Congenital absence of multiple primary teeth.

Idiopathic agenesis of primary dentition is very rare. This is a case report of a 2-year and 6-month-old girl child who presented with 14 missing primary teeth. A review of the previous case reports is done and the management of these cases is discussed.

Use of neutron reflection method to assay nuclear materials in solutions.

Neutron reflection methods are used in the chemical analysis of bulk samples, especially for the determination of contents in hydrogenous solutions. In these techniques albedo is measured by measuring either the activation of a foil, or count rate from a neutron detector. In the present paper Monte Carlo simulations are performed using this method for the possibility of detecting inadvertent criticality in the reprocessing plants and also estimation of 10B in heavy water, which is used as a moderator in PHWRs.

Glycogenic effect of an alkali soluble fraction from sepia shell.

The alkali soluble fraction of the sepia shell possesses both anticonvulsant and hypoglycemic effect. The investigation regarding the fate of the blood sugar during the hypoglycemia revealed that the sepia shell extract acts as a glycogenic agent by mobilising the blood sugar towards liver glycogen reserve through the modulation of the enzymes glycogen phosphorylase a and ab in normal and streptozotocin diabetic mice. The glucose tolerance test (GTT) showed a depression in the GTT curve in experimental mice. The available literature on the biochemistry of the shell reveals that it contains glucosamines and some amino acid residues. The presence of amine group may resemble the sulfonylureas like tolbutamide which also possesses both anticonvulsant and hypoglycemic effect.

Antiarrhythmic and pharmacokinetic evaluation of intravenous recainam in patients with frequent ventricular premature complexes and unsustained ventricular tachycardia.

The pharmacokinetics, antiarrhythmic activity and safety of intravenously administered recainam were evaluated in 15 men and 3 women. All patients had frequent (> 30/hour) ventricular premature complexes (VPCs) and unsustained ventricular tachycardia. Recainam was administered at a loading dose of 4.5 mg/kg/hour over 40 minutes, followed by a maintenance infusion of 0.9 mg/kg/hour for 23 hours and 20 minutes. Sixteen patients had satisfactory efficacy data. The mean frequency of total VPCs decreased by 92.6% and the mean frequency of runs decreased by 99.9% during the maintenance infusion. Suppressions of > or = 70% of total VPCs and > or = 90% of runs were maintained over the 23-hour, 20-minute maintenance infusion period in 16 of the 18 patients. During the maintenance infusion, hourly group plasma recainam concentrations ranged from mean +/- SD 2.6 +/- 0.7 to 3.4 +/- 0.9 micrograms/ml. Patients were observed for 24 hours after termination of the infusion. Periodic blood samples were obtained during and after termination of the infusion to determine recainam concentration. Urine specimens were collected over scheduled intervals to determine urinary excretion of recainam. A 2-compartment pharmacokinetic model was used to analyze the data. The following pharmacokinetic parameters were obtained: terminal elimination half-life, 5.0 +/- 0.8 hours; systemic clearance, 0.27 +/- 0.08 liter/hour/kg; and central and steady-state volume of distribution, 0.32 +/- 0.11 and 1.4 +/- 0.4 liter/kg, respectively. Adverse experiences were reported in 4 of the 18 patients, possibly drug-related in 2; none was considered severe or required discontinuation of recainam.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone.

Amiodarone is an antiarrhythmic agent with unique electrophysiological and pharmacokinetic properties and a wide spectrum of antiarrhythmic activity. Its clinical efficacy is not confined to ventricular arrhythmias but extends to supraventricular arrhythmias including those associated with Wolff-Parkinson-White Syndrome. Though a highly effective drug, amiodarone causes significant side effects. In this article, the electrophysiologic and pharmacokinetic properties, the clinical efficacy, and the adverse effects of amiodarone are reviewed.

Clinical approach to antiarrhythmic therapy in patients with ventricular arrhythmia.

Ventricular arrhythmias can be categorized into three broad groups, namely, benign, malignant, and potentially malignant based on the presence or absence and the severity of underlying heart disease. The benign group does not require treatment, the benefits of treatment in the potentially malignant group are unproven, and the malignant group benefits the most from antiarrhythmic therapy. Because there is no ideal antiarrhythmic drug and all drugs have limitations, selection of an antiarrhythmic drug should be based on the therapeutic goal and the relative efficacies and toxicity profiles of various agents. In the absence of demonstrated beneficial effect from suppression of ventricular arrhythmia in many cardiac patients, antiarrhythmic drug therapy should be confined to patients with serious symptoms, patients with recurrent sustained ventricular tachycardia, and those resuscitated from cardiac arrest.

