Encyclopedias as Topic
Intracoronary flecainide induces ST alternans and reentrant arrhythmia on intact canine heart: A role of 4-aminopyridine-sensitive current. (1/169)BACKGROUND: The electrical alternans shown on an ST segment, ST alternans, is known as one of the most important predictors of ventricular fibrillation (VF). It has also been reported that sodium channel inhibition changes action potential configuration, especially on the repolarization phase. Thus, the sodium channel blocker may produce ST alternans and trigger reentrant arrhythmia. METHODS AND RESULTS: A sodium channel blocker (disopyramide, lidocaine, or flecainide) was infused selectively into the left anterior descending coronary artery in anesthetized, open-chest dogs. Sixty unipolar electrograms were simultaneously recorded from the entire cardiac surface of the heart. The amplitude of ST alternans (STa) was determined as the difference in the ST-segment magnitude between 2 consecutive electrograms. We accepted the greatest STa among 60 leads for evaluation. High-dose flecainide (100 microg. kg-1. min-1) increased STa and evoked a spontaneous VF. The STa in high-dose flecainide loading (8.7+/-3.4 mV; mean+/-SEM) was significantly greater than that in disopyramide or lidocaine (0. 9+/-0.4 and 0.8+/-0.2 mV, P<0.05). Treatment of 4-aminopyridine (4-AP) suppressed the increase in STa and the occurrence of VF evoked by flecainide, while E4031 or verapamil did not inhibit those. CONCLUSIONS: Flecainide caused the ST alternans that was closely correlated to the occurrence of VF. Because the ST alternans was suppressed by 4-AP treatment, a 4-AP-sensitive current such as Ito or Isus may play an important role on this phenomenon. (+info)
Disopyramide improves hypoxia in patients with tetralogy of Fallot through a negative inotropic action. (2/169)The hemodynamic and right ventricular volumetric effects of disopyramide were investigated in patients with tetralogy of Fallot (TF). Intracardiac pressure and oxygen saturation were measured, before and after intravenous administration of disopyramide (2 mg/kg) in 7 patients who had not had previous surgery. Right ventricular volume and the diameter of its outflow tract were analyzed in these 7 and in a further 4 patients with a previous shunt. Aortic oxygen saturation increased from 90.4+/-7.5 (mean+/-SD) to 94.1+/-5.5% (p<0.05) with an increase in pulmonary blood flow and pressure. The systolic pressure gradient between the main pulmonary artery and the right ventricle decreased from 59+/-8 to 42+/-9 mmHg (p<0.01). Aortic pressure fell from 77+/-5 to 67+/-4 mmHg (p<0.05). Systemic vascular resistance increased from 15.3+/-2.2 to 19.4+/-3.3 u x m2 (p<0.05). Pulmonary vascular resistance remained unchanged. The diastolic and systolic diameter indices of the right ventricular outflow tract increased from 17.8+/-3.8 to 20.5+/-3.4 and from 6.5+/-3.0 to 10.4+/-2.2 mm/m2, respectively (p<0.01), whereas the right ventricular ejection fraction decreased. Disopyramide improves systemic oxygen saturation in patients with TF through its negative inotropic action on the right ventricle. (+info)
Serum alpha 1-acid glycoprotein, sialic acid, and protein binding of disopyramide in normal subjects and cardiac patients. (3/169)AIM: To study influence of congestive heart failure (CHF) and acute myocardial infarction (AMI) on alpha 1-acid glycoprotein (AGP) and sialic acid (SA) concentration, and binding of AGP to disopyramide (Dis). METHODS: Sera from 85 healthy subjects, 6 patients with CHF, and 6 patients with AMI were determined by immunochemistry for AGP, by HPLC method for sialic acid (SA), and by ultrafiltration and HPLC for the free fraction of Dis. RESULTS: Serum AGP concentrations (g.L-1) were 0.74 +/- 0.16 (healthy), 1.18 +/- 0.40 (d 1, CHF) and 0.90 +/- 0.24 (d 14, CHF), 1.53 +/- 0.26 (d 5, AMI) and 1.08 (d 14, AMI). The free Dis were 1.76 +/- 0.62 (d 1) and 2.14 +/- 0.48 (d 14), in CHF patients, 1.66 +/- 0.52 (d 5) and 1.77 (d 14) in AMI patients. The changes of serum SA and AGP concentrations showed the same tendency. CONCLUSION: The free Dis in serum was affected by the change of AGP binding in CHF and AMI patients. (+info)
