, systematically arranged, usually in alphabetic or classed order, giving address, affiliations, etc., for individuals, and giving address, officers, functions, and similar data for organizations. (ALA Glossary of Library and Information Science, 1983)Phytochemicals: A broad range of biologically active compounds which occur naturally in plants having important medicinal and nutritional properties.Manufactured Materials: Substances and materials manufactured for use in various technologies and industries and for domestic use.Industry: Any enterprise centered on the processing, assembly, production, or marketing of a line of products, services, commodities, or merchandise, in a particular field often named after its principal product. Examples include the automobile, fishing, music, publishing, insurance, and textile industries.Industrial Oils: Oils which are used in industrial or commercial applications.Organic Chemicals: A broad class of substances containing carbon and its derivatives. Many of these chemicals will frequently contain hydrogen with or without oxygen, nitrogen, sulfur, phosphorus, and other elements. They exist in either carbon chain or carbon ring form.Particle Size: Relating to the size of solids.Volatile Organic Compounds: Organic compounds that have a relatively high VAPOR PRESSURE at room temperature.Chemistry, Organic: The study of the structure, preparation, properties, and reactions of carbon compounds. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Water Pollutants, Chemical: Chemical compounds which pollute the water of rivers, streams, lakes, the sea, reservoirs, or other bodies of water.Cosmic Dust: Finely divided solid matter with particle sizes smaller than a micrometeorite, thus with diameters much smaller than a millimeter, moving in interplanetary space. (NASA Thesaurus, 1994)Meteoroids: Any solid objects moving in interplanetary space that are smaller than a planet or asteroid but larger than a molecule. Meteorites are any meteoroid that has fallen to a planetary surface. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Domperidone: A specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms.Galactogogues: Substances that induce LACTATION.Gastrointestinal Motility: The motor activity of the GASTROINTESTINAL TRACT.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Gastroesophageal Reflux: Retrograde flow of gastric juice (GASTRIC ACID) and/or duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the distal ESOPHAGUS, commonly due to incompetence of the LOWER ESOPHAGEAL SPHINCTER.Suppositories: Medicated dosage forms that are designed to be inserted into the rectal, vaginal, or urethral orifice of the body for absorption. Generally, the active ingredients are packaged in dosage forms containing fatty bases such as cocoa butter, hydrogenated oil, or glycerogelatin that are solid at room temperature but melt or dissolve at body temperature.Gastrointestinal Diseases: Diseases in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.Alcohols: Alkyl compounds containing a hydroxyl group. They are classified according to relation of the carbon atom: primary alcohols, R-CH2OH; secondary alcohols, R2-CHOH; tertiary alcohols, R3-COH. (From Grant & Hackh's Chemical Dictionary, 5th ed)Alcohol Drinking: Behaviors associated with the ingesting of alcoholic beverages, including social drinking.Alcohol Dehydrogenase: A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.KetonesAlcohol Oxidoreductases: A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).Butanols: Isomeric forms and derivatives of butanol (C4H9OH).PropaneDrug Information Services: Services providing pharmaceutic and therapeutic drug information and consultation.Pamphlets: Printed publications usually having a format with no binding and no cover and having fewer than some set number of pages. They are often devoted to a single subject.Drug Labeling: Use of written, printed, or graphic materials upon or accompanying a drug container or wrapper. It includes contents, indications, effects, dosages, routes, methods, frequency and duration of administration, warnings, hazards, contraindications, side effects, precautions, and other relevant information.Patient Education as Topic: The teaching or training of patients concerning their own health needs.Formularies as Topic: Works about lists of drugs or collections of recipes, formulas, and prescriptions for the compounding of medicinal preparations. Formularies differ from PHARMACOPOEIAS in that they are less complete, lacking full descriptions of the drugs, their formulations, analytic composition, chemical properties, etc. In hospitals, formularies list all drugs commonly stocked in the hospital pharmacy.Drug Industry: That segment of commercial enterprise devoted to the design, development, and manufacture of chemical products for use in the diagnosis and treatment of disease, disability, or other dysfunction, or to improve function.Medical Records Systems, Computerized: Computer-based systems for input, storage, display, retrieval, and printing of information contained in a patient's medical record.Facial Muscles: Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)Diplopia: A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE.Migraine Disorders: A class of disabling primary headache disorders, characterized by recurrent unilateral pulsatile headaches. The two major subtypes are common migraine (without aura) and classic migraine (with aura or neurological symptoms). (International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004: suppl 1)Tryptamines: Decarboxylated monoamine derivatives of TRYPTOPHAN.Chest Pain: Pressure, burning, or numbness in the chest.Jaw: Bony structure of the mouth that holds the teeth. It consists of the MANDIBLE and the MAXILLA.Universal Precautions: Prudent standard preventive measures to be taken by professional and other health personnel in contact with persons afflicted with a communicable disease, to avoid contracting the disease by contagion or infection. Precautions are especially applicable in the diagnosis and care of AIDS patients.

ATP- and glutathione-dependent transport of chemotherapeutic drugs by the multidrug resistance protein MRP1. (1/40)

The present study was performed to investigate the ability of the multidrug resistance protein (MRPI) to transport different cationic substrates in comparison with MDR1-P-glycoprotein (MDR1). Transport studies were performed with isolated membrane vesicles from in vitro selected multidrug resistant cell lines overexpressing MDR1 (A2780AD) or MRP1 (GLC4/Adr) and a MRP1-transfected cell line (S1(MRP)). As substrates we used 3H-labelled derivatives of the hydrophilic monoquaternary cation N-(4',4'-azo-in-pentyl)-21-deoxy-ajmalinium (APDA), the basic drug vincristine and the more hydrophobic basic drug daunorubicin. All three are known MDR1-substrates. MRP1 did not mediate transport of these substrates per se. In the presence of reduced glutathione (GSH), there was an ATP-dependent uptake of vincristine and daunorubicin, but not of APDA, into GLC4/Adr and S1(MRP) membrane vesicles which could be inhibited by the MRP1-inhibitor MK571. ATP- and GSH-dependent transport of daunorubicin and vincristine into GLC4/Adr membrane vesicles was inhibited by the MRP1-specific monoclonal antibody QCRL-3. MRP1-mediated daunorubicin transport rates were dependent on the concentration of GSH and were maximal at concentrations > or = 10 mM. The apparent KM value for GSH was 2.7 mM. Transport of daunorubicin in the presence of 10 mM GSH was inhibited by MK571 with an IC50 of 0.4 microM. In conclusion, these results demonstrate that MRP1 transports vincristine and daunorubicin in an ATP- and GSH-dependent manner. APDA is not a substrate for MRP1.  (+info)

Sudden death in patients and relatives with the syndrome of right bundle branch block, ST segment elevation in the precordial leads V(1)to V(3)and sudden death. (2/40)

BACKGROUND: The syndrome with an electrocardiographic pattern of right bundle branch block, ST segment elevation in leads V(1)to V(3)and sudden death is genetically determined and caused by mutations in the cardiac sodium channel. The inheritance of the disease is autosomal dominant. Sudden death may, however, occur from a variety of causes in relatives and patients with this syndrome. PATIENTS AND METHODS: Twenty-five Flemish families with this syndrome with a total of 334 members were studied. Affected members were recognized by means of a typical electrocardiogram either occurring spontaneously or after the intravenous administration of antiarrhythmic drugs. Sudden deaths in these families were classified as related or not to the syndrome by analysis of the data at the time of the event, mode of inheritance of the disease, and data provided by survivors. Results Of the 25 families with the syndrome, 18 were symptomatic (at least one sudden death related to the syndrome) and seven were asymptomatic (no sudden deaths related to the syndrome). In total, there were 42 sudden cardiac deaths (12% incidence). Twenty-four sudden deaths were related to the syndrome and all occurred in symptomatic families. Eighteen sudden deaths (43% of total sudden deaths) were not related to the syndrome (nine cases) or were of unclear cause (nine cases). Three of them occurred in two asymptomatic families and the remaining 15 in five symptomatic families. Twenty-four of the 50 affected members (47%) suffered (aborted) sudden death and 18 of the 284 unaffected members (6%). This difference in the incidence of sudden death was statistically significant (P<0.0001). Patients with (aborted) sudden death caused by the syndrome were younger than patients with sudden death of other or unclear causes (38+/-4 years vs 59+/-3 years respectively, P=0.0003). CONCLUSIONS: In families at high risk of sudden death because of genetically determined diseases, the main cause of sudden death remains the disease. However, almost the half of sudden deaths are caused by unrelated diseases or are of unclear cause. Accurate classification of the causes of sudden death is mandatory for appropriate analysis of the causes of death when designing preventive treatments.  (+info)

Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads. (3/40)

OBJECTIVE: The aim of this study was to perform quantitative signal analysis of high-resolution body surface potential mapping (BSPM) recordings to assess its usefulness for the electrocardiographic characterization of patients with Brugada syndrome. The diagnostic value of the QRS integral and of the gradient of the ST segment have not been elucidated in Brugada syndrome. METHODS: In 27 subjects (16 with Brugada syndrome and 11 healthy subjects), 120-lead BSPMs were recorded at baseline and after pharmacological provocation with intravenous administration of ajmaline (1 mg/kg). The recordings were analyzed for two regions outside the positions of the standard ECG leads: the right precordial leads (RPL) on the second and third intercostal space (high RPL) and the left precordial leads (LPL) between the fifth and seventh intercostal space (low LPL). RESULTS: At baseline, in high RPL regions, patients with Brugada syndrome showed more positive QRS integrals (-5+/-8 vs. -16+/-8 mV ms) and a steeper negative ST segment gradient (-0.62+/-0.41 vs. -0.29+/-0.40 mV/s) compared to healthy subjects, P<0.001. In contrast, in low LPL regions, reduced QRS integrals and positive ST segment gradients were observed. These ECG signs were even more pronounced after intravenous ajmaline and showed a better discrimination for patients with Brugada syndrome than differences in RPL or LPL during baseline, respectively. CONCLUSIONS: In the left precordial leads, patients with Brugada syndrome showed ECG changes which were reversed in relation to the ECG changes observed in right precordial leads. BSPM measurement is a useful tool to improve the understanding of the electrocardiographic changes in the Brugada syndrome.  (+info)

Antiarrhythmic effect of aprindine on several types of ventricular arrhythmias. (4/40)

The antiarrhythmic effect of aprindine was compared with those of lidocaine and propranolol on several ventricular arrhythmias-epinephrine arrhythmias in cats, ouabain arrhythmias in cats and guinea pigs, ischemic ventricular arrhythmias in coronary-ligated Beagle dogs. Antiarrhythmic effects of aprindine and lidocaine were observed both in ouagain and ischemic arrhythmias, but not in epinephrine arrhythmias. While propranolol had a strong antiarrhythmic effect against epinephrine and ouabain arrhythmias, it did not increase sinus beats in ischemic arrhythmias. Marked anti-arrhythmic effects of aprindine in ischemic arrhythmias were observed in dogs using either single intravenous administration (4 mg/kg) or intravenous infusion (200 mug/kg/min, 2 mg/kg). Antiarrhythmic activity of aprindine is considered to be about twice as strong as that of lidocaine, but lidocaine is less toxic in experimental animals.  (+info)

The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. (5/40)

AIMS: The diagnostic ECG pattern in Brugada syndrome (BS) can transiently normalize and may be unmasked by sodium channel blockers such as ajmaline. Proarrhythmic effects of the drug have been well documented in the literature. A detailed protocol for the ajmaline challenge in Brugada syndrome has not yet been described. Therefore, we prospectively studied the risks of a standardized ajmaline test. METHODS AND RESULTS: During a period of 60 months, 158 patients underwent the ajmaline test in our institution. Ajmaline was given intravenously in fractions (10mg every two minutes) up to a target dose of 1mg/kg. In 37 patients (23%) the typical coved-type ECG pattern of BS was unmasked. During the test, symptomatic VT appeared in 2 patients (1.3%). In all other patients, the drug challenge did not induce VT if the target dose, QRS prolongation >30%, presence/appearance of the typical ECG, or the occurrence of premature ventricular ectopy were considered as end points of the test. A positive response to ajmaline was induced in 2 of 94 patients (2%) with a normal baseline ECG, who underwent evaluation solely for syncope of unknown origin. CONCLUSION: The ajmaline challenge using a protocol with fractionated drug administration is a safe method to diagnose BS. Because of the potential induction of VT, it should be performed under continuous medical surveillance with advanced life-support facilities. Due to the prognostic importance all patients with aborted sudden death or unexplained syncope without demonstrable structural heart disease and family members of affected individuals should presently undergo drug testing for unmasking BS.  (+info)

Unusual response to the ajmaline test in a patient with Brugada syndrome. (6/40)

We present a Brugada syndrome patient who suffered an aborted sudden death. The ajmaline test (1 mg/kg body weight) induced accentuated alternans ST-segment elevation in V1-V2 without ventricular arrhythmias. It could represent silent ischaemia not detected before, failure of myocardial regions to repolarize in alternate beats due to transmural dispersion of conduction and refractoriness in the right ventricular outflow tract or a rate dependent sodium channel block by ajmaline. We need more studies to know whether this electrocardiographic sign is a risk factor for life-threatening ventricular arrhythmias in Brugada syndrome patients.  (+info)

Value of electrocardiographic parameters and ajmaline test in the diagnosis of Brugada syndrome caused by SCN5A mutations. (7/40)

BACKGROUND: The Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene, SCN5A. The electrocardiographic pattern characteristic of the syndrome is dynamic and is often absent in affected individuals. Sodium channel blockers are effective in unmasking carriers of the disease. However, the value of the test remains controversial. METHODS AND RESULTS: We studied 147 individuals representing 4 large families with SCN5A mutations. Of these, 104 were determined to be at possible risk for Brugada syndrome and underwent both electrocardiographic and genetic evaluation. Twenty-four individuals displayed an ECG diagnostic of Brugada syndrome at baseline. Of the remaining, 71 received intravenous ajmaline. Of the 35 genetic carriers who received ajmaline, 28 had a positive test and 7 a negative ajmaline test. The sensitivity, specificity, and positive and negative predictive values of the drug challenge were 80% (28:35), 94.4% (34:36), 93.3% (28:30), and 82.9% (34:41), respectively. Penetrance of the disease phenotype increased from 32.7% to 78.6% with the use of sodium channel blockers. In the absence of ST-segment elevation under baseline conditions, a prolonged P-R interval, but not incomplete right bundle-branch block or early repolarization patterns, indicates a high probability of an SCN5A mutation carrier. CONCLUSIONS: In families with Brugada syndrome, the data suggest that ajmaline testing is valuable in the diagnosis of SCN5A carriers. In the absence of ST-segment elevation at baseline, family members with first-degree atrioventricular block should be suspected of carrying the mutation. An ajmaline test is often the key to making the proper diagnosis in these patients.  (+info)

Crystal structure of vinorine synthase, the first representative of the BAHD superfamily. (8/40)

Vinorine synthase is an acetyltransferase that occupies a central role in the biosynthesis of the antiarrhythmic monoterpenoid indole alkaloid ajmaline in the plant Rauvolfia. Vinorine synthase belongs to the benzylalcohol acetyl-, anthocyanin-O-hydroxy-cinnamoyl-, anthranilate-N-hydroxy-cinnamoyl/benzoyl-, deacetylvindoline acetyltransferase (BAHD) enzyme superfamily, members of which are involved in the biosynthesis of several important drugs, such as morphine, Taxol, or vindoline, a precursor of the anti-cancer drugs vincaleucoblastine and vincristine. The x-ray structure of vinorine synthase is described at 2.6-angstrom resolution. Despite low sequence identity, the two-domain structure of vinorine synthase shows surprising similarity with structures of several CoA-dependent acyltransferases such as dihydrolipoyl transacetylase, polyketide-associated protein A5, and carnitine acetyltransferase. All conserved residues typical for the BAHD family are found in domain 1. His160 of the HXXXD motif functions as a general base during catalysis. It is located in the center of the reaction channel at the interface of both domains and is accessible from both sides. The channel runs through the entire molecule, allowing the substrate and co-substrate to bind independently. Asp164 points away from the catalytic site and seems to be of structural rather than catalytic importance. Surprisingly, the DFGWG motif, which is indispensable for the catalyzed reaction and unique to the BAHD family, is located far away from the active site and seems to play only a structural role. Vinorine synthase represents the first solved protein structure of the BAHD superfamily.  (+info)

