Amiodarone
Anti-Arrhythmia Agents
Atrial Fibrillation
Tachycardia
Tachycardia, Ventricular
Thyrotoxicosis
Ventricular Fibrillation
Arrhythmias, Cardiac
Electric Countershock
Propafenone
Electrocardiography
Tachycardia, Ectopic Junctional
Effects of cycloprotobuxine-A on atrial fibrillation. (1/719)
AIM: To study the effects of cycloprotobuxine-A (Cyc-A) on atrial fibrillation. METHODS: Atrial fibrillations in vivo and in vitro were induced by arrhythmogenic drugs. Action potentials were measured by the standard microelectrode technique. RESULTS: Cyc-A, similar to or slightly stronger than amiodarone (Ami), decreased incidences of atrial fibrillation elicited by CaCl2-acetylcholine in mice and increased doses of aconitine, ouabain, or adrenaline to elicit atrial fibrillation in isolated guinea pig atria. Cyc-A 0.3-100 mumol.L-1 decreased the normal automaticity and 0.3-30 mumol.L-1 attenuated or almost abolished the isoprenaline-induced abnormal increase in automaticity in sinus nodal cells. In isolated left atria, Cyc-A 0.3-30 mumol.L-1 inhibited the abnormal rhythmic activity elicited by adrenaline, prolonged action potential duration (APD) and effective refractory period, and reduced excitability. At 3-30 mumol.L-1, Cyc-A also decreased the maximal velocity of depolarization (Vmax). Cyc-A antagonized the acetylcholine-induced shortening of APD. These electrophysiologic effects were similar to those of amiodarone, but Ami did not affect the Vmax. CONCLUSION: Cyc-A produces a protective effect against experimental atrial fibrillation via a prolongation of repolarization, a decease of automaticity, and an inhibition of excitability. (+info)Retinal stimulates ATP hydrolysis by purified and reconstituted ABCR, the photoreceptor-specific ATP-binding cassette transporter responsible for Stargardt disease. (2/719)
Many substrates for P-glycoprotein, an ABC transporter that mediates multidrug resistance in mammalian cells, have been shown to stimulate its ATPase activity in vitro. In the present study, we used this property as a criterion to search for natural and artificial substrates and/or allosteric regulators of ABCR, the rod photoreceptor-specific ABC transporter responsible for Stargardt disease, an early onset macular degeneration. ABCR was immunoaffinity purified to apparent homogeneity from bovine rod outer segments and reconstituted into liposomes. All-trans-retinal, a candidate ligand, stimulates the ATPase activity of ABCR 3-4-fold, with a half-maximal effect at 10-15 microM. 11-cis- and 13-cis-retinal show similar activity. All-trans-retinal stimulates the ATPase activity of ABCR with Michaelis-Menten behavior indicative of simple noncooperative binding that is associated with a rate-limiting enzyme-substrate intermediate in the pathway of ATP hydrolysis. Among 37 structurally diverse non-retinoid compounds, including nine previously characterized substrates or sensitizers of P-glycoprotein, only four show significant ATPase stimulation when tested at 20 microM. The dose-response curves of these four compounds are indicative of multiple binding sites and/or modes of interaction with ABCR. Two of these compounds, amiodarone and digitonin, can act synergistically with all-trans-retinal, implying that they interact with a site or sites on ABCR different from the one with which all-trans-retinal interacts. Unlike retinal, amiodarone appears to interact with both free and ATP-bound ABCR. Together with clinical observations on Stargardt disease and the localization of ABCR to rod outer segment disc membranes, these data suggest that retinoids, and most likely retinal, are the natural substrates for transport by ABCR in rod outer segments. These observations have significant implications for understanding the visual cycle and the pathogenesis of Stargardt disease and for the identification of compounds that could modify the natural history of Stargardt disease or other retinopathies associated with impaired ABCR function. (+info)Fetal tachycardias: management and outcome of 127 consecutive cases. (3/719)
OBJECTIVE: To review the management and outcome of fetal tachycardia, and to determine the problems encountered with various treatment protocols. STUDY DESIGN: Retrospective analysis. SUBJECTS: 127 consecutive fetuses with a tachycardia presenting between 1980 and 1996 to a single tertiary centre for fetal cardiology. The median gestational age at presentation was 32 weeks (range 18 to 42). RESULTS: 105 fetuses had a supraventricular tachycardia and 22 had atrial flutter. Overall, 52 fetuses were hydropic and 75 non-hydropic. Prenatal control of the tachycardia was achieved in 83% of treated non-hydropic fetuses compared with 66% of the treated hydropic fetuses. Digoxin monotherapy converted most (62%) of the treated non-hydropic fetuses, and 96% survived through the neonatal period. First line drug treatment for hydropic fetuses was more diverse, including digoxin (n = 5), digoxin plus verapamil (n = 14), and flecainide (n = 27). The response rates to these drugs were 20%, 57%, and 59%, respectively, confirming that digoxin monotherapy is a poor choice for the hydropic fetus. Response to flecainide was faster than to the other drugs. Direct fetal treatment was used in four fetuses, of whom two survived. Overall, 73% (n = 38) of the hydropic fetuses survived. Postnatally, 4% of the non-hydropic group had ECG evidence of pre-excitation, compared with 16% of the hydropic group; 57% of non-hydropic fetuses were treated with long term anti-arrhythmics compared with 79% of hydropic fetuses. CONCLUSIONS: Non-hydropic fetuses with tachycardias have a very good prognosis with transplacental treatment. Most arrhythmias associated with fetal hydrops can be controlled with transplacental treatment, but the mortality in this group is 27%. At present, there is no ideal treatment protocol for these fetuses and a large prospective multicentre trial is required to optimise treatment of both hydropic and non-hydropic fetuses. (+info)Electrophysiologic effects of chronic amiodarone therapy and hypothyroidism, alone and in combination, on guinea pig ventricular myocytes. (4/719)