Mechanism of ventricular arrhythmias caused by increased dispersion of repolarization.

To explain the mechanism of arrhythmias dependent predominantly on increased dispersion of repolarization, we created a model in which increased dispersion was induced by means of generalized hypothermia (29 degrees C) and regional warm blood (38-43 degrees C) perfusion (RWBP) via a coronary artery branch. In 23 open-chest dogs, hypothermia plus RWBP increased maximum dispersion of repolarization from 13 +/- 10 to 111 +/- 16 ms (P less than 0.001) due predominantly to the increased monophasic action potential duration (MAP) difference of six simultaneously recorded MAP's from the ventricular surface, from 10 +/- 15 to 97 +/- 16 ms (P less than 0.001). The maximal difference between activation times was not significantly changed while QRS duration increased from 47 +/- 6 to 52 +/- 7 ms (P less than 0.01). Ventricular arrhythmia (VA) did not occur spontaneously but was induced by a single ventricular premature stimulus (VPS) in all 23 dogs during hypothermia plus RWBP when dispersion reached a critical magnitude. The requirement of this critical magnitude of dispersion for the induction of VA was documented in 16 dogs by means of stepwise increments or decrements of dispersion. In four dogs an increase in atrial pacing rate by 24 beats/min-1 prevented induction of VA by decreasing dispersion from a critical magnitude of 103 +/- 5 ms to a nonarrhythmogenic value of 86 +/- 9 ms (P less than 0.05). In six dogs, we compared the stimulation-site dependent effects of VPS applied in the region with short and long MAPD. In all dogs VA was inducible only by VPS from the region with short MAPD.(ABSTRACT TRUNCATED AT 250 WORDS)

Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes.

The effect of two consecutive ventricular premature stimuli (S1S2) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 +/- 7 msec (activation time difference 4 +/- 6 msec, MAP duration difference 25 +/- 8 msec), that after S1 at paraseptal the site was 81 +/- 8 msec (activation time difference 73 +/- 12 msec, MAP duration difference 8 +/- 5 msec), and that after S1S2 was 148 +/- 27 msec (activation time difference 103 +/- 21, MAP duration difference 44 +/- 26 msec). Neither S1 nor S1S2 induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 +/- 22 msec (activation time difference 9 +/- 3 msec, MAP duration difference 61 +/- 19 msec). During hypothermia and regional warm blood reperfusion, S1 produced a dispersion of repolarization of 149 +/- 29 msec (activation time difference 85 +/- 8 msec, MAP duration difference 64 +/- 23 msec) and did not induce ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Asystole during treatment with amiodarone in a patient with persistent atrial tachycardia.

During treatment with amiodarone, digoxin and nadolol, asystole occurred repeatedly in a patient with chronic persistent automatic atrial tachycardia. Asystole did not occur after discontinuation of drug therapy, and rechallenge with amiodarone alone produced marked overdrive suppression of all pacemakers resulting in asystole. Amiodarone serum level was within therapeutic range. The possible electrophysiologic mechanisms by which amiodarone might suppress both normal and abnormal pacemakers are discussed. The occurrence of asystole at therapeutic serum concentration of amiodarone suggests that this drug should be used with caution.

Effect of amiodarone on electric induction, morphology, and rate of ventricular tachycardia and its relation to clinical efficacy.

Using His bundle electrograms and programmed ventricular stimulation, the effects of chronic amiodarone treatment on induction, morphology, and the rate of ventricular tachycardia (VT) were studied in 17 consecutive patients treated with amiodarone for control of recurrent sustained VT or ventricular fibrillation. Studies were done before and after treatment with amiodarone for an average duration of 5.3 (range 2 to 18) months. During the control study, sustained VT could be induced in 16 patients. VT was initiated by single or double right ventricular (RV) extrastimuli in 14 patients, by double left ventricular (LV) extrastimuli in 1 patient, and by RV burst pacing in 1 patient. Only one pattern (morphology) of VT similar to that of spontaneous VT was induced in 12 patients and two patterns of VT in 4 patients. The average cycle length (CL) (mean +/- SD) of induced VT was 325.8 +/- 61.2 ms. After amiodarone, VT could be induced in 7 of 17 patients and was initiated by single RV extrastimuli in 5 patients, double RV extrastimuli in 1 patient, and RV burst pacing in 1 patient. In 3 of 5 patients in whom VT could be initiated by single RV extrastimuli, initiation of VT required double RV or double LV extrastimuli in the control study; in 1 of 5 patients VT could not be induced in the control study. Amiodarone induced nonclinical, polymorphic VT in 4 patients in whom only clinical VT could be induced during the control study. Compared to control, the CL of induced VT was significantly longer (322 +/- 65.7 vs 416 +/- 41.5 ms; P less than 0.001).+

Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia.

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H2A2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated in 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 +/- 27 vs 352 +/- 40 ms, p less than 0.01), but prolonged H2A2 interval in only 5 of 11 patients (37 +/- 6 vs 60 +/- 31 ms, p less than 0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H2A2 interval was prolonged. Correlation between the paced cycle length which induced VA block, the shortest V1H2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H2A2 or H-Ae interval, the shortest V1H2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of amiodarone on retrograde conduction and refractoriness of the His-Purkinje system in man.

The effects of long term treatment with oral amiodarone on retrograde conduction ( S2H2 interval) and refractoriness of the His-Purkinje system were studied in 11 patients using His bundle electrograms and the ventricular extrastimulus method. Ten patients had ventricular tachycardia and one supraventricular tachycardia. Electrophysiological studies were carried out before and after the patients had been taking their maintenance dose for a mean duration of 84 days. After amiodarone treatment the HV interval was prolonged in seven patients and unchanged in four. At comparable S1S2 intervals, the S2H2 intervals were longer after treatment with amiodarone in all patients than before. Similarly, the longest S2H2 intervals achieved after amiodarone were longer than the control values. Amiodarone significantly increased the relative, effective, and functional refractory periods of the His-Purkinje system. Thus amiodarone exerts important effects on the His-Purkinje system.

Intravenous disopyramide: safety and efficacy of a new dosage regimen.

The efficacy and safety of a new dosage regimen of intravenous disopyramide in ventricular arrhythmias were evaluated in 10 patients. Each had at least four premature ventricular contractions (PVCs)/min during a 30-min period before dosing. By the classification of Lown et al., grade III arrhythmia was present in four patients, grade IVA in three patients, and grade IVB in three patients. Disopyramide was injected intravenously as a bolus of 0.5 mg/kg over 5 min. Each patient received two to three additional boluses of same strength with 5-min intervals between each dosing during the first hour. Continuous intravenous infusion was started with the first bolus and continued at a rate of 1 mg/kg/hr for 3 hr and at 0.4 mg/kg/hr for 15 hr. All patients had continuous Holter monitoring throughout the 18-hr treatment period and for 30 to 60 min before treatment. In eight patients the grade of arrhythmia after drug decreased and the frequency of PVCs fell by 70% to 100% (greater than 85% in six patients and less than 85% in two patients), and the response persisted during the continuous infusion. In two patients PVC frequency increased. For the group as a whole, PVC frequency decreased on the average by 68.4%. Therapeutic serum levels (greater than 2 micrograms/ml) were reached after the first or second bolus and were maintained during the continuous infusion period. There were no side effects necessitating termination of disopyramide infusion. The dosage regimen of intravenous disopyramide evaluated was effective in 60% of patients with ventricular arrhythmia, induced no severe toxic effects, and rapidly achieved therapeutic serum levels that were maintained during continuous infusion.

Treatment of ventricular tachycardia using an automatic scanning extrastimulus pacemaker.

A patient with recurrent sustained ventricular tachycardia that was resistant to both conventional and experimental antiarrhythmic agents was treated with a programmable automatic scanning extrastimulus pacemaker. The antitachycardia pacemaker was implanted only after many episodes of spontaneous and laboratory-induced ventricular tachycardia were reliably and reproducibly terminated with programmed ventricular extrastimuli. In the 6 months since implantation of the automatic scanning pacemaker, all episodes of ventricular tachycardia have been terminated successfully by the pacemaker. Acceleration of rate of ventricular tachycardia or induction of ventricular fibrillation did not occur at any time during attempted termination of ventricular tachycardia by the pacemaker. The advantages of the automatic scanning extrastimulus pacemaker over other antitachycardia pacemakers are discussed.