Hypoglycemia induced by interaction between clarithromycin and disopyramide. (4/169)A 59-year-old man receiving hemodialysis was hospitalized due to severe hypoglycemic attack. The patient had been treated with disopyramide (50 mg/day) because of paroxysmal atrial fibrillation. Hypoglycemia occurred after taking clarithromycin (CAM, 600 mg/day), a macrolide antibiotic. The serum disopyramide concentration reached 8.0 micrograms/ml (23.6 microM) in the presence of CAM, while it was 1.5 micrograms/ml before the addition of CAM. A 75 g oral glucose tolerance test and daily profiles of blood glucose value showed that blood glucose levels were significantly lower in the presence of CAM and disopyramide compared to that in the absence of these drugs. The Turner index in the presence of CAM and disopyramide was significantly higher than that in the absence of these drugs, suggesting that a toxic concentration of disopyramide enhanced insulin secretion, resulting in the induction of hypoglycemic attacks, in which the inhibitory effects of CAM on the hepatic chytochrome P-450 might be involved. QT and QTc intervals were prolonged in the presence of CAM and disopyramide, but torsades de points were not observed in this patient receiving nicorandil (15 mg/day). Thus, it should be taken into account that life-threatening hypoglycemia may result from the interaction between clarithromycin and disopyramide. (+info)
Mechanism of transient outward K(+) channel block by disopyramide. (5/169)The block of the transient outward K(+) current (I(to)) by disopyramide was studied in isolated rat right ventricular myocytes using whole cell patch-clamp techniques. Disopyramide at a concentration of 10 to 1000 microM reduced peak I(to) and accelerated the apparent rate of current inactivation. The onset of block was assessed using a double pulse protocol with steps from -70 to +50 mV. As the duration of the first (conditioning) pulse was increased from 1 to 50 ms, block was increased. Further prolongation of the conditioning pulse resulted in relief of block, which was nearly complete with a 1-s conditioning pulse. In the absence of drug, the recovery from inactivation of I(to) at -70 mV was fast and best fit with a single exponential function having a time constant of 33 +/- 13 ms. In contrast, in the presence of 100 microM disopyramide, recovery from apparent inactivation was biexponential with time constants of 35 +/- 13 ms and 7.16 +/- 1.5 s. The time course of the slow component was used to estimate recovery of channels from block by disopyramide. Recovery from block was voltage-dependent, suggesting that disopyramide was trapped by the open channel. Taken together, these results suggest that disopyramide rapidly blocks channels in the open state and that unblock occurs from the inactivated state. (+info)
Transverse conduction capabilities of the crista terminalis in patients with atrial flutter and atrial fibrillation. (6/169)OBJECTIVES: In this study, the transverse conduction capabilities of the crista terminalis (CT) were determined during pacing in sinus rhythm in patients with atrial flutter and atrial fibrillation. BACKGROUND: It has been demonstrated that the CT is a barrier to transverse conduction during typical atrial flutter. Mapping studies in animal models provide evidence that this is functional. The influence of transverse conduction capabilities of the CT on the development of atrial flutter remains unclear. METHODS: The CT was identified by intracardiac echocardiography. The atrial activation at the CT was determined during programmed stimulation with one extrastimulus at five pacing sites anteriorly to the CT in 10 patients with atrial flutter and 10 patients with atrial fibrillation before and after intravenous administration of 2 mg/kg disopyramide. Subsequently, atrial arrhythmias were reinduced. RESULTS: At baseline, pacing with longer coupling intervals resulted in a transverse pulse propagation across the CT. During shorter coupling intervals, split electrograms and a marked alteration of the activation sequence of its second component were found, indicating a functional conduction block. In patients with atrial flutter, the longest coupling interval that resulted in a complete transverse conduction block at the CT was significantly longer than that in patients with atrial fibrillation (285 +/- 49 ms vs. 221 +/- 28 ms; p < 0.05). After disopyramide administration, a transverse conduction block occurred at longer coupling intervals as compared with baseline (287 +/- 68 ms vs. 250 +/- 52 ms; p < 0.05). Subsequently, a sustained atrial arrhythmia was inducible in 15 of 20 patients. This was atrial flutter in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients. CONCLUSIONS: It was found that the CT provides transverse conduction capabilities and that the conduction block during atrial flutter is functional. Limited transverse conduction capabilities of the CT seem to contribute to the development of atrial flutter. (+info)
