A major metabolite of PROCAINAMIDE. Its anti-arrhythmic action may cause cardiac toxicity in kidney failure.
A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
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.
Surgery performed on the heart.
A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016).
An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.

Prediction of N-acetylprocainamide disposition kinetics in rat by combination of gamma variate and physiological pharmacokinetic model. (1/13)

Clearances and tissue/blood drug concentration ratios of N-acetylprocainamide (NAPA) in rats were determined. The clearances of NAPA in rat blood, liver, and kidney were 13.1, 4.88, and 8.24 ml.kg-1.min-1, respectively. Disposition kinetics of NAPA in rats was predicted with combination of gamma variate and physiological pharmacokinetic model. Equation for estimating the concentration of NAPA in rat blood following iv NAPA 40 mg.kg-1 was C = 55.06t(-0.220) exp(-0.00713t). Using r2 value as a criterion, we found a good agreement between predicted and observed concentrations in blood, lung, small intestine, heart, brain, and skin.  (+info)

Effects of antiarrhythmic drugs on phospholipid metabolism in Jurkat T cells. The potassium channel blocker, clofilium, specifically increases phosphatidylserine synthesis. (2/13)

Five antiarrhythmic drugs (bretylium, clofilium, propranolol, N-acetylprocainamide and amiodarone) were tested for their ability to modify phospholipid metabolism in Jurkat T lymphocytes. The five drugs, decreased in a dose-dependent mode the biosynthesis of both phosphatidylcholine and phosphatidylethanolamine, this effect was essentially due to impairment of either choline or ethanolamine uptake by the cells. The efficiency of the drugs to inhibit phosphatidylcholine and phosphatidylethanolamine synthesis was in the order: clofilium greater than amiodarone much greater than propranolol = bretylium much greater than N-acetylprocainamide. The IC50 varied from 3-5 microM for clofilium to greater than 200 microM for N-acetylprocainamide. In contrast, only clofilium, a voltage-gated K(+)-channel blocker, was able to increase phosphatidylserine synthesis with an EC50 = 50 microM. The effect of clofilium on phosphatidylserine synthesis thus mimics the effect of three other K(+)-channel blockers, quinine, 4-aminopyridine and tetraethylammonium, suggesting close relationships between phosphatidylserine synthesis and K+ channel activity.  (+info)

Levofloxacin and ciprofloxacin decrease procainamide and N-acetylprocainamide renal clearances. (3/13)

Ten healthy adults participated in a randomized, crossover drug interaction study testing procainamide only, procainamide plus levofloxacin, and procainamide plus ciprofloxacin. During levofloxacin therapy, most procainamide and N-acetylprocainamide (NAPA) pharmacokinetic parameters, including decreased renal clearances and renal clearance/creatinine clearance ratios, changed (P < 0.05). During ciprofloxacin treatment, only procainamide and NAPA renal clearances decreased significantly.  (+info)

Application of a generic physiologically based pharmacokinetic model to the estimation of xenobiotic levels in human plasma. (4/13)

Estimation of xenobiotic kinetics in humans frequently relies upon extrapolation from experimental data generated in animals. In an accompanying paper, we have presented a unique, generic, physiologically based pharmacokinetic model and described its application to the prediction of rat plasma pharmacokinetics from in vitro data alone. Here we demonstrate the application of the same model, parameterized for human physiology, to the estimation of plasma pharmacokinetics in humans and report a comparative evaluation against some recently published predictive methods that involve scaling from in vivo animal data. The model was parameterized through an optimization process, using a training set of in vivo data taken from the literature, and validated using a separate test set of published in vivo data. On average, the vertical divergence of the predicted plasma concentrations from the observed data, on a semilog concentration-time plot, was 0.47 log unit. For the training set, more than 80% of the predicted values of a standardized measure of the area under the concentration-time curve were within 3-fold of the observed values; over 70% of the test set predictions were within the same margin. Furthermore, in terms of predicting human clearance for the test set, the model was found to match or exceed the performance of three published interspecies scaling methods, all of which showed a distinct bias toward overprediction. We conclude that the generic physiologically based pharmacokinetic model, as a means of integrating readily determined in vitro and/or in silico data, is potentially a powerful, cost-effective tool for predicting human xenobiotic kinetics in drug discovery and risk assessment.  (+info)

