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.
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.
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.
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.
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.
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.
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.

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)

The syndrome is caused by abnormal electrical activity in the heart, which can lead to a potentially life-threatening arrhythmia called ventricular fibrillation. This occurs when the ventricles of the heart beat irregularly and rapidly, leading to a loss of effective cardiac function.

Individuals with Brugada syndrome may experience palpitations, shortness of breath, and dizziness, and in some cases, the condition can lead to sudden cardiac death. The diagnosis of Brugada syndrome is based on the presence of a specific ECG pattern, known as a coved-type ST segment elevation, which is characterized by a rounded notch in the ST segment of the ECG tracing.

There is no cure for Brugada syndrome, but medications and implantable devices such as an implantable cardioverter-defibrillator (ICD) can be used to manage the condition and prevent complications. In some cases, surgery may be necessary to remove any underlying causes of the arrhythmia.

Overall, Brugada syndrome is a rare and potentially life-threatening cardiac disorder that requires careful monitoring and management to prevent complications and improve quality of life for affected individuals.

There are three main types of bundle branch blocks:

1. Right bundle branch block (RBBB): This occurs when the electrical conduction bundle that carries the heart's rhythm from the right atrium to the right ventricle is damaged or diseased.
2. Left bundle branch block (LBBB): This occurs when the electrical conduction bundle that carries the heart's rhythm from the left atrium to the left ventricle is damaged or diseased.
3. Bifascicular bundle branch block: This occurs when two of the electrical conduction bundles are damaged or diseased.

Symptoms of bundle branch block may include:

* Heart palpitations
* Slow or irregular heartbeat
* Shortness of breath
* Fatigue
* Dizziness or lightheadedness
* Chest pain or discomfort

Diagnosis of bundle branch block is typically made using an electrocardiogram (ECG) test, which measures the electrical activity of the heart. Treatment options for BBB may include medications to regulate the heartbeat, cardiac resynchronization therapy (CRT) to help both ventricles beat together, or implantable cardioverter-defibrillator (ICD) to prevent life-threatening arrhythmias. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

It is important to note that bundle branch block can increase the risk of developing other cardiac conditions such as heart failure, atrial fibrillation, and ventricular tachycardia. Therefore, it is essential for individuals with BBB to work closely with their healthcare provider to manage their condition and reduce the risk of complications.

