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Biomedical subjects

E Piccolo

Publications and source records attributed to E Piccolo.

At least 55 records · Page 3Linked 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

[Electrocardiographic changes and echocardiography variations in ventricular morphology in left ventricular overload].

In order to compare the ECG patterns to several echocardiographic morphological indexes in different left ventricular overloadings, 15 cases of systolic left ventricular overloading (SLVO) and 17 cases of diastolic left ventricular overloading (DLVO) were analyzed. The current ECG changes of left ventricular hypertrophy and some original parameters of ventricular repolarization have been correlated with volumes, ejection fraction and mass of the left ventricle (calculated by Reichek's formula) and with left ventricular diastolic and systolic eccentricity indexes, derived by the application of Fishl's formula to the 2D echocardiographic four or two chamber apical view. In both SLVO and DLVO we found a correlation between the left ventricular mass and Romhilt-Estes point score system (p = 0.02) as well as the degree of ventricular repolarization abnormalities (p = 0.01). In SLVO we found a direct correlation between negative P wave deflection on lead V1 and diastolic as well as systolic eccentricity index: that is, the more negative P wave the more elongated left ventricular geometry. Moreover, in SLVO we found an interesting apposite correlation, compared with DLVO, between the systolic eccentricity index and the degree of ventricular repolarization abnormalities: in SLVO ST depression or T wave inversion on left limb or left precordial leads was associated with the maintenance of an elongated shape of left ventricle, while in DLVO the same ventricular repolarization abnormalities were associated with the loss of the elongated geometry of left ventricle which became spheric. Thus ECG correlates with echocardiographic left ventricular mass if poliparametric voltage indexes are considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1986

[Hypertrophic cardiomyopathy. Correlation between the morphologic-quantitative data of the 2-dimensional echocardiogram and electro-vectorcardiographic aspects].

39 patients affected with hypertrophic cardiomyopathy (ICM) have been studied by M-mode and two-dimensional echocardiography (1 and 2D Echo), standard electrocardiogram (ECG) and vectorcardiogram (VCG). For each patient we have outlined the anatomical shape of the left ventricle and we have tried to measure the myocardial hypertrophy by a score system that determines its size and extent. For this reason we have followed the echocardiographic segmental analysis procedure suggested by Edward (1981) but we have modified it dividing the left ventricle into 11 segments and measuring the value of the apex three times. We have given each patient a hypertrophy score by assigning a value 0 to any segment with a thickness less than or equal to 12 mm, a value 1 if the thickness was greater than 12 less than or equal to 17 mm, a value 2 if it was greater than 17 less than or equal to 22 mm, a value 3 if greater than 22 mm. We have also calculated the distribution index of the hypertrophy dividing the number of the hypertrophied segments by the number of the ventricular segments. We have identified five patterns of hypertrophic cardiomyopathy: 7 cases with a partial involvement of the interventricular septum (IVS) (pattern 1), 7 cases with a full involvement of the IVS (pattern 2), 22 cases with involvement of the free wall of the left ventricle (pattern 3), 2 cases with involvement of the distal IVS and the apex (pattern 4), 1 case with involvement of the inferior and lateral wall (pattern 5). The highest hypertrophy score and distribution index was noticed in the third anatomical pattern (p less than 0.001). Comparing the three more frequent anatomical patterns with their Ecg-Vcg aspects, we have found a higher prevalence of the left anterior hemiblock in pattern 1, of the pathological Q waves in pattern 2, of the left ventricular hypertrophy in pattern 3. However this correlation was not significant while the correlation between the Ecg-Vcg aspects and the myocardial hypertrophy score and distribution index was extremely significant (p less than 0.001). Consequently the size and distribution of the myocardial hypertrophy could differentiate the Ecg-Vcg aspects better than the anatomical shape of the left ventricle; when hypertrophy was moderate the left anterior hemiblock and the pathological Q waves were more frequent. On the contrary when hypertrophy was high and widespread the prevailing Ecg-Vcg aspect was the left ventricle hypertrophy.

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

[Post-ischemic inversion of the T wave].

The significance of new T wave inversion (so called post-ischemic T wave inversion) in the basal electrocardiogram of patients suffering from unstable angina is still controversial. Some AA suggest that the patients who develop this ecg pattern represent a subgroup with poor prognosis, particularly when to deep negative T waves (greater than 3 mm) a long QT interval is associated (giant negative T waves). On the contrary other AA suggest that there is not a different prognosis between patients which develop and which do not develop post-ischemic T waves (post-I T waves). We studied 113 patients with unstable angina: 95 patients were reviewed retrospectively (group I), 18 patients were studied perspectively (group II). In group I 63/95 developed post-I T waves (49 in anterior, 9 in inferior and 5 in both anterior and inferior leads) while 32/95 did not develop post-ischemic T waves. In group II all 18 patients developed post-ischemic T waves according to the characteristics of giant negative T waves. Follow up periods were 62 +/- 36 months in group I and 11 +/- 7 months in group II. In 61 cases (45 of group I and 16 of group II) the electrocardiogram was registered during anginal pain. ST increase and/or pseudonormalization of T wave from negative to positive, indicating transmural ischemia, was observed in 59% of patients with post-ischemic T waves vs 30% of pts without post-ischemic T waves (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1984

Diagnostic value of electrocardiogram and vectorcardiogram in postinfarction ventricular asynergy.

The ability of ECG-VCG to predict the severity of postinfarction LV asynergy was evaluated in 152 patients with previous myocardial infarction who underwent left cineventriculography in the right anterior oblique view. Various ECG and VCG signs were examined in order to predict the existence of severe asynergy in general (dyskinesia or akinesia or severe hypokinesia) and of dyskinesia in particular. In patients with inferior myocardial infarction (Group A) persistent ST segment elevation was the only specific ECG sign (100%) of severe asynergy; it had a poor sensitivity (6.2%). Four frontal VCG signs (presence of terminal bite, y- greater than 0.18 mV, maximum early superior vector along x axis = MESV greater than or equal to 1.3 mV, duration of initial superior forces = DISF greater than 50 msec) increased the sensitivity of the ECG-VCG method to 75.8% while maintaining a 100% specificity. Regarding the diagnosis of dyskinesia, only the ECG sign of persistent ST segment elevation and the VCG sign of y- greater than or equal to 0.3 mV had a 100% specificity. The sensitivity of the ECG-VCG method was 33.3% (16.6% ECG and 16.6% VCG). In patients with anterior myocardial infarction (Group B), concerning the diagnosis of severe asynergy, the ECG signs of sigma ST greater than 3 mm in anterior leads; pathologic Q wave in four or more anterior leads (including D1 and aVL); and the presence of LAH or LAH + RBBB, had a 100% specificity and a good sensitivity (60.5%). The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 71% while maintaining a 100% specificity. As for the diagnosis of dyskinesia, the ECG signs with a 100% specificity were sigma ST greater than or equal to 5 mm in anterior leads, a pathologic Q wave in more than five anterior leads (including I and a VL) and RBBB + LAH; these variables had a sensitivity of 48.3%. The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 79.3% while maintaining a 100% specificity. In patients with inferior plus anterior myocardial infarction (Group A + B) the signs mentioned above for each group were evaluated, confirming a 100% specificity. Regarding the diagnosis of severe asynergy, the ECG signs had a sensitivity of 61.3%, while VCG increased the sensitivity of the ECG-VCG method to 90.3%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
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↗