Amiodarone is a widely used antiarrhythmic drug, the mechanisms of action of which remain incompletely understood. Indirect evidence suggests that the class III properties of amiodarone may be mediated by cardiac antithyroid effects. We sought to determine whether the effects of chronic amiodarone on repolarization in guinea pig hearts can be attributed to an antithyroid action by studying the changes in dofetilide-sensitive rapid (IKr) and dofetilide-resistant slow (IKs) delayed rectifier currents, inward rectifier K+ current (IK1), and action potentials of ventricular myocytes from five groups of guinea pigs: control, hypothyroid, amiodarone-treated for 7 days, hypothyroid plus amiodarone, and vehicle (dimethyl sulfoxide) treated. IKs was reduced by amiodarone (to 61% of control, P <.05, at 50 mV) but was more strongly reduced by hypothyroidism (to 35% of control, P <.01, 50 mV). Amiodarone significantly reduced IKr and IK1 (by 55 and 64% at 10 mV and -50 mV, respectively), which were unaffected by hypothyroidism. Amiodarone alone and hypothyroidism alone had similar action potential-prolonging actions. Hypothyroid animals treated with amiodarone showed a combination of ionic effects (strong IKs reduction, similar to hypothyroidism alone; reduced IKr and IK1, similar to amiodarone alone), along with action potential prolongation significantly greater than that caused by either intervention alone. We conclude that chronic amiodarone and hypothyroidism have different effects on ionic currents and that their combination prolongs action potential duration to a greater extent than either alone in guinea pig hearts, suggesting that the class III actions of amiodarone are not mediated by a cardiac hypothyroid state. (+info)Amiodarone versus propafenone for conversion of chronic atrial fibrillation: results of a randomized, controlled study. (5/719)
OBJECTIVES: The purpose of this study was to investigate the efficacy and safety of amiodarone and propafenone in the conversion of chronic atrial fibrillation in a prospective, randomized, placebo-controlled study. BACKGROUND: The effectiveness of amiodarone and propafenone in the treatment of patients with chronic atrial fibrillation has not been adequately studied. METHODS: One hundred one patients (48 men, mean age 64 +/- 9 years) with atrial fibrillation lasting >3 weeks participated in the study. Thirty-four patients received amiodarone (300 mg intravenously over 1 h, followed by 20 mg/kg over the next 24 h plus 600 mg orally, in three doses, for 1 week, then 400 mg/day orally, for three weeks), 32 received propafenone (2 mg/kg intravenously over 15 min, followed by 10 mg/kg over 24 h and then 450 mg/day orally, for one month) and the remaining 35 served as control subjects. All patients received digoxin and anticoagulant treatment as indicated (International Normalized Ratio 2 to 3). RESULTS: Conversion to sinus rhythm was achieved in 16 (47.05%) patients who received amiodarone, in 13 (40.62%) who received propafenone and in none of the control subjects (p < 0.001 for both groups vs. control subjects). Those who converted had smaller atria than those who did not and atrial fibrillation of shorter duration in both the amiodarone and propafenone groups. Treatment was discontinued in one patient of the propafenone group because of significant QRS widening. CONCLUSIONS: Amiodarone and propafenone appear to be safe and equally effective in the termination of chronic atrial fibrillation. Left atrial diameter and arrhythmia duration are independent predictors of conversion. (+info)Effect of intravenous amiodarone on electrophysiologic variables and on the modes of termination of atrioventricular reciprocating tachycardia in Wolff-Parkinson-White syndrome. (6/719)
Atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White (WPW) syndrome, sometimes terminates spontaneously, generally sustains and eventually becomes drug resistant. Amiodarone is a potent antiarrhythmic drug that is sometimes effective in patients with AVRT which is resistant to conventional antiarrhythmic drugs. However, systematic studies concerning the effects of amiodarone on AVRT have not been reported. This study evaluated the effects of intravenous amiodarone on electrophysiologic variables, and on the sites and the modes of termination of AVRT. Fifteen WPW patients were studied. Nine had overt, and 6 had concealed WPW syndrome. Measurements of electrophysiologic variables and the induction of AVRT were performed by atrial and/or ventricular programmed stimulations. Amiodarone was then administered at a dose of 5 mg/kg over 5 min. The effective refractory periods (ERP) of the atrial, atrioventricular node, ventricular and accessory pathway were increased significantly by amiodarone. The conduction times of all the components were significantly lengthened by amiodarone, except for the His-ventricular (HV) interval in concealed WPW patients. AVRT was induced in all patients, and was terminated by amiodarone in 12 of 13 patients with sustained AVRT. After amiodarone, AVRT was induced in 9 patients. Spontaneous termination was observed 11 times in 3 of the 9 patients in whom AVRT was still induced. In these cases, the modes and sites of termination were the same as during the baseline state. The ERPs and conduction times of all components of AVRT, except the HV interval, were significantly lengthened by amiodarone. Amiodarone is efficacious for terminating AVRT wherever weak links exist. However, sites of spontaneous termination are not significantly affected by amiodarone. (+info)Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease. (7/719)
