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PubMed1984

[Pharmacokinetics and plasma concentrations of anti-arrhythmic drugs].

The efficacy of antiarrhythmic drug treatment and the risk of toxicity can be evaluated by studying the relationship between these agents effects and their plasma concentrations. Optimal drug surveillance is not possible, however, unless: an effect-concentration relationship can be demonstrated; therapeutic and toxic plasma concentrations have been established; plasma concentrations in different patients demonstrate adequate dosage when measured after the administration of standard doses; a reliable and specific dosing method can be easily performed at a reasonable cost. Lidocaine, quinidine, and procainamide are among the commonly employed antiarrhythmic agents which fulfill all these requirements. Clinical pharmacologic studies are underway for disopyramide, amiodarone, mexiletine, propafenone and flecainide, and certain findings are already of value in hospital settings.

Anti-Arrhythmia Agents↗
PubMed1983

Effects of MD770207 (carocainide) on experimental ventricular arrhythmias.

Administered by intravenous or oral route, carocainide, MD770207, abolished experimental ventricular arrhythmias in anaesthetized and conscious dogs. Slow rate intravenous infusion (0.5 mg/kg/min) studies in conscious coronary ligated dogs demonstrated a good arrhythmia conversion as well as a wide margin of safety; mean conversion to 95% of normal sinus rhythm was achieved at 10.5 +/- 2.1 mg/kg while first signs of reversible neuro and cardio-toxicity occurred at 37.8 +/- 8 mg/kg. The reference agents disopyramide and lidocaine showed less favourable safety margin. Carocainide reduced epicardial ST-segment elevation produced by short coronary artery occlusion and prevented the occurrence of ventricular fibrillation resulting from reperfusion after acute coronary artery ligation. At antiarrhythmic dose levels there were no undesirable effects noted on cardiovascular function. Given intravenously the compound increased the ventricular fibrillation threshold in spontaneously hypertensive rats.

Administration, Oral↗
PubMed1983

Measurement of flecainide acetate in human plasma by an extraction spectrophotofluorometric method.

A fluorometric method for the quantitation of 2,5-bis-(2,2,2-trifluoroethoxy)-N-(2-piperidylmethyl)benzamide acetate (R-818, flecainide acetate) in human plasma has been developed. The minimum quantifiable concentration of flecainide acetate by this method is 25 ng/ml with a 2 ml plasma sample; a slightly modified procedure which also requires the use of a microcell in the spectrophotofluorometer further increases the maximum sensitivity to 12.5 ng/ml. The precision, expressed as relative standard deviation is 2.9, 0.7, 5.6, 3.5, and 4.3% for 75, 150, 250, 500, and 700 ng flecainide acetate/ml, respectively. The accuracy, expressed as relative error, is -6.7, -3.3, -0.4, +4.4, and -0.4%, respectively, for the corresponding concentrations specified above. The relative standard deviations for the inter-day variation are 19, 7, 9, 9, 8, 10, 13, 12, and 9% for the 25, 50, 100, 200, 300, 400, 600, 800, and 1000 ng/ml standards, respectively. Preliminary data indicate that propranolol and quinidine interfere with this method while procainamide, disopyramide, hydralazine, methyldopa, diazepam, hydrochlorothiazide, and sulfinpyrazone exhibit little or no interference. The results of the analyses of clinical samples by the fluorometric method agree well with an established GLC method. Thus, the quality of the fluorometric method is considered adequate for estimating plasma flecainide acetate levels during drug therapy in most non-research settings, if careful consideration is given to possible interference by other drugs.

Chromatography, Gas↗
PubMed1984

Double-blind crossover randomized trial of intravenously administered verapamil. Its use for atrial fibrillation and flutter following open heart surgery.

Fourteen patients with onset of atrial fibrillation (11) or flutter (three) and ventricular rate over 120 beats per minute following cardiac surgery were treated with intravenous (IV) doses of verapamil hydrochloride or placebo in a double-blind crossover protocol. Patients with poor left ventricular function, hypotension, atrioventricular block, and taking beta-blockers and disopyramide were excluded. The dosages were 0.075 mg/kg and 0.15 mg/kg given 15 minutes apart, with termination of study on achieving an end point (conversion to sinus rhythm or slowing of ventricular rate to below 100 beats per minute). None reached the end point with placebo but all with verapamil. Baseline ventricular rate was 144 +/- 20 beats per minute, after placebo 143 +/- 16 beats per minute, and after verapamil 89 +/- 7 beats per minute (mean +/- SD). Thus, IV verapamil briefly slows the ventricular rate of atrial tachyarrhythmias following cardiac surgery.