... is widely dispersed among 25 plant genera, but is of significant concentration in the Apocynaceae family. Ajmaline is ... In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. When ajmaline ... Finally, norajmaline methyl transferase (NAMT) methylates norajmaline resulting in our desired compound: ajmaline. Ajmaline was ... Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the ...
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". ...
... and ajmaline. In the 1970s, the bark from stems and roots was harvested from which reserpine was extracted and sold for human ...
Medications such as ajmaline may be used to reveal the ECG changes. Similar ECG patterns may be seen in certain electrolyte ... The most commonly used drugs for this purpose are ajmaline, flecainide, and procainamide, with some suggestions indicating that ... "Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome". Heart Rhythm. 2 (3): 254-60. doi: ... ajmaline may be the most effective. Precaution must be taken in giving these medications as there is a small risk of causing ...
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 ...
... is an alkaloid that is an intermediate chemical in the biosynthesis of ajmaline. von Schumann, Gerald; Gao, Shujuan ... a novel enzyme catalyzing a crucial step in the biosynthesis of the therapeutically applied antiarrhythmic alkaloid ajmaline". ...
"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 ...
... including ajmaline, ajmalicine, reserpine, and serpentine, among others. Rauvolfia serpentina may be useful in treating ... ajmaline, and ajmalicine in Rauvolfia serpentina by reversed-phase high-performance liquid chromatography". Journal of ...
"A newly-detected reductase from Rauvolfia closes a gap in the biosynthesis of the antiarrhythmic alkaloid ajmaline". Planta ...
His superiors allegedly did not act on these suspicions, even when four empty vials of gilurytmal (ajmaline) surfaced in ... On 28 August 2017, police said that Högel had used five different drugs, including ajmaline, sotalol, lidocaine, amiodarone and ... Ajmaline), Sotalex (Sotalol), Xylocain (Lidocaine) and Cordarex (Amiodarone). The main trial at Landgericht Oldenburg commenced ... colleagues caught Högel intentionally manipulating a patient's syringe pump to improperly administer ajmaline. The incident ...
... and electrophysiological observations in patients with myotonic muscle disease and the therapeutic effect of N-propyl-ajmaline ...
It is derived from ajmaline, an alkaloid from the roots of Rauvolfia serpentina, by synthetically adding a chloroacetate ...
... a novel enzyme catalyzing a crucial step in the biosynthesis of the therapeutically applied antiarrhythmic alkaloid ajmaline". ...
Hairy root: ajmaline, ajmalacine, reserpine, reserpiline, sarpagine, and serpentine Root bark: aunamine and neosarpagine Other ... Sudha, C. G.; Obul Reddy, B.; Ravishankar, G. A.; Seeni, S. (2003). "Production of Ajmalicine and Ajmaline in Hairy Root ...
Ajmaline itself is named after Hakim Ajmal Khan, a distinguished practitioner of the Unani school of traditional medicine in ... The stereochemistry is the same as that in naturally occurring ajmaline, and corresponds to (2R,3S,5S,7S,15S,16R,20S) using ... The name is derived from ajmaline, an antiarrhythmic alkaloid isolated from the roots of Rauvolfia serpentina which is formally ...
Ruppert M, Woll J, Giritch A, Genady E, Ma X, Stöckigt J (November 2005). "Functional expression of an ajmaline pathway- ... acetate This plant enzyme mediates the last stages in the biosynthesis of the indole alkaloid ajmaline. Polz L, Schübel H, ... a specific enzyme involved in the biosynthesis of the Rauwolfia alkaloid ajmaline". Zeitschrift für Naturforschung C. 42 (4): ... ajmaline + acetate (2) 17-O-acetylnorajmaline + H2O ⇌ {\displaystyle \rightleftharpoons } norajmaline + ...
... and he could also show the anti-arrhytmic effects of ajmaline. As he did not give his acceptance to the Berlin Wall he had to ...
Other drugs that affect the cardiovascular system include ajmaline, which is a Class I antiarrhythmic agents, and ajmalicine, ...
Falkenhagen H, Stockligt J (1995). "Enzymatic biosynthesis of vomilenine, a key intermediate of the ajmaline pathway, catalysed ...
H+ The biosynthesis of raucaffrinoline from perakine is a side route of the ajmaline biosynthesis pathway. Sun L, Ruppert M, ...
... ajmaline MeSH D03.132.436.681.077.650 - prajmaline MeSH D03.132.436.681.333 - ellipticines MeSH D03.132.436.681.444 - ibogaine ... ajmaline MeSH D03.438.473.402.681.077.650 - prajmaline MeSH D03.438.473.402.681.333 - ellipticines MeSH D03.438.473.402.681.444 ...
Cymarin C01AX02 Peruvoside C01BA01 Quinidine C01BA02 Procainamide C01BA03 Disopyramide C01BA04 Sparteine C01BA05 Ajmaline ...
The molecular formula C20H26N2O2 (molar mass: 326.4 g/mol) may refer to: Ajmaline Dihydroquinidine Dihydroquinine Epsiprantel ...
Antiarrhythmic agents Type I (sodium channel blockers) Type Ia Ajmaline Procainamide Quinidine Type Ib Lidocaine Phenytoin Type ...
... ajmaline, procainamide, disopyramide) Class Ib - Sodium channels (lidocaine, phenytoin, mexiletine, tocainide) Class Ic - ...
ajmaline. *dexketoprofen. *Sulfanilamide has no known mild interactions with other drugs.. The drug interactions listed above ...
Intrahepatic cholestatic hepatitis following diagnostic ajmaline challenge. Mellor G, Fellows I, Williams I. Mellor G, et al. ...
Brugada, J., Brugada, P. & Brugada, R. Ajmaline unmasks right bundle branch block-like and ST segment elevation in V1-V3 in ...
Ajmaline - Preferred Concept UI. M0000613. Scope note. An alkaloid found in the root of RAUWOLFIA SERPENTINA, among other plant ... Ajmaline Hydrochloride - Narrower Concept UI. M0584206. Scope note. An alkaloid found in the root of RAUWOLFIA SERPENTINA, ... Ajmaline Hydrochloride. Aritmina. Cardiorythmine. Gilurtymal. Rauverid. Serenol. Tachmalin. Wolfina. Tree number(s):. D03.132. ...