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AIMS: Sodium-channel blockers (SCBs) are associated with arrhythmia, but variability of cardiac electrical response remains unexplained. We sought to identify predictors of ajmaline-induced PR and QRS changes and Type I Brugada syndrome (BrS) electrocardiogram (ECG). METHODS AND RESULTS: In 1368 patients that underwent ajmaline infusion for suspected BrS, we performed measurements of 26 721 ECGs, dose-response mixed modelling and genotyping. We calculated polygenic risk scores (PRS) for PR interval (PRSPR), QRS duration (PRSQRS), and Brugada syndrome (PRSBrS) derived from published genome-wide association studies and used regression analysis to identify predictors of ajmaline dose related PR change (slope) and QRS slope. We derived and validated using bootstrapping a predictive model for ajmaline-induced Type I BrS ECG. Higher PRSPR, baseline PR, and female sex are associated with more pronounced PR slope, while PRSQRS and age are positively associated with QRS slope (P , 0.01 for all). PRSBrS, ...
The classic finding here is the "j-wave" found in V1->V3 at the end of the QRS complex. The "J-point" is where the QRS ends and the ST segment begins. This EKG is classic for a profoundly positive (>2 mm) J wave (not just J point) with its associated convex-up ST segment, followed by a negative last 1/2 of the T wave, suggestive of a Type I Brugada syndrome. More can be found about the EKG criteria here. Realize the ST segment and J-wave amplitude can be dynamic, so if they are not as prominent as this, a Type I antiarrhythmic can be used to provoke the findings - hence the procainamide, flecainide, or ajmaline challenge tests. ...
All consecutive patients with suspected BrS-ECG pattern will perform an ajmaline testing (1mg/kg in 5 min). A total of 30 patients with positive testing and 30 patients with negative testing will be selected and enrolled. Patients will perform cardiac magnetic resonance and 3D echocardiography imaging to evaluate and compare morphological and functional characteristics of the 2 groups before and after ajmaline. Patients with positive testing will also perform a standardized programmed ventricular stimulation protocol ...
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.. Handling Instructions Tel: +1-832-582-8158 Ext:3 If you have any other enquiries, please leave a message.. ...
A 51 year old man, with a previous history of 15 years of hypertension treated with β blockers, complained of nocturnal and early morning seizures. One year ago, he had a syncope thought to be caused by bradycardia. β Blockers were reduced in a first step, and then discontinued. Serial neurological investigations were normal. Therapeutic challenges using sodium valproate or phenytoin did not had any favourable influence. Glucose metabolism was normal.. Cardiac investigations including carotid sinus massage, recording of late potentials, repetitive 24 hour Holter monitoring, and tilt table testing were normal. At electrophysiological testing, AH interval was 80 ms, and HV interval was 42 ms. Sinus node function and anterograde atrioventricular conduction were normal. Programmed atrial and ventricular stimulation did not induce any sustained arrhythmia. The ajmaline test was negative.. A Reveal Plus implantable loop recorder (Medtronic) was implanted. One month later, at the follow up visit, the ...
Brugada ECGs have been characterised into three patterns (Figure 1). A type 1 Brugada ECG has coved ST elevation of , 0.2mm followed by a negative T-wave (Figure 1A). A downsloping ST segment from an elevated J point with an STJ/ST80 (80ms after J point) ratio ,1 is found in the Type 1 ECG pattern. The type 2 ECG has a saddleback morphology with high take-off ST elevation followed by a biphasic (Figure 1B) or positive (Figure 1C) T-wave. A type 3 ECG has either a coved or saddleback morphology with J point elevation ,2mm but the terminal portion of ST segment ,1mm. Type 2 and Type 3 patterns can be confused with partial RBBB but measuring the angle between the upslope of the S wave and downslope of the r wave (β in Figure 2) can be helpful with an angle ,58° having a sensitivity of 92% and specificity of 87% in those without structural heart disease (12). Pharmacological testing with a class 1C antiarrhythmic such as Ajmaline can unmask the typical ECG, however it is non-diagnostic in up to ...
Literature data and results of our studies performed in 1979-1993 were summarized. The major outcome of our investigations was the establishment of novel cell strains-producents and the development of conditions for their maintaining that increased the accumulation of indoline alkaloid, ajmaline, up to 6-8 % and occasionally up to 20 %. This is 100-fold higher that of inherent to 5-7 old plants growing in tropics ...
Alkaloids, Catharanthus, Catharanthus Roseus, Plants, Secretion, Metabolism, Ajmaline, Concentrations, Tissues, Abc Transporters, Arabidopsis, Coa, Diurnal Rhythm, Diurnal Rhythms, Exudates, Flavonoids, Gene, Gene Expression, Genes, Ligases
Dear Doctor, I have been diagnost with an incomplete right bundle branch block. I am 45 and 108 punds. All physical, stress test and blood work is fine. The doctor tells me not to worry. However ...
Introduction: While it has been proposed that T wave inversions (TWI) in the anterior precordial leads can be a normal finding in the ECGs of Afro-Caribbean athletes, it is uncertain whether this holds true for African-Americans. Hypothesis: TWI in the anterior precordial leads can be a non-specific marker of cardiac disease, and as a result, assuming a benign nature for TWI in the anterior leads in African-American athletes may not be appropriate. Methods: To begin to investigate this notion, we evaluated the incidence of cardiovascular death (CVD) in apparently healthy African- Americans with anterior TWI over an 11 year period. We analyzed the ECGs and CV deaths in 5334 ambulatory African Americans (average age 50 years, 8% female, average follow up of 8 years) seen at the Palo Alto VA Health Care system from 1986 until 1997. T waves were coded as inverted in V2, V3, V4 and V5 if TWI were noted to be more than 1 mm below the PR segment. The leads coded as inverted were summed to create a ...
As a result of exhaustive investigation on the subject, some of the genetic basis and pathophysiologic substrate of arrhythmias in BS have been unravelled. Mutations in 4 genes have been linked to BS: SCN5A, encoding for the α-subunit of the cardiac sodium (Na+) channel31 , and resulting in loss of function of the mentioned channel by different mechanisms32 (being responsible for up to 30% of BS cases5) ; glycerol-3-phosphate dehydrogenase 1-like gene (GPD1L), which reduce the inward Na+ current by affecting the trafficking of the cardiac Na+ channel to the cell surface33, 34; finally, mutations in genes encoding the α1-(CACNA1C) and β- (CACNB2b) subunits of the L-type cardiac calcium (Ca+2) channel result in a combined Brugada/short QT syndrome35 (it has not been established yet which percentage of BS patients present these three last types of mutations ...
ABUD, Atilio M. et al. Retrospective Analysis of Patients with Brugada Syndrome and Implantable Cardioverter Defibrillator. Rev. argent. cardiol. [online]. 2014, vol.82, n.1, pp.21-25. ISSN 1850-3748.. Introduction The Brugada syndrome is an inherited, electrical anomaly, with increased risk of sudden cardiac death. Automatic cardioverter defibrillators are the only effective treatment to prevent sudden cardiac death, while therapy management in asymptomatic patients is still controversial. Objectives The aims of the study were to evaluate the incidence and causes of appropriate and inappropriate shocks and the complications related to the device, and to identify the relation of clinical and electrophysiological study variables with the incidence of appropriate shocks. Methods This was a single-center, retrospective registry of patients with Brugada syndrome, with type-1 electrocardiographic pattern, either spontaneous or induced by ajmaline infusion, who were recipients of automatic implantable ...
As the terminology implies this is a block in the right bundle branch. Does this cause the heart to slow down like we see in some AV blocks? No, because we still have the left bundle working the electrical impulse simply travels down the left side and then spreads across to the right ventricle. Ok, its not as efficient as both bundles working at the same time, but its still enough to make both ventricles contract albeit in a different direction from the norm and with a slight delay. How does this manifest on the ECG? Well, perhaps the most obvious sign is a change in the QRS morphology in the right precordial leads - namely the typical RSR pattern. Why the RSR pattern? Well, its all about vectors. The second R wave is produced by the wave of depolarisation spreading from the left ventricle to the right ventricle i.e. toward the right precordial leads. Anything that moves toward a lead will produce a positive complex. Dont forget that in a normal ECG V1 should be predominantly negative. There ...