Adult↗
PubMed1982

Comparison of the antiarrhythmic activity of mexiletine and lorcainide on ventricular arrhythmias.

In a blind cross-over study, 12 patients with ventricular arrhythmias (VPC's; Lown Grades II-IVB) resistant to a daily dose of quinidine 1.2 g, disopyramide 0.8 g, N-propyl-ajmaline 0.1 g were randomly given, each dose for one week, placebo (PL), mexiletine (MEX; 400, 600, 800 mg daily) and lorcainide (LOR; 200, 300, 400 mg daily). On the last day of each treatment period, patients were evaluated by 24-h continuous ambulatory monitoring, 6-channel surface ECG, plasma concentrations and side-effects. During PL I (before) and PL II (after drug treatment), the mean number of VPCs per hour was 670 and 701. VPCs were reduced in 5 of the 12 patients with MEX by 43% (400 mg), 74% (600 mg) and 91% (800 mg). VPCs were reduced in 10 patients with LOR by 60% (200 mg), 78% (300 mg) and 93% (400 mg). Log. lin. plasma conc. effect relationships were constructed for MEX and LOR. Vomiting, nausea, and abdominal pain were seen in 2 patients with MEX; insomnia and feeling heat in 10 patients with LOR. At the end of the LOR-treatment, these side-effects were less in 5 and absent in 5 patients. In this study, LOR seems superior to MEX in refractory ventricular arrhythmias.

Adult↗
PubMedDate not supplied

[Electrophysiological evaluation of the treatment of patients with recurrent ventricular tachycardia].

In order to asses the predictive value of serial electrophysiologic studies in the selection of an effective long-term effective antiarrhythmic regimen, we studied 16 patients with recurrent sustained ventricular tachycardia (VT), resistant to conventional medical treatment. (group 1) Eleven patients in this group had chronic chagas myocarditis, and several hospitalizations and cardioversions had been required for therapy of VT. In addition, 35 patients (group 2: control) underwent electrophysiological studies to evaluate rhythm disturbances differences to TV. Ventricular Tachycardia was successfully initiated and terminate with programmed electrical stimulation of the right ventricle only in the group 1. After control studies, the effects of several drugs (ajmalin, amiodarone, carbamazepine, disopyramide, diphenilhydantoin, mexiletine, procainamide, propranolol, quinidine and verapamil on the ability to initiate VT were assessed. A drug was considered effective only if it prevented the initiation of VT and allowed long-term suppression o clinical VT. All the patients of group 1 were placed on chronic oral therapy with the effective agent and were followed for an average period of 16 months (range 5 to 47 months). In all 16 patients we could document complete long-term prophylaxis against VT. This method offers advantage in terms of morbidity, mortality, duration of therapy, and promptness of choosing an effective drug add expense to the patient over traditional empirical methods of drug selection.

Adolescent↗
PubMed1980

Factors affecting the plasma protein binding of verapamil and norverapamil in man.

The in vitro and vivo binding of the antiarrhythmic agent verapamil and its active metabolite norverapamil to human plasma proteins was determined under different conditions at 37 degrees C by equilibrium dialysis. The binding of verapamil was considerable (free fraction of about 0.10) and was independent of plasma concentration over the range of 50 ng/ml to 1500 ng/ml. Norverapamil was also extensively bound to plasma proteins. Verapamil binding was reduced significantly upon plasma dilution and upon addition of three of its major metabolites (norverapamil and metabolites A and B). Therapeutic concentrations of several drugs including disopyramide (12 micrograms/ml), diazepam (2 micrograms/ml), lidocaine (4 micrograms/ml), propranolol (150 ng/ml), and salicylate (250 microgram/ml) also significantly increased the free fraction of verapamil. The results of in vivo protein binding studies using plasma samples collected during a steady-state dosing interval from a patient receiving 80 mg of verapamil orally every 6 hr were similar to those obtained from vitro binding studies.

