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.
Recording of the moment-to-moment electromotive forces of the heart on a plane of the body surface delineated as a vector function of time.
A characteristic symptom complex.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of CARDIOMYOCYTES. Defects in the SCN5A gene, which codes for the alpha subunit of this sodium channel, are associated with a variety of CARDIAC DISEASES that result from loss of sodium channel function.
Persistent and disabling ANXIETY.
Formed by the articulation of the talus with the calcaneus.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.

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)

Ajmaline is a type of medication known as a Class I antiarrhythmic agent, which is used to treat certain types of abnormal heart rhythms. It works by blocking the sodium channels in the heart muscle, which helps to slow down the conduction of electrical signals within the heart and can help to restore a normal heart rhythm.

Ajmaline is typically administered intravenously (through a vein) in a hospital setting, as it acts quickly and its effects can be closely monitored by healthcare professionals. It may be used to diagnose certain types of heart rhythm disturbances or to treat acute episodes of arrhythmias that are not responding to other treatments.

Like all medications, ajmaline can have side effects, including dizziness, headache, nausea, and chest pain. It is important for patients to be closely monitored while taking this medication and to report any unusual symptoms to their healthcare provider. Ajmaline should only be used under the close supervision of a qualified healthcare professional.

"Rauwolfia" is the name of a genus of plants in the dogbane family (Apocynaceae). It includes several species that have been used in traditional medicine for various purposes. The most well-known species is probably Rauwolfia serpentina, also known as Indian snakeroot or sarpagandha.

Extracts from the roots of Rauwolfia serpentina contain a number of alkaloids with pharmacological activity, including reserpine, which has been used in modern medicine to treat high blood pressure and some psychiatric disorders. However, due to its side effects, it is not commonly used today.

It's important to note that the use of Rauwolfia and its extracts should be done under medical supervision, as they can have significant effects on various body systems, including the heart, blood pressure, and nervous system.

Brugada Syndrome is a genetic disorder characterized by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death. It is typically caused by a mutation in the SCN5A gene, which encodes for a sodium channel protein in the heart. This mutation can lead to abnormal ion transport in the heart cells, causing changes in the electrical activity of the heart that can trigger dangerous arrhythmias.

The ECG findings associated with Brugada Syndrome include a distinct pattern of ST-segment elevation in the right precordial leads (V1-V3), which can appear spontaneously or be induced by certain medications. The syndrome is often classified into two types based on the presence or absence of symptoms:

* Type 1 Brugada Syndrome: This type is characterized by a coved-type ST-segment elevation of at least 2 mm in height in at least one right precordial lead, with a negative T wave. This pattern must be present to make the diagnosis, and it should not be transient or induced by any medication or condition. Type 1 Brugada Syndrome is associated with a higher risk of sudden cardiac death.
* Type 2 Brugada Syndrome: This type is characterized by a saddleback-type ST-segment elevation of at least 2 mm in height in at least one right precordial lead, with a positive or biphasic T wave. The ST segment should return to the baseline level or below within 0.08 seconds after the J point (the junction between the QRS complex and the ST segment). Type 2 Brugada Syndrome is associated with a lower risk of sudden cardiac death compared to Type 1, but it can still pose a significant risk in some individuals.

Brugada Syndrome can affect people of any age, gender, or ethnicity, although it is more commonly diagnosed in middle-aged men of Asian descent. The syndrome can be inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutation from a parent who carries the gene. However, not all individuals with the genetic mutation will develop symptoms or have abnormal ECG findings.

Treatment for Brugada Syndrome typically involves implanting a cardioverter-defibrillator (ICD) to prevent sudden cardiac death. Medications such as quinidine or isoproterenol may also be used to reduce the risk of arrhythmias. Lifestyle modifications, such as avoiding alcohol and certain medications that can trigger arrhythmias, may also be recommended.

