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PubMed1990

Modification of human atrioventricular nodal function by selective atrioventricular nodal artery catheterization.

The hypothesis that human atrioventricular (AV) nodal function can be modulated selectively with a new technique of AV nodal artery catheterization was tested in eight subjects referred for diagnostic cardiac catheterization or electrophysiological studies. Three patients had no history of arrhythmias. Three patients had supraventricular tachycardia (SVT) due to reentry confined to the AV node (AVNRT). One patient had SVT due to reentry over a concealed AV bypass tract (AVRT-CBT), and one patient had nonsustained ventricular tachycardia. In each subject, sinus cycle length, AH interval, HV interval, AV nodal effective refractory period (AVN-ERP), and Wenckebach paced cycle length were measured in a control state. A flexible infusion catheter was then positioned selectively in the AV nodal artery of each subject. Through this catheter, a constant infusion of 0.1 mg/min procainamide at a flow rate of 0.125 ml/min (n = 1) or 50 micrograms/min acetylcholine at a flow rate of 0.25 ml/min (n = 4) was administered. Electrophysiological parameters were determined again during selective AV nodal artery drug infusion and during infusion of saline at identical rates. Two subjects developed transient AV nodal block during selective AV nodal catheterization alone and did not receive an infusion of drug or saline. A stable position of the AV nodal artery catheter could not be achieved in one other subject, who also received no drug or saline. In the other five subjects, drug infusion caused an increase in AVN-ERP from a control value of 312 +/- 52 msec to a value of 543 +/- 228 msec (p less than 0.05) and an increase in Wenckebach paced cycle length from a control value of 360 +/- 47 msec to a value of 572 +/- 217 msec (p less than 0.05). These parameters were unchanged from control during selective saline infusion. In two patients with AVNRT, drug infusion abolished SVT by causing complete blockade of ventriculoatrial conduction as well as lengthening of anterograde AVN-ERP. In the patient with AVRT-CBT, drug infusion abolished SVT by preventing repetitive anterograde AV conduction. Saline had no effect on SVT inducibility. Selective AV nodal artery catheterization enables AV nodal function to be modulated exclusively. Delivery of ablative agents to the AV node by this technique may be useful in patients with refractory SVT.

Acetylcholine↗

PubMed1992

Iontophoretic transmyocardial drug delivery. A novel approach to antiarrhythmic drug therapy.

BACKGROUND: Antiarrhythmic drugs often fail to achieve therapeutic effects without toxic systemic levels. Direct transport of drugs into the myocardium may circumvent this problem and may also provide new insights into antiarrhythmic drug effect on arrhythmogenic tissues. In a canine model, procainamide (PA) was delivered iontophoretically using pulsed current synchronized with the ventricular depolarization via an implantable defibrillator patch electrode that was modified to contain a 3.6-ml chamber. Myocardial tissue concentrations of PA were evaluated in 7-day myocardial infarcts (n = 16) that were exposed to 10 minutes of iontophoretic PA delivery and compared with passive diffusion (n = 5) and intravenous (n = 16) PA. These dogs were followed for 3 hours. The infarcted tissue PA levels were compared with normal myocardium. Coronary and systemic blood levels of PA, effective refractory period (ERP), diastolic threshold, and efficacy of ventricular tachycardia (VT) suppression were evaluated throughout the follow-up period. METHODS AND RESULTS: Three hours after 10 minutes of iontophoretic, passive, and intravenous PA, the epicardial layer concentration in the center of the infarcted zone was 840 +/- 853 micrograms/g, 93 +/- 90 micrograms/g, and 15 +/- 8 micrograms/g of tissue, respectively. In the endocardial layer, the PA concentrations with iontophoresis were 38 +/- 57 micrograms/g and were significantly higher than those achieved with either passive diffusion 38 +/- (4 +/- 2 micrograms/g) or with intravenous delivery (11 +/- 5 micrograms/g) (p less than 0.05). Epicardial tissue PA concentrations 3 hours after iontophoresis, passive diffusion, and intravenous PA in the normally perfused tissues were 14 +/- 13 micrograms/g, 3 +/- 2 micrograms/g, and 16 +/- 8 micrograms/g of PA, respectively. Venous blood levels were 2 +/- 3 micrograms/ml 3 hours after iontophoresis, 1 +/- 1 microgram/ml 3 hours after passive PA delivery, and 11 +/- 7 micrograms/ml with intravenous administration (p less than 0.05 intravenous versus passive and iontophoresis). Iontophoretic delivery of PA resulted in 22 +/- 29 msec ERP prolongation intramurally in the infarcted zone with no significant normal tissue ERP prolongation. Passive delivery of PA produced no significant changes in ERP. After intravenous infusion, the ERP in the infarcted zone increased by 35 +/- 29 msec and 13 +/- 12 msec in the normal tissue. Sustained monomorphic VT was induced in 20 animals. In one of these animals, only nonsustained VT could be induced at baseline; however, after intravenous PA, VT could be induced and remained inducible throughout the 3-hour follow-up period. In the iontophoretic delivery group, PA suppressed VT in all of the animals, with termination time ranging from 20 seconds to 7 minutes. In three cases, sustained monomorphic VT could be reinduced, two after 60 minutes and one after 120 minutes. However, in seven dogs, VT could not be induced during the 3-hour follow-up period. None of the dogs in which PA was delivered iontophoretically into the infarcted myocardium developed VT that was not induced before delivery of the drug. Intravenous PA administration resulted in VT suppression in one of 10 dogs. In two dogs, VT could not be induced before intravenous infusion of PA. However, after intravenous PA, VT could be induced. Immunohistochemical mapping of the PA within the infarcted tissue revealed transmural PA distribution. CONCLUSIONS: These data show that 1) the delivery of high transmural concentrations of PA directly into infarcted myocardium is both feasible and effective...

