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Biomedical subjects

M Di Biase

Publications and source records attributed to M Di Biase.

At least 19 recordsLinked to original sources
PubMed1992

Ventricular premature beats in young subjects without evidence of cardiac disease: histological findings.

This report describes the results of right ventricle endomyocardial biopsies from 26 subjects (mean age 27 +/- 10 years) with premature ventricular beats and normal cardiac anatomy and mechanical function. Light microscopy examination revealed normal myocardium in 10 subjects (38%), acute myocarditis in two (7%), borderline myocarditis in one (3.5%), non-specific histological abnormalities including cellular hypertrophy, fibrosis and degenerative changes in 11 (42%), vasculitis in one (3.5%) and findings compatible with right ventricular dysplasia in the final subject (3.5%). The frequency of ventricular premature beats, as assessed by Holter monitoring, and the results of electrophysiological testing did not correlate with histopathological findings and their severity. These data indicate that some young subjects with premature ventricular beats of unknown origin have abnormal right ventricular biopsy findings. Adequate follow-up will probably demonstrate the clinical utility of these observations.

Acute Disease↗
PubMed1991

Electrophysiologic evaluation of intravenous L-propionylcarnitine in man.

L-propionylcarnitine, a short-chain acylcarnitine, has been shown in experimental studies to induce, during acidic and hypoxic conditions, some electrophysiological changes such as an increase of duration of the action potential and of the effective refractory period. In this study, the acute electrophysiological effects of intravenous L-propionylcarnitine (30 mg/kg in 3 min) were studied in 12 subjects with estimated normal function of the sinus node and normal parameters for atrioventricular conduction. Statistically significant changes were observed 2 min after infusion. The sinus cycle length shortened (866 +/- 138 vs 818 +/- 124 msec, P less than 0.05) while refractory periods of the atrioventricular node increased (effective by 30-50 msec in four cases; functional from 425 +/- 52 to 436 +/- 55 msec, P less than 0.05). Sinuatrial conduction time, atrial refractory periods, infranodal conduction, bundle branch, His-Purkinje system and ventricular refractoriness were unchanged. Systolic and diastolic blood pressure were also unchanged. Because of the limited effects on electrophysiological parameters, L-propionylcarnitine should be used as a metabolic drug even in patients with mild disturbances of conduction.

Blood Pressure↗
PubMed1991

Echo-Doppler evaluation of the effects of heart rate increments on left atrial pump function in normal human subjects.

It is commonly believed that the atrial contribution to left ventricular filling increases during heart rate increments. However, the relative contribution of the pump function (atrial systole) and of the passive role (diastasis and reservoir) of the atrium to end-diastolic left ventricular filling is not well known. In order to investigate this problem, we performed a two-dimensional echo-Doppler study during right atrial pacing. Transmitral flow velocity curves were obtained by means of pulsed Doppler. Pacing was performed (1) at the lowest heart rate at which it was possible to obtain a stable capture of the atria, (2) at the heart rate at which the early and late Doppler filling waves almost completely overlapped. In both stages pacing was interrupted for a few seconds to obtain some post-pacing beats. Doppler tracing recorded at rest, during pacing and in the immediate post-pacing beats were analysed to obtain well-known parameters of atrial contribution; atrial peak flow velocity, early to atrial peak flow velocity ratio, and time-velocity integral of the atrial wave. Furthermore, in order to distinguish end-diastolic passive flow from the active contribution of atrial systole to filling, we superimposed the envelope of the last Doppler curve obtained during atrial pacing over the envelope of the first post-pacing curve. In this way the area of the atrial wave of the paced beat was divided by the mid-diastolic part of the post-pacing one into two areas, the integrals of which correspond to the active and passive atrial contribution respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Electrocardiographic patterns during Holter monitoring in patients with first and second degree A-V block due to 'dual A-V nodal pathways'.

