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Biomedical subjects

A Raviele

Publications and source records attributed to A Raviele.

At least 73 records · Page 4Linked to original sources
PubMed1987

[Different degrees of risk of high-frequency atrial fibrillation in symptomatic and asymptomatic WPW syndrome. Electrophysiologic evaluation].

Sudden death in WPW pattern can occur when atrial fibrillation (a.f.) with rapid ventricular response develops. This event seems to be the final result of three concomitant conditions: the appearance of an orthodromic atrio-ventricular reciprocating tachycardia, the most common form of tachycardia in these patients; a high atrial vulnerability, which makes possible that reciprocating tachycardia degenerates into atrial fibrillation and a short anterograde refractory period of the Kent bundle. With the purpose of evaluating the risk to develop high frequency a.f., 36 WPW subjects were electrophysiologically studied. 22 were symptomatic for palpitations (Group I) and 14 were totally asymptomatic (Group II). 3/22 patients of Group I had experienced clinical atrial fibrillation (Subgroup I A), which was never documented in the remaining 19/22 (Subgroup I B). In all cases the following parameters were analyzed: the presence or absence of the retrograde conduction of the anomalous pathway, essential for the occurrence of orthodromic reciprocating atrio-ventricular tachycardia; the presence or absence of a high atrial vulnerability and the presence of RR intervals between pre-excited complexes during induced a.f. less than 250 msec. As an index of atrial vulnerability were considered the spontaneous degeneration into atrial fibrillation of an electrophysiologically induced reciprocating tachycardia and/or the induction of a sustained a.f. by programmed right atrial stimulation during sinus rhythm and/or during 600 and 400 ms atrial driving and/or by 160-250/m' atrial bursts. Results--Retrograde conduction of Kent bundle was documented in 100% of Gr. I vs 22% of Gr. II (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Value of serial electropharmacologic tests in the treatment of sustained ventricular arrhythmias].

The value of electropharmacological testing in patients (pts) with sustained ventricular tachyarrhythmias was studied in 46 consecutive pts (24 with sustained ventricular tachycardia (SVT) and 22 with cardiac arrest due to a ventricular tachyarrhythmia. Forty-two pts underwent a baseline electrophysiological study. The ventricular stimulation protocol included up to 3 extrastimuli during spontaneous rhythm and during paced ventricular rhythm at 100/min, 130/min, 160/min and brief bursts pacing at 2 ventricular sites. Ventricular tachycardia was induced in 37/42 pts (88%) (sustained in 32 pts and non sustained in 5 pts). Twenty nine pts underwent 79 trials of different drug regimens (mean 2.72 per pt, range 1-8). A totally successful drug regimen was found in 15/29 pts (51.7%) and a partially successful drug regimen in 11/29 pts (37.9%). Twenty-three pts were discharged on a drug regimen successful during serial electropharmacological testing (Group I) and 23 pts were discharged on an empiric drug regimen (Group II). Each pt was followed-up for a mean period of 15 months (range 1-74). Group I pts had fewer arrhythmia recurrence (SVT and/or sudden death) than Group II pts (2/23 vs 13/23 p less than 0.01). In conclusion electropharmacological testing is an useful tool in the therapy of pts with sustained ventricular tachyarrhythmias.

Adolescent↗
PubMed1985

[Idiopathic ventricular tachycardia responsive to verapamil. Presentation of 3 cases and review of the literature].