Animals↗

PubMed1998

Tachycardia-induced change of atrial refractory period in humans: rate dependency and effects of antiarrhythmic drugs.

BACKGROUND: Atrial fibrillation (AF) has been shown to shorten the atrial effective refractory period (ERP) and make the atrium more vulnerable to AF. This study investigated the effect of atrial rate and antiarrhythmic drugs on ERP shortening induced by tachycardia. METHODS AND RESULTS: Seventy adult patients without structural heart disease were included. For the first part of the study, right atrial ERP was measured with a drive cycle length of 500 ms before and after 10 minutes of rapid atrial pacing using five pacing cycle lengths (450, 400, 350, 300, and 250 ms) in 10 patients. For the second part of the study, the remaining 60 patients were included to study the effects of antiarrhythmic drugs on changes in atrial ERP induced by AF. Atrial ERP was measured with a drive cycle of 500 ms before and after an episode of pacing-induced AF. After the patients were randomized to receive one of six antiarrhythmic drugs (procainamide, propafenone, propranolol, dl-sotalol, amiodarone, and verapamil), atrial ERP was measured before and after another episode of pacing-induced AF. In the first part of the study, atrial ERP shortened significantly after 10 minutes of rapid atrial pacing, and the degree of shortening was correlated with pacing cycle length. The second part of the study showed that atrial ERP shortened after conversion of AF (172+/-15 versus 202+/-14 ms, P<0.0001) and that ERP shortening was attenuated after verapamil infusion (-4.6+/-1.2% versus -15.1+/-3.4%, P<0.001) but was unchanged after infusion of the other antiarrhythmic drugs. Furthermore, all of these antiarrhythmic drugs could decrease the incidence and duration of secondary AF. CONCLUSIONS: The atrial ERP shortening induced by tachycardia was a rate-dependent response. Verapamil, but not other antiarrhythmic drugs, could markedly attenuate this effect. However, verapamil and the other drugs could decrease the incidence and duration of secondary AF.

Adult↗

PubMed1980

The effect of antiarrhythmic drugs on depressed conduction and unidirectional block in sheep Purkinje fibers.

We studied the effect of therapeutic concentrations of lidocaine, procainamide, quinidine, propranolol, and diphenylhydantoin on two models of depressed conduction and unidirectional block produced by asymmetric focal cooling and crushing in sheep Purkinje fibers. All drugs were shown to induce reversible deterioration of conduction. Unidirectional block was converted to bidirectional block with each drug. Improvement of conduction was rare and conversion of unidirectional block to bidirectional conduction never was observed. These experiments suggest that all five drugs may act by a uniform mechanism of action in some reentrant ventricular arrhythmias involving a zone of depressed conduction or unidirectional block within the Purkinje network.

Animals↗

PubMed1994

Subthreshold stimulation of Purkinje fibers interrupts ventricular tachycardia in intact hearts. Experimental study with voltage-sensitive dyes and imaging techniques.