AIM: To compare the efficacy of sotalol versus amiodarone for long-term treatment of ventricular tachyarrhythmias. METHODS: Patients (n=75) with spontaneous, sustained ventricular tachyarrhythmias secondary to remote myocardial infarction were studied. After intravenous electrophysiological testing, both sotalol and amiodarone were predicted to be ineffective in 50 (67%) patients. Five patients were excluded. Forty-five patients were randomized to receive sotalol (n=22) or amiodarone (n=23) for maintenance therapy. The primary outcome variable was the time to first recurrence of sustained ventricular tachyarrhythmia. RESULTS: At 36 months. 75% of those allocated sotalol remained free of ventricular tachyarrhythmia compared with 38% of those allocated amiodarone (P=0.05). On multivariate analysis the risk of recurrence of ventricular tachyarrhythmia for patients on amiodarone was 5.9 times higher (P=0.008) than that for patients on sotalol. CONCLUSION: Sotalol is superior to amiodarone for long-term treatment of ventricular tachyarrhythmia secondary to coronary artery disease when both drugs have been predicted to be ineffective at intravenous electrophysiological testing. Randomized trials in larger numbers of patients with ventricular tachyarrhythmia need to be performed comparing the two agents directly. (+info)Amiodarone compared with iodine exhibits a potent and persistent inhibitory effect on TSH-stimulated cAMP production in vitro: a possible mechanism to explain amiodarone-induced hypothyroidism. (8/719)
Amiodarone (AMD) is a powerful anti-arrhythmic drug used for the treatment of a wide variety of cardiac arrhythmias and its most striking feature is its high iodine content. Thyroid dysfunction is a limiting side-effect of the drug and both AMD-induced hypothyroidism (AIH) and AMD-induced thyrotoxicosis (AIT) are reported. To examine the hypothesis that altered bioavailability of iodine is a contributing event in the pathogenesis of AIH, we compared the effects of AMD and inorganic iodine in vitro on events involved in the process of thyroid autoregulation. FRTL-5 cells and JP26 CHO cells (transfected with the human TSH receptor) were exposed to AMD or NaI in the presence of TSH, and cAMP production was measured as an indicator of cellular function. Forskolin and cholera toxin were also used to determine the possible target sites of AMD and iodide. Our results indicated that there was a difference between the effects of AMD versus those of physiological doses of iodide. The inhibitory effects of AMD occurred at lower concentrations of iodide than those seen in the NaI-treated cells. The effects of AMD were irreversible indicating a possible persistence of the Wolff-Chaikoff effect due to a constant high intracellular iodide level. The inhibitory effects of AMD (also seen at supraphysiological doses of iodide) were partially overcome by forskolin but not by cholera toxin indicating an effect on TSH receptor interactions with the other signal transduction elements such as G proteins and adenylate cyclase. The persistence of the Wolff-Chaikoff effect through loss of autoregulation may be a mechanism of the observed hypothyroidism in some patients taking AMD. The combined effects of the constant release of iodide together with the drug toxicity may be the mechanism for the observed effects. (+info)There are several risk factors for developing AF, including:
1. Age: The risk of developing AF increases with age, with the majority of cases occurring in people over the age of 65.
2. Hypertension (high blood pressure): High blood pressure can damage the heart and increase the risk of developing AF.
3. Heart disease: People with heart disease, such as coronary artery disease or heart failure, are at higher risk of developing AF.
4. Diabetes mellitus: Diabetes can increase the risk of developing AF.
5. Sleep apnea: Sleep apnea can increase the risk of developing AF.
6. Certain medications: Certain medications, such as thyroid medications and asthma medications, can increase the risk of developing AF.
7. Alcohol consumption: Excessive alcohol consumption has been linked to an increased risk of developing AF.
8. Smoking: Smoking is a risk factor for many cardiovascular conditions, including AF.
9. Obesity: Obesity is a risk factor for many cardiovascular conditions, including AF.
Symptoms of AF can include:
1. Palpitations (rapid or irregular heartbeat)
2. Shortness of breath
3. Fatigue
4. Dizziness or lightheadedness
5. Chest pain or discomfort
AF can be diagnosed with the help of several tests, including:
1. Electrocardiogram (ECG): This is a non-invasive test that measures the electrical activity of the heart.
2. Holter monitor: This is a portable device that records the heart's rhythm over a 24-hour period.
3. Event monitor: This is a portable device that records the heart's rhythm over a longer period of time, usually 1-2 weeks.
4. Echocardiogram: This is an imaging test that uses sound waves to create pictures of the heart.
5. Cardiac MRI: This is an imaging test that uses magnetic fields and radio waves to create detailed pictures of the heart.
Treatment for AF depends on the underlying cause and may include medications, such as:
1. Beta blockers: These medications slow the heart rate and reduce the force of the heart's contractions.
2. Antiarrhythmics: These medications help regulate the heart's rhythm.
3. Blood thinners: These medications prevent blood clots from forming and can help reduce the risk of stroke.
4. Calcium channel blockers: These medications slow the entry of calcium into the heart muscle cells, which can help slow the heart rate and reduce the force of the heart's contractions.
In some cases, catheter ablation may be recommended to destroy the abnormal electrical pathway causing AF. This is a minimally invasive procedure that involves inserting a catheter through a vein in the leg and guiding it to the heart using x-ray imaging. Once the catheter is in place, energy is applied to the abnormal electrical pathway to destroy it and restore a normal heart rhythm.
It's important to note that AF can increase the risk of stroke, so anticoagulation therapy may be recommended to reduce this risk. This can include medications such as warfarin or aspirin, or in some cases, implantable devices such as a left atrial appendage closure device.