Blood Proteins↗
PubMed1995

[Acute and chronic sequential atrioventricular pacing in patients with obstructive-type hypertrophic myocardiopathy resistant to medical therapy].

An evaluation was undertaken regarding two female patients suffering from obstructive hypertrophic cardiomyopathy, with high and strongly symptomatic gradients, as well as evidencing a resistance to medication with beta-blockers, verapamil and disopyramide when administered in maximal doses. These patients were provided with the implant of a definitive type DDD pacemaker, with an auricular electrocatheter placed on the right auricular appendix, and with a bipolar ventricular catheter placed on the apex of the right ventricle. The generator was programmed with a short AV so as to ensure that the ventricular stimulation would at any given time be the result of the ventricular contraction would be initiated at the apex portion of the right ventricle. With these therapeutics, we observed not only a reduction or even the gradient, but also the complete elimination of the existing symptoms--angor, dyspnea, dizziness, palpitations and fainting--with the resulting normalcy of the quality of life of the patients. All taken into account we are of the opinion that these therapeutics are, in the case of patients suffering from obstructive hypertrophic cardiomyopathy, a valid alternative for surgical treatment by means of myectomy or myotomy, but without the morbidity and mortality rates presented by such methods.

Adult↗
PubMed1995

[Tilt-table test in the diagnosis of syncope of unknown origin].

71 patients with unexplained syncope was examined by 60 grade of head up tilt table test with or without administration of isoproterenol during 25 minutes interval. The mean age of patients was 71.44 +/- 16.40 (12-86) years. 38 (54%) were female and 33 (46%) were male. The underlying heart disease were 27 (38%) coronary artery disease, 12 (17%) arterial hypertension, 6 (8%) diabetes mellitus, 3 (4%) valvular heart disease and 14 (20%) patients had other diseases. Nine (13%) patients had no organic disease. During head up tilt table test positive reaction was found in 13 (18%) patients. Four (6%) patients were vaso-vagal syncope with classic signs, and 9 (13%) patients were vasodepressor type of syncope, without changes in the heart rate. Isoproterenol was given to 16 (23%) patients, and in 4 (6%) (2 vasodepressor and 2 mixed type of syncope) patients occurred the positive test during isoproterenol administration. Orthostatic reaction occurred during head up tilt table test in 14 (20%) patients. Normal was the result of tilt table test in 42 (59%) patients, and two (3%) patients had autonome neuropathy. The vasovagal syncope was treated by metoprolol, atenolol and disopyramid with success. The head up tilt table testing is a good, simple, useful test for evaluation of syncope patients, especially the diagnosis of vasovagal syndrome.

Adolescent↗
PubMed1993

[The circadian profile of ventricular extrasystole].

STUDY OBJECTIVE: to determine the existence of circadian variability (CV) of single ventricular premature beats (VPBs) and study its relationship with the heart rate variation; to compare sub-groups of patients (Pts) with and without antiarrhythmic therapy and with ischemic cardiopathy versus a free structural cardiopathy group. DESIGN: retrospective study. PATIENTS AND METHODS: the CV of VPBs was analyzed by Holter monitoring in 147 Pts, 93 male and 54 female with a mean age of 59 +/- 14.6. Seventy seven Pts were not taking antiarrhythmic drugs while 70 were doing it: Amiodarone 23, Propafenone 30, B-Blockers 9, Quinidine and Disopyramide 7, Flecainide 1. Sixty five Pts had ischemic cardiopathy and 37 were free of any structural abnormality. The selection criteria consisted in: 1--more than 100 VPBs/24h; 2--distribution over more than 12 hours; 3--absence of any hour with more than 35% of the total VPBs in the recording. Data were presented in a percentage form and the results evaluation was made by using single and two-harmonic regression models. MAIN RESULTS: a CV was found to the single VPBs, with minimum values during the nocturnal period and maximum values in the morning, with a significant adjustment to the two-harmonic regression model, defined by the equation y = 4.2 - Q,559 sen (2 pi T/24) - 0.604 cos (2 pi T/24) - 0.417 sen (4 pi T/24) + 0,272 cos (4 pi T/24) (p < 0.001). A strong positive correlation was observed between VPBs and heart rate variability (r = 0.95; p < 0.001). The sub-groups of Pts, whether taking antiarrhythmic drugs or not, also showed a CV with a statistically significant two-harmonic regression pattern, with a major morning increase of VPBs in the antiarrhythmic group. The free structural cardiopathy sub-group displayed a best adjustment to the single harmonic regression model while the ischemic group exhibited a two-harmonic regression pattern. CONCLUSIONS: a significant circadian variability of VPBs with a bi-modality expression was determined. The majority of the analyzed sub-groups showed the same kind of variation. A strong positive correlation with the heart rate variability was observed.

