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Biomedical subjects

D Bracchetti

Publications and source records attributed to D Bracchetti.

At least 55 records · Page 3Linked to original sources
PubMed1984

[Comparative study on the efficacy of disopyramide and propafenone in the prevention of the recurrence of ventricular tachycardia].

The purpose of our study was to assess the efficacy of Propafenon in comparison with Disopyramide in the long-term treatment of repetitive ventricular tachycardia. We studied 34 patients suffering from episodes of repetitive ventricular tachycardia of different etiology. Propafenon and Disopyramide was administered in doses of 300 mg and 200 mg three times a day respectively. The number of ventricular tachycardias has been evaluated during a period of 4 months of basal observation and during two periods of 4 months each of treatment respectively with Disopyramide and Propafenon. Moreover a dynamic electrocardiogram was recorded to assess the efficacy of Propafenon in suppressing ventricular ectopic beats in 17 patients. We conclude that Propafenon shows greater efficacy than Disopyramide in the treatment of repetitive ventricular tachycardias and a comparable efficacy in the control of ventricular ectopic beats. Moreover Propafenon shows also a minor incidence of side effects.

Anti-Arrhythmia Agents↗
PubMed1984

Epicardial, endocardial and transmural mapping in assessing electrophysiological effects of 14-C lidocaine and 14-C propafenone on activation times in experimental chronic myocardial infarction. Correlations with myocardial drugs concentrations.

The electrophysiological effects of lidocaine (L) and propafenone (P) in chronic myocardial infarction in relation to tissue drug concentrations (TDC) are unknown. Thus of 16 dogs with one week old myocardial infarction, 8 received propafenone 2 mg/kg and 8 lidocaine 5 mg/kg followed by 0.2 mg/kg/min of either drug for 60 min. Epicardial (EPI) mapping (greater than 30 points) was performed with a bipolar electrode. Endocardial (ENDO) and transmural (TRANS) mapping (greater than 20 points) were performed with 4 pairs of needle mounted bipolar electrodes. The % change in activation times (% delta AT) in EPI, ENDO and TRANS was evaluated in normal (N) and infarcted (I) zones at control and 60 min after drugs. Ventricular arrhythmias (VA) were studied with programmed extra stimulation. Results (P less than 0.01 to L, P less than 0.01 to N zone, # P less than 0.05 to ENDO): (Table: see text) At 60' ventricular tachycardia and ventricular fibrillation were both still inducible in 50% in the lidocaine group (37% in control), while only in 16% in the propafenone group (62% in control). Despite lower drug concentrations in the infarct, the effects on AT are comparable to normal zones for both drugs. In conclusion lidocaine reduces and propafenone increases AT, affecting in opposite directions the inducibility of reentrant ventricular arrhythmias.

Animals↗
PubMed1983

Propranolol v. verapamil in the treatment of unstable angina. A double-blind cross-over study.

A double-blind, cross-over study was performed in 23 consecutive patients with unstable angina at rest in order to compare the efficacy of verapamil (480 mg/day) and propranolol (240 mg/day) in reducing the number of anginal crises and nitroglycerin (NTG) consumption. Twenty patients, 15 men and five women, mean age 59.7 (range 45-68) years completed the study. The mean daily number of attacks was 3.1 in the two-day run-in period and 2.9 in a subsequent two-day placebo period immediately preceding the treatment periods. Propranolol reduced the number of attacks to 1.6 (P less than 0.01 compared to the run-in and placebo periods). Verapamil reduced the crises to 0.2/day (P less than 0.01 compared to the run-in placebo and propranolol periods). The NTG consumption behaved in a similar way. Adverse reactions to verapamil were observed in two patients. Although there are objective difficulties in performing correct trials in these kinds of patients, the results of this study indicate the efficacy of verapamil in preventing anginal pains during the "warm phase' of the unstable form and stress the superiority of this calcium antagonist when compared to propranolol.

Aged↗
PubMed1983

[Hemodynamic aspects of torsade de pointes: echocardiographic study of a case].

In a patient with complete heart block complicated by "Torsade de point" (T.D.P.) we were able to record an M-mode echocardiogram during an attack of this peculiar ventricular tachyarrhythmia. The aortic valve opening was inconstant, incomplete and unequal during the T.D.P. (13 sec.), although the rate of the tachyarrhythmia was almost constant. On the other hand, during a subsequent ventricular pacing at a comparable rate like, the aortic valve opening was constant and complete. On the basis of these observations we conclude that the reduction of stroke volume, observed in T.D.P., is mainly due to mechanical failure as a result of partial desynchronization of the ventricular activation, as in ventricular fibrillation in which, however, the desynchronization is complete.

Aged↗
PubMed1982

[Drug treatment of a trial fibrillation in patients with Wolff-Parkinson-White syndrome].

In 10 patients with ventricular preexcitation (Kent bundle), in whom atrial fibrillation (A.F.) was present, the effect of some common antiarrhythmic drugs on the conduction through the anomalous pathway, and on the ventricular rate was estimated. Procainamide caused transient complete block in the accessory pathway (disappearance of the aberrant QRS) and marked reduction of the average ventricular rate in all instances. Lidocaine caused incomplete block in the accessory pathway (reduction of the number of the aberrant QRS) and significant reduction of the average ventricular rate in all tested subjects. Amiodarone slowed the ventricular rate (increase of the average and minimum R-R intervals between wide QRS complexes) in two patients, but it did not block the anomalous pathway (all QRS complexes remained aberrant); whereas in 1 patient the ventricular rate became faster and regular and the patient had syncope, while the QRS remained always aberrant. This response was probably due to the change of A.F. into atrial flutter with atrio-ventricular conduction through the anomalous pathway only. Digitalis increased the average ventricular rate and shortened the minimum R-R interval between aberrant QRS complexes 3 out of 3 times. On the basis of our experience and of the data in the literature, we conclude that, in the management of A.F. in patients with W.P.W. syndrome:--the most effective drugs are those of the 1st group of Singh and Hauswirth classification (especially Procainamide and Ajmaline);--Lidocaine is less effective, but not ineffective and its utilization may be recommended whenever the previous drugs may be hazardous;--Amiodarone, although capable of modifying the electrophysiologic properties both of the anomalous pathway and of the A-V node, seems to be less reliable;--the drugs which influence only the A-V node (Verapamil, beta-Blockers, etc.) are quite ineffective;--finally, the Digitalis is not suitable because this drug increases the ventricular rate by decreasing the effective refractory period (ERP) of the anomalous pathway.