The electrocardiographic patterns, observed during 24-h Holter monitoring, of 10 patients (mean age 35 +/- 22 years) with first and second degree A-V block due to dual A-V nodal pathways are reported. Recordings were selected according to the presence of: sudden and persistent prolongation of the PR interval: sudden normalization of the PR interval: 'atypical' Wenckebach sequences showing sudden and pronounced prolongation of any PR interval prior to the blocked P wave. Besides the already recognized pattern, new aspects were identified: (1) Wenckebach sequences in the slow and fast pathways characterized by a progressive increase in the PR interval until a blocked P wave occurred during long and short PR interval periods, respectively; (2) Wenckebach periods first in the slow and then in the fast pathway; (3) 2:1 A-V block with a normal PR interval in the conducted beat after a Wenckebach sequence in the slow pathway; (4) Wenckebach in the fast pathway and, subsequently, in the slow one characterized by a slight prolongation of the PR interval for some beats followed by a sudden and pronounced increase in the PR interval of one beat and a subsequent progressive slight PR prolongation until a blocked P wave occurred; (5) Wenckebach sequence in the fast pathway with subsequent conduction over the slow pathway without a blocked P wave; (6) blocked P waves during both long and short PR interval periods with slight prolongation of the preceding PR interval. The electrophysiological mechanisms involved in these electrocardiographic patterns together with the nature (anatomical or functional) of the intranodal pathways and the clinical significance of this type of block are discussed.

Adolescent↗
PubMed1991

[Localization of the accessory pathways using surface ECG in Wolff-Parkinson-White syndrome].

During recent years criteria for localization of bypass tracts in the Wolff-Parkinson-White syndrome from the conventional ECG have been acquired utilizing epicardial and endocardial mapping data. The polarity of delta wave and QRS in the frontal and horizontal plane and the morphology of retrograde P waves during orthodromic reciprocating tachycardia, are the most indicative elements. An accurate analysis of QRS complexes during atrial fibrillation confirms the site of pre-excitation and could suggest the presence of 2 or more accessory pathways with sufficient spatial separation. Some criteria for identifying multiple accessory pathways are discussed.

Atrial Fibrillation↗
PubMed1991

[Transesophageal study in the diagnostic evaluation of pre-excitation].

Electrophysiologic non-invasive transesophageal testing is compared to intracardiac study in the management of patients with Wolff-Parkinson-White (WPW) syndrome. Transesophageal study can be reliably used to identify the participation of the accessory pathway in reciprocating supraventricular tachycardia and to determine the anterograde conduction properties of the accessory pathway. Using the shortest pre-excited interval during induced atrial fibrillation, or programmed and continuous atrial transesophageal stimulation can markedly reduce the need of intracardiac evaluation. The greater safety and economy of transesophageal compared to the intracardiac technique justify its wider use in preliminary screening of all WPW patients, unless ablative treatment has been clinically indicated, and in evaluating long-term drug protection against a potential deleterious ventricular response during atrial tachyarrhythmias.

Cardiac Pacing, Artificial↗
PubMed1991

[The role of metabolic therapy in myocardial infarct].

During acute myocardial ischemia the metabolism of free fatty acids is impaired. Since the rate of beta-oxidation is reduced, the levels of acil-CoA and long-chain acyl-carnitine increase. The activity of carnitine, which permits the transport of fatty acids into the mitochondria, is reduced both by its transformation in acyl-carnitine and by its release from the cells induced by acute ischemia. The accumulation of fatty acids induces a deterioration of hemodynamic parameters and some impulse formation and conduction disturbances. Since in experimental studies L-carnitine prevents the occurrence of hemodynamic and arrhythmic complications, clinical studies with this compound have been performed during acute ischemia in man. In patients with acute myocardial infarction high doses of L-carnitine induce: a statistically significant increase in urinary concentrations of long- and short-chain carnitine esters; a statistically significant reduction of ventricular arrhythmias during the second day after the onset of symptoms; a reduction of the necrotic area as assessed by electrocardiographic and enzymatic methods.

Adenosine Triphosphate↗
PubMed1990

The nature and evolution of ventricular arrhythmias in acute myocardial infarction.

The natural evolution of ventricular arrhythmias complicating a first episode of acute myocardial infarction has been studied in a group of 56 consecutive patients, who were admitted to the Coronary Care Unit within three hours of the onset of symptoms, and in whom drug administration (digitalis, antiarrhythmics, diuretics and heparin) was limited. Ventricular arrhythmias have been evaluated by means of Holter monitoring performed during the first 24 hours, the second 24 hours, the eighth day, the 18th day and two years after discharge when antiarrhythmic drugs has been discontinued for at least five half-lives. The overall incidence and prevalence of ventricular arrhythmias showed a steady and statistically significant reduction from the first to the eighth day, and a not statistically significant increase from the eighth to the 18th day. The latter increase was still present at the two-year follow-up. The one-by-one behaviour analysis of discharged patients delineated three different patterns: patients who presented a steady reduction in ventricular arrhythmias from the first to the 18th day (44%); patients who showed an almost constant incidence of ventricular arrhythmias during all phases of acute myocardial infarction (24%); and patients who presented both a decrease and an increase in their ventricular arrhythmias (31%). The follow-up at two years showed that the majority of patients, especially those discharged in a high Lown class, had the same arrhythmias as at their follow-up on the 18th day. Correlation of ventricular arrhythmias with the extent of the infarcted area demonstrated that only the peak and mean values of lactic dehydrogenase correlated with the severity of ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1989

Electrophysiologic evaluation of intravenous nicardipine in man.