Procainamide, but not N-acetylprocainamide, induces protein free radical formation on myeloperoxidase: a potential mechanism of agranulocytosis. (5/13)

 (+info)

More-sensitive enzyme-multiplied immunoassay technique for procainamide and N-acetylprocainamide in plasma, serum, and urine. (6/13)

A commercially available (Syva Co.) enzyme-multiplied immunoassay technique (EMIT) for the quantitative determination of procainamide (PA) and N-acetylprocainamide (NAPA) was modified to allow automated quantitative analysis of approximately 100 samples per day, in a working range of 0.1 to 2.0 micrograms/mL. Such a test was needed to evaluate the pharmacokinetic characteristics of controlled-release dosage forms characterized by long half-lives at low plasma concentration. Analytical recovery of PA and NAPA from serum, plasma, and urine was satisfactory, but at extreme ratios for PA:NAPA the accuracy of determining the lower-concentration component became unsatisfactory. In fact, however, we found no such ratios in 5400 clinical samples assayed by this procedure.  (+info)

Metabolites of procainamide and practolol inhibit complement components C3 and C4. (7/13)

Drug-induced systemic lupus erythematosus arises from toxic side-effects of administration of hydralazine, isoniazid, procainamide and practolol. Hydralazine and isoniazid are nucleophilic drugs and inhibit the covalent binding reaction of complement components, C3 and C4, an effect likely to lead to deposition of immune complexes (a feature of systemic lupus erythematosus). Procainamide and practolol do not themselves inhibit C3 and C4. A range of metabolites and putative metabolites of procainamide and practolol were synthesized, and tested for their ability to inhibit the covalent binding reactions of C3 and C4. The highly nucleophilic hydroxylamine metabolite of procainamide was strongly inhibitory in both tests, as was a putative hydroxylamine metabolite of practolol. These studies indicate a potential role for the hydroxylamine metabolites in mediating the toxic side-effects of procainamide and practolol, and emphasize the need for adequate measurements of hydroxylamine metabolites in human tissue.  (+info)

Four fluorescence polarization immunoassays for therapeutic drug monitoring evaluated. (8/13)

We evaluated four fluorescence polarization immunoassays--those for phenytoin, procainamide, N-acetylprocainamide (NAPA), and quinidine--from Roche Diagnostic Systems, done in the Cobas Bio FP centrifugal analyzer. The assays for phenytoin, NAPA, and quinidine demonstrated a linear response over the expected ranges of concentrations, and analytical recovery of test drug added to drug-free sera was greater than 90%. However, recovery in the procainamide assay was poor (69-82%) for samples containing greater than 8 mg/L, owing to nonlinearity. Results of method-comparison studies of the four assays paralleled the recovery studies, although the quinidine assay demonstrated a bias (1.0 mg/L higher) when compared with EMIT (Syva). The precision of the phenytoin assay was acceptable at all concentrations tested (total CV less than 7.0%). Imprecision of the other assays was significant at certain concentrations: total CV greater than 10.0% at subtherapeutic values for NAPA and quinidine, and greater than 9.0% for low (2.4 mg/L) and moderate concentrations (9.6 mg/L) of procainamide. Interferences were not significant for hemolyzed, icteric, or lipemic specimens or for specimens with added drug metabolites. The calibration curves for all four assays had good stability (greater than 60 days).  (+info)

Acecainide is a Class IC antiarrhythmic drug that was used to treat certain types of irregular heart rhythms (ventricular arrhythmias). It works by blocking the signals that cause the heart to beat irregularly. However, acecainide is no longer available in the market due to its potential to cause serious side effects, including a decreased survival rate in patients with heart disease.

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.

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.

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.

