Disopyramide: A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.Mexiletine: Antiarrhythmic agent pharmacologically similar to LIDOCAINE. It may have some anticonvulsant properties.Anti-Arrhythmia Agents: 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.Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.Procainamide: A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.OrosomucoidParasympatholytics: Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.Tocainide: An antiarrhythmic agent which exerts a potential- and frequency-dependent block of SODIUM CHANNELS.Cross Circulation: The circulation in a portion of the body of one individual of blood supplied from another individual.Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.Encyclopedias as Topic: 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)Sodium Channels: Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.Myocardial Contraction: Contractile activity of the MYOCARDIUM.Capsules: Hard or soft soluble containers used for the oral administration of medicine.Delayed-Action Preparations: Dosage forms of a drug that act over a period of time by controlled-release processes or technology.Terminology as Topic: The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.Safety: Freedom from exposure to danger and protection from the occurrence or risk of injury or loss. It suggests optimal precautions in the workplace, on the street, in the home, etc., and includes personal safety as well as the safety of property.Phosphates: Inorganic salts of phosphoric acid.Accidents, Occupational: Unforeseen occurrences, especially injuries in the course of work-related activities.Databases, Chemical: Databases devoted to knowledge about specific chemicals.Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)Phenytoin: An anticonvulsant that is used to treat a wide variety of seizures. It is also an anti-arrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs.Antipyrine: An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29)Enzyme Induction: An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.Sick Sinus Syndrome: A condition caused by dysfunctions related to the SINOATRIAL NODE including impulse generation (CARDIAC SINUS ARREST) and impulse conduction (SINOATRIAL EXIT BLOCK). It is characterized by persistent BRADYCARDIA, chronic ATRIAL FIBRILLATION, and failure to resume sinus rhythm following CARDIOVERSION. This syndrome can be congenital or acquired, particularly after surgical correction for heart defects.Electrocardiography: Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.Medicare Part C: The Balanced Budget Act (BBA) of 1997 establishes a Medicare+Choice program under part C of Title XVIII, Section 4001, of the Social Security Act. Under this program, an eligible individual may elect to receive Medicare benefits through enrollment in a Medicare+Choice plan. Beneficiaries may choose to use private pay options, establish medical savings accounts, use managed care plans, or join provider-sponsored plans.Fitness Centers: Facilities having programs intended to promote and maintain a state of physical well-being for optimal performance and health.Insurance Carriers: Organizations which assume the financial responsibility for the risks of policyholders.Medicare: Federal program, created by Public Law 89-97, Title XVIII-Health Insurance for the Aged, a 1965 amendment to the Social Security Act, that provides health insurance benefits to persons over the age of 65 and others eligible for Social Security benefits. It consists of two separate but coordinated programs: hospital insurance (MEDICARE PART A) and supplementary medical insurance (MEDICARE PART B). (Hospital Administration Terminology, AHA, 2d ed and A Discursive Dictionary of Health Care, US House of Representatives, 1976)United StatesAppointments and Schedules: The different methods of scheduling patient visits, appointment systems, individual or group appointments, waiting times, waiting lists for hospitals, walk-in clinics, etc.Medicare Part D: A stand-alone drug plan offered by insurers and other private companies to beneficiaries that receive their Medicare Part A and/or B benefits through the Original Medicare Plan. It includes Medicare Private Fee-for-Service Plans that do not offer prescription drug coverage and Medicare Cost Plans offering Medicare prescription drug coverage. The plan was enacted as the Medicare Prescription Drug, Improvement and Modernization Act of 2003 with coverage beginning January 1, 2006.