Sovaldi is being hailed as breakthrough treatment for the more than 3 million Americans with hepatitis C. But while the pricey prescription pill has given new hope to patients, it has had a detrimental impact on the state budget.
Annals of Case Reports is an open access, peer-reviewed international scientific journal that publishes case series, interesting cases, the latest findings in all areas of medicine.
dear mr. Smith, how can I contact you? can I send you my ECG? Im male, 25 years old, Im in Vietnam. I was dianosed to have Brugada type II since 5 years ago, after test with Flecanide. And sice that day, my life is so terrible. There was nothing happen to me but I keep imagining about the death. I want to ask you, is there any case in wrong dianose in history? I really neeed your counsel, please tell me how to send you my ECG. thank you so much, god bless you.. ReplyDelete ...
Very interesting. I read the articles, also. I just have a problem with any recommendation that requires that I be successfully resuscitated from a cardiac arrest caused by a KNOWN entity that I am KNOWN to have and that is KNOWN to cause cardiac arrest before an ICD should be recommended. In this case, it is a fact that around 3% of these people with confirmed Brugada Type 1 are going to arrest. What I really have a problem with is the rather strange assumption that these people are going to be in a place where they can be immediately resuscitated and, even if they are, that the resuscitation attempt will be successful. I really believe there are ethical issues here.. ReplyDelete ...
Clinical By study definition, all patients developed ST elevation in at least one anterior precordial lead during coronary occlusion. No patient developed ST
Veja grátis o arquivo Precordial%20palpation enviado para a disciplina de Propedêutica Clínica Categoria: Anotações - 2 - 959808
An example of bilateral bundle-branch block (RBBB) in the presence of WPW syndrome in which diagnosis was established with the aid of His bundle recordings is presented. Complete RBBB and intermittent block of the superior and inferior divisions of the left bundle branch were coexistent for at least 2 years before complete heart block (trifascicular block) occurred. It was demonstrated that the preexcitation pathway conducted and blocked together with the normal pathways. It is suggested that the anomalous bundle in this case traveled with the normal pathways and that this close relationship is more common than has been suspected.. Retrograde V-A conduction at 1:1 ratio was present during electrical stimulation of the right ventricle and the anomalous bundle was used for retrograde spread of activation from the ventricles to the atria. The retrograde P waves, thus produced, conducted antegrade through the His bundle (reciprocation) but reached the ventricles only when they appeared near the end ...
Prajmaline (Neo-gilurythmal) is a class Ia antiarrhythmic agent which has been available since the 1970s. Class Ia drugs increase the time one action potential lasts in the heart. Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor. It acts to stop arrhythmias of the heart through a frequency-dependent block of cardiac sodium channels. Prajmaline causes a resting block in the heart. A resting block is the depression of a persons Vmax after a resting period. This effect is seen more in the atrium than the ventricle. The effects of some Class I antiarrhythmics are only seen in a patient who has a normal heart rate (~1 Hz). This is due to the effect of a phenomenon called reverse use dependence. The higher the heart rate, the less effect Prajmaline will have. The drug Prajmaline has been used to treat a number of cardiac disorders. These include: coronary artery disease, angina, paroxysmal tachycardia and Wolff-Parkinson-White syndrome. ...
Right bundle branch block Differential diagnosis of right bundle branch block / causes of right bundle branch block are : -pulmonary embolism
authors, ,mainauthor= [[user:Pgpostema,P.G. Postema, MD]] ,supervisor= ,coauthor= [[user:Drj,J.S.S.G. de Jong, MD]] ,moderator= [[user:Pgpostema,P.G. Postema, MD]] ,editor= }} [[Image:Brugada.png,thumb,Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]] [[Image:Brugada_ecg_characteristics.png,thumb, Typical ECG abnormalities in Brugada syndrome]] [[Image:brugada.jpg,thumb, Dr. Pedro Brugada. Pedro and Josep Brugada described in 1992 a landmark publication with a case-series of 8 patients with sudden cardiac death. ,cite>Brugada,/cite> Currently, three brothers of the Brugada family (Pedro, Josep and Ramon Brugada) conduct research in the syndrome that has been named after them.]] [[Image:scn5a.jpg,thumb, The SCN5a gen is located on the short arm (p) of chromosome 3]] The Brugada syndrome is an hereditary disease that is associated with high risk of sudden cardiac death. It is characterized by typical ECG abnormalities: ST segment elevation in the ...
Brugada syndrome is a disorder characterized by sudden death associated with one of several ECG patterns characterized by incomplete right bundle-branch block and ST-segment elevations in the anterior precordial leads. See the image below.
Brugada syndrome is a disorder characterized by sudden death associated with one of several ECG patterns characterized by incomplete right bundle-branch block and ST-segment elevations in the anterior precordial leads. See the image below.
Brugada syndrome is a rare but highly informative condition of susceptibility to potentially lethal ventricular tachyarrhythmias that provides an important model for understanding the pathomechanism underlying more common arrhythmia syndromes.22 23 Perhaps the most attractive and well-substantiated hypothesis to explain the cellular basis of Brugada syndrome involves reduced myocardial Na+ current and the resultant imbalance of inward and outward currents particularly in the right ventricular epicardium where disproportionate expression of the transient outward current creates a transmural voltage gradient and dispersion of repolarization.8 24 This hypothesis has been validated by experimental animal models and by computational methods.9 12 The theory helps to explain the characteristic ECG pattern observed in patients with Brugada syndrome, provides a basis for understanding the effects of Na+-channel blocking agents to aggravate this phenotype, and may illustrate mechanisms underlying acquired ...
BACKGROUND AND PURPOSE: Understanding drug effects on the heart is key to safety pharmacology assessment and anti-arrhythmic therapy development. Here our goal is to demonstrate the ability of computational models to simulate the effect of drug action on the electrical activity of the heart, at the level of the ion-channel, cell, heart and ECG body surface potential. EXPERIMENTAL APPROACH: We use the state-of-the-art mathematical models governing the electrical activity of the heart. A drug model is introduced using an ion channel conductance block for the hERG and fast sodium channels, depending on the IC(50) value and the drug dose. We simulate the ECG measurements at the body surface and compare biomarkers under different drug actions. KEY RESULTS: Introducing a 50% hERG-channel current block results in 8% prolongation of the APD(90) and 6% QT interval prolongation, hERG block does not affect the QRS interval. Introducing 50% fast sodium current block prolongs the QRS and the QT intervals by 12% and
The non-invasive localization of focal heart activity via body surface potential measurements (BSPM) could greatly benefit the understanding and treatment of arrhythmic heart diseases. However, the in vivo validation of source localization algorithms
Right bundle branch block treatment is not always necessary but it can be essential to ensure the condition doesnt exacerbate. Complication and prevention is also available.
Genetic testing for up to 20 genes that cause Brugada syndrome, an arrhythmia that can cause fainting, seizure-like episodes, or cardiac arrest.
... is a genetic disorder that causes an irregular heartbeat. This rare, but life threatening condition is more common in people of Asian descent.
The researchers performed a 5-year retrospective chart review of patients with historical allergic drug reactions who underwent single-blind, placebo-controlled graded drug challenges at an outpatient drug allergy clinic. "We provided evaluation of penicillin and other antibiotic allergies by using standard of care (skin test and challenges) and adding placebo," explains Dr. Jerschow. "The addition of placebo was thought to be necessary as many patients (about 11% to 12% in our study) experience subjective reactions that are often not due to medication, but due to the anticipation effect. Adding placebo helped to distinguish between symptoms due to placebo and due to drug.". The study team found that beta-lactams were the most commonly challenged drug class (70.8%), followed by NSAIDs (17.5%). Reaction rates to drug and placebo were similar during beta-lactam challenges (9.4% vs 8.2%) and during NSAID challenges (14.0% vs 7.0%), respectively. Only 4.4% of patients had objective findings during ...