Secologanin tryptamine alkaloids are a type of alkaloid compound that is derived from the combination of secologanin (a metabolite found in certain plants) and tryptamine (an organic compound that is a building block for several neurotransmitters). These alkaloids have been identified in various plant species, including those in the genera *Psychotria* and *Uncaria*, and are known to exhibit a range of pharmacological activities. Some examples of secologanin tryptamine alkaloids include ajmalicine, reserpine, and yohimbine, which have been used in traditional medicine for their sedative, antihypertensive, and aphrodisiac properties, respectively. However, it is important to note that these compounds can also have toxic effects and should only be used under the guidance of a medical professional.

Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:

1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.

It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.

Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.

During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.

ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.

Bundle-branch block (BBB) is a type of conduction delay or block in the heart's electrical system that affects the way electrical impulses travel through the ventricles (the lower chambers of the heart). In BBB, one of the two main bundle branches that conduct electrical impulses to the ventricles is partially or completely blocked, causing a delay in the contraction of one of the ventricles.

There are two types of bundle-branch block: right bundle-branch block (RBBB) and left bundle-branch block (LBBB). In RBBB, the right bundle branch is affected, while in LBBB, the left bundle branch is affected. The symptoms and severity of BBB can vary depending on the underlying cause and the presence of other heart conditions.

In some cases, BBB may not cause any noticeable symptoms and may only be detected during a routine electrocardiogram (ECG). However, if BBB occurs along with other heart conditions such as coronary artery disease, heart failure, or cardiomyopathy, it can increase the risk of serious complications such as arrhythmias, syncope, and even sudden cardiac death.

Treatment for bundle-branch block depends on the underlying cause and the severity of the condition. In some cases, no treatment may be necessary, while in others, medications, pacemakers, or other treatments may be recommended to manage symptoms and prevent complications.

Vectorcardiography (VCG) is a type of graphical recording that depicts the vector magnitude and direction of the electrical activity of the heart over time. It provides a three-dimensional view of the electrical activation pattern of the heart, as opposed to the one-dimensional view offered by a standard electrocardiogram (ECG).

In VCG, the electrical potentials are recorded using a special array of electrodes placed on the body surface. These potentials are then mathematically converted into vectors and plotted on a vector loop or a series of loops that represent different planes of the heart's electrical activity. The resulting tracing provides information about the magnitude, direction, and timing of the electrical activation of the heart, which can be helpful in diagnosing various cardiac arrhythmias, ischemic heart disease, and other cardiac conditions.

Overall, vectorcardiography offers a more detailed and comprehensive view of the heart's electrical activity than traditional ECG, making it a valuable tool in clinical cardiology.

A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.

For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.

It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.

NAV1.5, also known as SCN5A, is a specific type of voltage-gated sodium channel found in the heart muscle cells (cardiomyocytes). These channels play a crucial role in the generation and transmission of electrical signals that coordinate the contraction of the heart.

More specifically, NAV1.5 channels are responsible for the rapid influx of sodium ions into cardiomyocytes during the initial phase of the action potential, which is the electrical excitation of the cell. This rapid influx of sodium ions helps to initiate and propagate the action potential throughout the heart muscle, allowing for coordinated contraction and proper heart function.

Mutations in the SCN5A gene, which encodes the NAV1.5 channel, have been associated with various cardiac arrhythmias, including long QT syndrome, Brugada syndrome, and familial atrial fibrillation, among others. These genetic disorders can lead to abnormal heart rhythms, syncope, and in some cases, sudden cardiac death.

Anxiety disorders are a category of mental health disorders characterized by feelings of excessive and persistent worry, fear, or anxiety that interfere with daily activities. They include several different types of disorders, such as:

1. Generalized Anxiety Disorder (GAD): This is characterized by chronic and exaggerated worry and tension, even when there is little or nothing to provoke it.
2. Panic Disorder: This is characterized by recurring unexpected panic attacks and fear of experiencing more panic attacks.
3. Social Anxiety Disorder (SAD): Also known as social phobia, this is characterized by excessive fear, anxiety, or avoidance of social situations due to feelings of embarrassment, self-consciousness, and concern about being judged or viewed negatively by others.
4. Phobias: These are intense, irrational fears of certain objects, places, or situations. When a person with a phobia encounters the object or situation they fear, they may experience panic attacks or other severe anxiety responses.
5. Agoraphobia: This is a fear of being in places where it may be difficult to escape or get help if one has a panic attack or other embarrassing or incapacitating symptoms.
6. Separation Anxiety Disorder (SAD): This is characterized by excessive anxiety about separation from home or from people to whom the individual has a strong emotional attachment (such as a parent, sibling, or partner).
7. Selective Mutism: This is a disorder where a child becomes mute in certain situations, such as at school, but can speak normally at home or with close family members.