Cardiac surgical procedures are operations that are performed on the heart or great vessels (the aorta and vena cava) by cardiothoracic surgeons. These surgeries are often complex and require a high level of skill and expertise. Some common reasons for cardiac surgical procedures include:

1. Coronary artery bypass grafting (CABG): This is a surgery to improve blood flow to the heart in patients with coronary artery disease. During the procedure, a healthy blood vessel from another part of the body is used to create a detour around the blocked or narrowed portion of the coronary artery.
2. Valve repair or replacement: The heart has four valves that control blood flow through and out of the heart. If one or more of these valves become damaged or diseased, they may need to be repaired or replaced. This can be done using artificial valves or valves from animal or human donors.
3. Aneurysm repair: An aneurysm is a weakened area in the wall of an artery that can bulge out and potentially rupture. If an aneurysm occurs in the aorta, it may require surgical repair to prevent rupture.
4. Heart transplantation: In some cases, heart failure may be so severe that a heart transplant is necessary. This involves removing the diseased heart and replacing it with a healthy donor heart.
5. Arrhythmia surgery: Certain types of abnormal heart rhythms (arrhythmias) may require surgical treatment. One such procedure is called the Maze procedure, which involves creating a pattern of scar tissue in the heart to disrupt the abnormal electrical signals that cause the arrhythmia.
6. Congenital heart defect repair: Some people are born with structural problems in their hearts that require surgical correction. These may include holes between the chambers of the heart or abnormal blood vessels.

Cardiac surgical procedures carry risks, including bleeding, infection, stroke, and death. However, for many patients, these surgeries can significantly improve their quality of life and longevity.

Procaine is a local anesthetic drug that is used to reduce the feeling of pain in a specific area of the body. It works by blocking the nerves from transmitting painful sensations to the brain. Procaine is often used during minor surgical procedures, dental work, or when a patient needs to have a wound cleaned or stitched up. It can also be used as a diagnostic tool to help determine the source of pain.

Procaine is administered via injection directly into the area that requires anesthesia. The effects of procaine are relatively short-lived, typically lasting between 30 minutes and two hours, depending on the dose and the individual's metabolism. Procaine may also cause a brief period of heightened sensory perception or euphoria following injection, known as "procaine rush."

It is important to note that procaine should only be administered by trained medical professionals, as improper use can lead to serious complications such as allergic reactions, respiratory depression, and even death.

Sotalol is a non-selective beta blocker and class III antiarrhythmic drug. It works by blocking the action of certain natural substances in your body, such as adrenaline, on the heart. This helps to decrease the heart's workload, slow the heart rate, and regulate certain types of irregular heartbeats (such as atrial fibrillation).

Sotalol is used to treat various types of irregular heartbeats (atrial fibrillation/flutter, ventricular tachycardia) and may also be used to help maintain a normal heart rhythm after a heart attack. It is important to note that Sotalol should only be prescribed by a healthcare professional who has experience in treating heart rhythm disorders.

This medical definition is based on the information provided by the National Library of Medicine (NLM).