The effects of subthreshold stimulation (STS) delivered during right atrial pacing and ventricular tachycardia (VT) were investigated in Langendorff-perfused guinea pig hearts. The hearts were stained with a voltage-sensitive dye (RH 421) to map the propagation of optical action potentials. Sustained VT was reliably induced by 5-second trains (cycle length [CL], 25 to 50 milliseconds; duration, 0.5 to 10 milliseconds; and voltage, 2x threshold voltage) of impulses (n = 12 hearts) or a single premature beat (n = 6). The location of extrastimuli was not critical to the induction of VT, but the diameter of the heart had to be > or = 14.5 mm. During VT, heart rate increased from 200 to 600 beats per minute; action potential durations decreased from 112 to 175 milliseconds to 60 to 105 milliseconds, with no diastolic interval. Activation on the epicardium spread anisotropically, but VT decreased the "apparent" maximum conduction velocity (theta max) by 68% and altered the orientation of the major axis from beat to beat. Activation patterns and theta max measured during VT were similar to patterns recorded during direct pacing of the ventricle and indicated that Purkinje fibers no longer propelled ventricular excitation. STS (CL, 25 to 50 milliseconds; duration, 0.5 to 25 milliseconds; and voltage, 0.5x to 0.8x threshold; trains of 2.0 to 2.5 seconds) interrupted VT when applied to Purkinje fibers lining the endocardium (n = 6) but failed to interrupt VT when applied to the epicardium (n = 8). In atrial pacing, STS delivered to the endocardium increased theta max from 2.44 +/- 0.32 (mean +/- SEM) to 3.63 +/- 0.21 m/s in a local region surrounding the first activation sites (n = 4). Alternatively, VT could be terminated by reducing theta max (approximately 55%) with procainamide (10 mumol/L) (n = 6). STS terminates VT by synchronizing ventricular excitation most likely by increasing local conduction and/or improving the coupling between Purkinje and ventricular cells.

Action Potentials↗

PubMed1999

Electrical restitution and spatiotemporal organization during ventricular fibrillation.

Despite recent advances in our understanding of the mechanism for ventricular fibrillation (VF), important electrophysiological aspects of the development of VF still are poorly defined. It has been suggested that the onset of VF involves the disintegration of a single spiral wave into many self-perpetuating waves. It has been further suggested that such a process requires that the slope of the electrical restitution relation be >/=1. The same theory anticipates that a single spiral wave will be stable (not disintegrate) if the maximum slope of the restitution relation is <1. We have shown previously that the slope of the restitution relation during rapid pacing and during VF is >/=1 in canine ventricle. We now show that drugs that reduce the slope of the restitution relation (diacetyl monoxime and verapamil) prevent the induction of VF and convert existing VF into a periodic rhythm. In contrast, a drug that does not reduce the slope of the restitution relation (procainamide) does not prevent the induction of VF, nor does it regularize VF. These results indicate that the kinetics of electrical restitution is a key determinant of VF. Moreover, they suggest novel approaches to preventing the induction or maintenance of VF.

Action Potentials↗

PubMed2003

Inhaled nitric oxide modifies left ventricular diastolic stress in the presence of vasoactive agents in heart failure.

Nitric oxide (NO) inhalation therapy has been widely used in several diseases with pulmonary hypertension. However, application of NO inhalation therapy remains controversial in heart failure. Cardiovascular effects of inhaled NO (iNO) were evaluated in dogs before and after induction of heart failure with and without infusion of vasoactive agents. iNO did not affect the baseline left ventricular (LV) function or the response to isoproterenol in control conditions or heart failure induced by procainamide. Pulmonary vascular resistance was significantly decreased by iNO in heart failure with infusion of vasoactive agents. Unexpectedly, LV end-diastolic pressure was significantly elevated by iNO in heart failure in the presence of infusion of vasoactive agents independent of their types; either the vasodilating agents of acetylcholine and nitroglycerin or the vasoconstricting agents of norepinephrine and angiotensin-II. The end-diastolic LV dimension and wall stress were also significantly increased by iNO, however, those at end systole were not affected. These results suggested that NO inhalation therapy reduced pulmonary vascular resistance, whereas in the presence of additional stress of vasoactive agents, it increased LV preload and end-diastolic wall stress in heart failure.

Acetylcholine↗

PubMed1978

Antibodies to histones in drug-induced and idiopathic lupus erythematosus.