These disorders are treatable with a combination of medication and psychotherapy (cognitive-behavioral therapy, exposure therapy). It's important to seek professional help if you suspect that you or someone you know may have an anxiety disorder.

The subtalar joint is a joint in the foot that is located between the talus and calcaneus (heel) bones. It is called a "joint" because it allows for movement, specifically inversion and eversion, which are the movements that allow the foot to roll inward or outward. The subtalar joint plays an essential role in the biomechanics of the foot and ankle, helping to absorb shock during walking and running, and contributing to the stability of the foot during standing and walking. Issues with the subtalar joint can lead to various foot and ankle problems, such as flatfoot or chronic ankle instability.

Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.

An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.

There are several types of cardiac arrhythmias, including:

1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.

Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.

Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.

... 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 ... colleagues caught Högel intentionally manipulating a patient's syringe pump to improperly administer ajmaline. He was arrested ...
... 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-arrhythmic 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 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 ...
Structure, properties, spectra, suppliers and links for: AJMALINE, 4360-12-7.
Wolfina - tablet, oral (50mg) - Ajmaline (Wolfina) CureHunter Inc. provides medical information and specifically does NOT ...
... ajmaline, oxamniquine, and argatroban. To explore the generality of this protocol, a number of indoline and tetrahydroquinoline ...
Platycodon fluidextract, glycyrrhiza extract, plantago herb extract, peony root extract and dihydrocodeine phosphate ,JP ...
The researchers identified the anti-arrhythmia drug ajmaline as one potential Ebola treatment. ...
1994) Efficacy of ajmaline and propafenone in patients with accessory pathways: a prospective randomized study. J Cardiovasc ...
9] Cocaine consumption or the use of the antiarrhythmic drugs propafenone, ajmaline, flecainide, or procainamide may reveal ECG ...
Sequential isolation of superoxide dismutase and ajmaline from tissue culture of Rauwolfia serpentina Benth. Prikl. Biokhim. ...
Ajmaline. The risk or severity of QTc prolongation can be increased when Famotidine is combined with Ajmaline. ...
ajmaline. Some of these alkaloids act similar to beta blockers. In their 2009 book, "Medicinal Plants of the World," botanist ... Another alkaloid, ajmaline, has anti-arrhythmic action and inhibits ventricular arrhythmias. Indian snakeroot has tranquilizing ...
Rolf S, Bruns HJ, Wichter T, Kirchhof P, Ribbing M, Wasmer K, Paul M, Breithardt G, Haverkamp W, Eckardt L: The ajmaline ... Vinblastine is clinically used for the treatment of leukemia, Hodgkins lymphoma and other cancers [12-15]. Ajmaline of ... Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome. Heart Rhythm. 2005, 3: 254-260. ...
One study used ajmaline provocation to elicit a type 1 Brugada ECG pattern in 91 patients, and found that the repolarization ... and body surface potential maps during ajmaline provocation. J Am Coll Cardiol. 2010 Feb 23. 55(8):789-97. [QxMD MEDLINE Link] ...
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. ...
Ajmaline, Arbre aux Serpents, Arbre de Serpents, Bois de Couleuvre, Chandrika, Chota-Chand, Covanamilpori, Dhanburua, Pagla-Ka- ...
Ajmaline. Sodium channel protein type 5 subunit alpha. target. Almitrine. Sodium/potassium-transporting ATPase subunit alpha-1 ... Ajmaline. An antiarrhythmic used to manage a variety of forms of tachycardias. ...
Pharmacological testing with a class 1C antiarrhythmic such as Ajmaline can unmask the typical ECG, however it is non- ...
Ajmaline. ; (15α,17R,21α)-Ajmalan-17,21-diol(IUPAC). ; Ajmalan-17,21-diol, (15α,17R,21α)-(CAS). ; Ajmaline [Wiki]. ; Aritmina. ...