Some acecainide can convert to procainamide. The deacetylation clearance of acecainide is 0.39 L/h compare to a total NAPA ... acecainide can cause cardiac toxicity that effects in torsades de pointes. Also acecainide can decrease renal function when it ... Acecainide is considered comparable in activity to its parent compound; however, acecainide levels will vary widely. Serum ... However, hypotension has been reported in association with a rapid injection of acecainide. In animals, acecainide has positive ...
... acecainide MeSH D02.241.223.100.054.055.105 - benzocaine MeSH D02.241.223.100.054.055.650 - procainamide MeSH D02.241.223.100. ...
... acecainide (INN) acecarbromal (INN) aceclidine (INN) aceclofenac (INN) acedapsone (INN) acediasulfone (INN) acedoben (INN) ...
... acecainide), an anti-arrhythmic heart drug NAPA Auto Parts, an American retailers' cooperative National Academy of Public ...
Some acecainide can convert to procainamide. The deacetylation clearance of acecainide is 0.39 L/h compare to a total NAPA ... acecainide can cause cardiac toxicity that effects in torsades de pointes. Also acecainide can decrease renal function when it ... Acecainide is considered comparable in activity to its parent compound; however, acecainide levels will vary widely. Serum ... However, hypotension has been reported in association with a rapid injection of acecainide. In animals, acecainide has positive ...
This medicine comes with a patient information insert. Read and follow these instructions carefully. Ask your doctor or pharmacist if you have any questions. The solution comes in small containers that are only used one time. Throw the empty container away after putting the medicine into your ear(s). This medicine should be used only inside the ear. Do not put it in the eyes or nose, and do not take it by mouth. If this medicine is swallowed by accident or gets into your eyes, call your doctor right away. It is important that the infected ear remain clean and dry. When bathing, avoid getting the infected ear wet. Avoid swimming unless your doctor has instructed you otherwise. To use the ear drops:. ...
Detailed drug Information for Duo-Vil 2-25. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
The steady-state pharmacokinetics and pharmacodynamics of procainamide and its active N-acetyl metabolite (NAPA) were assessed alone and in combination with trimethoprim. Eight healthy men received oral sustained-release procainamide, 500 mg every 6 hours for 3 days, alone and with oral trimethoprim …
Acecainide Acecainide Hydrochloride use Acecainide Acecainide Monohydrochloride use Acecainide Acedapsone Acedoxin use ...
Acecainide Acecainide Hydrochloride use Acecainide Acecainide Monohydrochloride use Acecainide Acedapsone Acedoxin use ...
Acecainide Acecainide Hydrochloride use Acecainide Acecainide Monohydrochloride use Acecainide Acedapsone Acedoxin use ...
Acecainide Acecainide Hydrochloride use Acecainide Acecainide Monohydrochloride use Acecainide Acedapsone Acedoxin use ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
Acecainide [D02.455.426.559.389.127.085.033] * Aminohippuric Acids [D02.455.426.559.389.127.085.067] * Amisulpride [D02.455. ...
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This graph shows the total number of publications written about "Sulpiride" by people in this website by year, and whether "Sulpiride" was a major or minor topic of these publications ...
Acecainide [D02.455.426.559.389.127.020.937.625] * 4-Aminobenzoic Acid [D02.455.426.559.389.127.020.937.640] ...
Detailed drug Information for Amiodarone (Intravenous). Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Acecainide, unlike procainamide, is an agent whose pharmacokinetics allow long-term therapy on a practical schedule. It is ... The mean half-life of elimination after a single 500 mg dose of acecainide was 7.5 hours; this had prolonged significantly (p ... The mean plasma concentration of acecainide associated with efficacy was 14.3 micrograms/ml (range 9.4 to 19.5) and with side ... No variable examined (including acetylator phenotype) was found to be a predictor of responsiveness to acecainide. Outpatient ...
Acecainide,create,22-AUG-08,(null),(null) C75126,Acecainide_Hydrochloride,create,22-AUG-08,(null),(null) C75127,Ciprafamide, ...
Acecainide Acecainide Hydrochloride use Acecainide Acecainide Monohydrochloride use Acecainide Acedapsone Acedoxin use ...