When tissue sections are extracted with 0.1 N HCl, cellular nuclear proteins, including histones, are removed but nuclear DNA is retained. Histones can be reconstituted back to nuclear DNA in acid-extracted tissue sections so that the resulting nuclear substrate is composed only of DNA and histones and does not contain acidic nuclear protein antigens. The resulting DNA-histone tissue substrate can be used in the immunofluorescent method for specific detention of antibodies to histones. Sera from 23 patients with drug-induced lupus erythematosus (procainamide 19, isoniazid 2, nitrofurantoin 2) and 20 patients with idiopathic (not drug-induced) systemic lupus erythematosus (SLE) were studied. All 23 patients with drug-induced lupus erythematosus (LE) lost nuclear staining on acid-extracted sections. In contrast, only 12 of 20 with idiopathic SLE lost nuclear staining on acid-extracted tissues, and in the remaining 8, there was no significant fall in titer. In the drug-induced LE group, loss of nuclear staining was due to the absence of histones on the substrate because with histone-reconstituted sections, 22 of 23 again became positive for nuclear staining at titers equal to or at one doubling dilution below titers on unextracted tissues. In contrast, of the 12 idiopathic SLE sera which lost nuclear staining, only 5 regained nuclear staining on histone-reconstituted tissue sections. In idiopathic SLE, antinuclear antibodies are heterogeneous in specificities and may consist of antibodies to native DNA, histones, or nonhistone proteins. In contrast, antinuclear antibodies in drug-induced LE are less heterogeneous and mainly consist of antibodies to histones.

Antibodies, Antinuclear↗

PubMed2004

Epigenetic regulation of 11 beta-hydroxysteroid dehydrogenase type 2 expression.

The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD2) is selectively expressed in aldosterone target tissues, where it confers aldosterone selectivity for the mineralocorticoid receptor by inactivating 11 beta-hydroxyglucocorticoids. Variable activity of 11 beta HSD2 is relevant for blood pressure control and hypertension. The present investigation aimed to elucidate whether an epigenetic mechanism, DNA methylation, accounts for the rigorous control of expression of the gene encoding 11 beta HSD2, HSD11B2. CpG islands covering the promoter and exon 1 of HSD11B2 were found to be densely methylated in tissues and cell lines with low expression but not those with high expression of HSD11B2. Demethylation induced by 5-aza-2'-deoxycytidine and procainamide enhanced the transcription and activity of the 11 beta HSD2 enzyme in human cells in vitro and in rats in vivo. Methylation of HSD11B2 promoter-luciferase constructs decreased transcriptional activity. Methylation of recognition sequences of transcription factors, including those for Sp1/Sp3, Arnt, and nuclear factor 1 (NF1) diminished their DNA-binding activity. Herein NF1 was identified as a strong HSD11B2 stimulatory factor. The effect of NF1 was dependent on the position of CpGs and the combination of CpGs methylated. A methylated-CpG-binding protein complex 1 transcriptional repression interacted directly with the methylated HSD11B2 promoter. These results indicate a role for DNA methylation in HSD11B2 gene repression and suggest an epigenetic mechanism affecting this gene causally linked with hypertension.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗

PubMed1994

Comparison of popliteal lymph node responses in various strains of rats.

Outbred (namely Wistar and Sprague-Dawley) and inbred (Wistar-Furth, Lewis, Fisher 344 and Brown-Norway) strains of rats were screened for their responses to reference compounds in the popliteal lymph node (PLN) assay. Streptozotocin and diphenylhydantoin gave positive responses as evidenced by increased weight and cellularity indices in all strains used whereas procainamide, isoniazid and barbital consistently gave negative responses. Although these findings overall are in agreement with previous investigations involving these compounds, the lack of marked interstrain differences in PLN responses argues against a strong immunogenetically controlled mechanism as could be assumed in presumably auto-immune reactions. The question is raised whether drug-induced side-effects predicted by the PLN assay are basically non-autoimmune as suggested by clinical and immunological findings in man.

Animals↗

PubMed2001

Thymus function in drug-induced lupus.

Autoimmunity develops when a lupus-inducing drug is introduced into the thymus of normal mice, but the relevance of this model to the human disorder is unclear in part because it is widely assumed that the thymus is non-functional in the adult. We compared thymus function in 10 patients with symptomatic procainamide-induced lupus to that in 13 asymptomatic patients who only developed drug-induced autoantibodies. T cell output from the thymus was quantified using a competitive polymerase chain reaction that detects T cell receptor DNA excision circles in peripheral blood lymphocytes. Despite the advanced age of the patient population under study, newly generated T cells were detected in all subjects. Although there was no overall quantitative difference between the symptomatic and asymptomatic patients, we found a positive correlation between the level of T cell receptor excision circles in peripheral lymphocytes and serum IgG anti-chromatin antibody activity in patients with drug-induced lupus. The association between autoantibodies and nascent peripheral T cells supports the requirement for T cells in autoantibody production. Our observations are consistent with findings in mice in which autoreactive T cells derived from drug-induced abnormalities in T cell development in the thymus.

