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PubMed2001

Pattern of inheritance in three sudden unexplained death syndrome ("Lai-tai") families.

Sudden Unexplained Death Syndrome (SUDS) (or Lai-tai) is sudden death in previously healthy young adults without any structural cause of death from autopsy findings. Our previous data showed that familial SUDS is not X-linked recessive. The objective of this study was to determine the pattern of inheritance in familial SUDS using the ECG markers of Brugada syndrome (RBBB and ST-segment elevation in V1 to V3), SUDS and presumptive SUDS as phenotypes. We employed the standard 12-lead ECG and higher intercostal space (ICS) V1 to V3 (-V1 to -V3 and -2V1 to -2V3) leads ECG in SUDS relatives after procainamide and drew the pedigree. We studied 62 relatives of 9 SUDS victims who died in Singapore and selected 3 families (n = 34) for the procainamide test and ECG. The mean age was 36.4 +/- 23.6 years (4-78 years). Three SUDS families showed the same pattern of inheritance of autosomal dominant.

Autopsy↗
PubMed2003

Procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells.

Methylation-associated silencing of tumor suppressor genes is recognized as being a molecular hallmark of human cancer. Unlike genetic alterations, changes in DNA methylation are potentially reversible. This possibility has attracted considerable attention from a therapeutics standpoint. Nucleoside-analogue inhibitors of DNA methyltransferases, such as 5-aza-2'-deoxycytidine, are able to demethylate DNA and restore silenced gene expression. Unfortunately, the clinical utility of these compounds has not yet been fully realized, mainly because of their side effects. A few non-nucleoside inhibitors of DNA methyltransferases have been reported, including the anti-arrhythmia drug procainamide. Following this need to find new demethylating agents, we have tested the potential use of procaine, an anesthetic drug related to procainamide. Using the MCF-7 breast cancer cell line, we have found that procaine is a DNA-demethylating agent that produces a 40% reduction in 5-methylcytosine DNA content as determined by high-performance capillary electrophoresis or total DNA enzyme digestion. Procaine can also demethylate densely hypermethylated CpG islands, such as those located in the promoter region of the RAR beta 2 gene, restoring gene expression of epigenetically silenced genes. This property may be explained by our finding that procaine binds to CpG-enriched DNA. Finally, procaine also has growth-inhibitory effects in these cancer cells, causing mitotic arrest. Thus, procaine is a promising candidate agent for future cancer therapies based on epigenetics.

Antineoplastic Agents↗
PubMed2006

Monitoring of drugs with a narrow therapeutic range in ambulatory care.

OBJECTIVES: To describe the proportion of patients receiving drugs with a narrow therapeutic range who lacked serum drug concentration monitoring during a 1-year period of therapy and to identify patient characteristics associated with lack of monitoring. STUDY DESIGN: Retrospective cohort. METHODS: Ambulatory patients (n = 17,748) at 10 health maintenance organizations who were receiving ongoing continuous drug therapy with digoxin, carbamazepine, divalproex sodium, lithium carbonate, lithium citrate, phenobarbital sodium, phenytoin, phenytoin sodium, primidone, quinidine gluconate, quinidine sulfate, procainamide hydrochloride, theophylline, theophylline sodium glycinate, tacrolimus, or cyclosporine for at least 12 months between January 1, 1999, and June 30, 2001, were identified. Serum drug concentration monitoring was assessed from administrative data and from medical record data. RESULTS: Fifty percent or more of patients receiving digoxin, theophylline, procainamide, quinidine, or primidone were not monitored, and 25% to 50% of patients receiving divalproex, carbamazepine, phenobarbital, phenytoin, or tacrolimus were not monitored. Younger age was associated with lack of monitoring for patients prescribed digoxin (adjusted odds ratio, 1.86; 95% confidence interval, 1.39-2.48) and theophylline (adjusted odds ratio, 1.58; 95% confidence interval, 1.23-2.04), while older age was associated with lack of monitoring for patients prescribed carbamazepine (adjusted odds ratio, 0.59; 95% confidence interval, 0.44-0.80) and divalproex (adjusted odds ratio, 0.50; 95% confidence interval, 0.38-0.66). Patients with fewer outpatient visits were also less likely to be monitored (P < .001). CONCLUSIONS: A substantial proportion of ambulatory patients receiving drugs with narrow intervals between doses resulting in beneficial and adverse effects did not have serum drug concentration monitoring during 1 year of use. Clinical implications of this finding need to be evaluated.