Dr. Stern responded: None necessary. No treatment necessary and it is not serious unless other |a href="/topics/heart" track_data="{
Sonic Genetics provides word-class genetic testing through specialised genetic laboratories across Australia, the UK, Europe and the USA.
How do the interpretation rules for ST segment proportionality, concordance and discordance apply to right bundle branch block in patients with chest pain ...
TY - JOUR. T1 - Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome. T2 - A prospective evaluation of 52 families. AU - Priori, Silvia G.. AU - Napolitano, Carlo. AU - Gasparini, Maurizio. AU - Pappone, Carlo. AU - Della Bella, Paolo. AU - Brignole, Michele. AU - Giordano, Umberto. AU - Giovannini, Tiziana. AU - Menozzi, Carlo. AU - Bloise, Raffaella. AU - Crotti, Lia. AU - Terreni, Liana. AU - Schwartz, Peter J.. PY - 2000/11/14. Y1 - 2000/11/14. N2 - Background - The ECG pattern of right bundle branch block and ST-segment elevation in leads V1 to V3 (Brugada syndrome) is associated with high risk of sudden death in patients with a normal heart. Current management and prognosis are based on a single study suggesting a high mortality risk within 3 years for symptomatic and asymptomatic patients alike. As a consequence, aggressive management (implantable cardioverter defibrillator) is recommended for both groups. Methods and Results - Sixty patients ...
Brugada syndrome can be caused by mutations in one of several genes. The most commonly mutated gene in this condition is SCN5A, which is altered in approximately 30 percent of affected individuals. This gene provides instructions for making a sodium channel, which normally transports positively charged sodium atoms (ions) into heart muscle cells. This type of ion channel plays a critical role in maintaining the hearts normal rhythm. Mutations in the SCN5A gene alter the structure or function of the channel, which reduces the flow of sodium ions into cells. A disruption in ion transport alters the way the heart beats, leading to the abnormal heart rhythm characteristic of Brugada syndrome.. Mutations in other genes can also cause Brugada syndrome. Together, these other genetic changes account for less than two percent of cases of the condition. Some of the additional genes involved in Brugada syndrome provide instructions for making proteins that ensure the correct location or function of sodium ...
The ECG patterns associated with typical Brugada syndrome were first reported by Martini et al. (17). Subsequent studies showed 3 different types of ECG changes to be associated with Brugada syndrome based on the morphology in V1 and V2 (18). Type-1 ECG is characterized by a ≥2-mm J-point elevation, coved type ST-T segment elevation, and inverted T-wave in leads V1 and V2 (Fig. 1A). Type-2 ECG is characterized by a ≥2-mm J-point elevation, ≥1-mm ST-segment elevation, saddleback ST-T segment, and a positive or biphasic T-wave. Type-3 ECG is the same as type 2, except that the ST-segment elevation is ,1 mm. Among these 3 types of ECGs, only the type 1 is diagnostic of Brugada syndrome. A simple method to document type-1 ECG is to move the V1 lead from the third intercostals space to the second intercostals space. However, the sensitivity and specificity of the diagnosis established with upward displacement of leads are unknown. Another method is to take an ECG after a large meal (19), ...
The most common causes of a right bundle branch block are a previous heart attack, a congenital deformity, cardiovascular disease...
The prevalence varies between 5-50:10.000, largely depending on geographic location. In some southeast Asian countries the disease is considered endemic and believed to be the second cause of death among young men (after car accidents). In these countries Brugada syndrome is believed to underly (in part) the Sudden Unexpected Death Syndrome (SUDS). This relation has, however, not been thoroughly investigated and there are almost no epidemiological studies into Brugada syndrome ECGs (apart from Japan). In different Asian countries, different names have been given to SUDS: in the Phillipines it is called bangungut (to rise and moan in sleep) and in Thailand lai tai (death during sleep ...
The other group consisted of 11 patients showing saddleback-type ST elevation who were referred to us for further evaluation. All were men, and the mean age was 54 ± 14 years. Two patients had episodes of presyncope, but none had a history of cardiac arrest or a family history of sudden cardiac death. Ventricular fibrillation was induced among 8 patients who underwent electrophysiologic study, and 5 received ICD implantation.. After admission, all patients received a pharmacological test for diagnosis of BS using pilsicainide. The drug was given at 1 mg/kg in 5 min, and at the final dose of 46.5 ± 15.6 mg, coved-type ST-segment elevation was induced in all patients. The conventional LP was positive in 8 of 11 patients before pilsicainide, whereas all patients showed saddleback-type ST elevation. When coved-type ST-segment elevation was induced, LP became positive in all. The fQRS complex prolonged from 158 ± 12 ms to 190 ± 12 ms, LAS40 from 31 ± 12 ms to 52 ± 11 ms, and RMS40 from 17.7 ± ...
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Abstract: The goal of this study was to describe normal electrocardiographic (ECG) patterns and... | Article from Journal of Avian Medicine and Surgery March 1, 2011
The main finding of this study is that abnormal ST segment elevation was presented following administration of class Ic drugs in five patients who experienced no previous syncope or ventricular fibrillation. Although the ST segment elevation was similar to that found in the Brugada syndrome, the relation between the ECG changes and the incidence of serious arrhythmias has not yet been sufficiently clarified. The mechanism of ST segment elevation in conjunction with the relevance of sodium channel blocking effects is discussed.. Class Ic drugs are known to be effective for the treatment of various arrhythmias.11 On the other hand, proarrhythmic effects and other adverse effects7 12 have also been reported. Recently, some cases of ST segment elevation in the right precordial leads following administration of class Ic drug were reported by our group5-7 and others.8 9 In recent studies, the mechanisms of ST segment elevation in the Brugada syndrome are thought to derive from the transmural ...
A novel clinical entity characterized by ST segment elevation in right precordial leads (V1 to V3), incomplete or complete right bundle branch block, and susceptibility to ventricular tachyarrhythmia and sudden cardiac death has been described by Brugada et al. in 1992. This disease is now frequently called Brugada syndrome (BrS). The prevalence of BrS in the general population is unknown. The suggested prevalence ranges from 5/1,000 (Caucasians) to 14/1,000 (Japanese). Syncope, typically occurring at rest or during sleep (in individuals in their third or fourth decades of life) is a common presentation of BrS. In some cases, tachycardia does not terminate spontaneously and it may degenerate into ventricular fibrillation and lead to sudden death. Both sporadic and familial cases have been reported and pedigree analysis suggests an autosomal dominant pattern of inheritance. In approximately 20% of the cases BrS is caused by mutations in the SCN5A gene on chromosome 3p21-23, encoding the cardiac sodium
Dromotropic derives from the Greek word "dromos", meaning running, a course, a race. A dromotropic agent is one which affects the conduction speed in the AV node, and subsequently the rate of electrical impulses in the heart. Agents that are dromotropic are often (but not always) inotropic and chronotropic. For instance, parasympathetic stimulation is usually negatively chronotropic and dromotropic, but because the vagus nerve does not innervate ventricular myocardium has no effect on inotropy. Non-dihydropyridine calcium channel blockers such as verapamil block the slow inward calcium current in cardiac tissues, thereby having a negatively dromotropic, chronotropic and inotropic effect. This (and other) pharmacological effect makes these drugs useful in the treatment of angina pectoris. Conversely, they can lead to symptomatic disturbances in cardiac conduction and bradyarrhythmias, and may aggravate left ventricular failure. Bathmotropic Chronotropic Inotrope Furukawa, Y.; Wallick, D. W.; ...
The Brugada syndrome is a genetic disease characterised by abnormal electrocardiogram findings and an increased risk of sudden cardiac death.
Build: Wed Jun 21 18:33:50 EDT 2017 (commit: 4a3b2dc). National Center for Advancing Translational Sciences (NCATS), 6701 Democracy Boulevard, Bethesda MD 20892-4874 • 301-435-0888. ...
