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Biomedical subjects

G Vergara

Publications and source records attributed to G Vergara.

At least 91 records · Page 5Linked to original sources
PubMed1984

Worsening of arrhythmias during pharmacological treatment.

The widespread use of antiarrhythmic agents to control severe life-threatening arrhythmias evidenced the possibility of a worsening of arrhythmias induced by the same drugs. We performed a retrospective analysis studying the worsening phenomenon in patients who underwent pharmacological invasive and non invasive antiarrhythmic tests to choose the drug to be administered in the chronic treatment. Particularly we reviewed: 101 acute pharmacologic non invasive tests for "stable" ventricular ectopic beats using computerized automatic continuous recording system which allows quantitative and qualitative evaluation of arrhythmias. The drugs tested were: Propafenone (25 patients), Disopiramide (25 patients), Tocainide (11 patients), Lorcainide (8 patients), Lorajmine (13 patients), Nadolol (9 patients). In accordance with Vallebit et al., we considered arrhythmias worsening criteria: the onset of non sustained or sustained ventricular tachycardia; an increase of four fold the number of ventricular ectopic beats and/or ten fold the repetitive forms. A worsening of arrhythmias was observed in 4/101 (3.9% patients); 1/9 treated with Nadolol, 1/25 with Propafenone, 1/35 with Disopiramide, 1/13 with Lorajmine. For one young patient the worsening phenomenon could be considered a toxic picture, because of the very high drug plasmatic levels (Lorajmine) observed for the whole duration of the sustained VT induced from the drug. For the remaining 3 patients the response resambles a paradox effect. 34 pharmacologic invasive tests in 30 patients with common recurrent ventricular tachycardia, during electrophysiologic endocavitary study. The drugs tested were: Propafenone (12 patients), Amiodarone (11 patients), Ajmaline (4 patients), Tocainide (3 patients), Lorcainide (2 patients), Lorajmine (1 patient), Disopiramide (1 patient).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

[Clinical experience with propafenone in paroxysmal supraventricular reciprocating tachycardias].

We studied the long term antiarrhythmic efficacy of Propafenon, (300-900 mg/day) in 25 patients (18 females, 7 males; mean age 37,6; follow-up 10 +/- 9,3 months) affected by episodes of disabling paroxysmal supraventricular reciprocating tachycardia. We performed an electrophysiologic study using cardiac catheterization in all 25 patients. Fifteen patients had a Wolff-Parkinson-White syndrome; in 8/25 pts the reentrant circuit was in the atrio-ventricular node and in 2/25 pts it was into the atrium. Ten of fifteen patients with Wolff-Parkinson-White syndrome and 5/8 patients with the reentrant circuit in the atrio-ventricular node have been treated with Propafenon according to the results of the acute test performed during electrophysiologic study. Good results (no recurrences of paroxysmal supraventricular reciprocating tachycardia or less frequent recurrences at a much slower heart rate) have been obtained in 13/15 patients with Wolff-Parkinson-White syndrome and in 5/8 patients with the reentrant circuit in the atrio-ventricular node. The acute drug test with Propafenon during electrophysiologic study was predictive of the clinical response in 100% of patients with Wolff-Parkinson-White syndrome and in 60% of patients with the reentrant circuit in the atrio-ventricular node. We conclude that: 1) Propafenon may be good alternative to Amiodarone in the chronic treatment of pts affected by paroxysmal supraventricular reciprocating tachycardia, especially in patients with Wolff-Parkinson-White syndrome; 2) electrophysiologic study to evaluate Propafenon efficacy is most valuable in patients with Wolff-Parkinson-White syndrome.

Anti-Arrhythmia Agents↗
PubMed1984

[Sustained ventricular tachycardia: induced polymorphism. Clinical and electrophysiological aspects; therapeutic implications].