Ambulatory Care↗
PubMed1991

[Family with predominance of cardiac involvement in Steinert's disease].

We report an affected family (mother and two children) with prominent cardiac form as reflected by the mother, 49, with neuromuscular signs (muscular atrophy os face, neck and distally in the extremities) who received an implantable pacemaker after 2 consecutive episodes of syncope and baseline EKG with P-R of 250 ms, QRS of 130 ms (LBBB) and conduction system intervals displaying overt widening (AH of 140 ms with a ERP of junction tissue of 590 ms, and Wenckebach point of 115 bpm; and HV of 80 ms before and 95 ms after pharmacological stress with procainamide). As long as its mode of inheritance is autosomal dominant, the cardiovascular examination of her two affected siblings (F1 and F2) revealed: F1 (male, 31), with P-R of 180 ms and QRS of 100 ms; F2 (female, 27), with P-R of 200 ms and QRS of 100 ms, both with left axis deviation. Echocardiographic studies were normal in both, but Holter studies showed remarkable bradycardia in both and intermittent rate-related (phase 3) LBBB in F2. Also for F1 and F2 conduction system intervals, except for AH (normal in both), displayed severe widening (HV of 70 ms in F1 and of 80 ms in F2, but only in this later with a procainamide stress extra widening to 130 ms). All three patients showed normal NS function, as usual for the disease. F2 is kept under close surveillance for the appearance of any symptom. In conclusion, although rarely symptomatic, the intensity of IV conduction system damage should not be disregarded in this condition.

Adult↗
PubMed1990

[Malignant ventricular arrhythmias in the subacute and late phases of myocardial infarction. Clinical arrhythmological characteristics and prognostic value].

The purposes of this study are as follows: 1) to describe the clinical and arrhythmological characteristics of 30 patients (23 male, 7 female, mean age: 61 years) who suffered from episodes of ventricular tachycardia and/or ventricular fibrillation between the 7th and the 90th day following acute myocardial infarction; 2) to evaluate the effectiveness of treatment with amiodarone also taking into account the results of electrophysiologic study; 3) to correlate our results with data from previous studies. The site of the acute myocardial infarction was anterior in 16 patients, inferior in 12, and anterior and inferior in 2. Twenty patients had early post-acute myocardial infarction complications (67%) such as cardiac failure (16), bundle branch blocks (9) and ventricular fibrillation in the first 48 hours (6). The mean ejection fraction was 33 +/- 8% and a left ventricular aneurysmatic evolution was observed in 13 patients (43%). The first episodes of spontaneous ventricular arrhythmias occurred after a mean interval of 32 +/- 24 days following acute myocardial infarction. These occurred in the form of ventricular fibrillation in 19 patients (63%) and of ventricular tachycardia in the other 11 (37%). The patients experienced 5.6 +/- 5 episodes of ventricular fibrillation or ventricular tachycardia. Of the 30 patients, 28 received amiodarone, 1 procainamide and 1 propafenone. Five of the 28 patients treated with amiodarone were also given either procainamide or propafenone due to the early recurrence of ventricular tachycardia or fibrillation. One patient underwent early left ventricular aneurysmatic resection due to refractory ventricular fibrillation. Two groups of patients were distinguished on the basis of the electrophysiologic study results obtained during anti-arrhythmic treatment: group A consisted of 17 cases in which a sustained ventricular tachycardia was inducible (57%), group B consisted of 13 cases in which a sustained ventricular tachycardia was not inducible (43%). During a mean follow-up period of 31.6 +/- 26 months the total mortality rate was 23% in group A and 46% in group B (p = ns), the incidence of sudden death was 17% in group A and 23% in group B (p = ns), the incidence of non fatal ventricular tachycardia or ventricular fibrillation recurrences was 24% in group A and 0% in group B (0.05 less than p less than 0.1). One group A patient successfully underwent a heart transplant. The negative predictive value of ventricular stimulation in relation to sudden death and to non-fatal arrhythmic recurrences was 77% and 100%; the positive predictive value was 17 and 28%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