The acute electrophysiological effects of intravenous nicardipine (0.014 mg/kg per min for 5 minutes) were studied in 12 subjects with estimated normal sinus node functions and atrioventricular conduction parameters. The most important effects were sinus cycle length shortening, increase of corrected sinus node recovery time and reduction of effective and functional refractory period of the atrioventricular node. Sinuatrial conduction time, atrial refractory periods, intranodal conduction, bundle branch refractoriness and ventricular refractoriness were unchanged. Systolic and diastolic blood pressure was reduced. The clinical implications of these properties of the drug are discussed and compared with those of verapamil, diltiazem and nifedipine.

Blood Pressure↗
PubMed1989

Usefulness of transesophageal atrial pacing in hyperkalemia-induced impulse formation and conduction disturbances.

This report describes the usefulness of transesophageal atrial pacing in the treatment of five patients with hyperkalemia-induced bradycardias. Three patients had marked sinus bradycardia while the other two had a regular rhythm with QRS of left bundle branch block morphology, with no P waves visible on the surface electrocardiogram. Four patients were in chronic hemodialysis three times a week, and one had severe post-traumatic hemorrhage. In three patients, hyperkalemia had been precipitated by food intoxication. In one case the cause was unknown while, in the last case, hyperkalemia was due to rapid infusion of stored blood and solutions containing high concentrations of potassium. Transesophageal atrial pacing was performed in all cases utilizing a bipolar catheter introduced into the esophagus and a constant current generator delivering square wave pulses of 10 msec duration and 19-28 mA intensity. Atrial capture, followed by impulse conduction to the ventricles, was constant in all cases, being performed for between 15 and 35 minutes until a normal sinus rhythm was restored. The procedure was well tolerated. The advantages of this procedure as opposed to invasive ventricular pacing are discussed.

Aged↗
PubMed1989

Programmed stimulation in patients with minor forms of right ventricular dysplasia.

Programmed electrical stimulation (PES) was performed in 17 patients, mean age 31 +/- 8 years, with minor forms of right ventricular dysplasia diagnosed because of (1) premature ventricular beats (PVBs) of left bundle branch block (LBBB) morphology; (2) no clinical or non-invasive evidence of cardiac abnormalities; (3) angiographic evidence of right ventricular wall motion abnormalities and bioptic findings of fibro-adipose infiltration. Fifteen patients had frequent and complex PVBs while two had sustained ventricular tachycardia (VT). During PES, sustained VT was induced in 2/2 patients with spontaneous sustained VT; ventricular repetitive responses were induced in 2/15 cases (13%) with complex and frequent PVBs. In conclusion, in minor forms of right ventricular dysplasia, PES induces VT only in patients with clinical VT; on the contrary, in patients with PVBs it is only possible to induce repetitive ventricular responses in a small proportion of cases; it is therefore not possible to select patients at high risk of developing severe ventricular arrhythmias.

Adult↗
PubMed1989

High doses of L-carnitine in acute myocardial infarction: metabolic and antiarrhythmic effects.

Fatty acids accumulate in the muscle cells in some carnitine deficiency syndromes due to a variety of genetic defects in intermediary metabolism. L-Carnitine administration may relieve this excess by transporting acyl compounds out of the cell as acylcarnitine. Similar fatty acid accumulation occurs during myocardial ischaemia because of the decreased rate of beta-oxidation, and this has been put forward as a cause of ventricular arrhythmias. This study was carried out to investigate whether administration of high doses of i.v. L-carnitine in patients with acute myocardial infarction could increase urinary excretion of acylcarnitine and reduce early ventricular arrhythmias. Fifty-six patients suffering from acute myocardial infarction, admitted to the Coronary Unit between 3 and 12 h after the onset of symptoms, were included in the study. The design of the study was double blind, parallel and placebo controlled. Allocation of treatment to patients was done randomly after stratification (time from onset of pain and site of infarction). The first group (28 patients) received intravenous L-carnitine at a dose of 100 mg kg-1 b.w. every 12 h for 36 h while the second group (28 patients) received placebo intravenously. Immediately before starting treatment two blood samples were taken (at 5-min intervals) and a further 16 samples were taken at regular intervals over the following 48 h. Patients' urine was collected over the same period of time. Concentrations of free carnitine, short chain acylcarnitine esters and long chain acylcarnitine esters in serum and urine were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Incidence of 'dual A-V nodal pathways' in first- and second-degree type I supra-His A-V block.