Age Factors↗
PubMed1995

A possible involvement of sodium channel blockade of class-I-type antiarrhythmic agents in postischemic contractile recovery of isolated, perfused hearts.

The present study was undertaken to test the hypothesis that the degree of sodium channel blockade by class-I-type antiarrhythmic agents accounts for enhancement of postischemic contractile recovery of ischemic/reperfused hearts. Electrophysiological studies showed that the class-I-type antiarrhythmic agents quinidine, disopyramide, procainamide, lidocaine, mexiletine, flecainide and pilsicainide suppressed the Vmax value of the rat left ventricular muscle cell, a marker of sodium channel blockade, in a concentration-dependent manner. Isolated rat hearts were subjected to 35 min of ischemia and 60 min of reperfusion. Postischemic contractile recovery, which was never detected in untreated hearts, was enhanced in hearts pretreated with these antiarrhythmic agents during the last 3 min before ischemia at concentrations ranging from 3 to 300 microM. Tissue Na, but not Ca, accumulation was also detected in the ischemic heart, and tissue Na and Ca accumulation was observed in the reperfused heart, which suggests that sodium overload occurs during ischemia, followed by sodium and calcium overload during reperfusion. The degree of postischemic contractile recovery seen in the presence of these antiarrhythmic agents was inversely related to tissue Na or Ca accumulation after reperfusion, which suggests that class-I-type antiarrhythmic agents inhibit sodium overload occurring in ischemic/reperfused myocardial cells. A close relationship between postischemic contractile recovery of the perfused heart and depression in the Vmax value of the ventricular muscle was also observed. These results suggest that the ability class-I-type antiarrhythmic agents to inhibit myocardial sodium channels plays a significant role in the enhancement of postischemic contractile recovery of the ischemic/reperfused heart.

Animals↗
PubMed1994

[Hypertrophic obstructive cardiomyopathy: current treatment, indications and results].

Global annual mortality in hospitalized patients with symptomatic hypertrophic obstructive cardiomyopathy is just under 5%. Several treatments have been proposed for this severe disease in order to improve diastolic function and reduce the intraventricular obstacle. The aim is to improve symptomatology and prognosis. The mainstay of treatment is drug therapy. The negative inotrope and bradytrope action of beta-blockers given at medium doses of 160 to 320 mg/day (propranolol) helps decrease the incidence of dyspnoea chest pain and the frequency of syncopes in 30 to 70% of the patients. Higher doses up to 1 g per day may be helpful in certain patients, but with the risk of sudden death. Calcium channel inhibitors at a dose of 360 mg/day for verapamil give very favourable results in patients managed medically and sometimes in those undergoing surgery. Amiodarone is essentially used as an antiarrhythmic drug in obstructive syndromes complicated by severe ventricular arrhythmias. Wider use is limited due to cardiac and extracardiac side effects. Other drugs including disopyramide, diuretics, digitalics and antivitamin K agents also have a role to play. The aim of surgery is to alleviate the intraventricular obstacle, correct mitral regurgitation and increase left ventricular compliance. There has been much controversy over the most adapted approach, but the most commonly used technique is currently septal myectomy which reduces the intraventricular gradient by 80 to 90%. Simple mitral valve replacement gives similar improvement in cardiac haemodynamics but exposes the patient to the complications inherent with mitral prostheses. Dual chamber sequential pacing has also been proven to be an effective means of treating hypertrophic obstructive cardiomyopathy, reducing the risk of sudden death as well as symptomatology in selected patients. Apical pre-stimulation using a short atrio-ventricular delay and the paradoxical septal movement induced by right ventricular stimulation decreases the sub-aortic obstruction and thus improves left ventricular performance. This method must be confirmed by mid- and long term results. We are in agreement with the Mayo Clinic recommendations that surgical myectomy remains the preferred treatment for most patients with severe hypertrophic obstructive cardiomyopathy who are unresponsive to medical treatment.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Comparative study of different classes of anti-arrhythmia agents on the vulnerability of ischemic ventricular fibrillation].