Characterization and antigenic specificity of chlorpromazine-induced antinuclear antibodies.

Prolonged treatment with chlorpromazine is often associated with the development of antinuclear antibodies, an immunoglobulin M lupus anticoagulant, and polyclonal serum IgM elevation, but not with clinical features of systemic lupus erythematosus (SLE). Sera from 62 long-term psychiatric patients given treatment daily with 100 mg or more of chlorpromazine for at least 1 year were screened for antinuclear antibodies by indirect immunoperoxidase assay using HEp-2 cells. In 26 samples, antinuclear antibody titers greater than or equal to 1:40 with a homogeneous pattern were seen when anti-human IgM was used as the second antibody, three sera samples reacted with IgG, and four samples reacted with both IgG and IgM antisera. The antinuclear antibody antigenic reactivity was investigated by using histone and nonhistone nuclear antigens by enzyme-linked immunosorbent assay and passive hemagglutination techniques. Forty serum samples reacted with histone. Twenty-five samples reacted with deoxyribonucleoprotein (DNP), 28 with single-stranded DNA, and two with double-stranded DNA. No reaction was obtained with the extractable nuclear antigens RNP or Sm. These results indicate that chlorpromazine-induced antinuclear antibodies, like the antinuclear antibodies induced by hydralazine and procainamide, react mainly with histone nuclear antigens. Unlike the hydralazine and procainamide response, in which both IgG and IgM antibodies are demonstrated, the chlorpromazine-induced autoantibodies are predominantly of the IgM class.

Antibodies, Antinuclear↗
PubMed1987

A review of the effects of disopyramide phosphate on left ventricular function and the peripheral circulation.

In the absence of preexistent myocardial dysfunction, the risk of producing cardiac decompensation in patients being treated with any of the conventional antiarrhythmic agents is low. The availability of disopyramide for clinical use in 1977 produced optimism for an effective antiarrhythmic agent that was free of the well-known immediate and late toxicities of quinidine and procainamide. Unfortunately, shortly after its clinical introduction, reports appeared that raised concern about the negative inotropic actions of disopyramide and the possible role of this drug in precipitating heart failure. In clinical use, the frequency of adverse effects on ventricular function appeared to be out of proportion to disopyramide's greater negative inotropic activity and the contrasting (augmenting) effect on the peripheral vascular resistance compared to that of either quinidine or procainamide, suggesting that the other factors contributed to these observations. Review of the reported literature reveals that certain factors encourage such adverse reactions. These primarily include the routine use of oral and especially intravenous loading dosages of disopyramide in an effort to attain rapid onset of action, the failure to adequately reduce dosages of disopyramide in the setting of compromised renal function, and, most importantly, the use of standard (and even loading) dosages in patients with active heart failure, compromised left ventricular function, or a history of heart failure. The avoidance of loading dosages of disopyramide, adequate reductions of maintenance dosages in the setting of renal insufficiency, gradual dose titration for additional drug action, and omission of patients with decompensated heart failure or significant left ventricular dysfunction should significantly enhance safety in the use of disopyramide.

Anti-Arrhythmia Agents↗
PubMed1986

Stability of amiodarone hydrochloride in admixtures with other injectable drugs.