In conclusion, atrial fibrillation is a common heart rhythm disorder that can increase the risk of stroke and heart failure. Treatment options depend on the underlying cause and may include medications, cardioversion, catheter ablation, or anticoagulation therapy. It's important to work closely with a healthcare provider to determine the best course of treatment for AF.
There are several types of tachycardia, including:
1. Sinus tachycardia: This is the most common type and is caused by an increase in the rate of the normal sinus node. It is often seen in response to physical activity or stress.
2. Atrial fibrillation: This is a type of arrhythmia where the heart's upper chambers (atria) contract irregularly and rapidly, leading to a rapid heart rate.
3. Ventricular tachycardia: This is a type of arrhythmia where the heart's lower chambers (ventricles) contract rapidly, often with a rate above 100 bpm.
4. Premature ventricular contractions (PVCs): These are early or extra beats that originate in the ventricles, causing a rapid heart rate.
Tachycardia can cause a range of symptoms, including palpitations, shortness of breath, chest pain, and dizziness. In severe cases, it can lead to cardiac arrhythmias, heart failure, and even death.
Diagnosis of tachycardia typically involves a physical examination, electrocardiogram (ECG), and other tests such as stress tests or echocardiography. Treatment options vary depending on the underlying cause, but may include medications to regulate the heart rate, cardioversion to restore a normal heart rhythm, or in severe cases, implantation of a pacemaker or defibrillator.
Tachycardia, ventricular can be classified into several types based on its duration and the presence of other symptoms. These include:
1. Paroxysmal ventricular tachycardia (PVT): This is a rapid heart rate that occurs in episodes lasting less than 30 seconds and may be accompanied by palpitations, shortness of breath, or dizziness.
2. Sustained ventricular tachycardia: This is a rapid heart rate that persists for more than 30 seconds and may require medical intervention to return the heart to normal rhythm.
3. Ventricular fibrillation (VF): This is a life-threatening condition in which the ventricles are unable to pump blood effectively due to rapid, disorganized electrical activity.
Symptoms of tachycardia, ventricular may include:
* Palpitations or rapid heartbeat
* Shortness of breath
* Dizziness or lightheadedness
* Chest pain or discomfort
* Fatigue or weakness
Diagnosis of tachycardia, ventricular is typically made based on a physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, or stress test. Treatment options may include medications to regulate heart rhythm, cardioversion to restore normal heart rhythm, and in some cases, implantation of a cardioverter-defibrillator (ICD) to prevent sudden death.
In summary, tachycardia, ventricular is a rapid heart rate that originates in the ventricles and can be caused by a variety of conditions. It is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, it is possible to manage the condition and improve quality of life.
The most common cause of thyrotoxicosis is an overactive thyroid gland, known as hyperthyroidism. This can be caused by a variety of factors, including:
* Graves' disease: An autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone.
* Toxic multinodular goiter: A condition in which one or more nodules in the thyroid gland become overactive and produce excessive amounts of thyroid hormone.
* Thyroid adenoma: A benign tumor of the thyroid gland that can cause hyperthyroidism.
* Thyroid cancer: A malignant tumor of the thyroid gland that can cause hyperthyroidism.
Symptoms of thyrotoxicosis can vary depending on the severity of the condition and the individual affected, but may include:
* Weight loss
* Increased heart rate
* Anxiety
* Sweating
* Tremors
* Nervousness
* Fatigue
* Heat intolerance
* Increased bowel movements
* Muscle weakness
Thyrotoxicosis can be diagnosed through a series of tests, including:
* Blood tests: To measure thyroid hormone levels in the blood.
* Thyroid scan: To visualize the thyroid gland and identify any nodules or tumors.
* Ultrasound: To evaluate the structure of the thyroid gland and detect any abnormalities.
Treatment for thyrotoxicosis depends on the underlying cause, but may include:
* Medications to reduce thyroid hormone production.
* Radioactive iodine therapy to destroy part or all of the thyroid gland.
* Surgery to remove part or all of the thyroid gland.
It is important to note that untreated thyrotoxicosis can lead to complications such as heart problems, osteoporosis, and eye problems, so it is important to seek medical attention if symptoms persist or worsen over time.
In Vfib, the electrical activity of the heart becomes disorganized, leading to a fibrillatory pattern of contraction. This means that the ventricles are contracting in a rapid, unsynchronized manner, rather than the coordinated, synchronized contractions that occur in normal heart function.
Vfib can be caused by a variety of factors, including coronary artery disease, heart attack, cardiomyopathy, and electrolyte imbalances. It can also be triggered by certain medications, such as digoxin, or by electrical shocks to the heart.
Symptoms of Vfib include palpitations, shortness of breath, chest pain, and loss of consciousness. If not treated promptly, Vfib can lead to cardiac arrest and death.
Treatment of Vfib typically involves electrical cardioversion, which involves delivering an electric shock to the heart to restore a normal heart rhythm. In some cases, medications may also be used to help regulate the heart rhythm. In more severe cases, surgery or other interventions may be necessary to address any underlying causes of Vfib.
Overall, ventricular fibrillation is a serious medical condition that requires prompt treatment to prevent complications and ensure effective cardiac function.
There are many different types of cardiac arrhythmias, including:
1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.
Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.
The symptoms of PAT can vary in severity and may include:
* Rapid heartbeats (tachycardia)
* Palpitations or pounding sensation in the chest
* Shortness of breath (dyspnea)
* Dizziness or lightheadedness
* Chest pain or discomfort
During an episode of PAT, the heart rate may exceed 100 beats per minute and can reach as high as 200-300 beats per minute. The episodes can last from a few seconds to several hours and may occur randomly throughout the day.
