[Arrhythmologic study of 50 patients with arrhythmogenic disease of the right ventricle: prognostic implications]. / Studio aritmologico in 50 pazienti con malattia aritmogena del ventricolo destro: implicazioni prognostiche.

UNLABELLED: Arrhythmogenic right ventricular disease is a syndrome which involves a wide spectrum of anatomo-clinical features. It is characterised by different levels of right ventricle anomaly, and by life-threatening "right" hyperkinetic ventricular arrhythmias. Fifty consecutive pts were retrospectively examined at the Arrhythmological Centre in Trento between 1977 and 1988. The results of rigorous arrhythmological, echocardiographic and angiographic criteria showed that all pts were affected by arrhythmogenic right ventricular disease. CASE STUDY: 39/50 (78%) males, 11/50 (22%) females; age 30.6 years (11-78) at the time of the first study. METHODS: clinical history in 50/50 pts, electrocardiogram in 50/50 pts, Holter monitoring in 50/50 pts, ergometric test in 49/50 pts, non-invasive analysis using signal-averaging QRS in 17/50 pts, 2D echocardiogram in 50/50 pts, angiography in 38/50 pts, electrophysiological endocavitary study in 35/50 pts. RESULTS: familial 2/50 (4%); 1/50 (2%) was in class II NYHA; first arrhythmia at 24.6 years (8-60); most severe arrhythmia at 27.7 years (9-74). Forty-three out of fifty patients (86%) were symptomatic for arrhythmias: 28/50 (56%) as a result of stress; 20/50 (40%) had life-threatening symptoms; 6/50 (12%) had aborted sudden death. Arrhythmogenic right ventricular disease was "localized" in 42/50 (84%) and "diffused" in 8/50 (16%) and was associated with anomalies of the left ventricle in 30/50 (60%). Electrocardiogram showed: right bundle branch block in 10/50 (20%), negative T wave on the right precordial leads in 19/50 (38%), delayed ventricular potentials in 4/17 (23.5%). Using the electrocardiogram, Holter monitoring and electrophysiological endocavitary study the following were documented: a) clinical ventricular tachycardia in 40/50 (80%): non-sustained ventricular tachycardia in 10/50 (20%), sustained ventricular tachycardia in 30/50 (60%); b) electrically induced ventricular tachycardia in 26/35 (74.2%): non-sustained ventricular tachycardia in 8/35 (22.8%), sustained ventricular tachycardia in 18/35 (51.4%) (clinical sustained ventricular tachycardia in 18/18); c) multiform ventricular tachycardia in 12/50 (24%) (diffused arrhythmogenic right ventricular disease in 3/12 and associated anomalies of the left ventricle in 11/12); d) pleomorphic sustained ventricular tachycardia in 9/30 (30%) (diffused arrhythmogenic right ventricular disease in 2/9, and associated anomalies of the left ventricle in 8/9). Forty-two out of fifty patients (84%) underwent antiarrhythmic treatment. When the study was carried out 6.6 years (1 month-22 years) had passed since the first symptom; follow-up was 2.1 years (1 month-11 years) while the interval between the first symptom and the last check-up was 8.4 years (1-30 years); 2/50 dropped out and 2/50 died suddenly.(ABSTRACT TRUNCATED AT 400 WORDS)

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)

[Clinical experience with propafenone in paroxysmal supraventricular reciprocating tachycardias]. / Esperienza clinica con il propafenone nelle tachicardie parossistiche sopraventricolari reciprocanti.

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.

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.

[Another type of interaction between blood levels of digitalis and anti-arrhythmic drugs: digoxin and amiodarone. Experience with long-term therapy]. / Un altro tipo di interazione fra livelli ematici della digitale e di farmaci antiaritmici: digoxina ed amiodarone. Esperienza di trattamento a lungo termine.

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.

[Acute changes of the mechanical function of the ischaemic left ventricle by sublingual nifedipine (author's transl)]. / Modificazioni acute della funzione meccanica del ventricolo sinistro ischemico indotte dalla nifedipina perlinguale.

In 20 patients, who had undergone a routine cardiac catheterization for the evaluation of anginal syndrome, some parameters of mechanical function of left ventricle (LV) were evaluated before and after left ventriculography was performed. Then, the same parameters were also measured, in identical technical conditions, after the administration of 20 mg of sublingual nifedipine (NIF). After NIF a significant decrease (P < 0.01) in left ventricular systolic and diastolic pressure, aortic diastolic pressure and left ventricular enddiastolic and endsystolic volumes was observed; while, heart rate, dP/dt max, stroke volume and ejection fraction were significantly increased (P < 0.01). Evaluation of LV segmental wall motion, after NIF, revealed no changes of wall motion in normal areas or in those with akinesis or dyskinesis; while, 68% of the areas with slight hypokinesis and 55% of those with severe hypokinesis were significantly improved after NIF (P < 0.005). Thus, we concluded that NIF does not cause a depression of LV mechanical function. The improvement of LV wall motion displayed by the areas with a transitory ischemic damage could be attributed to the reduction in preload and, more significantly, in afterload induced by NIF.