By induced polymorphism (I.P.) we mean the electrical induction during endocavitary electrophysiologic study (E.E.S.) either of two or more morphologically distinct types of Sustained Ventricular Tachycardia (S.V.T.) (i.e. different bundle branch block patterns or with shifting of QRS by greater than or equal to 90 degrees) or of one type of sustained ventricular tachycardia other than the spontaneous one. Twenty-two patients with clinical sustained ventricular tachycardia, in whom at least one episode of sustained ventricular tachycardia was induced during endocavitary electrophysiologic study, were divided into 2 groups depending on the presence or not of induced polymorphism: Group I consisted of 13 patients with induced polymorphism; Group II consisted of 9 patients without induced polymorphism. All the patients of the Group I had chronic ischemic heart disease (C.I.H.D.); 12/13 previously had myocardial infarction. Only 1 patient of the Group II had chronic ischemic heart disease. Intraventricular conduction defect was present in 9 patients of the Group I and in 2 of the Group II. An overall of 26 sustained ventricular tachycardia episodes were induced in patients of the Group I: 9 with RBBB, 10 with LBBB and 7 with "bizarre" QRS morphology. Sustained ventricular tachycardia reinduction was attempted in 10 patients of the Group I after acute drug testing (Ajmaline, Propafenone, Amiodarone): sustained ventricular tachycardia was no longer inducible in 6, but in 3 of those 4 in whom it was, a marked increase in polymorphism was observed as compared to pre-test pattern. Of the 11 alive patients of Group I, 10 are on Amiodarone alone or in combination with other antiarrhythmic drugs. We conclude as follows: different morphological types of sustained ventricular tachycardia can be quite commonly induced during endocavitary electrophysiologic study; according to our cases induced polymorphism is observed only in patients with chronic ischemic heart disease; patients with induced polymorphism often have intraventricular conduction defect; induced polymorphism furtherly accounts for reentry as the mechanism of sustained ventricular tachycardia in patients with chronic ischemic heart disease; a prevalent morphology of the endocavitary electrophysiologic study induced sustained ventricular tachycardia in patients with chronic ischemic heart disease was not observed at least in our patients; Amiodarone is the drug of choice for the treatment of induced polymorphic sustained ventricular tachycardia patients.

Adult↗
PubMed1984

[Use of transesophageal atrial stimulation in the treatment of atrial flutter. Clinical experience].

Transesophageal atrial pacing with relatively low current output and wide pulse duration has been recently reported. With this method supraventricular tachycardias can be successfully induced and terminated. In this study 23 episodes of spontaneous common atrial flutter (21 patients) were treated by rapid transesophageal atrial pacing (output of 16 Volts and pulse duration of 10 msec). Sinus rhythm resumption was obtained in 18 episodes (78.2%), directly after interruption of stimulation in 7 and following brief periods of atrial fibrillation in 11. All patients tolerated the procedure well with moderate discomfort; no complications were observed. Esophageal pacing offers a useful, rapid, minimally invasive, well tolerated method of terminating atrial flutter in the clinical practice.

Adult↗
PubMed1983

Familial endemic persistent atrial standstill in a small mountain community: review of eight cases.

Familial persistent atrial standstill (PAS) has been rarely documented. Five patients, three male and two female (mean age 46 years at first observation), with familial 'complete' PAS, all from a small mountain community (900 residents) have been studied. Diagnostic criteria were: absence of P wave in any lead of the standard electrocardiogram; no electrical activity of the atria with extremely slow junctional escape rhythm on the endocavitary recordings; lack of atrial excitability; absence of atrial wall movement at fluoroscopy; no mitral A wave on the echocardiogram. All patients had marked cardiac enlargement primarily due to atrial enlargement and all had impaired functional class. Some had bradycardia for many years but none had syncope. Permanent cardiac pacing was carried out in all. Two had cerebral embolism. In the same community there were three patients, one male and two female (mean age 34 years at first observation), with 'partial' atrial standstill characterized by absence of P waves in any lead of the standard electrocardiogram and by endocavitary recording of electrical activity limited to a localized region of the atrium. These three patients also had cardiac enlargement primarily due to atrial enlargement but to a lesser degree than the patients with complete PAS. One patient had cerebral embolism. The familial and endemic character of the disease is stressed. Cardiac enlargement due primarily to atrial enlargement seems to be a common feature of both the complete and partial form of the PAS syndrome.

Adult↗
PubMed1983

Evidence of a reentry circuit in the common type of atrial flutter in man.

To investigate the mechanism of atrial flutter (AF) in humans, we studied 13 patients during episodes of spontaneous common AF, with simultaneous multiple atrial endocavitary recordings and atrial programmed stimulation. In all patients, low paraseptal atrial activation preceded high right atrial activation, and the latter preceded mid- or low lateral right atrial activation (recorded in five patients). Programmed atrial stimulation resulted in early reset of the AF cycle, with an unchanged poststimulation AF activation pattern. The poststimulation cycle recorded from an even potential to the site of stimulation was always shorter than the basic flutter cycle length. The poststimulation cycle recorded at the site of stimulation was always equal to or longer than the flutter cycle length. These results strongly favor the existence of a reentry circuit to which the extrastimulus has access.

Adult↗
PubMed1983

Clinical evaluation of new antiarrhythmic agents: experiences with propafenone.