Recently a unique clinical entity has been suggested in subjects without apparent heart disease presenting with recurrent ventricular tachycardia (VT) characterized by RBBB + LAH electrocardiographic pattern, relatively slow rate, induction by atrial stimulation, and interruption by verapamil. According to these characteristics, three cases (2 M and 1 F, aged 18, 33 and 66 years) are presented in this study. They have had palpitations from one to twenty years, but not syncopal episodes. During VT the cycle length ranged from 300 to 480 msec. VT was terminated both by verapamil and by ajmaline. VT was inducible in 3/3 cases by incremental atrial pacing when cycle length of pacing became similar to that of spontaneous VT; in 2/3 cases VT was induced by programmed right atrial stimulation and in 2/3 cases by programmed ventricular stimulation. Serial electrophysiological studies for pharmacological and therapeutic evaluation applied to 1/3 cases showed: amiodarone given orally (200 mg/die) for two months prevented the induction of VT while verapamil, propranolol, mexiletine, and propafenone tested intravenously were ineffective. In the remaining two patients amiodarone, tested only intravenously, was not effective to prevent the induction of VT but lengthened its cycle length. All patients received amiodarone orally (200 mg/die) and were followed for 2,7 and 8 years respectively. Two of them had no more episodes of VT and one, while asymptomatic, continued to present with. The electrophysiological mechanism of this form of VT cannot be identified with certainty, but many data suggest a reentry in the posterior fascicle of left bundle branch as the most probable mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

[Predictive value of the ajmaline test in dysfunction of the sinus node. Prospective 4-year follow-up relative to 77 patients].

To establish the usefulness of Ajmaline test for the evaluation of sinus node function, 77 pts (47 M, 30 F, mean age +/- SD = 61 +/- 15 yrs) first underwent an electrophysiologic study and then were followed-up for a mean period of 46.3 months. The following parameters were determined before and after i.v. administration of Ajmaline (1 mg/kg in 1 minute): sinus cycle length (SCL), corrected sinus node recovery time (CSNRT) and sino-atrial conduction time (SACT). The pts were divided into 3 groups: Group A: 10 pts without clinical or electrocardiographic signs of sinus node dysfunction (SND) and with normal control CSNRT and SACT (less than or equal to 500 and less than or equal to 120 msec, respectively); Group B: 46 pts with clinical-electrocardiographic signs of suspected or apparently not severe SND (sinus bradycardia greater than or equal to 40 beats/min and/or syncopes with positive vagal manoeuvres) and/or slightly abnormal control CSNRT (greater than 500 less than or equal to 600 msec) and/or SACT (greater than 120 less than or equal to 150 msec); Group C: 21 pts with clinical-electrocardiographic signs of apparently severe SND (sinus bradycardia less than or equal to 39 beats/min, sino-atrial block, sinus arrest) and/or definitely prolonged control CSNRT and/or SACT (greater than 600 and greater than 150 msec, respectively). The Ajmaline test was considered negative for the presence of a severe SND if SCL was not prolonged after the administration of the drug more than 20% and CSNRT and SACT were not prolonged more than 50% compared to the control values. Otherwise the Ajmaline test was considered positive. Twenty-seven out of the 77 pts studied underwent permanent pacemaker implantation (23 immediately after the electrophysiologic study and 4 during the follow-up). The following results were obtained: the Ajmaline test was negative in 100% of group A, 87% of group B and 48% of group C pts and positive in 0% of group A, 13% of group B and 52% of group C pts; during the follow-up a negative test resulted predictive in 56 out of 60 pts (92%) and a positive test in 16 out of 17 pts (94%). The predictive accuracy of the test was, therefore, 93.5%. These results indicate that Ajmaline test is an useful provocative test for disclosing, during electrophysiologic studies, pts who have severe SND and for selecting those who need pacemaker implantation.

Adolescent↗
PubMed1984

Value of serial electropharmacological testing in managing patients resuscitated from cardiac arrest.