PAT is often diagnosed through a physical examination, electrocardiogram (ECG), or holter monitor. Treatment options for PAT may include medications to control heart rate and rhythm, lifestyle changes such as avoiding triggers, and in severe cases, implantable devices such as pacemakers or cardioverter-defibrillators.
In summary, paroxysmal tachycardia is a type of arrhythmia that is characterized by rapid heartbeats that come and go in episodes, and it can be triggered by various factors. It can cause symptoms such as palpitations, shortness of breath, and chest pain, and may require treatment with medications or implantable devices.
In EJ tachycardia, the heartbeats are initiated by abnormal electrical impulses that arise from the junctional tissue near the atrioventricular (AV) node. These impulses then spread to the rest of the heart, causing a rapid and irregular heartbeat.
EJ tachycardia can be caused by a variety of factors, including:
* Coronary artery disease
* Heart failure
* Cardiomyopathy
* Hypertension
* Certain medications
* Abnormal electrical pathways in the heart
Symptoms of EJ tachycardia can include palpitations, shortness of breath, and dizziness. In some cases, the arrhythmia may be asymptomatic and only detected during a physical examination or electrocardiogram (ECG).
Diagnosis of EJ tachycardia is typically made based on symptoms, physical examination findings, and results of diagnostic tests such as an ECG, echocardiogram, or stress test. Treatment options for EJ tachycardia depend on the underlying cause of the arrhythmia and may include medications to control heart rate and rhythm, cardioversion (electrical shock therapy) to restore a normal heart rhythm, or catheter ablation to destroy the abnormal electrical pathways in the heart. In some cases, implantation of a cardioverter-defibrillator (ICD) may be recommended to prevent sudden death.
Amiodarone
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HERG
Potassium channel blocker
CACNA2D2
Potassium channel
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Krukenberg's spindle
Anosmia
Simvastatin
Fabry disease
Budiodarone
Polysorbate 80
Sanofi
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Cordarone4
- Amiodarone (Cordarone)Taking papaya extract by mouth along with amiodarone might increase the amount of amiodarone in the body. (nih.gov)
- Amiodarone (Cordarone)Grapefruit juice can increase how much amiodarone the body absorbs. (nih.gov)
- Amiodarone (Cordarone) Amiodarone might increase sensitivity to sunlight. (nih.gov)
- Amiodarone is available in tablets of 200 and 400 mg in generic forms and under the brand names of Cordarone and Pacerone. (nih.gov)
Risks of taking ami1
- Talk to your doctor about the risks of taking amiodarone. (medlineplus.gov)
Arrhythmias9
- In animals, amiodarone is effective in the prevention or suppression of experimentally induced arrhythmias. (nih.gov)
- Amiodarone may cause your arrhythmia (irregular heart rhythm) to worsen or may cause you to develop new arrhythmias. (medlineplus.gov)
- Amiodarone is used to treat and prevent certain types of serious, life-threatening ventricular arrhythmias (a certain type of abnormal heart rhythm when other medications did not help or could not be tolerated. (medlineplus.gov)
- Amiodarone in the treatment of arrhythmias]. (nih.gov)
- Amiodarone is highly effective in suppressing ventricular arrhythmias and in maintaining sinus rhythm in patients with atrial fibrillation. (nih.gov)
- Reserve amiodarone hydrochloride for patients with the indicated life-threatening arrhythmias because its use is accompanied by substantial toxicity, some also life-threatening. (nih.gov)
- Amiodarone is used for the maintenance of sinus rhythm in patients with arrhythmias, but thyroid dysfunction (amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH)) is a common adverse effect. (bioscientifica.com)
- Amiodarone (brand name: Pacerone) is a prescription drug used to treat atrial and ventricular cardiac arrhythmias. (dangerousdrugs.com)
- Amiodarone is generally used to treat life-threatening arrhythmias or to prevent or treat heart rhythm disorders in people at risk of heart attack and other serious complications. (verywellhealth.com)
Atrial fibrillation2
- Amiodarone is also used off-label for suppression of atrial fibrillation and maintenance of normal sinus rhythm after cardioversion. (nih.gov)
- Amiodarone may also be useful in the treatment of atrial fibrillation. (medscape.com)
Discontinuation of amiodarone2
- These changes should not require discontinuation of amiodarone as they are evidence of its pharmacological action, although amiodarone can cause marked sinus bradycardia or sinus arrest and heart block. (nih.gov)
- 1%) leading to discontinuation of amiodarone hydrochloride tablets include pulmonary toxicity, paroxysmal ventricular tachycardia, congestive heart failure, and elevation of liver enzymes. (nih.gov)
Take amiodarone5
- Your doctor will monitor you carefully during this time and for as long as you continue to take amiodarone. (medlineplus.gov)
- Your doctor will order certain tests, such as blood tests, X-rays, and electrocardiograms (EKGs, tests that record the electrical activity of the heart) before and during your treatment to be sure that it is safe for you to take amiodarone and to check your body's response to the medication. (medlineplus.gov)
- You may take amiodarone either with or without food, but be sure to take it the same way each time.Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. (medlineplus.gov)
- Those who take amiodarone for over 6 months are also likely to develop small corneal deposits in the eye, which can cause vision to be blurred by a bluish spot. (drugsdb.com)