Part I. Ajmaline series. Journal of the Indian Chemical Society. 9. p. 539. Siddiqui, S. and Siddiqui, R.H. (1935). The ... Ajmaline series. Journal of the Indian Chemical Society. 12. p. 37. Siddiqui, S. (1942). A note on isolation of three new ... He named the newly discovered chemical compound as Ajmaline, after his mentor Hakim Ajmal Khan who was one of the illustrious ... "Value of Electrocardiographic Parameters and Ajmaline Test in the Diagnosis of Brugada Syndrome Caused by SCN5A Mutations". ...
... is a member of the sodium channel blocking class of antiepileptic drugs.[60] This may suppress the release of glutamate and aspartate, two of the dominant excitatory neurotransmitters in the CNS.[61] It is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[62] but it could have additional actions since it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not, possibly on account of its sigma receptor activity. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties.[63] It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and ...
The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial was designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28] The study randomized 90 mothers of preterm babies to receive either domperidone 10 mg orally three times daily for 28 days (Group A) or placebo 10 mg orally three times daily for 14 days followed by domperidone ...
... (DHP) is a molecule based upon pyridine, and the parent of a class of molecules that have been semi-saturated with two substituents replacing one double bond. They are particularly well known in pharmacology as L-type calcium channel blockers, used in the treatment of hypertension. Compared with certain other L-type calcium channel blockers (for example those of the phenylalkylamine class such as verapamil) that have significant action at the heart, they are relatively vascular selective in their mechanism of action in lowering blood pressure. ...
InChI=1S/C20H27N5O5S/c1-15-14-18(23-30-15)19(26)21-11-10-16-6-8-17(9-7-16)31(28,29)24-20(27)22-25-12-4-2-3-5-13-25/h6-9,14H,2-5,10-13H2,1H3,(H,21,26)(H2,22,24,27) ...
... (CBZ), sold under the trade name Tegretol among others, is an anticonvulsant medication used primarily in the treatment of epilepsy and neuropathic pain.[1] It is not effective for absence or myoclonic seizures.[1] It is used in schizophrenia along with other medications and as a second-line agent in bipolar disorder.[3][1] Carbamazepine appears to work as well as phenytoin and valproate for focal and generalised seizures.[4] Common side effects include nausea and drowsiness.[1] Serious side effects may include skin rashes, decreased bone marrow function, suicidal thoughts, or confusion.[1] It should not be used in those with a history of bone marrow problems.[1] Use during pregnancy may cause harm to the baby; however, stopping the medication in pregnant women with seizures is not recommended.[1] Its use during breastfeeding is not recommended.[1] Care should be taken in those with either kidney or liver problems.[1] Carbamazepine was discovered in 1953 by Swiss chemist Walter ...
A channel that is "inwardly-rectifying" is one that passes current (positive charge) more easily in the inward direction (into the cell) than in the outward direction (out of the cell). It is thought that this current may play an important role in regulating neuronal activity, by helping to stabilize the resting membrane potential of the cell. By convention, inward current (positive charge moving into the cell) is displayed in voltage clamp as a downward deflection, while an outward current (positive charge moving out of the cell) is shown as an upward deflection. At membrane potentials negative to potassium's reversal potential, inwardly rectifying K+ channels support the flow of positively charged K+ ions into the cell, pushing the membrane potential back to the resting potential. This can be seen in figure 1: when the membrane potential is clamped negative to the channel's resting potential (e.g. -60 mV), inward current flows (i.e. positive charge flows into the cell). However, when the ...
... also binds to and blocks α2δ subunit-containing VDCCs, similarly to gabapentin and pregabalin, and hence is a gabapentinoid.[9][16] Both (R)-phenibut and (S)-phenibut display this action with similar affinity (Ki = 23 and 39 μM, respectively).[9] Moreover, (R)-phenibut possesses 4-fold greater affinity for this site than for the GABAB receptor (Ki = 92 μM), while (S)-phenibut does not bind significantly to the GABAB receptor (Ki , 1 mM).[9] As such, based on the results of this study, phenibut would appear to have much greater potency in its interactions with α2δ subunit-containing VDCCs than with the GABAB receptor (between 5- to 10-fold).[9] For this reason, the actions of phenibut as a α2δ subunit-containing voltage-gated calcium channel blocker or gabapentinoid may be its true primary mechanism of action, and this may explain the differences between phenibut and its close relative baclofen (which, in contrast, has essentially insignificant activity as a gabapentinoid; Ki = 6 ...
InChI=1S/C24H34N2O/c1-21(2)19-27-20-24(25-15-9-10-16-25)18-26(23-13-7-4-8-14-23)17-22-11-5-3-6-12-22/h3-8,11-14,21,24H,9-10,15-20H2,1-2H3 ...
... (marketed as Depamide by Sanofi-Aventis) is a carboxamide derivative of valproic acid used in the treatment of epilepsy and some affective disorders. It is rapidly metabolised (80%) to valproic acid (another anticonvulsant) but has anticonvulsant properties itself. It may produce more stable plasma levels than valproic acid or sodium valproate and may be more effective at preventing febrile seizures. However, it is over one hundred times more potent as an inhibitor of liver microsomal epoxide hydrolase. This makes it incompatible with carbamazepine and can affect the ability of the body to remove other toxins. Valpromide is no safer during pregnancy than valproic acid. Valpromide is formed through the reaction of valproic acid and ammonia via an intermediate acid chloride. In pure form, valpromide is a white crystalline powder and has melting point 125-126 °C. It is practically insoluble in water but soluble in hot water. It is available on the market in some European countries. ...
Class Ib antiarrhythmic agents are sodium channel blockers. They have fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates. Class Ib agents shorten the action potential duration and reduce refractoriness. These agents will decrease Vmax in partially depolarized cells with fast response action potentials. They either do not change the action potential duration, or they may decrease the action potential duration. Class Ib drugs tend to be more specific for voltage gated Na channels than Ia. Lidocaine in particular is highly frequency dependent, in that it has more activity with increasing heart rates. This is because lidocaine selectively blocks Na channels in their open and inactive states and has little binding capability in the resting state. Class Ib agents are indicated for the treatment of ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation. Class Ib ...
... has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels.[1] How this effect is mediated and to what extent this mechanism is involved in the anxiolytic and analgesic effects of kavalactones on the central nervous system is unknown. Kavain's pharmacological activities have not been sufficiently investigated, and neither its effect as a serotonin reuptake inhibitor nor its monoamine (norepinephrine) uptake inhibitions and activation of NMDA receptors have been confirmed. The mechanism behind the psychotropic, sedative, and anxiolytic actions of kavain and related kavalactones is still debated. Direct binding to the benzodiazepine/flumazenil binding site of the GABA-A receptor does not occur with kavain enantiomers.[2] Many studies involved kava extracts from different plant parts and are, therefore, not applicable to kavain itself. In 2016, kavain was shown to bind at the α4β2δ GABAA receptor and ...
... has a potential for drug interactions; caution should be used in combining other medicines with it, including other antiepileptics and mood stabilizers.[12] Lower levels of carbamazepine are seen when administrated with phenobarbital, phenytoin, or primidone, which can result in breakthrough seizure activity. Carbamazepine, as a CYP450 inducer, may increase clearance of many drugs, decreasing their concentration in the blood to subtherapeutic levels and reducing their desired effects.[19] Drugs that are more rapidly metabolized with carbamazepine include warfarin, lamotrigine, phenytoin, theophylline, and valproic acid.[12] Drugs that decrease the metabolism of carbamazepine or otherwise increase its levels include erythromycin,[20] cimetidine, propoxyphene, and calcium channel blockers.[12] Carbamazepine also increases the metabolism of the hormones in birth control pills and can reduce their effectiveness, potentially leading to unexpected pregnancies.[12] As a drug that induces ...