The stability of amiodarone hydrochloride in intravenous admixtures was studied. Amiodarone hydrochloride 900 mg was mixed with 500 mL of either 5% dextrose injection or 0.9% sodium chloride injection in polyvinyl chloride or polyolefin containers; identical solutions were also mixed with either potassium chloride 20 meq, lidocaine hydrochloride 2000 mg, quinidine gluconate 500 mg, procainamide hydrochloride 2000 mg, verapamil hydrochloride 25 mg, or furosemide 100 mg. All admixtures were prepared in triplicate and stored for 24 hours at 24 degrees C. Amiodarone concentrations were determined using a stability-indicating high-performance liquid chromatographic assay immediately after admixture and at intervals during storage. Each solution was visually inspected and tested for pH. Amiodarone concentrations decreased less than 10% in all admixtures except those containing quinidine gluconate in polyvinyl chloride containers. The only visual incompatibility observed was in admixtures containing quinidine gluconate and 5% dextrose injection. In most solutions pH either decreased slightly or remained unchanged. Amiodarone hydrochloride is stable when mixed with either 5% dextrose injection or 0.9% sodium chloride injection in polyvinyl chloride or polyolefin containers alone or with potassium chloride, lidocaine, procainamide, verapamil, or furosemide and stored for 24 hours at 24 degrees C. Amiodarone should not be mixed with quinidine gluconate in polyvinyl chloride containers.

Amiodarone↗
PubMed1985

Effect of antiarrhythmic drugs on the premature action potential duration in canine cardiac Purkinje fibers.

We studied the effect of six class I antiarrhythmic drugs, i.e., quinidine (5 micrograms/ml), disopyramide (10 micrograms/ml), procainamide (30 micrograms/ml), flecainide (4 micrograms/ml), lidocaine (4 micrograms/ml) and mexiletine (4 micrograms/ml), on the durations of the basic action potential (APDb) at a cycle length of 500 ms and on the premature APD (APDt) elicited at progressively increasing diastolic intervals (DI) in canine Purkinje fibers. The difference between APDt elicited at diastolic intervals of 100 msec and the earliest APDt elicited at the onset of effective refractory period was defined as the range of APDt. In control this range was 98 +/- 1.8 ms (n = 59). Disopyramide and procainamide did not change the range significantly but the other four drugs decreased it significantly (P less than .01) as follows: quinidine by 50.2%, lidocaine by 60.2%, mexiletine by 61.6% and flecainide by 61.4%. The following four factors contributed to this decrease in range of APDt: shorter duration of APDb, increased effective refractory period/APD ratio, slower kinetics of APD restitution, and shift of normalized restitution curve toward longer APDt values. The magnitude of the contribution made by each of the above factors varied with different drugs. The greatest contributing factor for quinidine was an increased effective refractory period/APD ratio, for lidocaine a slower restitution and for flecainide and mexiletine the shift of the restitution curve. We concluded that antiarrhythmic drugs belonging to the same class have different effects on the range of premature APD and that these effects cannot be predicted from the effect of the drug on APDb alone.

Action Potentials↗
PubMed1977

[Example of dose finding in practice. Pharmacology of an antiarrhythmic agent (author's transl)].

Results of the pharmacological investigation of a new antiarrhythmic drug are presented. In the isolated guinea pig ileum the substance of the procainamide-quinidine type reveals strong activity in prolonging the relative refractory period. The safety index as to antiarrhythmic and negative-inotropic properties in relatively high. In the aconitine arrhythmia of the rat the substance is effective after i.v. or oral administration. Furthermore, in these experiments it shows a long-lasting action with these two modes of application. From experimental data in the conscious and anesthetized dog the oral efficacy can also be derived. An oral dose of the new substance for the first application in humans is proposed which refers to its pharmacological activity compared with procainamide and to the human dose of this latter substance.