Electrophysiologic studies were performed in 11 patients (9 men, 2 women; mean age: 59.9 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose of the studies was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. Ten of the patients were suffering from chronic ischemic heart disease with one or more previous myocardial infarctions while one had no evidence of structural heart disease. A ventricular aneurysm was present in four of them. During control electrophysiologic study, a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths plus bursts of rapid ventricular pacing) in nine of the ten patients (90%) who were studied while not receiving antiarrhythmic drugs; a non-sustained VT was induced in one of them (10%). In three patients (30%) VT could be initiated only by right ventricular stimulation at a side different from the apex (outflow tract). No arrhythmia was observed in the only patient who was studied while taking amiodarone orally (400 mg/day for more than three months). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in seven of the ten patients (70%) who underwent this procedure and a partially effective drug regimen (a sustained VT was no longer inducible; it was easier to interrupt and it was considerably slower) was found in two patients (20%). None of the nine patients who received chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14 months (range: 3-28) and only one had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of follow-up. These results indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest.

Adrenergic beta-Antagonists↗
PubMed1984

[Intrinsic function of the sinus node in patients with syncope and positive vagal maneuvers].

This study was undertaken to establish the nature (intrinsic or extrinsic) of sinus node dysfunction in patients presenting with syncope and abnormal response (sinus pause greater than 3'') to vagal manoeuvres (carotid sinus massage and/or eye-ball compression). To this purpose 29 patients (20 males, 9 females, aged 18-79 yrs, mean = 60) underwent an electrophysiologic study. In all we measured before and after autonomic blockade with Propranolol (0.2 mg/kg) and Atropine sulfate (0.04 mg/kg) the following parameters: sinus rate, corrected sinus node recovery time and sino-atrial conduction time. According to the presence or absence of electrocardiographic signs of sinus node dysfunction the patients were divided into three groups: Group A: 11 patients without electrocardiographic signs of sinus node dysfunction; Group B: 13 patients with borderline electrocardiographic signs of sinus node dysfunction (sinus bradycardia between 40 and 60 beats/min); Group C: 5 patients with definite electrocardiographic signs of sinus node dysfunction (sinus bradycardia less than or equal to 39 beats/min and/or sinoatrial block and/or sinus arrest). Fifteen patients (52%) had signs of organic heart disease. The main results obtained were: At least one electrophysiological test (sinus rate, corrected sinus node recovery time or sino-atrial conduction time) was abnormal in 10 patients (34,5%) before autonomic blockade and in 8 patients (27%) after autonomic blockade. Two of these 8 patients belonged to Group A (18%), 1 to Group B (8%) and 5 to Group C (100%). Six of these 8 patients were suffering from an organic heart disease and 2 were not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

[Value of a serial electropharmacologic study in survivors of a cardiac arrest secondary to ventricular tachycardia or ventricular fibrillation].

Electrophysiologic studies were performed in 10 patients (8 M, 2 F, mean age: 60.2 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. The cardiac arrest had always been sudden and unexpected. It occurred outside the hospital in 7 cases and in the hospital in 3 cases. Patients in whom cardiac arrest was associated with evidence of acute myocardial infarction were excluded from the study. Nine of the patients were suffering from chronic ischemic heart disease with 1 or more previous myocardial infarctions while 1 had no evidence of organic heart disease. A ventricular aneurysm was present in 4 of them. During control electrophysiologic study a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths + bursts of rapid ventricular pacing) in 9 of the 10 patients (90%) and a non sustained VT was induced in 1 of them (10%). In 3 patients (30%) VT could be initiated only by right ventricular stimulation at a site different from the apex (outflow tract). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in 6 of the 9 patients (66.7%) who underwent this procedure and a partially effective drug regimen (sustained VT no longer inducible, easier to interrupt and considerably slower) was found in 2 patients (22.2%). None of the patients who received a chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14.8 months (range: 3-29) and only 1 had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of the follow-up. It is also noteworthy that amiodarone, alone or in combination, was given chronically to 6 of our patients (60%). These results 1) indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest, and 2) suggest that amiodarone may be effective in preventing sudden death in these patients.

Adult↗
PubMed1984

Mid-diastolic intraventricular functional block. A new mechanism for intermittent intraventricular blocks?