Chronotropic, inotropic, dromotropic and coronary vasodilator effects of bisaramil, a new class I antiarrhythmic drug, assessed using canine isolated, blood-perfused heart preparations. (7/169)The cardiovascular effects of a new class I antiarrhythmic drug, bisaramil, were examined using canine isolated, blood-perfused heart preparations. Bisaramil exerted negative chronotropic, inotropic and dromotropic effects as well as coronary vasodilator action, which are qualitatively the same as those of classical class I drugs. The selectivity of bisaramil for the intraventricular conduction vs the other cardiac variables was compared with that of disopyramide and flecainide. Bisaramil was the most selective for intraventricular conduction, while it was the least selective for ventricular muscle contraction. We conclude that bisaramil may become a useful antiarrhythmic drug with less cardiac adverse effects. (+info)
Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide. (8/169)A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations. (+info)
Disopyramide is an antiarrhythmic medication that is primarily used to treat certain types of irregular heart rhythms (arrhythmias), such as ventricular tachycardia and atrial fibrillation. It works by blocking the activity of sodium channels in the heart, which helps to slow down and regulate the heart rate.
Disopyramide is available in immediate-release and extended-release forms, and it may be taken orally as a tablet or capsule. Common side effects of this medication include dry mouth, blurred vision, constipation, and difficulty urinating. More serious side effects can include dizziness, fainting, irregular heartbeat, and allergic reactions.
It is important to take disopyramide exactly as directed by a healthcare provider, as improper use or dosing can lead to serious complications. Additionally, individuals with certain medical conditions, such as heart failure, kidney disease, or myasthenia gravis, may not be able to safely take this medication.
Mexiletine is defined as an antiarrhythmic agent, classified as a Class IB medication. It works by blocking sodium channels in the heart, which helps to stabilize cardiac membranes and reduces the rate of firing of cardiac cells. This makes it useful for treating certain types of irregular heart rhythms (ventricular arrhythmias).
Mexiletine is also known to have analgesic properties and is sometimes used off-label for the treatment of neuropathic pain. It is available in oral form, and its use should be under the close supervision of a healthcare provider due to its potential side effects, which can include gastrointestinal symptoms, dizziness, tremors, and cardiac arrhythmias.
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.
Flecainide is an antiarrhythmic medication used to regularize abnormal heart rhythms, specifically certain types of irregular heartbeats called ventricular arrhythmias and paroxysmal atrial tachycardia/atrial fibrillation. It works by blocking sodium channels in the heart, which helps to slow down the conduction of electrical signals and reduces the likelihood of erratic heart rhythms.
Flecainide is available in oral forms such as tablets or capsules and is typically prescribed under the supervision of a healthcare professional experienced in managing heart rhythm disorders. It's important to note that flecainide can have serious side effects, including increasing the risk of dangerous arrhythmias in some patients, so it should only be used under close medical monitoring.
This definition is for informational purposes only and should not be considered a substitute for professional medical advice, diagnosis, or treatment. If you have any questions about your medications or health conditions, please consult with your healthcare provider.
Procainamide is an antiarrhythmic medication used to treat various types of irregular heart rhythms (arrhythmias), such as atrial fibrillation, atrial flutter, and ventricular tachycardia. It works by prolonging the duration of the cardiac action potential and decreasing the slope of the phase 0 depolarization, which helps to stabilize the heart's electrical activity and restore a normal rhythm.
Procainamide is classified as a Class Ia antiarrhythmic drug, according to the Vaughan Williams classification system. It primarily affects the fast sodium channels in the heart muscle cells, reducing their availability during depolarization. This results in a decreased rate of impulse generation and conduction velocity, which can help to suppress abnormal rhythms.
The medication is available as an oral formulation (procainamide hydrochloride) and as an injectable solution for intravenous use. Common side effects of procainamide include nausea, vomiting, diarrhea, headache, and dizziness. Procainamide can also cause a lupus-like syndrome, characterized by joint pain, skin rashes, and other autoimmune symptoms, in some patients who take the medication for an extended period.