Aconitine↗
PubMed1982

[Drug treatment of a trial fibrillation in patients with Wolff-Parkinson-White syndrome].

In 10 patients with ventricular preexcitation (Kent bundle), in whom atrial fibrillation (A.F.) was present, the effect of some common antiarrhythmic drugs on the conduction through the anomalous pathway, and on the ventricular rate was estimated. Procainamide caused transient complete block in the accessory pathway (disappearance of the aberrant QRS) and marked reduction of the average ventricular rate in all instances. Lidocaine caused incomplete block in the accessory pathway (reduction of the number of the aberrant QRS) and significant reduction of the average ventricular rate in all tested subjects. Amiodarone slowed the ventricular rate (increase of the average and minimum R-R intervals between wide QRS complexes) in two patients, but it did not block the anomalous pathway (all QRS complexes remained aberrant); whereas in 1 patient the ventricular rate became faster and regular and the patient had syncope, while the QRS remained always aberrant. This response was probably due to the change of A.F. into atrial flutter with atrio-ventricular conduction through the anomalous pathway only. Digitalis increased the average ventricular rate and shortened the minimum R-R interval between aberrant QRS complexes 3 out of 3 times. On the basis of our experience and of the data in the literature, we conclude that, in the management of A.F. in patients with W.P.W. syndrome:--the most effective drugs are those of the 1st group of Singh and Hauswirth classification (especially Procainamide and Ajmaline);--Lidocaine is less effective, but not ineffective and its utilization may be recommended whenever the previous drugs may be hazardous;--Amiodarone, although capable of modifying the electrophysiologic properties both of the anomalous pathway and of the A-V node, seems to be less reliable;--the drugs which influence only the A-V node (Verapamil, beta-Blockers, etc.) are quite ineffective;--finally, the Digitalis is not suitable because this drug increases the ventricular rate by decreasing the effective refractory period (ERP) of the anomalous pathway.

Adolescent↗
PubMedDate not supplied

Pirmenol hydrochloride (CI-845): antiarrhythmic profile in coronary artery ligated conscious dogs.

The antiarrhythmic profile of CI-845 (pirmenol hydrochloride) was assessed in conscious, coronary artery ligated dogs. In single-dose studies in these arrhythmic dogs, CI-845 administered by the intravenous, intranuscular, and oral routes was highly effective in restoring normal sinus rhythm. A 2.5 mg/kg dose was effective against the arrhythmias occurring on the second day after ligation, while 5 mg/kg was effective against the higher-rate arhythmias of the first day after ligation. The reference agents ajmaline, aprindine, disopyramide, lidocaine, mexiletine, procainamide, and quinidine were also tested, and in this model, CI-845 had greater efficacy, a longer duration of activity, and/or a wider safety margin. In slow rate intravenous infusion studies, 1-2 mg/kg/hr of CI-845 maintained near total arrhythmia conversion in first-day postligation dogs. Rapid rate intravenous infusion studies (10 mg/kg/hr) demonstrated a good correlation between the CI-845 dose, plasma level, and arrhythmia conversion, as well as a wide margin of safety. Mean conversions to 80% normal rhythm were achieved at 2.5 mg/kg, with associated plasma levels of 0.8 +/- 0.1 micron/ml, while first sings or gross toxicity occurred at 21.7 +/- 2.4 mg/kg at plasma levels of 6.2 +/- 0.4 micron/ml. There were minimal effects on cardiac conduction and blood pressure even at large doses. In drug interaction studies, CI-845 was safe and effective in combination with disopyramide, lidocaine, procainamide, propranolol, and quinidine. The results clearly show CI-845 to be an orally effective, long-acting antiarrhythmic agent with a favorable margin of safety in the coronary artery ligated dog model.

Administration, Oral↗
PubMed1983

[Comparative clinical study of the effectiveness of the new anti-arrhythmia agents, trimecaine and pyrromecaine].