- Women who are breastfeeding should not take amiodarone, since the benzyl alcohol present in the drug may induce what is called "gasping syndrome" in newborns, which is often fatal. (drugsdb.com)
Nexterone1
- NEXTERONE (amiodarone HCl) - Introducing the first ready-to-use premixed amiodarone from Baxter Healthcare Corporation. (mayfairdrugs.com)
Hydrochloride Tablets1
- These highlights do not include all the information needed to use AMIODARONE HYDROCHLORIDE TABLETS safely and effectively. (nih.gov)
Arrhythmia5
- Amiodarone is a potent arrhythmia suppressing agent that has been clearly linked to several distinct forms of drug induced liver disease. (nih.gov)
- Amiodarone is typically given in high loading doses of 800 to 1600 mg daily, either intravenously or orally until the arrhythmia is controlled, and as maintenance oral doses for long term therapy of 200 to 600 mg daily. (nih.gov)
- Once adequate arrhythmia control is achieved, or if side effects become prominent, reduce amiodarone hydrochloride tablet dose to 600 to 800 mg/day for one month and then to the maintenance dose, usually 400 mg/day. (nih.gov)
- Amiodarone is a drug used to treat a condition known as cardiac arrhythmia . (verywellhealth.com)
- Because amiodarone is prescribed to prevent or treat serious complications of cardiac arrhythmia, its benefits will almost always outweigh the risks of increased cholesterol. (verywellhealth.com)
Antiarrhythmics2
- Amiodarone is in a class of medications called antiarrhythmics. (medlineplus.gov)
- Avoid coadministration of amiodarone with other antiarrhythmics and drugs known to prolong the QT interval. (nih.gov)
Intravenous administration1
- In animal studies and after intravenous administration in man, amiodarone relaxes vascular smooth muscle, reduces peripheral vascular resistance (afterload), and slightly increases cardiac index. (nih.gov)
Acute3
- After acute intravenous dosing in man, amiodarone may have a mild negative inotropic effect. (nih.gov)
- Amiodarone, a Class III antiarrhythmic agent, used in the treatment of supraventricular and ventricular tachyarrhythmias, may cause acute hepatitis. (zenodo.org)
- Acute silica toxicity: attenuation by amiodarone-induced pulmonary phospholipidosis. (cdc.gov)
Drugs2
- Amiodarone hydrochloride is a member of a new class of antiarrhythmic drugs with predominantly Class III (Vaughan Williams' classification) effects. (nih.gov)
- We included patients with initial shockable rhythms who received the study drugs of amiodarone, lidocaine, or placebo before achieving return of spontaneous circulation. (nih.gov)
Benzofuran derivative2
Return of spontaneous circulation1
- How does amiodarone affect return of spontaneous circulation, survival, and neurological outcome following cardiac arrest? (rebelem.com)
Doses3
- The liver injury occurs more frequently with higher doses and prolonged therapy, and total cumulative dosage may be important as amiodarone can accumulate and can persist in liver tissue, even long after therapy is stopped. (nih.gov)
- A woman who took amiodarone with reducing doses of 600, 400 and 200 mg daily for one week at each dosage level during the last 3 weeks of pregnancy had milk amiodarone and desethylamiodarone levels of 0.5 to 1.8 mg/L and 0.4 to 0.8 mg/L, respectively, in 5 samples of colostrum obtained during days 2 and 3 postpartum. (nih.gov)
- You will receive your first few doses of amiodarone in a hospital setting where your heart can be monitored in case the medication causes serious side effects. (buystromectoln.com)
Hypothyroidism1
- It is also not uncommon for individuals to develop hypothyroidism or hyperthyroidism as a result of taking amiodarone. (drugsdb.com)
Desethylamiodarone7
- 7 , 8 ] Infant serum levels of amiodarone and desethylamiodarone may be useful for ruling out cardiac effects of the drug. (nih.gov)
- Amiodarone is an iodine-containing compound that is active and is also metabolized to the active metabolite desethylamiodarone. (nih.gov)
- In a mother who took amiodarone 200 mg daily for the last 5 weeks of pregnancy and for one week after delivery, milk amiodarone and desethylamiodarone levels were 0.55 and 0.44 mg/L, respectively, at 4 weeks postpartum and 0.030 and 0.002 mg/L at 6 weeks postpartum. (nih.gov)
- A mother who took amiodarone 200 mg daily throughout pregnancy and during breastfeeding had milk amiodarone and desethylamiodarone levels of 1.7 and 0.75 mg/L, respectively, 2 weeks postpartum and 3.0 and 1.8 mg/L 3 weeks postpartum. (nih.gov)
- Another mother who took amiodarone 200 mg daily throughout pregnancy had milk amiodarone and desethylamiodarone levels of 2.2 and 0.77 mg/L, respectively, at birth. (nih.gov)
- A woman who took amiodarone 400 mg daily from week 14 of pregnancy and throughout nursing had milk amiodarone levels that varied from 1.06 to 3.65 mg/L (average 2.52 mg/L) and milk desethylamiodarone levels that varied from 0.5 to 1.24 mg/L (average 0.9 mg/L) on 5 occasions during the month following delivery. (nih.gov)
- A woman who took amiodarone 800 mg daily for 1 week starting at week 34 of pregnancy, then 400 mg daily for the rest of her pregnancy and during breastfeeding had milk amiodarone levels that varied from 3.6 to 14.4 mg/L (average 10.4 mg/L) and milk desethylamiodarone levels that varied from 1.3 to 5.7 mg/L (average 4.1 mg/L) on days 9, 11 and 13 postpartum. (nih.gov)
Cardiac7
- Amiodarone prolongs the duration of the action potential of all cardiac fibers while causing minimal reduction of dV/dt (maximal upstroke velocity of the action potential). (nih.gov)
- Amiodarone increases the cardiac refractory period without influencing resting membrane potential, except in automatic cells where the slope of the prepotential is reduced, generally reducing automaticity. (nih.gov)