Experimental and clinical studies have demonstrated the existence of phase 3 and phase 4 functional blocks. In this report six cases are presented in which the electrophysiological study demonstrated the existence of a functional intraventricular block different from phase 3 and phase 4 blocks. In these cases the occurrence of the block was related to the presence in mid-diastole of a zone of block preceded and followed by intervals of unimpaired conduction. In two of 6 cases the functional block (infrahisian block) was not present in the basal tracing; it occurred during programmed atrial stimulation in a range of critical H1H2 coupling intervals delivered late in diastole, and did not appear after earlier stimuli. In the remaining four cases the conduction disturbance (2 RBBB, 2 infrahisian blocks) was present in the basal tracing, but disappeared both during early and late supraventricular extrastimuli, the first having short H1H2 intervals, the latter having H1H2 intervals longer than H1H1 basal cycle length. The width of the mid-diastolic zone of block varied from a few msec to hundreds of sec, and increased as heart rate increased. Two hypotheses are put forward in order to explain the electrophysiological mechanism responsible for the phenomenon: 1) a longitudinal dissociation in the conducting system, generating two different ways, one having a long refractory period, the other having a phase 4 spontaneous depolarization; they would be responsible of phase 3 and phase 4 blocks respectively. The early and late zones of conduction could be explained by an alternate conduction in one of the two ways, while the mid-diastolic zone of block could be due to a simultaneous block in both ways; 2) the existence of a diastolic oscillatory potential (late after-depolarization). In the latter case we can suppose that the mid-diastolic block was due to the stimulation of the cells of the conducting system before the restoration of the normal diastolic potential. Our electrophysiological data offer a new contribution to the understanding of intermittent intraventricular blocks. However further experimental and clinical studies are needed to confirm our electrophysiological hypotheses.

Adult↗
PubMed1983

Possible role of a ventricular conduction disturbance in the electrogenesis of the ECG-VCG signs of myocardial infarction.

The typical QRS patterns of myocardial infarction (MI-QRS) are commonly attributed to myocardial cellular death. However, observation of a transient appearance of MI-QRS during coronary insufficiency, the disappearance of MI-QRS after coronary by-pass surgery and the appearance of MI-QRS after intracranial hemorrhage suggest that a different electrophysiological mechanism may be at work. There is a single convincing explanation for all these observations. It seems possible, at least theoretically, that a localized conduction disturbance can generate or contribute to the generation of the MI-QRS. The results obtained in nine out of 194 cases studied by means of premature right atrial stimulation (PRAS) in our laboratory seem to confirm this hypothesis. In five of them we observed typical MI-QRS in the aberrant beats which were absent in the basal tracings. In the other four cases, MI-QRS which were present in basal tracings disappeared in the aberrant beats. In three of these a reduction in the duration of QRS was also observed, while in the fourth the duration of QRS did not change. In no case could the alterations of QRS (induction or disappearance of MI-QRS) be explained by a classical conduction disturbance, preexcitation or by a premature ventricular beat. While the induction of MI-QRS was clearly due to an aberrant conduction in the supraventricular beats, the disappearance of basal MI-QRS changes in premature supraventricular beats is more difficult to explain. One possible electrophysiological mechanism could be a supernormal phase conduction. If this is the case, the basal MI-QRS could be due to a ventricular conduction disturbance. In conclusion, our results suggest that MI-QRS can be generated, at least in our cases, by a localized conduction disturbance.

Adult↗
PubMed1983

[Clinical and prognostic significance of hyperkinetic ventricular arrhythmias].

