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Biomedical subjects

A Finzi

Publications and source records attributed to A Finzi.

At least 37 records · Page 2Linked to original sources
PubMed1987

Permanent form of junctional reciprocating tachycardia involving an atrio-hisian accessory pathway: electrophysiologic and histologic correlations.

We present clinical, electrophysiologic and morphologic correlations of a patient with a permanent form of junctional reciprocating tachycardia, who died from a lung tumor. At electrophysiologic study, the tachycardia circuit was suspected to involve an atrio-Hisian accessory pathway antegradely and the AV node retrogradely; a ventriculo-atrial accessory pathway was excluded. Pathologic examination revealed a right-sided atrio-Hisian accessory pathway and an area of abnormal dispersion in the distal His bundle fibers. This case is consistently different from another previously reported case in which a concealed, serpiginous, septal atrioventricular accessory pathway was demonstrated by anatomic examination. Thus, different substrates seem to be responsible for the permanent form of junctional reciprocating tachycardia.

Aged↗
PubMed1986

Long-term prognostic significance and electrophysiological evolution of intraventricular conduction disturbances complicating acute myocardial infarction.

Fifty-nine patients with post-infarctional, isolated intraventricular conduction disturbances (IVCD) who survived the acute stage of myocardial infarction were followed up after hospital discharge for a mean period of 11.4 +/- 4.8 months. Fourteen patients (24%) had HV interval prolongation (greater than 55 ms) during AMI (group A), and 45 patients had normal HV intervals (76%, group B). His bundle recordings were repeated during follow-up in 48 survivors after a mean period of 7.2 +/- 0.7 months. Infranodal conduction delay in the acute stage of infarction was correlated with a higher incidence of heart failure during AMI (78% of patients in group A vs 22% in group B, p less than 0.001), and with higher rate of cardiac mortality during follow-up (50% in group A vs 13% in group B, p less than 0.01). Survivors of group A showed a higher functional NYHA class, a higher incidence of CHF, and a higher prevalence of complex ventricular arrhythmias at Holter monitoring. No statistically significant difference in late sudden death was evident between the two groups of patients, and the global incidence of late AV block was 2%. At repeat His bundle recording no significant change (greater than 5 ms) in HV interval could be demonstrated in comparison to the acute phase recording, neither in patients with prolonged nor in patients with normal HV time. We conclude that HV prolongation in patients with isolated, post-infarctional IVCD is correlated with a worse prognosis, both during acute infarction and during the follow-up period, which presumably reflects wider anatomic damage in comparison to patients with normal HV time. The low incidence of late AV block and the electrophysiological demonstration of the stability of infranodal conduction several months after AMI indicate that these patients do not require permanent prophylactic pacing after acute myocardial infarction.

Adult↗
PubMed1985

Role of the polymorphonuclear neutrophils in the phototoxic reaction in porphyria cutanea tarda.

We have compared the superoxide production of polymorphonuclear cells (PMNLs) from healthy donors, when incubated with either control or porphyria cutanea tarda (PCT) sera at 4, 24 and 48 hours after exposure in vivo to UVA light. Serum from UVA-irradiated (1-5 J/cm2) PCT patients generated significantly greater amounts of superoxides from PMNLs than serum from UVA-irradiated (8-12 J/cm2) normal controls. This indicates that serum factors activated by porphyrin plus UVA stimulate neutrophilic granulocytes to liberate superoxides, triggering a series of events that cause tissue damage. The vascular lesions in patients with PCT could be, at least in part, due to this cytotoxic effect.

Adult↗
PubMed1984

[Hemodynamic effects of propafenone in acute myocardial infarct].

The hemodynamic effects of Propafenon were evaluated in 11 patients with acute myocardial infarction complicated by atrial and/or ventricular arrhythmias (atrial fibrillation in 4 cases, atrial premature beats in 3 cases, ventricular premature beats Class II-IVa in 4 and rapid sustained ventricular tachycardia in one case). Drug was administered as a bolus of 1-2 mg/kg in 5 min, followed by a 10-15 gamma/kg/min infusion for 24 hours in 7 patients. Serial measurements were taken of heart rate, systemic blood pressure, right atrial, pulmonary and capillary wedge pressure, cardiac output, cardiac index, total systemic resistances, left ventricular stroke work index, left ventricular ejection time and left ventricular mean ejection rate (LVMER) (8 cases) and PEP/LVET ratio (5 cases). After the intravenous bolus, a significant reduction of cardiac index (p less than 0.01) and LVMER (p less than 0.05) parallel to an increase of total systemic resistances and PEP/LVET ratio (p less than 0.01 and p less than 0.05 respectively); was observed no other parameter varied significantly. The peak hemodynamic effect was observed after 10 minutes and return to normal required from 30 minutes to 3-6 hours in the more severely affected patients. No late negative inotropic action was evident in 6 out of 7 patients who received long term infusion. Suppression or greater than 80% reduction of premature beats was evident in 9/12 cases. Sinus node function, atrioventricular and intraventricular conduction, and the QTc interval did not vary significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Hemodynamic effects of antiarrhythmic drugs in acute myocardial infarction.