A comparative study of the various classes of antiarrhythmic drugs as agents protecting against ischaemia-induced ventricular fibrillation was undertaken in the pig in situ heart, in anaesthetized animals which were subjected to complete temporary occlusion of the left anterior descending coronary artery. This occlusion resulted in fibrillation after a time which varied in inverse ratio to vulnerability to fibrillation. However, as this time did not exceed a few minutes, time to onset of fibrillation could be repeatedly measured in the course of an experiment, in the absence or in the presence of an antiarrhythmic drug. Under ventricular pacing at a constant rate, 180 beats/min, all the class I antiarrhythmic drugs, flecainide, disopyramide and lidocaine, in clinical dose range, reduced time to fibrillation to a large extent (25 to 50%) at the maximum of their action, with gradual return to control values within less than one hour. The enhancement of vulnerability to fibrillation was accompanied by reduction in intraventricular conduction velocity and fibrillation rate. With the same ventricular pacing, no change was observed in time to fibrillation under the influence of propranolol or amiodarone. As for verapamil, it lengthened this time considerably, up to 600%. However, bradycardia produced in usual circumstances ensures a real protection against ischaemic fibrillation with propranolol and amiodarone and enhances protection directly exerted by verapamil.

Animals↗
PubMed1994

Interaction of the stereoisomers of basic drugs with the uptake of tetraethylammonium by rat renal brush-border membrane vesicles.

Stereoselectivity in the renal clearance of drugs may be due to a stereoselective interaction with the organic cation/proton antiporter in the brush-border membrane of renal tubular epithelial cells. The interaction of the stereoisomers of chiral basic drugs with the uptake of [14C]tetraethylammonium was studied in rat renal brush-border membrane vesicles. No differences were observed in inhibition of [14C]tetraethylammonium uptake between the enantiomers of pindolol, disopyramide and bupivacaine or between (+/-)- and (+)-hydroxychloroquine and quinine/quinidine. Stereoselectivity was observed for the enantiomers of verapamil (IC50, R-verapamil 5.9 +/- 1.7 microM; S-verapamil, 3.4 +/- 1.7 microM). Stereoselectivity was also observed with the four stereoisomers of norephedrine and ephedrine in which the pairs of enantiomers differing in configuration at the carbon atom adjacent to the nitrogen atom showed stereoselectivity whereas those enantiomers having the same configuration at this carbon atom showed lack of stereoselectivity. It is concluded that when the center of chirality is adjacent to the basic functional group, the interaction with the transporter for organic cations is stereoselective. Further studies are required to elucidate the relationship between substrate stereochemistry and the organic cation transporter at both the basolateral and brush-border membranes of the renal tubular epithelial cells.

Animals↗
PubMed1994

Class I antiarrhythmic drugs: allosteric inhibitors of [3H] batrachotoxinin binding to rat cardiac sodium channels.

This study assessed whether class I antiarrhythmic drugs allosterically inhibit [3H]batrachotoxinin A 20-alpha-benzoate ([3H]BTXB) binding to sodium channels on freshly isolated rat cardiac myocytes. All class I drugs tested inhibited equilibrium [3H]BTXB binding in a concentration-dependent manner. Scatchard analysis showed that disopyramide, flecainide, transcainide, lidocaine and amiodarone reduced [3H]BTXB maximum binding (Bmax) whereas procainamide, mexiletine, quinidine, quinine, tocainide, propafenone, encainide and O-demethylencainide increased [3H]BTXB KD but had little effect on Bmax. Kinetic [3H]BTXB binding assays were used to assess the mechanism by which class I drugs inhibit [3H]BTXB binding. Drugs that increase the unidirectional dissociation rate constant (k-1) of [3H]BTXB probably bind to sodium channels to which [3H]BTXB is already bound. Although all class I drugs increased the k-1 of [3H]BTXB, they did so weakly and at concentrations above the IC50 values of the drugs. Thus, drug binding to [3H]BTXB-bound channels does not appear to be the predominant mechanism underlying their ability to inhibit [3H]BTXB binding. Conversely, drugs which allosterically decrease the unidirectional association rate constant (K+1) of [3H]BTXB probably bind to channels to which [3H]BTXB is not already bound. All class I drugs decreased the k+1 of [3H]BTXB, indicating drug binding to [3H]BTXB-free channels. The estimated affinities of drugs for [3H]BTXB-free channels correlated closely with the IC50 values of these drugs (r = 0.94, P < .001), suggesting that this effect is a common and major determinant in their ability to inhibit [3H]BTXB binding. The results are discussed in light of electrophysiologic theories of class I antiarrhythmic drug action.

