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Biomedical subjects

P Delise

Publications and source records attributed to P Delise.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Electrophysiological mechanisms of atrial tachyarrhythmia].

Both supraventricular and ventricular arrhythmias are generated by one of the following 2 mechanisms: increased automaticity and reentry. In this paper we will refer about the mechanisms of the commonest atrial tachyarrhythmias. Atrial parasystole: it is determined by an automatic focus protected by entrance block. In some cases the focus is only partially protected owing to a partial block or to the electrotonic influence of the sinus rhythm. Atrial tachycardia: it can be due both to increased automaticity and to reentry. Atrial flutter: it is generated by a counterclockwise macroreentry localized in the right atrium. The left atrium is passively activated. A critical delay of the circuit is present near the ostium of the coronary sinus. The lesion of this area by surgery or catheter ablation can interrupt and prevent the arrhythmia. Atrial fibrillation: it is generated by multiple wavelets which continuously change site and direction. The functional multiple reentry is made possible by dispersion of atrial refractoriness and by the existence of areas having delayed conduction. It is noteworthy that the same arrhythmia and the same atrial electrophysiologic alterations are present in many clinical conditions having very different anatomic backgrounds: subjects with no evident heart disease and normal atria, subjects with large atria, subjects with an anomalous pathway. These data suggest that some important informations are probably lacking about the genesis of this arrhythmia.

Atrial Fibrillation↗
PubMed1991

[The Wolff-Parkinson-White syndrome at risk].

Wolff-Parkinson-White (WPW) syndrome is characterized by a wide spectrum of clinical conditions: many subjects remain symptom free during the whole life, others suffer from paroxysmal episodes of reciprocating atrioventricular tachycardia, a minority of patients present with episodes of atrial fibrillation. The latter is the most dreadful arrhythmia because in the presence of a short refractory period of the Kent bundle it can produce very high ventricular rates, degenerate into ventricular fibrillation and cause sudden death. Sudden death however is very rare in the WPW syndrome. In 1988 the European registry on "sudden death in the WPW syndrome" collected 26 cases of various centres. This study demonstrated that sudden death occurs in 73% of cases in symptomatic subjects while in the remaining 27% it is an unexpected event in previously asymptomatic subjects. While sudden death is very rare, high frequency atrial fibrillation producing hemodynamic deterioration is not so rare, although its precise incidence is unknown. In hospitalized WPW patients it is reported in 10-30% of cases. One of the main problems in symptomatic and asymptomatic patients with the WPW pattern is to identify the subjects at risk of high frequency arrhythmias. Many Authors suggested that endocavitary or transesophageal electrophysiologic study can be useful in this regard if its results are evaluated by a multiparametric approach. In our opinion the main parameters to be evaluated are: presence or absence of retrograde conduction of the Kent bundle (which is necessary for the initiation of atrioventricular reciprocating tachycardia which is the commonest trigger of atrial fibrillation); atrial vulnerability; shortest and mean RR intervals during induced atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Supraventricular paroxysmal reentry tachycardia. Empirical and guided therapy].

The empirical therapy of reentrant supraventricular tachycardias (A-V and junctional tachycardia) is based on a preliminary diagnosis through standard ECG to evaluate, whenever possible, the relationship between P wave and QRS. In order to distinguish atrial tachycardias from other types, we must employ vagal manoeuvres or drugs. Often we use methods of recording and stimulation such as Holter monitoring and transesophageal technique which can provide useful information about the electrophysiological mechanisms and therefore can better guide our choice of drugs. The decision of undertaking pharmacologic treatment takes into account frequency, duration and tolerability of the crises and the patient's compliance. The most commonly used drugs are verapamil, diltiazem, propafenone, flecainide, sotalol and amiodarone. The percentage of success at 1 year ranges from 30 to 60%. Particularly in the Wolff-Parkinson-White (WPW) therapy must follow an accurate evaluation of the electrophysiological pattern through effort test, drugs test, transesophageal (ETS) or endocavitary (EPS) electrophysiological study. Indeed therapy aims not only at reducing arrhythmic relapses, but also preventing the potential risk of either death or severe damage. The useful drugs must have the property of acting at the same time upon at least one branch of the A-V circuit, on the atrium reducing its vulnerability and finally modifying the conductive anterograde capacity of the Kent bundle. They are quinidine, procainamide, propafenone (group I) sotalol and amiodarone (group III). The limitations of the empirical therapy are a high percentage of relapses and the difficulty in foreseeing the pro-arrhythmic effects. The guided by serial electrophysiologic testing implies artificial induction of spontaneous arrhythmia by repeating the test after acute or chronic assumption of drugs. Is this way it can be evaluated the efficacy as well as the tolerability of an antiarrhythmic drug which later will be taken for chronic prophylaxis. The percentage of inducibility of clinical arrhythmias is next to 100% both for EPS and TES. The number of patients for whom we can find an effective pharmacologic regimen through acute testing ranges from 30 to 100%, but is influenced by several factors such as aggressiveness of therapeutic protocol and type and dosage of drugs. The predictive value is high as it approaches 100% for a positive acute test. The elective indications for serial electrophysiologic study are: failure of empirical therapy; disabling and very frequent arrhythmias; arrhythmias provoking major disturbances (lipothymia, syncope, hypotension, shock); symptomatic WPW.