The authors propose a general design for the clinical evaluation of new antiarrhythmic agents with special reference to their experience with propafenone, a new Class 1 agent. The drug was studied in 61 patients affected by PSRT, VEBs or RVT often unresponsive to other drugs. Both acute i.v. sensitivity tests and evaluation of chronic oral treatment were carried out. The results indicate that propafenone is a highly effective drug and that its oral activity may be predicted in individual patients by an acute i.v. administration. The most frequent adverse reaction was a widening of QRS complex. However the drug had to be withdrawn due to impaired intraventricular conduction in one patient only. More frequently (four cases) its withdrawal was due to adverse extracardiac reactions.

Adolescent↗
PubMed1983

[Validity and limits of invasive pharmacological tests in the treatment of malignant ventricular hyperkinetic arrhythmias].

Programmed stimulation can now be safely performed for the evaluation of therapy for recurrent ventricular tachyarrhythmia. The initiation of ventricular tachycardia appears closely related to its actual spontaneous clinical occurrence. Serial electrophysiologic studies can be performed and are effective in prospectively evaluating the response to antiarrhythmic drugs. The efficacy of therapy based on the results of programmed stimulation appears to be good. On the other hand, Amiodarone can be effective in the chronic treatment as well as in patients with ineffective acute drug test.

Adult↗
PubMed1981

Overdrive and programmed atrial electrostimulation in the study of the electrogenetic mechanism of atrial flutter in man.

The response of atrial flutter (AF) to programmed atrial stimulation (PAS) (13 cases) and overdrive atrial pacing (OAP) ws studied in a total of 18 patients. During PAS the return cycle was equal to the basic cycle of AF in six patients, shorter in one patient, and slightly longer in six; it was never compensatory. ATrial flutter terminated in two patients by PAS and by OAP in three. In 4 patients, PAS resulted in an acceleration of the AF rate, followed by spontaneous interruption within 2 seconds. In the remaining patients, the stimulation either converted the AF into an uncommon type of AF (two patients) or into atrial fibrillation that was followed by spontaneous return to sinus rhythm. In two patients it was possible to reproduce the AF with PAS; in one of the patients another type of AF was induced. Some of the data observed suggest a re-entry circuit as the electrogenetic mechanism responsible for AF in man.

Adult↗
PubMed1981

[The phenomenon of accelerated A-V conduction. Electrophysiological study with a "selective" calcium antagonist (Verapamil)].

In order to discover slow response calcium dependent fibers within the structure with enhanced A-V conduction, an acute i.v. test with Verapamil (a highly selective calcium antagonist) was done in 13 patients with enhanced A-V conduction syndrome (4 had A-V by-pass, Kent type, associated). The action of Verapamil on the following parameters was studied: 1) A-H interval in sinus rhythms; 2) delta A-H interval (i.e. the maximum increment of A-H interval after incremental atrial pacing); 3) antegrade and retrograde function curves of the structure with enhanced A-V conduction; 4) R-R cycle of the reciprocating tachycardia, antegrade and retrograde conduction time (after identification of the reentry circuit) and pattern of induction and interruption of the tachycardia. Only in 1 patient a total atrio-hisian by-pass was identified. In all the other patients the electrophysiologic response to i.v. Verapamil suggested the presence of slow response calcium dependent fibers within the structure with enhanced A-V conduction which was always depressed by the drug even if to a lesser degree than in a normal A-V node. From these data and from the analysis of the epidemiology of enhanced A-V conduction, the Authors hypothesize that an infantile type A-V node could be in most cases the anatomical basis of enhanced A-V conduction while only rarely a total or partial A-V node by-pass.

Adolescent↗
PubMed1981

[Another type of interaction between blood levels of digitalis and anti-arrhythmic drugs: digoxin and amiodarone. Experience with long-term therapy].

In clinical Arrhythmology it is often necessary to associate digitalis and antiarrhythmic agents. This calls for study of possible interaction between the employed drugs. We found a statistically significant correlation between digitalis and amiodarone plasma level in patients on long term treatment with both drugs. A statistically significant linear correlation between plasma amiodarone level and digoxin (0.25 mg/day) or beta-methyldigoxin (0.20 mg/day) was documented in 33 patients. 23 patients had been treated with these drugs for paraxysmal reciprocating supraventricular tachycardia since an average of 52 months (computerized follow-up). (Amiodarone average weekly dose was 1078 +/- 168 mg after a loading dose of 12 gm given over one month). 10 patients were on chronic treatment with higher weekly doses of amiodarone (average dose 2380 +/- 731 mg per week). Thyroid function tests (T4; T3; T3UP; TSH; rT3) were checked in every patients. Further studies are warranted to understand the mechanism of the interaction between amiodarone and digitalis. As a clinical implication we point out that amiodarone-digoxin (or betamethyldigoxin) interaction in our patients has neither resulted in over-therapeutic plasma level nor in signs of digitalis toxicity.

Aged↗