... occludes the pore of calcium-activated voltage-gated shaker K+ channels by binding to one of four independent, overlapping binding sites.[6][7] It binds both to the open and the closed states. In addition, the block is enhanced as the ionic strength is lowered.[8] This block occurs as the Asn 30 on the CTX interacts with the Asp 381 on the K+ channel.[9] The blockade of K+ channels by the charybdotoxin peptide causes neuronal hyperexcitability. Mutations of the Lys31Gln and the Asn30Gln had the effect of lessening the CTX block of the pore on the shaker channel.[9] ...
... has several uses including the treatment of abnormal heart rhythms or arrhythmias, chronic pain, and myotonia. In general when treating arrhythmias, mexiletine is reserved for use in dangerous heart rhythm disturbances such as ventricular tachycardia.[2] It is of particular use when treating arrhythmias caused by long QT syndrome.[3] The LQT3 form of long QT syndrome is amenable to treatment with mexiletine as this form is caused by defective sodium channels that continue to release a sustained current rather than fully inactivating, however other forms of long QT syndrome can also be treated with this medication.[3] Mexiletine has been used to treat chronic pain and may also be used to treat muscle stiffness resulting from myotonic dystrophy (Steinert's disease) or nondystrophic myotonias such as myotonia congenita (Thomsen syndrome or Becker syndrome).[4][5] ...
... is available as a generic medication and usually not too expensive.[7] Wholesale it costs between US$0.003 and US$0.15 per dose.[8] A month of treatment is about US$30 in the United States.[2] Since September 2012, the marketing licence in the UK has been held by Flynn Pharma Ltd, of Dublin, Ireland, and the product, although identical, has been called Phenytoin Sodium xxmg Flynn Hard Capsules. (The xxmg in the name refers to the strength-for example "Phenytoin sodium 25 mg Flynn Hard Capsules").[49] The capsules are still made by Pfizer's Goedecke subsidiary's plant in Freiburg, Germany and they still have Epanutin printed on them.[50] After Pfizer's sale of the UK marketing licence to Flynn Pharma, the price of a 28-pack of 25 mg phenytoin sodium capsules marked Epanutin rose from 66p (about $0.88) to £15.74 (about $25.06). Capsules of other strengths also went up in price by the same factor-2384%,[51] costing the UK's National Health Service an extra £43 million (about $68.44 ...
... is effective for prevention of shivering during surgery or recovery from surgery.[5][6] Nefopam was significantly more effective than aspirin as an analgesic in one clinical trial,[7] although with a greater incidence of side effects such as sweating, dizziness and nausea, especially at higher doses.[8][9] The estimated relative potency of nefopam to morphine indicates that 20 mg of nefopam HCl is the approximate analgesic equal of 12 mg of morphine with comparable analgesic efficacy to morphine,[10][11][12] or oxycodone,[13] while Nefopam tends to produce fewer side effects, does not produce respiratory depression,[14] and has much less abuse potential, and so is useful either as an alternative to opioids, or as an adjunctive treatment for use alongside opioid(s) or other analgesics.[12][15] Nefopam is also used to treat severe hiccups.[16] ...
... is an intermediate chemical in the biosynthesis of ajmaline. Vomilenine reductase--a novel enzyme catalyzing a ... crucial step in the biosynthesis of the therapeutically applied antiarrhythmic alkaloid ajmaline. ...
Hinse C, Stöckigt J (July 2000). "The structure of the ring-opened N beta-propyl-ajmaline (Neo-Gilurytmal) at physiological pH ... Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor. It acts to ... Sowton E, Sullivan ID, Crick JC (1984). "Acute haemodynamic effects of ajmaline and prajmaline in patients with coronary heart ... is obviously responsible for its better absorption and bioavailability when compared with ajmaline (Gilurytmal)". Die Pharmazie ...
"Properties of vinorine synthase the Rauwolfia enzyme involved in the formation of the ajmaline skeleton". Z. Naturforsch. C: ...
Ajmaline, a class Ia antiarrhythmic agent and Ajmalan a parent hydride, are named after him. After the partition of India ...
... a key enzyme in the biosynthesis of sarpagine/ajmaline type alkaloids". Planta Med. 48 (8): 221-7. doi:10.1055/s-2007-969924. ...
Ruppert M, Woll J, Giritch A, Genady E, Ma X, Stockigt J (2005). "Functional expression of an ajmaline pathway-specific ...
"A newly-detected reductase from Rauvolfia closes a gap in the biosynthesis of the antiarrhythmic alkaloid ajmaline". Planta ...
Medications such as ajmaline may be used to reveal the ECG changes.[2] Similar ECG patterns may be seen in certain electrolyte ... with some suggestions indicating that ajmaline may be the most effective.[23] Precaution must be taken in giving these ... The most commonly used drugs for this purpose are ajmaline, flecainide, and procainamide, ... "Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome". Heart Rhythm. 2 (3): 254-60. doi ...
... the more important being two chemical classes known as the ajmaline and the serpentine group. The quantity of the total ...
A list of US medications equivalent to Ajmaline is available on the Drugs.com website. ... Ajmaline is a medicine available in a number of countries worldwide. ...
... ; Ritmos; 5H-6,10:11,12a-Dimethanoindolo[3,2-b]quinolizine, ajmalan-17,21-diol deriv.; NSC 15627 ...
In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. When ajmaline ... Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the ... Ajmaline can be found in most species of the Rauvolfia genus as well as Catharanthus roseus. In addition to Southeast Asia, ... Ajmaline was first discovered to lengthen the refractory period of the heart by blocking sodium ion channels, but it has also ...
Tags: buy Ajmaline , Ajmaline supplier , purchase Ajmaline , Ajmaline cost , Ajmaline manufacturer , order Ajmaline , Ajmaline ... Ajmaline, found in the root of Rauwolfia serpentina, is a class Ia antiarrhythmic agent.. ... Ajmaline, found in the root of Rauwolfia serpentina, is a class Ia antiarrhythmic agent. ...
... Author(s): Sorgente, A.; Yazaki, Y.; Capulzini, L.; ... We present an unusual transient pro-arrhythmic effect of ajmaline in a patient with resuscitated cardiac arrest and a left ... possible physio-pathological explanation for this new pro-arrhythmic effect linked to administration of intravenous ajmaline. ...
The preparation of Ajmaline should be 1mg/kg into a 20 ml syringe. Maximum dose is 100 mg. The administration of the drug ... The purpose of the Ajmaline Challenge is to diagnose Brugada Syndrome. ... The purpose of the Ajmaline Challenge is to diagnose Brugada Syndrome.. The preparation of Ajmaline should be 1mg/kg into a 20 ...
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What is a ajmaline challenge?. Ajmaline is a drug known as a sodium channel blocker. It is routinely used by doctors to prevent ... Is the ajmaline challenge safe?. Yes, the ajmaline challenge is safe. However, as with any procedure, there are potential risks ... Why do I need a ajmaline challenge?. Your doctor has advised you to undergo a ajmaline challenge to exclude Brugada syndrome. ... Ajmaline is used by doctors in this test as it blocks the faulty sodium channels and unmasks ECG changes in those patients who ...
The aim of the present study was to evaluate the prevalence of positive ajmaline challenge for BrS in a … ... Ajmaline Testing and the Brugada Syndrome Alessandro Rizzo 1 , Gianluca Borio 1 , Juan Sieira 1 , Sonia Van Dooren 2 , Ingrid ... In non-familial screening group (1,714) ajmaline testing resulted positive in 186 (10.9%). Indications for ajmaline testing ... Ajmaline Testing and the Brugada Syndrome Alessandro Rizzo et al. Am J Cardiol. 2020. . ...
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Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs.[60] This may suppress the release of glutamate and aspartate, two of the dominant excitatory neurotransmitters in the CNS.[61] It is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[62] but it could have additional actions since it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not, possibly on account of its sigma receptor activity. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties.[63] It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and ...
The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial was designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28] The study randomized 90 mothers of preterm babies to receive either domperidone 10 mg orally three times daily for 28 days (Group A) or placebo 10 mg orally three times daily for 14 days followed by domperidone ...
