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Biomedical subjects

V Bonatti

Publications and source records attributed to V Bonatti.

At least 19 recordsLinked to original sources
PubMed1988

[Efficacy of verapamil in the prevention of ventricular fibrillation in the acute phase of myocardial infarction].

The effectiveness of verapamil in preventing ventricular fibrillation caused by coronary occlusion or reperfusion has been well demonstrated in animal studies, but these experimental data have not yet been confirmed in man. In this study we evaluated the prevalence of ventricular arrhythmias (fibrillation, sustained tachycardia and frequent extrasystoles) in patients hospitalized for myocardial infarction and treated with or without verapamil. The records of patients admitted to our Coronary Intensive Care unit during a 5-year period were analyzed retrospectively. Strict selection criteria enabled us to divide our patients into two homogeneous groups. The control group (group A) consisted of 106 patients who received only continuous infusions of heparin. The treated group (group B) comprised 89 patients who received exclusively verapamil by intravenous injections followed by continuous infusions. The prevalence of ventricular arrhythmia of all types was significantly lower in group B (22 p. 100) than in group A patients (71 p. 100; p less than 0.001). Episodes of ventricular fibrillation, in particular, were considerably less frequent in group B patients (1 p. 100) than in group A patients (13 p. 100; p less than 0.001). It would appear from these results that verapamil is highly effective in preventing death due to cardiac arrhythmia in the acute phase of myocardial infarction.

Cardiac Complexes, Premature↗
PubMed1987

[Identification using thoracic electromapping of patients with sustained postinfarct ventricular tachycardia. Preliminary results of a new method of analysis of ST-T isoarea maps].

Recent studies have demonstrated that body surface maps (BSM) can be employed as non-invasive diagnostic tool for recognizing cardiac states at risk for repetitive ventricular arrhythmias in patients (pts) with old infarction. Our study reports preliminary results of a new method of statistical analysis of ST-T isoarea maps for identifying patients with post-infarction sustained ventricular tachycardia. 38 pts with previous myocardial infarction have been studied, 25 without and 13 with sustained ventricular tachycardia (VT). The two groups of pts did not differ significantly for age, site of infarction and ejection fraction. BSM have been recorded by means of an automated 35-channels instrument from 140 thoracic leads. For each lead ST-T deflection area has been calculated in microV.sec and taken as input variables for stepwise discriminant analysis which allowed identification of the integral values significantly discriminant (for F less than 0.15) between the two groups. Canonical analysis has been applied to identified values to obtain, by canonical coefficients, linear combination of the values for the highest correlation with the two groups of pts. To test the power of the method, the two groups of pts have been divided randomly in a learning set (17 pts without and 9 pts with VT) and a test set (8 pts without and 4 pts with VT).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Monophasic action potential studies in human subjects with prolonged ventricular repolarization and long QT syndromes.

In 58 human subjects monophasic action potentials (MAPs) were recorded with suction electrodes in several areas of the right ventricle (RV). Individual differences between the longest and the shortest RV MAP durations indicate that: normally (40 subjects) ventricular repolarization is almost synchronous; QT prolongation due either to bradycardia or to amiodarone treatment (eight cases) may be the result of a uniform lengthening of ventricular repolarization, when ventricular arrhythmias are not present; in long QT syndromes (LQTSs) of differing etiology (10 cases), in which severe ventricular arrhythmias are present, marked individual differences in RV MAP duration are present and correspond with pathological asynchrony of ventricular repolarization. Also observed in the LQTSs are morphological alterations (humps) in the terminal phase of the longest MAPs. Humps, interpreted as pathological delayed repolarization phenomena, may lead to focal re-excitation which seems to play a key role in the genesis of the arrhythmias complicating LQTSs.

Adolescent↗
PubMed1983

Recording of monophasic action potentials of the right ventricle in long QT syndromes complicated by severe ventricular arrhythmias.

Monophasic action potentials (MAPs) were recorded with intracardiac suction electrodes in several areas of the right ventricle in 10 patients with long QT syndromes (with "torsades de pointe') of different etiology. In all cases two characteristic electrophysiological features were observed: (1) a marked difference in MAP duration in the different areas of the right ventricle (asynchronous repolarization); (2) an alteration in the shape of the longest MAPs consisting in humps which occurred on the repolarization phase of MAP. Humps may be interpreted as delayed repolarization phenomena probably due to a decrease in potassium conductance of some ventricular cells. These may lead to focal re-excitation as a result of partial membrane depolarization. Focal re-excitation seems to play a key role in the genesis of severe arrhythmias occurring in the above mentioned syndromes.

Action Potentials↗
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↗
PubMed1982

[Electrophysiological effects of lidocaine on the QRS and ST segment during acute myocardial infarct. Evaluation with thoracic electromaps].