- In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countl. (bmj.com)
- Use of amiodarone in the treatment of cardiac dysrhythmias]. (nih.gov)
- Some investigators believe that breastfeeding can be undertaken during maternal amiodarone use with periodic monitoring of infant cardiac and thyroid function status,[ 5 , 6 ] especially if only a single dose of amiodarone is given. (nih.gov)
- BACKGROUND: Amiodarone and lidocaine have not been shown to have a clear survival benefit compared to placebo for out-of-hospital cardiac arrest (OHCA). (nih.gov)
- Subsequent studies have questioned the utility of amiodarone in cardiac arrest from the perspective of improving survival to hospital discharge or survival with a good neurological outcome. (rebelem.com)
Pulmonary3
- Amiodarone hydrochloride can cause pulmonary toxicity (hypersensitivity pneumonitis or interstitial/alveolar pneumonitis) that has resulted in clinically manifest disease at rates as high as 17% in some series of patients. (nih.gov)
- Obtain a baseline chest X-ray and pulmonary-function tests, including diffusion capacity, when amiodarone hydrochloride therapy is initiated. (nih.gov)
- For some time, the FDA was reluctant to approve amiodarone because of its link to serious pulmonary side effects. (dangerousdrugs.com)
Metabolite2
- Breastmilk and infant serum levels of amiodarone and its active metabolite are somewhat unpredictable, but can be high during breastfeeding. (nih.gov)
- Even if the drug were discontinued at birth, the mother would continue to excrete amiodarone and its metabolite (and possibly large amounts of iodine) into breastmilk for days to weeks. (nih.gov)
Medicines1
- The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. (bmj.com)
Shock-refractory1
- According to the advanced cardiovascular life support (ACLS) algorithm, amiodarone is still the recommended first-line medication for shock refractory VF/VT. (rebelem.com)
Antiarrhythmic effects2
- No data are available on the activity of DEA in humans, but in animals, it has significant electrophysiologic and antiarrhythmic effects generally similar to amiodarone itself. (nih.gov)
- Amiodarone may interact with thyroid nuclear receptors, but its antiarrhythmic effects are believed to be mediated by its action in blocking membrane ion channels via perturbation of the lipid environment in the membrane bilayer. (nih.gov)
Toxicity1
- The injury resembles alcoholic liver disease clinically and histologically, although serum ALT and AST are usually elevated to a similar degree in amiodarone toxicity in contrast to alcoholic liver injury. (nih.gov)
Tablet2
- Each amiodarone hydrochloride tablet intended for oral administration contains 200 mg of amiodarone hydrochloride. (nih.gov)
- Amiodarone comes as a tablet to take by mouth. (medlineplus.gov)
Hepatic1
- Intravenous amiodarone treatment is instituted, but at 12 hours after initiation of treatment, there is a significant increase in the level of hepatic transaminases. (zenodo.org)
Dose2
- The effects of food upon the bioavailability of amiodarone have been studied in 30 healthy subjects who received a single 600 mg dose immediately after consuming a high-fat meal and following an overnight fast. (nih.gov)
- Your doctor will probably start you on a high dose of amiodarone and gradually decrease your dose as the medication begins to work. (medlineplus.gov)
Body's2
- Amiodarone can cause a number of serious side effects pertaining to the body's major organs. (drugsdb.com)
- When mixed with amiodarone, MDMA can affect the body's ability to keep the correct temperature. (worldsbest.rehab)
Lidocaine4
- We sought to evaluate how timing from emergency medical services (EMS) arrival on scene to drug administration affects the efficacy of amiodarone and lidocaine compared to placebo. (nih.gov)
- METHOD: This is a secondary analysis of the 10-site, 55-EMS-agency double-blind randomized controlled amiodarone, lidocaine, or placebo in OHCA study. (nih.gov)
- We compared outcomes for amiodarone and lidocaine compared to placebo and adjust for potential confounders. (nih.gov)
- Evaluated effects of amiodarone compared with alternative treatments (lidocaine, nifekalant, or placebo) on the following outcomes: (1) ROSC (2) survival to hospital admission (3) survival to 24 hrs (4) survival to hospital discharge (5) neurological outcome. (rebelem.com)
Favorable2
- After we stopped the amiodarone administration, the evolution is favorable, with the remission of the cytolysis syndrome. (zenodo.org)
- This systematic review and meta-analysis demonstrates that while amiodarone significantly increased survival to hospital to admission compared with placebo or other antidysrhythmics for OHCA, it does not significantly improve favorable neurological outcome or survival to hospital discharge. (rebelem.com)
Tissues1
- Amiodarone is highly lipophilic and is concentrated in many tissues and cells, including hepatocytes in the liver. (nih.gov)
Allergic3
- Case report of amiodarone-associated allergic pneumonitis amidst the COVID-19 pandemic. (pneumotox.com)
- More serious side effects of amiodarone can indicate an allergic reaction. (drugsdb.com)
- Rapid weight loss and weight gain are associated with serious allergic reactions to amiodarone, so individuals experiencing large weight fluctuations in a very short period of time should contact their physician. (drugsdb.com)
CONCLUSIONS1
- CONCLUSIONS: The early administration of amiodarone, particularly within 8 min, is associated with greater survival to admission, survival to discharge, and functional survival compared to placebo in patients with an initial shockable rhythm. (nih.gov)
Thyroid function2