Aged↗

PubMed1994

Role of T cell DNA methylation in lupus syndromes.

Current theories postulate that exposure to certain environmental agents will induce lupus in genetically predisposed individuals. However, the mechanisms by which environmental agents interact with the immune system to trigger lupus is unclear. Recent work has shown that some environmental agents associated with lupus, such as procainamide, hydralazine and ultraviolet light, will inhibit T cell DNA methylation, increase LFA-1 expression and induce autoreactivity. In addition, T cells isolated from patients with active lupus have hypomethlated DNA, diminished DNA methyltransferase activity and overexpress LFA-1 on an autoreactive subset of cells which spontaneously lyses autologous macrophages. More recent work has shown that the adoptive transfer of murine T cells made autoreactive with DNA methylation inhibitors is sufficient to cause a lupus-like disease in otherwise healthy syngeneic recipients. Together, these results support a new model of autoimmunity, in which certain environmental agents modify T cells by inhibiting DNA methylation and altering expression of certain genes, thereby inducing autoreactivity. The autoreactive cells then interact with the host to produce a lupus-like disease.

Azacitidine↗

PubMed1983

Some consequences of drug choice and dosage regimen for patients with impaired kidney function.

The object of this article is to discuss difficulties in extrapolating the performances of a drug for which the kinetic parameters are derived in healthy volunteers, to patients with severely impaired kidney function. The theoretical background of some actual or probable background is given, and a possible solution for these problems is offered, that is, choosing another drug from the same drug group. In patients without kidney function, metabolism is the only pathway of elimination. When the elimination of the metabolite formed occurs by means of renal excretion only, this metabolite accumulates in patients with impaired or absent kidney function. When a metabolic pathway of the parent drug is part of a metabolic equilibrium, the metabolic return reaction results in an "apparent parent compound," with a half-life identical to that of the accumulated metabolite. In this way, the concentration of the "apparent" parent compound increases and the half-life of the sum of parent and "apparent" parent drug will change. Examples of this drug behavior are given for sulfamethoxazole, sulfametrole, sulfamethizole, procainamide, and N4-acetylprocainamide.

Drug Synergism↗

PubMed1986

Experience with intrainstitutional clinical evaluations of newly marketed preparations as a basis for drug-product selection to hospital formularies.

The decision to admit a new drug-product formulation (NDPF) to a hospital pharmacy formulary is a difficult task, particularly when minimal pharmacokinetic or clinical efficacy data are available. To provide objective information to the Pharmacy and Therapeutics (P&T) Committee, we implemented a procedure to evaluate these NDPFs at our institution. This procedure, termed clinical evaluation, was initiated at our institution in 1981. The clinical evaluations of two NDPFs were performed. The two NDPFs studied were a transdermal nitroglycerin preparation and a sustained-release procainamide preparation. The clinical assessment of the therapeutic and the pharmacokinetic performance of each preparation was made by clinical pharmacists. Following completion of the clinical evaluation, the data were presented at a regular meeting of the P&T committee. The presentation of clinical data derived from our patient population facilitated objective assessment by the P&T committee regarding formulary status. We conclude that the clinical evaluation represents a novel approach to acquire data necessary for objective decisions on NDPFs by the P&T committee.

Administration, Topical↗

PubMed1986

Drug-induced fever.

Humans maintain body temperature within a narrow range. Drug administration can upset the usual balance and cause a fever. The drug may interfere with heat dissipation peripherally, increase the rate of metabolism, evoke a cellular or humoral immune response, mimic endogenous pyrogen, or damage tissues. The fever may be a result of the pharmacological action of the drug or some other unrelated effect. Drug-induced fever is most commonly the result of a hypersensitivity reaction and its characteristics resemble those of an allergic reaction. The fever most commonly occurs after 7 to 10 days of drug administration, persists as long as the drug is continued, disappears soon after stopping the drug, and will rapidly reappear if the drug is restarted. The agents most commonly associated with causing fever include the penicillins, cephalosporins, antituberculars, quinidine, procainamide, methyldopa, and phenytoin.