Allosteric Regulation↗
PubMed1993

[Pregnancy and cardiac drugs].

Any treatment used in pregnant women must take into account the effects of the substance in question of the fetus and the particular sensitivity of the latter during the first three months of development. The majority of drugs used in cardiology can be prescribed during pregnancy: digitalis preparations, furosemide, certain beta-blockers, verapamil, nifedipine (except during the first three months), quinidine, disopyramide, lignocaine, flecainide, amiodarone, heparins (non-fragmented and low molecular weight), central antihypertensive agents, dipyridamole and aspirin. In contrast, some drugs should be avoided because of insufficient information regarding their maternal and fetal consequences (bumetamide, modamide, the most recent beta-blockers, cibenzoline, ticlopidine) or because of harmful adverse effects on the fetus (spironolactones, bipyridines, diltiazem) or the newborn infant (angiotensin converting enzyme inhibitors). Finally, with certain medications (propafenone, oral anticoagulants), it is important to be able to compare maternal risks due to the disease and fetal risks induced by the drug. Modification of the conditions of use of these drugs and very careful monitoring of the patient most often suffice to avoid untoward events or complications with potentially serious medicolegal consequences and which may implicate the liability of the prescriber.

Cardiovascular Agents↗
PubMed1993

[Simultaneous prescription of digoxin and an anti-arrhythmia agent, is it dangerous?].

Many anti-arrhythmic drugs modify the pharmacokinetics of digoxin and increase serum levels. This possibility is considered for the majority of main anti-arrhythmics on the basis of a review of the literature. Quinidine, propafenone, flecainide, amiodarone and verapamil increase blood digoxin levels, sometimes to twice their baseline values. Suggested mechanisms involve above all a decrease in clearance of digoxin and changes in its volume of distribution. Reported accidents considered to be a direct consequence of these interactions are nevertheless rare in the literature, and the need for modifying dose and increased cardiological surveillance in the case of such a combination is essentially a question of precaution. Disopyramide, procainamide and mexiletine do not appear to have any reported effects on the pharmacokinetics of digoxin, their combined prescription never having had any effect on blood digoxin levels.

Anti-Arrhythmia Agents↗
PubMed1995

Antiarrhythmic effect related to the plasma concentration of pentisomide in vivo and the antiarrhythmic-concentration relationship in vitro.

Pentisomide, 2-(2-diisopropylaminoethyl)-4-methyl-2-(pyridyl)- pentanamide, is a novel antiarrhythmic agent structurally related to disopyramide. Using a glass bead arrhythmic model, the authors studied the antiarrhythmic effect of pentisomide in dogs by monitoring the plasma concentrations. When pentisomide was infused at 1 mg/kg/min for 20 min, the ventricular tachycardia was significantly reduced at 5 min after starting the infusion; the arrhythmias were reduced to less than 5% at the end of the 20 min infusion. The plasma-free concentration of pentisomide was about 3 micrograms/ml at 5 min; it increased to about 10 micrograms/ml at the end of 20 min infusion. With 0.3 mg/kg/min infusion, the arrhythmias were reduced to about 60% but were not significant at 20 min of infusion. The plasma-free concentration of pentisomide did not reach 3 micrograms/ml until 20 min of infusion. The 3 micrograms/ml plasma-free concentration for pentisomide seems to be a critical concentration in inducing a significant antiarrhythmic effect. Pentisomide dose-dependently inhibited ischaemia-reperfusion arrhythmia at doses of 30 microM and higher concentrations in vitro. In conclusion, pentisomide inhibits arrhythmias dependent with the plasma concentration or with the concentration of the external solution. The critical plasma-free concentration for inhibition of arrhythmias was 3 micrograms/ml (not equal to 10 microM) and the in vitro effect also had a similar concentration. Therefore, the in vivo and in vitro antiarrhythmic concentrations were well correlated.

Animals↗