Anti-Arrhythmia Agents↗
PubMed1991

[Treatment of malignant ventricular tachyarrhythmia with amiodarone: comparison of empirical administration and administration guided by Holter or ventricular stimulation. Results of the parallel test].

To assess the most appropriate method of administering amiodarone and predicting its efficacy (empiric vs guided by Holter or by ventricular stimulation), 19 patients with sustained ventricular tachycardia or ventricular fibrillation underwent a "parallel study". Fifteen patients were men and 4 women, with a mean age of 65 years. A coronary artery disease with previous myocardial infarction was present in 15 patients, dilated cardiomyopathy in 3 and arrhythmogenic right ventricular dysplasia in 1 (mean left ventricular ejection fraction = 35%). All 19 patients had, as inclusion criteria, 1) frequent (greater than or equal to 30/hour) and/or repetitive (greater than or equal to 10/24 hours) ventricular premature beats during 24-hour Holter monitoring and 2) inducible sustained (greater than 30/sec) ventricular arrhythmias during programmed ventricular stimulation (1-3 extrastimuli from 2 right ventricular sites). Amiodarone was given at an initial dosage of 15 mg/kg/day for 2 weeks and then at a dosage of 5 mg/kg/day. After 15 days 24-hour Holter monitoring and programmed ventricular stimulation were repeated. The data of these tests, however, were not used to guide the therapy that remained empiric, but served only to assess retrospectively the predictive value of Holter monitoring and ventricular stimulation. The following main results were obtained: The mean duration of follow-up was 25 +/- 13 months. During this period 6 patients (32%) died, 3 from sudden and 3 from non-sudden cardiac death. Two other patients had recurrence of sustained ventricular arrhythmias. After 15 days of therapy amiodarone was effective at Holter monitoring in 15 patients (79%) and not effective in 4 (21%). Two of the 15 patients considered responders died suddenly during the follow-up and 2 had arrhythmic recurrence, vs 1 of the 4 non-responder patients who died suddenly (negative predictive value of Holter monitoring: 73%; positive predictive value: 25%; predictive accuracy: 63%). After 15 days of therapy amiodarone was effective at ventricular stimulation in 10 patients (53%) and not effective in 9 (47%). None of the 10 patients considered responders had arrhythmic events during the follow-up, vs 5 of the 9 non-responders, 3 of whom died suddenly and 2 of whom had arrhythmic recurrences (negative predictive value of ventricular stimulation: 100%; positive predictive value: 56%; predictive accuracy: 79%). Only 1 patient discontinued amiodarone after 25 months of follow-up because of development of an important blue-grey skin discoloration.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study.

The vasovagal nature of syncope, which remained unexplained despite full clinical and electrophysiologic investigation, was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (17 men and 13 women, mean age 65 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5) episodes of syncope of unknown origin were studied. Head-up tilt test was considered positive if syncope developed in association with hypotension, bradycardia, or both. During baseline head-up tilt 15 patients (50%) had a positive response. Ten patients had a vasodepressor response (marked hypotension without marked bradycardia) and 5 had a mixed response (marked hypotension with marked bradycardia). None of 8 control subjects became symptomatic during the test. Baseline head-up tilt test was positively reproducible in 10 of 14 patients (71%). Nine of these 10 patients underwent serial head-up tilt tests after drug administration to determine the pathogenesis of vasovagal syncope. Atropine prevented tilt-induced syncope in 3 of 8 patients (37.5%), propranolol in 2 of 8 (25%) and etilephrine in 7 of 7 (100%). Seven patients received long-term drug treatment with drugs selected on the basis of acute drug testing. One responder to atropine received transdermal scopolamine and 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 12 months. Head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vasovagal reaction in patients with syncope of unknown origin. Withdrawal of alpha-sympathetic stimulation is a principal mechanism responsible for vasodilation and syncope during head-up tilt.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1990

Electrogenesis of the S1S2S3 electrocardiographic pattern. A study in humans based on body surface potential and right ventricular endocardial mapping.