Anti-Bacterial Agents↗

PubMedDate not supplied

Malignant hyperthermia associated with enflurane anesthesia: a case report.

Malignant hyperthermia syndrome associated with various anesthetic agents has been well documented, but none has been reported with enflurane (Ethrane). This particular case is the first involving exposure for the second time to enflurane anesthesia after a six-month interval in which malignant hyperthermia resulted. A patient subject to malignant hyperthermia does not necessarily develop rigidity after succinylcholine for the intubation as noticed in this case. However, with the abnormal production of heat in the soda lime canister with tachycardia, tachypnea, rapidly rising body temperature and hypertonicity of skeletal muscles during anesthesia one should suspect malignant hyperthermia. The treatment of malignant hyperthermia involves cooling procedures, correction of acidosis, use of steroids and procainamide, and acetaminophen to facilitate lowering the body temperature.

Acetaminophen↗

PubMed1983

Availability of electrophysiological approach to the selection and assessment of antiarrhythmic drugs for recurrent ventricular tachycardia.

We performed serial electrophysiological-pharmacological studies on 21 patients with recurrent sustained or non-sustained ventricular tachycardia (VT). In 8 of 11 patients with recurrent sustained VT, VT could be induced repeatedly by programmed electrical stimulation and terminated by ventricular burst pacing. In 13 of the 21 patients, repetitive ventricular response (RVR) was successfully induced. In the 8 patients with induced VT, the efficacy of several antiarrhythmic drugs intravenously administered was assessed. Procainamide prevented the initiation of VT in 57%, disopyramide in 50% and mexiletine in 40%. However, lidocaine, propranolol and verapamil could not prevent VT in any of 5, 3 and 6 patients, respectively. Verapamil in combination with quinidine prevented the initiation of VT in one case. Each of disopyramide, propranolol and verapamil increased the VT zone in 2 patients. The drugs belonging to the same group classified by their electrophysiological properties were not interchangeable in 2 patients. Their ability to terminate induced VT did not always correlate with that to prevent its initiation in 2 patients. The effects of specific drugs were rather variable and unpredictable in each patients, and especially those of combination regimens using more than 2 antiarrhythmic drugs were more unpredictable. In all patients, the induced VT was morphologically identical to the spontaneously occurring VT and its rate was ranged within 13% of that of the spontaneously VT. In 10 of 13 patients with RVR, QRS configuration of RVR was not similar to the spontaneously occurring arrhythmia. The pharmacological suppression of RVR as an index for prevention against spontaneous VT remains controversial. This study concludes that the serial electrophysiological-pharmacological study provides a rapid prediction of effectiveness of a particular regimen and combination and a rapid identification of the deleterious effects of certain drugs in patients with recurrent sustained VT.

Adolescent↗

PubMed1983

The usefulness of Holter monitoring in the evaluation of antiarrhythmic drug efficacy for tachycardia.

Using Holter monitoring tachycardia was found in 145 out of 2058 patients suffering from various underlying diseases. Three thousand seven hundred and forty monitorings were performed. The mean age of patients was 54.5 years with a range of 19 to 83 years. The observed tachycardia was classified into three types: tachycardia with short duration, tachycardia with long duration and tachycardia with complex form. The attacks of tachycardia were more frequently observed during periods of physical activity than during sleeping periods. The relationship of the number of tachycardia with short duration between 24-hour Holter monitorings was examined in order to establish day to day variability of the attacks. The 95% confidence interval about the resultant regression line was calculated and the percent reduction required for the evaluation of drug efficacy to avoid the chances of interference of spontaneous variation was found to be about 44.0, 55.0 and 82% when the total number of attacks during a 24-hour period were 50, 100 and 1,000, respectively. Holter monitoring showed higher positive results as compared to exercise testing for detection of tachycardia. Higher correlation coefficients between numbers of premature ventricular contractions (PVCs) and the plasma concentrations of procainamide or N-acetylprocainamide were observed in 3 or more successive PVCs than in individually occurring PVCs. Using repeated 24-hour Holter monitorings a significant reduction in the number of tachycardia was observed when the therapeutic concentration was reached after the combined or single administration of the drug. These results suggest that repeated Holter monitorings, exercise testing and determination of plasma level of the drug may be useful for the evaluation of antiarrhythmic drug efficacy for tachycardia.

Adult↗