Ventricular arrhythmias, mainly ventricular premature beats (VPBs) are omnipresent in the general population. They may be detected or induced by means of different techniques such as routine ECG, ambulatory ECG-monitoring, exercise testing and ventricular stimulation during an intracavitary electrophysiologic study. The prevalence and clinical-prognostic significance of VPBs are highly related to the presence and severity of an underlying heart disease. Simple and complex (bigeminal, multiform, repetitive or R on T) VPBs are much more frequent in cardiac patients than in normal subjects. Acute myocardial infarction (AMI), chronic coronary heart disease (CCHD), cardiomyopathies and mitral valve prolapse are the most common clinical conditions in which VPBs occur. In apparently healthy persons, the presence of VPBs does not seem to indicate a greater risk for the future development of cardiac disease. In patients with AMI frequent, and complex VPBs often precede primary ventricular fibrillation and appear to be directly related to the size of the infarct. In the posthospital phase of AMI, as well as in CCHD, the occurrence of high-grade VPBs usually indicates more advanced degrees of both coronary and left ventricular disease as well as the possibility of cardiac and/or sudden death. In cardiomyopathies and mitral valve prolapse the VPBs do not correlate with either clinical, electrocardiographic, echocardiographic or hemodynamic parameters but their complex patterns appear to be a good indicator of patients with high sudden death risk.

Adolescent↗
PubMed1982

[Clinical significance of corrected sinus node recovery time and natural and unnatural history of sinus node dysfunctions. A four-year prospective follow-up of 101 cases].

The clinical significance of corrected sinus node recovery time (CSNRT) and the natural and unnatural history of sinus node dysfunctions are not completely known. To gain some insight into this problem, 101 patients (pts) (54M, 47F, mean age +/- SD = 62.02 yrs +/- 14.42) with clinical and ECG signs of definite or suspected sick sinus syndrome (SSS) underwent an electrophysiologic study and then were prospectively followed for a mean period of 44.36 months +/- 18.96 (range: 2-78 months). The pts were divided into two groups: 1) Group A: 68 pts with prolonged CSNRT (greater than 500 msec); 2) Group B: 33 pts with normal CSNRT. Thirty-three pts of Group A (48.5%) and 2 pts of Group B (6.1%) received VVI pacemaker implantation (PM) immediately after the electrophysiologic study. The following results were obtained: 1) Pts of Group A showed a higher prevalence of organic heart disease and of ECG signs of definite SSS than pts of Group B. (p less than 0.05). Moreover, the higher the CSNRT in Group A pts, the more severe the ECG abnormalities of SSS. 2) Pts without PM, both of Group A and Group B, noted during the follow-up period a disappearance of neurological symptoms (syncopes and/or dizziness) and of ECG abnormalities of SSS in more than 50% of the cases. However, this was less evident in Group A pts compared with Group B pts (53.8% vs 78.6% regarding neurological symptoms and 54.3% vs 74.1% regarding ECG abnormalities of SSS) as well as in pts with organic heart disease in comparison with those with primitive SSS. Moreover, the number of pts who needed PM implantation during the follow-up period due to the worsening of clinical and ECG signs of SSS were higher in Group A than in Group B (20% vs 6.5%). The occurrence of cardiac death among the pts without PM was similar in pts of Group A (8.5%) and in those of Group B (9.7%). One pt of Group A without PM died suddenly (less than 1 hour). 3) Pts who required PM implantation were older (p less than 0.01) and showed a prevalence of organic heart disease higher (p less than 0.05) than those who did not require PM implantation. Pts with PM, both of Group A and Group B, showed a complete disappearance of syncopes and a clear-cut reduction of dizziness after implantation of it. On the contrary, dyspnea nearly always persisted and sometimes appeared when initially absent. Sudden and non-sudden cardiac death in PM pts (13.6%) was somewhat more frequent than in those without PM. 4) The incidence of stable atrial fibrillation was 12.1% in pts without PM and 27.2% in pts with PM. The occurrence of stable atrial fibrillation in pts without PM was generally not followed by clinical improvement. 5) The incidence of cerebrovascular accidents was approximately 8%. The accidents always occurred in pts with organic heart disease and often in the older pts (mean age: 75.1 yrs +/- 5.7) particularly in those with PM. A bradycardia-tachycardia syndrome was observed only in 3 pts who had a stroke...

Cardiac Pacing, Artificial↗