Adolescent↗
PubMed1982

Comparison of the efficacy of propafenone versus disopyramide for complex premature ventricular contractions. Evaluation with long-term monitoring.

Interpreting the results of this study, propafenone (Rytmonorm), administered orally in a dose of 900 mg daily, was more effective than disopyramide in a dose of 600 mg daily, in the treatment of patients with complex premature ventricular contractions (PVCs). The study was performed in 12 patients, with several Holter ECG monitorings to obtain quantitative data of the effectiveness in the same patient of the new drug propafenone in comparison with disopyramide in a documented effective oral regimen. A quantitative analysis of PVCs was obtained with a computer assisted detection. Clinical effectiveness, considered as 70--80% reduction of total number of PVCs, was obtained in 8/12 patients for propafenone and 6/12 for disopyramide, or as 50% reduction with suppression of all complex PVCs (couplets, repetitive, multiform and bigeminy) was obtained in 11/12 for propafenone and 9/12 for disopyramide.

Adolescent↗
PubMed1981

Comparison of acute haemodynamic effects of nifedipine and isosorbide dinitrate in patients with heart failure following acute myocardial infarction.

The acute haemodynamic effects of nifedipine (10 mg sublingually) and isosorbide dinitrate (5 mg sublingually) were compared in 13 patients with heart failure due to acute myocardial infarction. Nifedipine induced a significant reduction in systolic (from 122 +/- 5 to 107 +/- 3 mm Hg: mean +/- SEM; P less than 0.002) and diastolic blood pressure (from 85 +/- 3 to 75 +/- 2 mm Hg; P less than 0.01). Heart rate did not change significantly, nor did mean right atrial pressure. The mean pulmonary arterial pressure was lowered from 31 +/- 2 to 27 +/- 2 mm Hg (P less than 0.005). The left ventricular filling pressure decreased from 24 +/- 1 to 19 +/- 1 mm Hg (P less than 0.0001). A significant increase in cardiac index (from 2.33 +/- 0.13 to 2.69 +/- 0.15 l/min per m2; P less than 0.001) and in stroke volume index (from 24 +/- 2 to 28 +/- 2 ml/beats per m2; P less than 0.005) was registered. Systemic vascular resistance fell from 1742 +/- 145 to 1308 +/- 85 dynes/sec per cm-5 (P less than 0.00005). After isosorbide dinitrate was administered a significant reduction in mean right atrial pressure (from 9.5 +/- 1.6 to 5.1 +/- 1.2 mm Hg; P less than 0.0001), in mean pulmonary arterial pressure (from 32 +/- 1 to 23 +/- 1 mm Hg; P less than 0.00001) and in left ventricular filling pressure (from 23 +/- 1 to 16 +/- 1 mm Hg; P less than 0.0001) was seen. No significant change in systolic and diastolic blood pressure, heart rate, cardiac index, stroke volume index and systemic vascular resistance was registered. No side-effects were seen after nifedipine and isosorbide dinitrate were administered.

Adult↗
PubMed1981

[Dynamic electrocardiography evaluation of the effectiveness of prajmalium bitartrate, disopyramide and procainamide in patients with stabilized ventricular extrasystole].

20 patients with chronic premature ventricular contractions (P.V.Cs) underwent several Holter ECG monitorings to assess clinical effectiveness of three antiarrhythmic drugs: Prajmalium Bitartrate (P.B.) 80 mg/daily, Disopyramide (D.) 600 mg/daily and Procainamide (P.) 2400 mg/daily, to assess the most effective antiarrhythmic medication in every patient. Clinical effectiveness was considered as 80% reduction of P.V.Cs or 50% reduction with suppression of all complex ventricular ectopy (repetitive, polymorph, bigeminy). These results were observed respectively, for 80% reduction, in 5/20 patients for P.B., in 9/20 for D., and in 3/19 for P; and for 50% reduction in 11/20 for P.B., in 18/20 for D., and in 9/19 for P. Comparison in the same patient, using Holter ECG monitoring with a computer assisted analysis, of the effects of different antiarrhythmic medications, is a rational procedure to assess clinical efficacy of new antiarrhythmic drugs and to choose the most effective in each case.

Adolescent↗
PubMed1981

[Electrophysiologic demonstration of dual atrioventricular nodal pathways and final common pathway in a case of A-V nodal paroxysmal tachycardia. Considerations on the functional complexity of the A-V node (author's transl)].

The AA. studied the A-V nodal conduction using the technique of induced PAB in a patient with A-V reentrant paroxysmal tachycardia. They observed that the conduction through the A-V node failed when coupling intervals A1-A2 were between 280 and 260 msec and, after, recovered, with consistent slackening, when A1-A2 intervals were shortened, until the atrial ERP was reached. This uncommon response indicates the functional complexity of the A-V node and, particularly, suggests the presence of a final common pathway distal to the fast and slow A-V pathways, that are the anatomic-functional basis of the reentry circuit in A-V nodal paroxismal tachycardia.

Atrioventricular Node↗