The hemodynamic effects induced by an i.v. administration of Amiodarone (5 mg/Kg in 10 min + continuous infusion of 0.6 mg/min for 4-40 hrs), Propafenone (1-2 mg/Kg in 5 min + continuous infusion of 10-15 mcg/Kg/min for 24 hrs) and Mexiletine (250 mg in 15 min + 250 mg in 1 hr) have been evaluated in patients with acute myocardial infarction complicated by sinus tachycardia and hyperdynamic pattern, ventricular or supraventricular arrhythmias. The hemodynamic serial determinations have been comprehensive of: heart rate; systolic, diastolic and mean pressure; central venous pressure; arterial and wedge pulmonary pressure; cardiac output and cardiac index; vascular systemic resistences; left ventricular stroke work index; left ventricular mean ejection rate; double and triple product. In all of the three groups we observed: a reduction of cardiac index associated with an increase of left and right ventricular filling pressure and a reduction either of left ventricular stroke work index and left ventricular mean ejection rate; these hemodynamic changes were less significant after Mexiletine than after Amiodarone or Propafenone. These data confirm the negative inotropic effect of the three drugs; anyhow, these changes are usually well tolerated by patients affected by AMI with a sufficiently preserved ventricular function. The authors, however, reccommend an accurate hemodynamic monitoring of the effects of the drugs also to identify patients with a not overt ventricular failure which may become manifest after drug administration.

Amiodarone↗
PubMed1982

[Electrophysiologic study of the intraventricular conduction disorders complicating acute myocardial infarct. Evaluation in the acute phase and follow-up].

In order to investigate the natural history and to evaluate the long-term risk of progression of the intraventricular (IV) conduction disturbances (CD) that complicate acute myocardial infarction (AMI), we prospectively followed the electrophysiological evolution of the IVCD in 47 patients admitted to our CCU in the years 1978-81 (34 anterior wall AMI, 13 inferior wall AMI; LAFB in 7, RBBB in 12, RBBB + LAFB in 13, RBBB + LPFB in 7, and LBBB in 8 cases). Only patients who acquired the IVCD after AMI and who did not develop 2 or 3 or 3 degrees degree AV blocks during the acute phase were considered. A His bundle recording (HBR) was obtained in every patient at the time of IVCD appearance. The HV interval was greater than 55 msec in 13 and less than or equal to 55 msec in 34. The study was repeated in 37 survivors after 3-20 months, mean 12. No significant change in infra His bundle conduction time was demonstrated at repeat HBR; the HV interval remained to be prolonged in all 8 patients with previously prolonged HV interval, and normal in all 29 patients with previously normal infra His bundle conduction time. The incidence of infra His bundle conduction delays was correlated with the degree of cardiac functional impairment, either during the acute phase or at follow-up. Late cardiac mortality rate was significantly higher for patients with HV prolongation during AMI (6/13 = 46%), compared to patients with normal HV interval (5/34 = 14%), (p less than 0.01). Two patients died suddenly during the follow-up period, both had had HV prolongation during AMI; all other deaths were due to reinfarction or to congestive heart failure. Our data indicate that patients who develop an IVCD, without advanced AV block, during AMI, do not exhibit late progressive deterioration of their infra His bundle conduction, whether it was normal or prolonged during AMI. The risk of late AV block seems to be negligible for patients with normal HV interval, while it cannot be overlooked in patients with prolonged HV interval during the acute phase of myocardial infarction.

Adult↗
PubMed1977

[Electrophysiological mechanisms of tachyarrhythmias associated with the sick sinus syndrome (author's transl)].

Atrail programmed stimulation (APS) and His bundle recordings were performed in 24 patients with assessed sick sinus syndrome, 14 of whom had previously suffered from bouts of spontaneous paroxysmal tachycardias (Group I) and 10 with no history of previous similar complication (Group II). APS reproduced re-entry arrhythmias in 13 cases of Group I (92%). In 6 cases, junctional reciprocating tachycardia was elicited and the atrioventricular node function curve showed a typical steplike profile, consistent with longitudinal dissociation of the node itself as a cause of reciprocation. In 7 cases with previous paroxysmal atrial tachycardias, APS elicited intra-atrial re-entry arrhythmias. Absolutely no arrhythmia was elicited by APS in the 10 cases of Group II. High incidence of basal prolongation of conduction intervals was observed in both Groups (11 cases in Group I, 6 cases in Group II). Intra-atrial and/or atrio-nodel conduction delays were recognized in all the cases with intra-atrial re-entry arrhythmias. These results suggest that so called bradycardia-tachycardia syndrome should be regarded as an independent clinical form from the sick sinus syndrome, sharing with the latter the sinusal disfunction only. Re-entry mechanisms seems to be mainly responsible for the inititation of paroxysmal tachyarrhythmias: re-entry in the atrium, based on stable conduction delays, is probably correlated with scattered lesions of the same degenerative process affecting the sinus node. On the contrary, the frequent association of sick sinus syndrome with junctional paroxysmal tachycardia and its comples dissociation mechanism of the a-v node, raises the suspicion that, in such cases, two completely different processes are merely coexisting: a degenerative lesion of the sinus node and an anatomical or functional anomaly of a separate portion of the conduction system.

Adult↗