The antiarrythmic effects of trimecain and pyromecain were studied in 53 patients with frequent ventricular premature beats. Trimecain was given to 22 patients and pyromecain was given to 31. The efficiency of both intravenous and oral drug administration was considered. Comparative drugs--lidocain, mexityl, procainamid were parallely used. The efficiency criterion was the decrease in mean ventricular premature beats per hour by 50% or more during ECG-monitoring. A positive antiarrhythmic effect of intravenous trimecain was observed in 35.3% of the patients, that of pyromecain was in 18.2% and after administration of a related compound lidocain, it was seen in 30.0% and 26.7%, respectively. Trimecain in tablets proved to be efficacious in 15.4% of the patients in a single dose and in 18.2% after its long-term therapy, while mexityl, a comparative agent was efficacious in 63.6%. Pyromecain in tablets did not lead to decrease in ectopia either during an "acute" test or during the long-term therapy whereas procainamid was effective in 37.3% of the patients studied.

Acetanilides↗
PubMedDate not supplied

Influence of the restoration of vagal tone by intracisternal injection of dextromoramide on the cardiac effects of the antiarrhythmic drugs.

The effects of four antiarrhythmic drugs, quinidine, procainamide, amiodarone and verapamil were studied on sinus rate, conduction time and, when possible, effective refractory period (ERP) in atrioventricular node (AV node), and finally atrial muscle ERP. This study was made under two types of conditions, vagal tone being absent or present after restoration in the anesthetized dog by a new technique, the intracisternal injection of dextromoramide. Quinidine and procainamide which tend to slow down sinus rate and conduction in the former case accelerate them considerably in the latter by opposing the effects of acetylcholine released by vagal endings. The prolongation of atrial ERP also induced by these drugs results from both this process and their own capacity. Amiodarone and verapamil, usually responsible for bradycardia, notable delay in AV node conduction and lengthening of AV node ERP are, however, liable to elicit opposite effects, especially amiodarone when vagal tone is very high. The reduction of vagal influence is, in the case of these drugs, the only factor in the prolongation of atrial ERP. In any case, the response of both specialized and common tissue of the heart to antiarrhythmic drugs should not be interpreted unless the degree of vagal tone is known.

Amiodarone↗
PubMed1982

Identification of genetically homozygous rapid and slow acetylators of drugs and environmental carcinogens among established inbred rabbit strains.

Liver and gut mucosa N-acetyltransferase (NAT) cytosol (105,000 x g) was prepared from selected lines of New Zealand White rapid and slow acetylator rabbits bred and housed at the University of Michigan, and from inbred and partially inbred rabbits obtained from The Jackson Laboratory. Liver NAT activity was determined with p-aminobenzoic acid, p-aminosalicyclic acid, procainamide, sulfamethazine, isoniazid and 2-aminofluorene as substrates. Gut mucosal NAT activity was determined with 2-aminofluorene. A gene dose-response relationship was observed for both liver NAT and gut mucosa NAT with all substrates tested. Highest levels were always observed in homozygous rapid acetylator inbred strains (B/J, III/J, IIIC/J, III/DwJ, IIIEP/J and IIIVO/J), lower levels in obligate heterozygous rapid acetylator rabbits and lowest levels in homozygous slow acetylator inbred (ACEP/J, III/cdJ, IIIVO/ahJ, and IIIVO/vptJ) and outbred rabbits. The differences in magnitude of liver NAT activity level between acetylator genotypes was dependent on the substrate employed, progressively increasing in the following order: p-aminobenzoic acid, p-aminosalicyclic acid, procainamide, sulfamethazine, isoniazid, 2-aminofluorene. The determination of kinetic constants for liver p-aminosalicyclic acid NAT activity indicated a 2-fold difference in apparent Vmax between rapid acetylator genotypes and a 30-fold difference between rapid and slow acetylator phenotypes. In addition, the apparent Km for p-aminosalicyclic acid was significantly lower in the slow acetylators than in the rapid acetylators.