It is essential to monitor procainamide levels in the blood during treatment to ensure that the drug is within the therapeutic range and to minimize the risk of adverse effects. Healthcare providers should also regularly assess patients' renal function, as procainamide and its active metabolite, N-acetylprocainamide (NAPA), are primarily excreted by the kidneys.
Quinidine is a Class IA antiarrhythmic medication that is primarily used to treat and prevent various types of cardiac arrhythmias (abnormal heart rhythms). It works by blocking the rapid sodium channels in the heart, which helps to slow down the conduction of electrical signals within the heart and stabilize its rhythm.
Quinidine is derived from the bark of the Cinchona tree and has been used for centuries as a treatment for malaria. However, its antiarrhythmic properties were discovered later, and it became an important medication in cardiology.
In addition to its use in treating arrhythmias, quinidine may also be used off-label for other indications such as the treatment of nocturnal leg cramps or myasthenia gravis. It is available in various forms, including tablets and injectable solutions.
It's important to note that quinidine has a narrow therapeutic index, meaning that there is only a small difference between an effective dose and a toxic one. Therefore, it must be carefully monitored to ensure that the patient is receiving a safe and effective dose. Common side effects of quinidine include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as visual disturbances, headache, and dizziness. More serious side effects can include QT prolongation, which can lead to dangerous arrhythmias, and hypersensitivity reactions.
I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).
In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.
Orosomucoid, also known as α-1-acid glycoprotein or AAG, is a protein found in human plasma. It's a member of the acute phase proteins, which are produced in higher amounts during inflammation and infection. Orosomucoid has a molecular weight of approximately 41-43 kDa and is composed of a single polypeptide chain with five N-linked glycosylation sites. It plays a role in protecting tissues from various harmful substances, such as proteases and oxidants, by binding to them and preventing their interaction with cells. Additionally, orosomucoid has been studied as a potential biomarker for several diseases due to its altered levels during inflammation and cancer.
Parasympatholytics are a type of medication that blocks the action of the parasympathetic nervous system. The parasympathetic nervous system is responsible for the body's rest and digest response, which includes slowing the heart rate, increasing intestinal and glandular activity, and promoting urination and defecation.
Parasympatholytics work by selectively binding to muscarinic receptors, which are found in various organs throughout the body, including the heart, lungs, and digestive system. By blocking these receptors, parasympatholytics can cause a range of effects, such as an increased heart rate, decreased glandular secretions, and reduced intestinal motility.
Some common examples of parasympatholytics include atropine, scopolamine, and ipratropium. These medications are often used to treat conditions such as bradycardia (slow heart rate), excessive salivation, and gastrointestinal cramping or diarrhea. However, because they can have significant side effects, parasympatholytics are typically used only when necessary and under the close supervision of a healthcare provider.
Tocainide is an antiarrhythmic medication, which means it's used to treat irregular heart rhythms. It works by stabilizing the electrical activity of the heart and helping to restore a normal heartbeat. Tocainide belongs to a class of medications called Class Ib antiarrhythmics.
It is important to note that tocainide has been associated with serious side effects, including an increased risk of potentially life-threatening heart rhythm abnormalities, and its use is generally reserved for situations where other treatments have not been effective. It's also worth mentioning that tocainide is no longer commonly used due to these safety concerns and has been largely replaced by newer antiarrhythmic medications with more favorable side effect profiles.
Cross circulation is a medical procedure in which blood from one person (the donor) is circulated through the body of another person (the recipient) by connecting their cardiovascular systems. This technique was first developed and used in open-heart surgery during the 1950s, before the invention of heart-lung machines.
In cross circulation, the donor's and recipient's circulatory systems are connected through anastomoses (surgical connections) between their blood vessels. The most common configuration involved connecting the donor's femoral artery to the recipient's aorta and the donor's femoral vein to the recipient's vena cava. This allowed the donor's heart to pump oxygenated blood to both the donor and the recipient during the surgery.
Cross circulation was used as a temporary measure to maintain the recipient's circulation and oxygenation while their own heart was stopped and repaired during open-heart surgery. However, this technique had several limitations and risks, including potential complications for the donor (such as bleeding, infection, or reactions to the recipient's blood) and ethical concerns related to using one person as a "human bridge" to save another.