Acecainide / therapeutic use Actions. * Search in PubMed * Search in MeSH * Add to Search ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
Acecainide Hydrochloride Narrower Concept UI. M0000194. Registry Number. B9K738KX14. Terms. Acecainide Hydrochloride Preferred ... Acecainide Hydrochloride Acecainide Monohydrochloride Acetylprocainamide N-Acetylprocainamide Pharm Action. Anti-Arrhythmia ... Acecainide Preferred Term Term UI T000367. Date01/01/1999. LexicalTag NON. ThesaurusID ... Acecainide Preferred Concept UI. M0000193. Registry Number. 910Q707V6F. Related Numbers. 32795-44-1. 34118-92-8. B9K738KX14. ...
Acecainide Hydrochloride Narrower Concept UI. M0000194. Registry Number. B9K738KX14. Terms. Acecainide Hydrochloride Preferred ... Acecainide Hydrochloride Acecainide Monohydrochloride Acetylprocainamide N-Acetylprocainamide Pharm Action. Anti-Arrhythmia ... Acecainide Preferred Term Term UI T000367. Date01/01/1999. LexicalTag NON. ThesaurusID ... Acecainide Preferred Concept UI. M0000193. Registry Number. 910Q707V6F. Related Numbers. 32795-44-1. 34118-92-8. B9K738KX14. ...
Acecainide Current Synonym true false 159396014 N-acetylprocainamide Current Synonym true false ...
... blur bepotastine side effects eye drops alongside them bibliographic acecainide, whreas subdued from relocate among their ...
ANTI-ARRHYTHMIA AGENTS ACECAINIDE ANTI-ARRHYTHMIA AGENTS ACETYLDIGITOXINS ANTI-ARRHYTHMIA AGENTS ACETYLDIGOXINS ANTI-ARRHYTHMIA ... CARDIOVASCULAR AGENTS ACECAINIDE CARDIOVASCULAR AGENTS ACETYLCHOLINE CARDIOVASCULAR AGENTS ACETYLDIGITOXINS CARDIOVASCULAR ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
D2.455.426.559.389.127.20.937.640 Acecainide D2.241.223.100.54.55.15 D2.241.223.100.50.500.625 D2.241.223.100.100.33 D2.455. ...
This graph shows the total number of publications written about "Sulpiride" by people in this website by year, and whether "Sulpiride" was a major or minor topic of these publications ...
Acecainide [D02.455.426.559.389.127.085.033] * Aminohippuric Acids [D02.455.426.559.389.127.085.067] * Amisulpride [D02.455. ...
  • Along with the discovery of procainamide came the discovery of its metabolite acecainide. (wikipedia.org)
  • Procainamide is metabolized in the liver to acecainide by N-acetyltransferase, an enzyme that is genetically determined. (wikipedia.org)
  • Acecainide is the major metabolite of the antiarrhythmic drug, procainamide. (wikipedia.org)
  • Monitoring acecainide levels along with the procainamide is recommended during procainamide therapy. (wikipedia.org)
  • Serum levels of acecainide increase in patients on chronic procainamide therapy, particularly in those with renal impairment. (wikipedia.org)
  • The average serum concentration ratio of acecainide to procainamide is 0.8 to 1.2, depending on a genetically determined tendency to acetylate procainamide rapidly or slowly. (wikipedia.org)
  • Because the ratio varies from patient to patient, measuring serum acecainide and procainamide together helps to achieve an optimum anti-arrhythmic effect and reduce the risk of toxicity. (wikipedia.org)
  • The pharmacokinetic properties of acecainide, an active metabolite of procainamide, have been studied in healthy people and patients with cardiomyopathy in elderly and younger patients. (wikipedia.org)
  • Acecainide (N-acetylprocainamide, NAPA) is an antiarrhythmic drug. (wikipedia.org)
  • Acecainide is the major metabolite of the antiarrhythmic drug, procainamide. (wikipedia.org)
  • Acecainide is a potassium-channel blocker like Class III antiarrhythmic compounds. (wikipedia.org)
  • Acecainide is pharmacologically active as an antiarrhythmic agent. (wikipedia.org)
  • this finding implies that estimates of the antiarrhythmic contribution of acecainide concentrations achieved during long-term procainamide therapy are unlikely to be meaningful in a given person. (nih.gov)
  • Monitoring acecainide levels along with the procainamide is recommended during procainamide therapy. (wikipedia.org)
  • Serum levels of acecainide increase in patients on chronic procainamide therapy, particularly in those with renal impairment. (wikipedia.org)
  • The average serum concentration ratio of acecainide to procainamide is 0.8 to 1.2, depending on a genetically determined tendency to acetylate procainamide rapidly or slowly. (wikipedia.org)
  • The mean plasma concentration of acecainide associated with efficacy was 14.3 micrograms/ml (range 9.4 to 19.5) and with side effects (primarily gastrointestinal) was 22.5 micrograms/ml (10.6 to 37.9). (nih.gov)