Acetylation↗
PubMed1982

Canine-effective plasma concentrations of antiarrhythmic drugs on the two-stage coronary ligation arrhythmia.

Seven drugs were tested for their antiarrhythmic effects on ventricular arrhythmias 24 and 48 hr after two-stage coronary ligation in conscious beagles. Venous blood samples were drawn for plasma drug assays. Minimum effective plasma concentrations of drugs were calculated from derived concentration-time curves. Effective drugs and their minimum effective concentrations for the suppression of arrhythmias 24 and 48 hr after coronary ligation were: disopyramide, 4.2 and 2.3 micrograms/ml; procainamide, 26.4 and 27.0 micrograms/ml; phenytoin, 8.4 and 6.4 micrograms/ml; and a new beta-blocker, N-696, 7.6 and 8.7 micrograms/ml. The concentrations of disopyramide and phenytoin were almost the same as those reported for human antiarrhythmic concentrations, but those of procainamide were higher than those reported for man. Lidocaine, verapamil and a new beta-blocker, OPC-1427, were ineffective. Membrane-stabilizing effects seem to be important in suppressing the canine two-stage coronary ligation arrhythmia.

Animals↗
PubMed1994

Diagnosis and management of arrhythmias associated with Wolff-Parkinson-White syndrome.

Because of the emergency nature of the arrhythmias associated with WPW syndrome, nurses are often called upon for diagnosis and intervention in critical settings. In such cases the nurse's understanding of mechanisms, ECG recognition, and emergency treatment guarantees the patient the best possible outcome, not only in the critical setting, but in the long term as well. The most common arrhythmias of WPW syndrome are PSVT and atrial fibrillation. In PSVT a differential diagnosis is made on the ECG between (1) CMT using the AV node anterogradely and an accessory pathway retrogradely and (2) AV nodal reentry tachycardia. Helpful clues are location of the P' wave, presence of QRS alternans, the initiating P'R interval, and presence of aberrancy. Atrial fibrillation with an accessory pathway has the morphology of VT but is differentiated because the rhythm is irregular and the rate is more than 200 beats per minute. Emergency treatment consists of blocking the accessory pathway with procainamide. Emergency treatment for both types of PSVT consists of breaking the reentry circuit at the AV node (eg, vagal maneuver, adenosine, or verapamil). Procainamide can also be used to block the retrograde fast pathway in the AV node and to terminate CMT by blocking the accessory pathway. Symptomatic patients with accessory pathways are referred for evaluation and possible radio-frequency ablation.

Atrial Fibrillation↗
PubMedDate not supplied

Acute management of ventricular arrhythmias: role of antiarrhythmic agents.

When treating life-threatening ventricular arrhythmias such as symptomatic ventricular tachycardia and ventricular fibrillation (VT/VF), the nature of the arrhythmia must be precisely defined and the approach must be tailored to it. For hemodynamically unstable ventricular arrhythmias, DC cardioversion or high-energy defibrillation remains the approach of choice. Determining the specific role of intravenous drugs in acute conversion of VT/VF and the most appropriate long-term therapy (pharmacologic or nonpharmacologic) to prevent recurrence can be difficult. Pharmacologic conversion of stable VT/VF presents an even greater challenge, as the role of lidocaine considered the first-line agent for many decades, is now being reevaluated. Lidocaine appears to be effective in converting no more than 20% of stable VTs, compared with 70% for intravenous sotalol. The precise efficacies of parenteral procainamide, beta-blockers, and newer class III agents, including intravenous amiodarone, remain to be defined; however, intravenous amiodarone, available recently, can control unstable, recurrent VT/VF that is resistant to lidocaine or procainamide. A standard regimen of concomitant intravenous and oral amiodarone may be given for rapid and sustained control, and allows oral amiodarone to be continued in a significant number of patients.

Amiodarone↗