In drug-induced hepatitis caused by a heterogenous group of drugs consisting of ajmaline, aminopterine, isaxonine, isoniazid, ...
In patients with no EPS diagnosis, tests with pharmacological stressors using infra-his stressordrugs (ajmaline 1 mg/kg to a ...
While reserpine is used as a hypotensive and tranquillizer, ajmaline is used as antiarrhythmic agent.[/p]. [h1]TULSI[/h1]. [p][ ... p]Roots of Rauvolfia vomitoria also contain a large number of alkaloids, most important of which are ajmaline, alstonine, ... Other alkaloids which are found in this plant but are not isolated commercially are ajmaline, ajmalicine and serpentine. ... However, out of these alkaloids, only ajmaline and reserpine are isolated commercially from Rauvolfia vomitoria. Total alkaloid ...
Ajmaline blocks INa and IKr without eliciting differences between Brugada syndrome patient and control human pluripotent stem ...
Ajmaline blocks INa and IKr without eliciting differences between Brugada syndrome patient and control human pluripotent stem ...
When cells were treated with VBL and each alkaloid for 30 min, reserpine, rescinnamine, syrosingopine, and ajmaline markedly ...
Ajmaline. An alkaloid found in the root of RAUWOLFIA SERPENTINA, among other plant sources. It is a class Ia antiarrhythmic ... Ajmaline is a medication used in the medical field to treat certain types of arrhythmias, which are abnormal heart rhythms. It ... Ajmaline is typically administered intravenously and is used to diagnose and treat certain types of arrhythmias, such as Wolff- ... Myeloma ProteinsBoronic AcidsPyrazinesThalidomideAjmalineMelphalanDexamethasoneSyndecan-1Antineoplastic AgentsBence Jones ...
Ajmaline. Salicylates may intensify Ajmalines harmful or toxic effects. In particular, there may be an elevated risk for ...
Ajmaline. 0.94. 0.00022. Antiarrhythmic agent. 4. 5707885. 0.87. 0.00044. Unknown. 6. Carbimazole. 0.90. 0.00182. Imidazole- ...
AJMALINE. Predisposing factors may increase risk of arrhythmias. Moderate Risk: Minimise risk. Take action necessary to reduce ...
  • Ajmaline (also known by trade names Gilurytmal, Ritmos, and Aritmina) is an alkaloid that is classified as a 1-A antiarrhythmic agent. (wikipedia.org)
  • Ajmaline is a monoterpenoid indole alkaloid, composed of an indole from tryptophan and a terpenoid from iridoid glucoside secologanin. (wikipedia.org)
  • Another alkaloid, ajmaline, has anti-arrhythmic action and inhibits ventricular arrhythmias. (healthfully.com)
  • Högel was found to have injected them with a variety of drugs that included the heart medicines ajmaline, amiodarone and sotalol, along with potassium and the anesthetic lidocaine. (wypr.org)
  • Ajmaline is used intravenously to test for Brugada syndrome since they both affect the sodium ion channel. (wikipedia.org)
  • OBJECTIVE: This study aimed to investigate the predictive value of T-peak to T-end interval and corrected T-peak to T-end interval for predicting the positive response of the ajmaline challenge test in suspected Brugada syndrome patients. (bvsalud.org)
  • CONCLUSIONS: The T-peak to T-end interval and corrected T-peak to T-end interval could not predict the positive response of the ajmaline challenge test in suspected Brugada syndrome patients. (bvsalud.org)
  • Ajmaline was first discovered to lengthen the refractory period of the heart by blocking sodium ion channels, but it has also been noted that it is also able to interfere with the hERG (human Ether-a-go-go-Related Gene) potassium ion channel. (wikipedia.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)
  • Ajmaline is superior to flecainide and procainamide to provoke BrS. (bvsalud.org)
  • While 86 alkaloids have been discovered throughout Rauvolfia vomitoria, ajmaline is mainly isolated from the stem bark and roots of the plant. (wikipedia.org)
  • Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the membrane to depolarize in the first case. (wikipedia.org)
  • Clinical characteristics and electrocardiographic parameters were analyzed, including TpTe, corrected TpTe, QT, corrected QT(QTc) interval, and S-wave duration, compared with the result of the ajmaline challenge test. (bvsalud.org)