- Metabolism also releases 6 mg of free iodine for each 100 mg of amiodarone which can affect thyroid function. (nih.gov)
- This study provides data to reconsider the yield of regular testing of thyroid function to predict overt thyroid dysfunction in amiodarone treated patients. (bioscientifica.com)
Treatment5
- You will probably be hospitalized for one week or longer when you begin your treatment with amiodarone. (medlineplus.gov)
- Your doctor or pharmacist will give you the manufacturer's patient information sheet (Medication Guide) when you begin treatment with amiodarone and each time you refill your prescription. (medlineplus.gov)
- There is an increased risk also when doctors prescribe amiodarone for off-label use, without informing the patient about the possible side effects, or that the FDA had not approved its treatment as safe and effective. (dangerousdrugs.com)
- While some of these side effects can manifest soon after beginning treatment, it is possible for them to appear months after a patient starts taking amiodarone (and even months after treatment ends), so it important for individuals to closely monitor themselves after discontinuing use of the drug. (drugsdb.com)
- We discuss a case of an eight-year-old child with Ebstein's anomaly who presented with supraventricular tachycardia and was effectively treated with amiodarone after initial treatment with adenosine failed to reduce the heart rate . (bvsalud.org)
Dosage1
- The average milk amiodarone concentration was 3.5 mg/L. The authors calculated that her infant would have received an average of 18% and a maximum of 26% of the maternal weight-adjusted dosage of amiodarone. (nih.gov)
Accumulation3
- Amiodarone has a very large but variable volume of distribution, averaging about 60 L/kg, because of extensive accumulation in various sites, especially adipose tissue and highly perfused organs, such as the liver, lung, and spleen. (nih.gov)
- The development of maximal ventricular Class III effects after oral amiodarone administration in humans correlates more closely with DEA accumulation over time than with amiodarone accumulation. (nih.gov)
- Often these elevations resolve despite continuation of amiodarone, and liver biopsy may reveal minimal changes, or accumulation of granular material in macrophages without other evidence of injury. (nih.gov)
Dysfunction1
- As the onset of AIT and AIH may be unpredictable, the value of long-term regular monitoring of amiodarone treated patients for thyroid dysfunction is still uncertain. (bioscientifica.com)
Patients6
- After oral dosing, however, amiodarone produces no significant change in left ventricular ejection fraction (LVEF), even in patients with depressed LVEF. (nih.gov)
- Patients taking amiodarone are recommended to have ALT and AST values taken at baseline and then every six months, and to discontinue therapy if levels are persistently greater than twice the upper limit of the normal range. (nih.gov)
- Clinically apparent liver disease arises in up to 1% of amiodarone treated patients annually. (nih.gov)
- This case highlights the need for careful monitoring of patients receiving intravenous amiodarone to identify any potential for hepatotoxicity. (zenodo.org)
- We included 303 patients treated with amiodarone between 1984 and 2007. (bioscientifica.com)
- In 2004, Amiodarone was prescribed to 2.3 million patients, and 82 percent of these were not for approved conditions. (dangerousdrugs.com)
Rhythms1
- Amiodarone is a medicine which prevents abnormal heart rhythms. (nih.gov)
Epididymitis1
- However, in some cases amiodarone has been found to trigger epididymitis in men, which is an inflammation of the scrotal tissue. (drugsdb.com)
Side effects2
- Generally, men and women experience similar common side effects of amiodarone. (drugsdb.com)
- Amiodarone is associated with a wide range of side effects. (verywellhealth.com)
Significantly1
- Amiodarone significantly improves survival to hospital admission. (rebelem.com)
Placebo1
- However, amiodarone does not improve survival to discharge or neurological outcomes compared to placebo or other antidysrhythmics. (rebelem.com)
Slowly1
- Following oral administration in man, amiodarone is slowly and variably absorbed. (nih.gov)
Situations1
- Amiodarone is for use only in life-threatening situations. (dangerousdrugs.com)
Concentration1
- The area under the plasma concentration-time curve (AUC) and the peak plasma concentration (C max ) of amiodarone increased by 2.3 (range 1.7 to 3.6) and 3.8 (range 2.7 to 4.4) times, respectively, in the presence of food. (nih.gov)
Affect1
- Amiodarone is a substrate for CYP3A and CYP2C8, so inhibitors and inducers affect amiodarone exposure. (nih.gov)
Survival1
- These recommendations stem from two hallmark studies which demonstrated improved ROSC and survival rates to admission after amiodarone was administered ( Dorian 2002 , Kudenchuk 1999 ). (rebelem.com)
Interval1
- amiodarone and trimethoprim both increase QTc interval. (medscape.com)
Effects2
- Little conclusive evidence has been drawn regarding the effects of amiodarone during the gestational stage. (drugsdb.com)
- MDMA on its own and even without amiodarone can have many of the same effects as other stimulants like cocaine and amphetamines. (worldsbest.rehab)
Abnormal1
- Additionally, some men have also reported gynecomastia (an abnormal development of mammary glands) as a result of taking amiodarone. (drugsdb.com)
Peripheral1
- Surely this is a case of the dangers of peripheral amiodarone being exagerated? (bmj.com)
Heart1
- In addition to pregnant women, amiodarone is not recommended for those who have been diagnosed with clogged arteries, abnormally low heart rate, a preexisting respiratory condition, or those who have been fitted with a pacemaker. (drugsdb.com)