Ajmaline D3.438.473.402.681.77 D3.633.100.473.402.681.77 Alarmins D12.644.276.87 D23.35 D12.776.467.87 D23.529.87 Albendazole ...
Ajmaline Hydrochloride Narrower Concept UI. M0584206. Registry Number. 140MW6WGAF. Terms. Ajmaline Hydrochloride Preferred Term ... Ajmaline [D03.633.100.473.402.681.077] * Lorajmine [D03.633.100.473.402.681.077.324] * Prajmaline [D03.633.100.473.402.681. ... Ajmaline [D03.633.100.496.500.500.681.077] * Lorajmine [D03.633.100.496.500.500.681.077.324] * Prajmaline [D03.633.100.496. ... Ajmaline Preferred Concept UI. M0000613. Registry Number. 1PON08459R. Related Numbers. 140MW6WGAF. 4360-12-7. Scope Note. An ...
Högel was found to have injected them with a variety of drugs that included the heart medicines ajmaline, amiodarone and ... even after a colleague saw him inject a patient with ajmaline. ...
Miles, C., Finocchiaro, G., Papadakis, M., Gray, B., Westaby, J., Ensam, B., Basu, J., Parry-Williams, G., Papatheodorou, E., Paterson, C., Malhotra, A., Robertus, J. L., Ware, J. S., Cook, S. A., Asimaki, A., Witney, A., Ster, I. C., Tome, M., Sharma, S., Behr, E. R., & 1 othersSheppard, M. N., 9 Apr 2019, In: Circulation. 139, 15, p. 1786-1797 12 p.. Research output: Contribution to journal › Article › peer-review ...
... activation or repression tadalafil cialis from india Ajmaline Sulfonamides may enhance the adverse toxic effect of Ajmaline ...
Santa clara university essay prompt 2022 for ajmaline synthesis essay. To what extent the ir existence depends upon noticing ...
The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. Eur Heart J. 2003;24(12):1104- ...
Oxcarbazepine, sold under the brand name Trileptal among others, is a medication used to treat epilepsy and bipolar disorder.[1] For epilepsy it is used for both focal seizures and generalized seizures.[5] It has been used both alone and as add-on therapy in people with bipolar who have had no success with other treatments.[6][1] It is taken by mouth.[1] Common side effects include nausea, vomiting, dizziness, drowsiness, double vision and trouble with walking.[2] Serious side effects may include anaphylaxis, liver problems, pancreatitis, suicide, and an abnormal heart beat.[2][5] While use during pregnancy may harm the baby, use may be less risky than having a seizure.[7] Use is not recommended during breastfeeding.[7] In those with an allergy to carbamazepine there is a 25% risk of problems with oxcarbazepine.[2] How it works is not entirely clear.[1] Oxcarbazepine was patented in 1969 and came into medical use in 1990.[8] It is available as a generic medication.[5] A month supply in the ...
Adenosine (phosphate); Ajmaline; Amiodarone; Antidysrhythmic NEC; Aprindine; Bretylium tosilate; Bunaftine; Cardiac; ...
... at baseline and during ajmaline testing for BrS diagnosis. METHODS: Consecutive patients diagnosed with BrS during ajmaline ... During ajmaline testing, BrS with VAs presented longer QRS duration [159 ± 34 ms versus 138 (122-155) ms, p = 0.006], higher ... ECG recordings during ajmaline or isoproterenol test were divided in two timeframes from which ECG parameters were calculated: ... CONCLUSIONS: Ajmaline induced important HRV changes similar to those observed during isoproterenol. Increased mTWA was observed ...
Ajmaline Testing and the Brugada Syndrome. Rizzo Alessandro et al. The American journal of cardiology 2020 Aug ...
ឱសថព្យាបាលជំងឺទាក់ទងនឹងចង្វាក់បេះដូង(Disopyramide, Procainamide, Ajmaline, Amiodarone, Quinidine, Propafenone, ជាដើម) - ...
AILANTHUS ALTISSIMA POLLEN C85091 5G78C6GB5E AILANTHUS ALTISSIMA WHOLE C72232 K21NZZ5Y0B AIR C73434 1PON08459R AJMALINE C83524 ...
21-di-monochloroacetyl-ajmaline in the prevention and therapy of cardiac arrhythmias]. PMID- 5098894 TI - [Need to develop ... Therapeutic comparison of ajmaline and quinidine compounds in arrhythmias in absence of organic cardiopathy]. PMID- 5098893 TI ...
A monochloroacetyl derivative of ajmaline. It is a class Ia antiarrhythmic agent that is rapidly hydrolyzed to ajmaline by ... HN - 2014; use AJMALINE 1973-2013 MH - Lujo virus UI - D063927 MN - B4.820.57.70.100.525 MN - B4.909.777.80.70.100.525 MS - A ...
In-silico characterization of the atrial mode of action of ajmaline and vernakalant and their effect on spiral waves. ...
As with other class I antiarrhythmic drugs, such as quinidine, ajmaline, and procainamide, the mechanism of action of ...
It could, for example, be a medicine that is licensed as a medicine abroad (e.g. ajmaline), or it could be a nutritional ...
Ajmaline D3.438.473.402.681.77 D3.633.100.473.402.681.77 Alarmins D12.644.276.87 D23.35 D12.776.467.87 D23.529.87 Albendazole ...
":"Ajmaline","data":{"category":"Medicine","linkRef":"Ajmaline"}},{"value":"Albendazole","data":{"category":"Medicine","linkRef ... ":"RS1001 - Ajmaline","data":{"category":"RS Form","linkRef":"RS1001"}},{"value":"RS1005 - Ezetimibe","data":{"category":"RS ...
Ajmaline [D03.633.100.496.500.500.681.077] * Ellipticines [D03.633.100.496.500.500.681.333] * Ibogaine [D03.633.100.496.500.500 ...
ajmaline and sarpagine biosynthesis. *Biosynthesis of secondary metabolites. *Indole alkaloid biosynthesis. gardneral + acetyl- ...
Inhibition of vasomotor reflexes by ajmaline.. DAS GUPTA, S R; WERNER, G. ...
  • The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. (bvsalud.org)
  • The aim of the present study was to evaluate the prevalence of positive ajmaline challenge for BrS in a cohort of consecutive patients who underwent electrophysiological evaluation for different clinical reasons. (nih.gov)
  • Study population was investigated by ajmaline challenge and echocardiographic assessment over time. (bvsalud.org)
  • Systematic investigations, including genetic testing and ajmaline challenge, can lead to the achievement of a specific diagnosis in up to 20% of patients. (bvsalud.org)