With the development of more advanced and safer heart-lung machines in the early 1960s, cross circulation became obsolete in cardiac surgery. Nowadays, it is rarely used and mainly of historical interest.
Lidocaine is a type of local anesthetic that numbs painful areas and is used to prevent pain during certain medical procedures. It works by blocking the nerves that transmit pain signals to the brain. In addition to its use as an anesthetic, lidocaine can also be used to treat irregular heart rates and relieve itching caused by allergic reactions or skin conditions such as eczema.
Lidocaine is available in various forms, including creams, gels, ointments, sprays, solutions, and injectable preparations. It can be applied directly to the skin or mucous membranes, or it can be administered by injection into a muscle or vein. The specific dosage and method of administration will depend on the reason for its use and the individual patient's medical history and current health status.
Like all medications, lidocaine can have side effects, including allergic reactions, numbness that lasts too long, and in rare cases, heart problems or seizures. It is important to follow the instructions of a healthcare provider carefully when using lidocaine to minimize the risk of adverse effects.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Sodium channels are specialized protein structures that are embedded in the membranes of excitable cells, such as nerve and muscle cells. They play a crucial role in the generation and transmission of electrical signals in these cells. Sodium channels are responsible for the rapid influx of sodium ions into the cell during the initial phase of an action potential, which is the electrical signal that travels along the membrane of a neuron or muscle fiber. This sudden influx of sodium ions causes the membrane potential to rapidly reverse, leading to the depolarization of the cell. After the action potential, the sodium channels close and become inactivated, preventing further entry of sodium ions and helping to restore the resting membrane potential.
Sodium channels are composed of a large alpha subunit and one or two smaller beta subunits. The alpha subunit forms the ion-conducting pore, while the beta subunits play a role in modulating the function and stability of the channel. Mutations in sodium channel genes have been associated with various inherited diseases, including certain forms of epilepsy, cardiac arrhythmias, and muscle disorders.
Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.
During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.
Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.
Sodium channel blocker
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Torsades de pointes
Drug-induced QT prolongation
List of MeSH codes (D03)
Brazilian Controlled Drugs and Substances Act
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List of drugs: Df-Di
Outline of cardiology
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Treatment of Atrial Fibrillation | Effective Health Care (EHC) Program
- Disopyramide (INN, trade names Norpace and Rythmodan) is an antiarrhythmic medication used in the treatment of ventricular tachycardia. (wikipedia.org)
Stop taking disop1
- Do not stop taking disopyramide without talking to your doctor. (medlineplus.gov)
Allergic to disopyramide1
- tell your doctor and pharmacist if you are allergic to disopyramide, any other medications, or any of the ingredients in disopyramide capsules. (medlineplus.gov)
- As a result, the use of disopyramide may reduce contractile force up to 42% at low doses and up to 100% in higher doses compared to quinidine. (wikipedia.org)
- The anticholinergic effect of drugs such as tri- and tetracyclic antidepressants, antihistamines, quinidine, amantadine, antipsychotics (e.g. butyrophenones, phenothiazines), disopyramide and other anticholinergics (e.g. tiotropium, ipratropium, atropine-like compounds) may be intensified by Buscopan. (janusinfo.se)
- 1.Rythmodan (disopyramide) Australian prescribing information. (webmd.com)
- Disopyramide (Rythmodan®)100mg capsules are out of stock until late October 2023. (middlesexlpcs.org.uk)
- Disopyramide (Rythmodan®) 250mg prolonged release tablets are out of stock until mid-December 2023 but parallel imports remain available and can fully cover demand. (middlesexlpcs.org.uk)
- The post Medicine Supply Notification: Disopyramide (Rythmodan®)100mg capsules appeared first on Community Pharmacy England . (middlesexlpcs.org.uk)
- Disopyramide has a negative inotropic effect on the ventricular myocardium, significantly decreasing the contractility. (wikipedia.org)