The incidence of 'dual A-V nodal pathways', diagnosed on the basis of spontaneous or induced modifications in the PR interval, has been assessed in a group of 168 consecutive patients with first- (77) and second-degree (91) type I supra-His block. 'Dual A-V nodal pathways' were found in 12 cases (16%) with first-degree and in 7 cases (7.7%) with second-degree type I supra-His A-V block. His bundle recording confirmed the hypothesis that PR interval variations observed in these cases are due to modifications in the AH interval and thus to changes in A-V nodal conduction velocity. The electrophysiologic study also showed that the phenomenon was easily reproduced by atrial stimulation. The frequent association between 'dual A-V nodal pathways' and supra-His blocks suggests that the block mechanism should be studied in depth as it could have prognostic and therapeutic implications.

Adolescent↗
PubMed1987

Role of QT prolongation secondary to a postextrasystolic pause as a possible mechanism for the induction of ventricular fibrillation. Report of two cases.

Two patients developed ventricular fibrillation (VF) while undergoing continuous electrocardiographic monitoring. Analysis showed that VF appeared only when a particular combination of circumstances occurred: a postextrasystolic pause, QT prolongation of the subsequent beat and a premature ventricular beat that did not have a short coupling interval. The relevance of this sequence as a trigger mechanism of VF is discussed.

Aged↗
PubMed1987

Ventricular fibrillation induced by transesophageal atrial pacing in hypertrophic cardiomyopathy.

Sudden death is a rather frequent occurrence in patients with hypertrophic cardiomyopathy, yet the mechanism is uncertain in most cases. We describe a case of an 18 years old patient with a family history of hypertrophic cardiomyopathy and sudden death in whom ventricular fibrillation could be repeatedly induced by means of transesophageal atrial stimulation with 1:1 AV conduction at a rate of 200 beats min-1 and prevented by pharmacological depression of AV node. The not particularly high ventricular rate at which VF occurred could suggest that in hypertrophic cardiomyopathy a major role in favouring VF induction is played by the electrophysiological properties of the myocardium and that sudden death can occur as a consequence of different atrial tachyarrhythmias.

Adolescent↗
PubMed1985

Effect of adenosine and adenosine-5'-triphosphate on atrioventricular conduction in patients.

This study was carried out to further elucidate the effects of adenosine and adenosine-5'-triphosphate (ATP) on atrioventricular (AV) conduction in patients. Adenosine (0.24 mg/kg) and ATP (0.28 mg/kg) were administered intravenously to 37 patients undergoing intracardiac electrophysiologic evaluation. Both adenosine and ATP depressed AV conduction by lengthening the atrial to His bundle (AH) interval. The effects of adenosine and ATP after rapid intravenous bolus administration were fast in onset (15 +/- 0.5 and 15 +/- 1.5 s, respectively), but transient in duration (10.5 +/- 0.5 s for ATP and 17 +/- 3 s for adenosine). Although muscarinic blockade with 0.04 mg/kg atropine shortened the AH interval from a control value of 123 +/- 12 to 74 +/- 4 ms, it did not modify the effects of adenosine or ATP, or both (that is, latency and duration of the effects were not significantly different from before atropine administration). In contrast, aminophylline, a competitive antagonist of adenosine, completely prevented the effects of adenosine and ATP. Aminophylline alone also shortened the AH interval from a control value of 98 +/- 9 to 74 +/- 9 ms. This decrease was blocked by propranolol (0.1 mg/kg), whereas propranolol did not influence the ability of aminophylline to antagonize the effects of adenosine or ATP, or both. Thus, the catecholamines released by aminophylline are unlikely to account for the ability of aminophylline to antagonize the effects of adenosine and ATP. In conclusion, these findings indicate that intravenously administered adenosine and ATP are equally effective in producing AV block that is antagonized by aminophylline but not by atropine.

Adenosine↗