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Ajmaline challenge. Ajmaline (1 mg/kg) was administered intravenously over a 5-min period to unmask the diagnostic ECG pattern ... Ajmaline challenge. From 1992 to 2013, a total of 169 individuals ≤12 years of age underwent an ajmaline challenge for ... Among them, ajmaline challenge revealed a Brugada ECG type 1 in 40 children (24%). ECG parameters before and after ajmaline ... Ajmaline challenge. Ajmaline challenge is an established tool to unmask the diagnostic Brugada ECG pattern in patients with ...
alcohol secundario (es); 第2級アルコール (ja); Alcool secondaire (fr); alkohol drugorzędowy (pl); вторичный спирт (ru); 仲醇 (lzh); 이차 알코올 (ko); secondary alcohol (en); sekundara alkoholo (eo); sekundární alkohol (cs); 仲醇 (zh) każdy alkohol, w którym grupa hydroksylowa przyłączona jest do drugorzędowego atomu węgla (pl) вторичные спирты (ru); Alcool Secondaire (fr); 2차 알코올 (ko); secondary alcohols (en); alkohole drugorzędowe (pl ...
Detailed drug Information for Pediazole. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Check with your doctor if you used this medicine and your migraine did not go away, or if your migraine got worse or started occurring more often. This medicine may increase your risk of having abnormal heart rhythm, heart attack, angina, or stroke. This is more likely to occur if you or a family member already has heart disease, if you have diabetes, high blood pressure, or if you smoke. Call your doctor right away if you have any symptoms of a heart problem, such as chest pain or discomfort, an uneven heartbeat, nausea or vomiting, pain or discomfort in the shoulders, arms, jaw, back, or neck, shortness of breath, or sweating. Call your doctor right away if you have any symptoms of a stroke, such as confusion, difficulty with speaking, double vision, headaches, an inability to move the arms, legs, or facial muscles, an inability to speak, or slow speech. Check with your doctor right away if you have chest discomfort, jaw or neck tightness after taking this medicine. Also, tell your doctor if ...
This medicine will add to the effects of alcohol and other CNS depressants (medicines that make you drowsy or less alert). Some examples of CNS depressants are antihistamines or medicine for allergies or colds, sedatives, tranquilizers, or sleeping medicine, prescription pain medicine or narcotics, medicine for seizures or barbiturates, muscle relaxants, or anesthetics, including some dental anesthetics. Check with your doctor before taking any of the above while you are using this medicine. This medicine may cause some people to become dizzy, drowsy, or may cause trouble with thinking or controlling body movements, which may lead to falls, fractures or other injuries. Even if you take haloperidol at bedtime, you may feel drowsy or less alert on arising. Make sure you know how you react to this medicine before you drive, use machines, or do anything else that could be dangerous if you are dizzy or not alert. Dizziness, lightheadedness, or fainting may occur, especially when you get up from a ...
Ajmaline 17-(Chloroacetate) Monohydrochloride. Drug: Ajmaline 17-(Chloroacetate) Monohydrochloride Ajmaline 17-(Chloroacetate) ... Ajmaline 17-(Chloroacetate) Monohydrochloride. Drug: Ajmaline 17-(Chloroacetate) Monohydrochloride Ajmaline 17-(Chloroacetate) ... Ajmaline. Lorajmine. Anti-Arrhythmia Agents. Voltage-Gated Sodium Channel Blockers. Sodium Channel Blockers. Membrane Transport ... All consecutive patients with suspected BrS-ECG pattern will perform an ajmaline testing (1mg/kg in 5 min). A total of 30 ...
The monomeric units belong to the sarpagine, ajmaline, macroline, vobasine, and pleiocarpamine series. An up-to-date discussion ... The monomeric units belong to the sarpagine, ajmaline, macroline, vobasine, and pleiocarpamine series. An up-to-date discussion ... Keywords: Alstonia genus; Apocynaceae family; sarpagine; macroline; ajmaline; bisindole alkaloids; biomimetic synthesis; ... ajmaline; bisindole alkaloids; biomimetic synthesis; partial and total synthesis; enantiospecific and regiospecific synthesis ...
Immunological protection against ajmaline toxicity.. Descotes J, Cadot R, Evreux JC, Grenot C, Cuilleron CY. ...
Ajmaline test Q&A with Dr Michael Papadakis. Dr Michael Papadakis answers some of your questions about their recent research ... Characterization of early repolarization during ajmaline provocation and exercise tolerance testing. Bastiaenen, R., Raju, H., ... "Characterization of early repolarization during ajmaline provocation and exercise tolerance testing." Heart Rhythm October 2012 ... death to the CRY Centre for Inherited Cardiac Conditions at St Georges Hospital would they always/usually have the ajmaline ...
Omega, delta and kappa families of conotoxins have a knottin or inhibitor cystine knot scaffold. The knottin scaffold is a very special disulfide-through-disulfide knot, in which the III-VI disulfide bond crosses the macrocycle formed by two other disulfide bonds (I-IV and II-V) and the interconnecting backbone segments, where I-VI indicates the six cysteine residues starting from the N-terminus. The cysteine arrangements are the same for omega, delta and kappa families, even though omega conotoxins are calcium channel blockers, whereas delta conotoxins delay the inactivation of sodium channels, and kappa conotoxins are potassium channel blockers.[7] ...
Importantly, our data emphasize the potential for confounding possibly false-positive ajmaline responses in this population, ... a positive ajmaline response was observed in a large proportion of UCA/SUD families. ... Ventricular arrhythmia during ajmaline challenge for the Brugada syndrome. Dobbels B, De Cleen D, Ector J. Dobbels B, et al. ... We assessed ajmaline test response and genetic testing results in 637 individuals from 482 families who underwent ajmaline ...
  • 1995) and most have carbon chains of the ajmaline, reserpine and yohimbine types (Carlos, 2007). (scielo.br)
  • He named it ajmaline, after Hakim Ajmal Khan, one of the most illustrious practitioners of Unani medicine in South Asia. (wikipedia.org)
  • He named the newly discovered chemical compound as Ajmaline, after his mentor Hakim Ajmal Khan who was one of the illustrious practitioners of Unani system of medicine in South Asia. (wikipedia.org)
  • In an afflicted person who was induced with ajmaline, the electrocardiogram would show the characteristic pattern of the syndrome where the ST segment is abnormally elevated above the baseline. (wikipedia.org)
  • We present an unusual transient pro-arrhythmic effect of ajmaline in a patient with resuscitated cardiac arrest and a left ventricular apical aneurysm. (ru.nl)
  • This study evaluated the yield of ajmaline testing and assessed the occurrence of confounding responses in a large cohort of families with unexplained cardiac arrest (UCA) or sudden unexplained death (SUD). (cdc.gov)
  • (8) reviewed the results of 637 ajmaline tests performed on 54 probands with unexplained cardiac arrest and on 583 family members. (onlinejacc.org)
  • In total, 14% of all ajmaline tests performed were positive, including 20% of the tests of cardiac arrest survivors. (onlinejacc.org)
  • Due to the low bioavailability of ajmaline, a semisynthetic propyl derivative called prajmaline (trade name Neo-gilurythmal) was developed that induces similar effects to its predecessor but has better bioavailability and absorption. (wikipedia.org)
  • Ajmaline was seen to be more effective than lidocaine (an accepted drug for treatment) in terminating ventricular tachycardia for acute treatment or emergency therapy for people with recurring symptoms. (wikipedia.org)
  • We discuss the clinical presentation and the possible physio-pathological explanation for this new pro-arrhythmic effect linked to administration of intravenous ajmaline. (ru.nl)
  • It is common to experience a metallic taste in your mouth during the administration of the ajmaline. (heartrhythmclinic.com)
  • The effects of ajmaline in experimental and clinical arrhythmias and their relation to some electrophysiological parameters of the heart. (aspetjournals.org)
  • Considering the renowned expertise of the investigators, it is fair to say that these "confounding ajmaline tests" simply represent false-positive test results. (onlinejacc.org)
  • When ajmaline reversibly blocks hERG, repolarization occurs more slowly because it is harder for potassium to get out due to less unblocked channels, therefore making the RS interval longer. (wikipedia.org)
  • Listing your company for AJMALINE - PHYTOCHEMICALS allows buyers to find your information through our directory pages which appear in the top positions when a search is conducted in Google, Yahoo! (poulvet.com)
  • We derived and validated using bootstrapping a predictive model for ajmaline-induced Type I BrS ECG. (eur.nl)
  • In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. (wikipedia.org)
  • Ajmaline causes action potentials to be prolonged, therefore slowing down firing of the conducting myocytes which ultimately slows the beating of the heart. (wikipedia.org)