  • RESULTS: The study found that TpTe and corrected TpTe interval in suspected BrS patients were not significantly associated with a positive response to the ajmaline challenge test. (bvsalud.org)
  • 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)
  • Some hospital employees in Delmenhorst, near Bremen, were charged with negligent manslaughter for not taking quick and decisive action to stop Högel - even after a colleague saw him inject a patient with ajmaline. (wypr.org)
  • Ajmaline can be found in most species of the genus Rauvolfia as well as Catharanthus roseus. (wikipedia.org)
  • Due to complications that could arise with the ajmaline challenge, a specialized doctor should perform the administration in a specialized center capable of extracorporeal membrane oxygenator support Hellmuth Kleinsorge (1920-2001) German medical doctor Siddiqui S, Siddiqui RH (1931). (wikipedia.org)
  • METHODS: Patients who underwent the ajmaline test in our center were enrolled. (bvsalud.org)
  • Ajmaline in combination with other hypotensive agents, is used in the treatment of HTN complicated with sarrythmia. (sdach.ac.in)
  • A total of seventeen alkaloids, comprising six macroline (including alstofolinine A, a macroline indole incorporating a butyrolactone ring-E), two ajmaline, one sarpagine, and eight akuammiline alkaloids, were isolated from the stem-bark and leaf extracts of the Malayan Alstonia macrophylla. (afpm.org.my)
  • While you are having an ECG test you will be given an injection of ajmaline or flecainide (antiarrhythmic drugs). (myheart.org.uk)
  • Ajmaline is superior to flecainide and procainamide to provoke BrS. (bvsalud.org)
  • Sodium channel blocker antiarrhythmic drugs (flecainide, procainamide, ajmaline) can unmask the pattern. (empendium.com)
  • He named it ajmaline, after Hakim Ajmal Khan, one of the most illustrious practitioners of Unani medicine in South Asia. (wikipedia.org)
  • He named it "Ajmaline" after the great Hakim Ajmal Khan. (ajmal.pk)
  • Ajmaline (also known by trade names Gilurytmal, Ritmos, and Aritmina) is an alkaloid that is classified as a 1-A antiarrhythmic agent. (wikipedia.org)
  • According to them, the roots of this herb contain several alkaloids, the more important being two chemical classes known as the ajmaline and the serpentine group. (pioneerherbal.com)
  • Ajmaline is a monoterpenoid indole alkaloid, composed of an indole from tryptophan and a terpenoid from iridoid glucoside secologanin. (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)
  • The biosynthesis of raucaffrinoline from perakine is a side route of the ajmaline biosynthesis pathway. (enzyme-database.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)
  • All consecutive patients from 2008 to 2019 who underwent ajmaline testing were prospectively included. (nih.gov)
  • A total of 2,456 patients underwent ajmaline testing, 742 (30.2%) in the context of familial screening for BrS. (nih.gov)
  • METHODS: Patients who underwent the ajmaline test in our center were enrolled. (bvsalud.org)
  • Sodium channel blockers (SCBs), such as ajmaline, are used to unmask the characteristic type 1 Brugada electrocardiographic pattern. (nih.gov)
  • 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)
  • Ajmaline blocks the faulty sodium channels and unmasks electrocardiogram (ECG) changes in those patients who have Brugada. (heartrhythmclinic.com)
  • Ajmaline was first discovered to lengthen the refractory period of the heart by blocking sodium ion channels, but it has also been noted that it is also able to interfere with the hERG (human Ether-a-go-go-Related Gene) potassium ion channel. (wikipedia.org)
  • Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the membrane to depolarize in the first case. (wikipedia.org)
  • Ajmaline is a drug known as a sodium channel blocker. (heartrhythmclinic.com)
  • In patients with normal cardiac cells ajmaline has little or no effect on the ECG. (heartrhythmclinic.com)
  • 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)