We have evaluated the effects of lidocaine on the main haemodynamic parameters, the QTc interval, the ST segment elevation (sigma ST) and the R wave sum (Max sigma pos), studied by automatic recording of thoracic maps, in 9 patients with acute anterior myocardial infarction, admitted to the CCU within 6 hours from pain onset. Lidocaine has been given at the dosage of 2 mg/kg as an i.v. bolus, followed by continuous infusion at 2 mg/min. Haemodynamic parameters, QTc interval and ECG maps have been recorded before and after 5, 15 and 30 min from the beginning of the therapy. Heart rate, systolic and diastolic arterial pressure and cardiac output have not been significantly affected by Lidocaine. The QTc interval has showed a significant reduction of the control ECG from 0.364 +/- 0.059 sec to 0.352 +/- 0.051 at 5 min, 0.353 +/- 0.053 at 15 min and 0.0355 +/- 0.058 sec and 30 min (P less than 0.05). The sigma ST segment decreased significantly after Lidocaine at 5 and 15 min. (from 126 +/- 26 mV to 109 +/- 23 mV and to 112 +/- 23 mV; P less than 0.01 and, respectively, P less than 0.025), whereas at 30 min. sigma ST was not different from control value. There were no significant changes of max sigma pos. Lidocaine did not significantly modify the main haemodynamic determinants of oxygen consumption. We therefore believe that the observed reduction of ST segment elevation was not caused by a decrease of the ischemic damage but was probably due to a primary electrophysiological effect. This drugs, which affects in a different way the action potentials of normal and ischemic cells, could abolish their differences, thus reducing the systolic current of injury.

Aged↗
PubMed1981

[Comparative study of the anti-arrhythmic activity of mexiletine and lidocaine in ventricular hyperkinetic arrhythmias].

The present study has been carried out on 50 patients admitted to C.C.U. for cardiovascular diseases of various ethiology (44 patients with ischemic heart disease) who required antiarrhythmic theory for different types of ventricular arrhythmias: monofocal ventricular extrasistoles greater than 6/min, bigeminal ventricular extrasistoles, polifocal and/or repetitive ventricular tachycardias. The patients have been randomly allocated into two groups of 25 subjects: the first one has been treated with Mexiletine and the second with Lidocaine. In Mexiletine treated group the following results have been obtained: 19 excellent (76%), 4 good (16%) and 2 ineffective (8%). In Lidocaine treated group: 11 excellent (44%), 5 good (20%) and 9 ineffective (36%). Statistical analysis by chi square test has shown significant prevalence of favourable results in Mexiletine treated patients (p less than 0.02; X(2) = 5.33). Moreover, in relation to the type of arrhythmias, Mexiletine succeded in a greater number of cases of complicated ventricular extrasistoles (bigeminal, polifocal and/or ripetitive) and in ventricular tachicardias. Mexiletine also has induced significant reduction of QTc and significant increase of cardiac rate, whereas it did not affect significantly the PR interval and blood pressure. None of these parameters has been influenced significantly by Lidocaine. Side effects have been similar for both drugs and generally mild. On the basis of results and in accord with the electrophysiological properties, the Authors discuss the possible mechanism of action and the role of Mexiletine in the treatment of ventricular arrhythmias particularly those complicating acute phase of myocardial infarction.

Aged↗
PubMed1981

[Treatment of acute myocardial infarction with verapamil. Hemodynamic effects and electrical changes studied by body surface maps (author's transl)].

The effects of Verapamil on main haemodinamic parameters and on Max sigma pos., sigma Q15, Max sigma pos./Max sigma neg. and sigma ST, studied by automatic recording of thoracic maps, were evaluated in 11 patients with acute myocardial infarction within 6 hours from pain onset. Verapamil was given at the dose of 0.1 mg/Kg followed by infusion of 0.035 mg/min. Hemodynamic measurements were made before and 15 minutes after Verapamil; the maps were recorded before and 5, 15 and 30 minutes after Verapamil. Heart rate and sistolic arterial pressure were reduced, though not significantly: right atrial pressure, pulmonary pressures and capillary pulmonary pressure remained unchanged. On the contrary, the reduction of diastolic arterial pressure (from 94 +/- 4.2 to 88 +/- 4.5 mmHg; P less than 0.05) and of cardiac index (from 3.1 +/- 0.11 to 3 +/- 0.11; P less than 0.05) was important. Max sigma pos. increased after 15 minutes from 11619 +/- 1970 to 12349 +/- 2151 microV (P less than 0.01), but il decreased after 30 minutes to 11037 +/- 2042 microV (P less than 0.05). Max sigma pos./Max sigma neg. ratio increased significantly after 5 and 15 minutes. Sigma Q15 increased significantly only after 30 minutes (from 7198 +/- 1643 to 8688 +/- 1541 microV; P less than 0.05). Sigma ST showed a transient, non significant increase after 5 minutes, but decreased significantly after 30 minutes (from 76664 +/- 19505 to 67157 +/- 18581 microV; P less than 0.05). The results show that Verapamil does not cause worsening of main haemodinamic parameters during acute, non complicated myocardial infarction and reduces significantly ST segment elevation. The Authors discuss also a possible electrophysiological effect of Verapamil on action potential of ischemic cells, responsible for early increase of sigma ST observed in some patients.

Aged↗