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)

  • Taking antiarrhythmic drugs, including disopyramide, may increase the risk of death. (medlineplus.gov)
  • What other drugs will affect disopyramide? (cigna.com)
  • Many drugs can interact with disopyramide. (cigna.com)
  • The pharmacology of disopyramide, potential advantages and disadvantages of the use of sustained- (or controlled-)release formulations of drugs, and the preliminary finding of our use of controlled-release disopyramide are described. (ebscohost.com)
  • Disopyramide can interact with some other drugs that you are taken and, depending on the situation, it may be best to avoid some combinations altogether. (medicinehow.com)
  • The effects of the antiarrhythmic agent disopyramide was studied on responses from voltage-clamped endplates at the neuromuscular junction of the garter snake. (strath.ac.uk)
  • Immunoassay reagents intended to perform quantitative analyses on a body fluid sample (e.g., serum, urine) to measure levels of disopyramide (a class I antiarrhythmic agent [one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent] with a depressant action on the heart similar to that of guanidine) present in the sample. (ophthalmologymanagement.com)
  • Simulation of serum disopyramide concentrations during transfer from steady-state immediate-release (IR) disopyramide to a sustained-release disopyramide preparation was performed based on pharmacokinetic parameters obtained from fit disopyramide and serum concentrations measured following an. (ebscohost.com)
  • 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)
  • In animal studies Disopyramide decreases the rate of diastolic depolarization (phase 4) in cells with augmented automaticity, decreases the upstroke velocity (phase 0) and increases the action potential duration of normal cardiac cells, decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium, and has no effect on alpha- or beta-adrenergic receptors. (drugs.com)
  • Intravenous Disopyramide may cause cardiac depression with an approximate mean 10% reduction of cardiac output, which is more pronounced in patients with cardiac dysfunction. (drugs.com)
  • After the oral administration of 200 mg of Disopyramide to 10 cardiac patients with borderline to moderate heart failure, the time to peak serum concentration of 2.3 ± 1.5 hours (mean ± SD) was increased, and the mean peak serum concentration of 4.8 ± 1.6 mcg/mL was higher than in healthy volunteers. (drugs.com)
  • There were no cardiac events within 3 months of disopyramide initiation. (ahajournals.org)
  • Conclusions Initiation of disopyramide in the outpatient setting is safe and the risk of subsequent sudden cardiac death is low. (ahajournals.org)
  • As a result, the use of disopyramide may reduce contractile force up to 42% at low doses and up to 100% in higher doses leading to heart failure. (wikipedia.org)
  • This combination increases acceptance of higher disopyramide dosing, important since there is a dose-response correlation in obstructive HCM, higher doses yielding lower gradients. (wikipedia.org)
  • 1 The effects of rifampicin, phenytoin, and disopyramide treatments on the metabolism of disopyramide were studied in patients and volunteers. (nih.gov)
  • Phenytoin can decrease the concentration of disopyramide in your body so that it doesn't work as well. (medicinehow.com)
  • 4 The metabolism of disopyramide seemed fastest in the patient group with the higher dose of disopyramide. (nih.gov)
  • Disopyramide in our clinic is usually initiated at a dose of 300 mg daily and titrated during follow‐up. (ahajournals.org)
  • Disopyramide caused dose-related negative chronotropic and inotropic effects in a dose range of 30-1000 microgram when injected directly into the cannulated sinus node artery of the isolated atrium. (meta.org)
  • Do not use disopyramide to treat any heart rhythm disorder that has not been checked and diagnosed by your doctor. (cigna.com)
  • Disopyramide is available in both oral and intravenous forms, and has a low degree of toxicity. (wikipedia.org)
  • In a second study of the oral administration of Disopyramide to 7 patients with heart disease, including left ventricular dysfunction, the mean plasma half-life was slightly prolonged to 7.8 ± 1.9 hours (range of 5 to 9.5 hours). (drugs.com)
  • A placebo-controlled trial of intravenous and oral disopyramide for prevention of neurally mediated syncope induced by head-up tilt. (thefreedictionary.com)
  • The pharmacokinetics of disopyramide and its effects on the electrocardiogram were studied in five healthy male volunteers after intravenous (50 mg) and oral (200 mg) administration. (elsevier.com)
  • With intravenous Disopyramide, either increases in systolic/diastolic or decreases in systolic blood pressure have been reported, depending on the infusion rate and the patient population. (drugs.com)
  • We have evaluated the influence of several factors on the binding of disopyramide to protein in human serum using a new ultrafiltration system and the enzyme multiplied immunoassay technique (EMIT) for disopyramide immuno-assay. (ebscohost.com)
  • From a small start-up operation founded in 1990 with just three products (extended-release potassium chloride, disopyramide phosphate and nitroglycerine) and first year sales of $5 million, Ethex is expected to top the $30 million mark in sales by the end of fiscal 1995. (thefreedictionary.com)
  • 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)
  • In six patients with impaired renal function (creatinine clearance less than 40 mL/min), Disopyramide half-life values were 8 to 18 hours. (drugs.com)
  • Both in patients and volunteers a significant increase occurred in the urinary mono-N-dealkyldisopyramide/disopyramide ratio during the first week of disopyramide therapy. (nih.gov)
  • These investigators found that disopyramide rendered 34% of the patients noninducible. (annals.org)
  • Disopyramide has the potential to suppress sinus node function and, therefore, must be used cautiously in patients with the sick sinus syndrome. (annals.org)
  • Methods and Results All charts of patients seen in the outpatient hypertrophic cardiomyopathy clinic between 2010 and 2014 were screened for initiation of disopyramide and data were extracted. (ahajournals.org)
  • A total of 2015 patients were seen in the clinic, including 168 who were started on disopyramide. (ahajournals.org)
  • Of the patients continuing disopyramide long term, 63% remained free of septal reduction interventions at end of follow‐up. (ahajournals.org)
  • 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)
  • Indeed, for relief of resistant symptoms, the European Society of Cardiology 5 and American Heart Association/American College of cardiology 6 guidelines rate disopyramide with a class I and IIa recommendation, respectively. (ahajournals.org)