- Disopyramide does not act as a blocking agent for beta or alpha adrenergic receptors, but does have a significant negative inotropic effect on the ventricular myocardium. (wikipedia.org)
- Disopyramide may produce side effects associated with negative inotropic action. (kembara.co)
- Levites proposed a possible secondary mode of action for disopyramide, against reentrant arrhythmias after an ischemic insult. (wikipedia.org)
- Disopyramide may increase the chance of having arrhythmias (irregular heartbeats) and has not been proven to help people without life-threatening arrhythmias to live longer. (medlineplus.gov)
- Disopyramide treats abnormal heart rhythms (arrhythmias). (rxwiki.com)
- Disopyramide is a prescription medication used to treat life-threatening abnormal heart rhythms (arrhythmias). (rxwiki.com)
- Disopyramide is a prescription medications used to treat life-threatening ventricular (lower chambers of the heart) arrhythmias. (rxwiki.com)
- showed that pyridostigmine used in combination with disopyramide substantially alleviates vagolytic side effects without compromising antiarrhythmic efficacy. (wikipedia.org)
- Taking antiarrhythmic drugs, including disopyramide, may increase the risk of death. (medlineplus.gov)
- Disopyramide is in a class of medications called antiarrhythmic medications. (medlineplus.gov)
- Disopyramide depresses the increase in sodium permeability of the cardiac myocyte during Phase 0 of the cardiac action potential, in turn decreasing the inward sodium current. (wikipedia.org)
- 2023. https://www.drugguide.com/ddo/view/Davis-Drug-Guide/51229/all/disopyramide. (drugguide.com)
- Treatment is with beta-blockers, verapamil , disopyramide , mavacamten , and sometimes chemical reduction or surgical removal of outflow tract obstruction. (msdmanuals.com)
- Older adults should not usually take disopyramide because it is not as safe or effective as other medications that can be used to treat the same condition. (medlineplus.gov)
- This is not a complete list of disopyramide drug interactions. (rxwiki.com)
- Disopyramide also has an anticholinergic effect on the heart which accounts for many adverse side effects. (wikipedia.org)
- Alcohol can make the side effects from disopyramide worse. (medlineplus.gov)
- See the "Disopyramide Precautions" section. (rxwiki.com)
- Disopyramide will block the opening of the Na+ channel and lead to inactivation of the sodium ion channel in the cell membrane. (kembara.co)
- Donnez-nous votre avis Association entre RIFABUTINE et DISOPYRAMIDE Interaction entre : -1- Substance : RIFABUTINE -2- Produit : DISOPYRAMIDE Conseil : A SURVEILLER Surveillance clinique, ECG et taux plasmatiques du disopyramide. (biam2.org)
- Disopyramide is class Ia anti arrhythmic agent. (kembara.co)
- Disopyramide may cause or worsen congestive heart failure or produce severe low blood pressure. (rxwiki.com)
- Many investigators and clinicians believe that disopyramide controlled release is the most potent agent available for reducing resting pressure gradients and improving symptoms. (wikipedia.org)
- Disopyramide, despite its efficacy, has one main side effect that has limited its use in the US, though it has seen wider application in Canada, UK and Japan. (wikipedia.org)
- Disopyramide may cause side effects. (medlineplus.gov)
- Serious side effects have been reported with disopyramide. (rxwiki.com)
- This is not a complete list of disopyramide side effects. (rxwiki.com)
- Disopyramide administration for obstructive HCM has a IB recommendation in the 2020 American Heart Association/American College of Cardiology Foundation guidelines for treatment of obstructive HCM. (wikipedia.org)
- When used in patients resistant to beta-blockade, disopyramide is effective in 60% of cases, reducing symptoms and gradient to the extent that invasive procedures such as surgical septal myectomy are not required. (wikipedia.org)
- INTERVENTIONS: Administration of disopyramide was effective in preventing syncope. (bvsalud.org)
- If first degree block develops, your doctor will reduce your disopyramide dose. (rxwiki.com)
- Some clinicians prescribe pyridostigmine sustained release (marketed in the US as Mestinon Timespan) to every patient begun on disopyramide. (wikipedia.org)
- Disopyramide helps control your condition but will not cure it. (medlineplus.gov)
- Talk to your doctor about the risks of taking disopyramide. (medlineplus.gov)
- If you become pregnant while taking disopyramide, call your doctor. (medlineplus.gov)
- ask your doctor about the safe use of alcoholic beverages while you are taking disopyramide. (medlineplus.gov)
- If this happens, your doctor will stop disopyramide. (rxwiki.com)