To study the electrogenesis of the S1S2S3 pattern, seven patients had body surface potential mapping and endocardial mapping of inflow tract, outflow tract, and apex of the right ventricle. QRS duration was longer in S1S2S3 versus controls (94 +/- 14 vs. 84 +/- 14 msec). Surface mapping was similar in S1S2S3 patients and in controls during the first 30-40 msec of QRS, but S1S2S3 patients subsequently presented the following differences: (1) earlier time of onset (34 +/- 3 vs. 44 +/- 6 msec) and a lower voltage (1,242 +/- 468 vs. 1,649 +/- 31 mV) of peak positive anterior maximum; (2) earlier dorsal migration (45 +/- 3 vs. 55 +/- 7 msec) of the maximum; (3) a second peak positive maximum at 58 +/- 3 msec, located on the dorsal spine; (4) the appearance of a right subclavicular positive area at 51 +/- 6 msec, which in controls was absent or appeared later (66 +/- 7 msec). At the end of QRS, the maximum was located in all but two S1S2S3 cases on the upper sternum. Right ventricular endocardial mapping showed a similar activation time of the apex in S1S2S3 patients and controls, but in the former a significant inflow (56 +/- 21 vs. 36 +/- 9 msec) and outflow tract (79 +/- 13 vs. 39 +/- 8 msec) activation delay was documented. The data obtained using body surface potential mapping suggest that an anomalous wavefront rightward and superiorly oriented is present in the S1S2S3 pattern, which is able to oppose the electrical forces of ventricular free walls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Syncope of undetermined nature after electrophysiologic study. Usefulness of the head-up tilt test in the diagnosis of vaso-vagal origin and in the choice of treatment].

The vaso-vagal nature of syncopes which remained unexplained despite full clinical and electrophysiological investigation was evaluated by means of 60 degrees head-up tilt test for 60 minutes. Thirty patients (16 men and 14 women, mean age 63.6 years, 19 with and 11 without organic heart disease) with 1 to 28 (mean 5.1) episodes of syncope of unknown origin were studied together with 11 asymptomatic control subjects. Head-up tilt test was considered positive if syncope developed in association with hypotension and/or bradycardia. During baseline head-up tilt 15 patients (50%) showed a positive test, with vasodepressor response (marked hypotension without marked bradycardia) in 10 cases and with mixed response (marked hypotension with marked bradycardia) in 5 cases. None of the control subjects became symptomatic during the test. Mean time to syncope was 24.9 minutes. Baseline head-up tilt test was reproducibly positive in 10 out of 14 patients (71%). Eight of these 10 patients underwent serial head-up tilt tests after atropine (0.04 mg/Kg i.v. in 1 minute), propranolol (0.2 mg/Kg i.v. in 3 minutes) and etilefrin (15-30 mg/day orally for 2-3 days) to determine the pathogenesis of vaso-vagal syncope. Atropine prevented tilt-induced syncope in 3 out of 7 patients (43%), propranolol in 2 out of 7 (29%) and etilephrine in 6 out of 6 (100%). Seven patients were chronically treated with drugs selected on the basis of acute drug testing. One patient-responder to atropine received transdermal scopolamine and the other 6 received etilephrine. None of these 7 patients had syncopal recurrences or death during a mean follow-up of 7.7 months, except 1 who experienced another episode of syncope after having discontinued etilephrine 4 months before. These results suggest that: 1) head-up tilt is a very sensitive and highly specific test to unmask susceptibility to vaso-vagal reaction in patients with syncope of unknown origin; 2) withdrawal of alpha-sympathetic stimulation is the principal mechanism responsible for vasodilation and syncope during head-up tilt; 3) alpha-sympathomimetic agents, such as etilephrine, are effective in preventing spontaneous episodes of vaso-vagal syncope during a short-term follow-up.

Adolescent↗
PubMed1990

[Empiric treatment with amiodarone in patients with sustained ventricular tachyarrhythmia. Results of a long-term follow-up].

The long-term follow-up of 52 pts (36 M, 16 F, mean age: 62 years) with sustained ventricular tachyarrhythmias (SVT) was analyzed to assess the efficacy and feasibility of empiric amiodarone treatment. Forty-five pts had organic heart disease (mean EF: 38.3%) and 7 pts no overt heart disease. Twenty pts suffered from syncope or cardiac arrest secondary to sustained ventricular tachyarrhythmias (mean: 2.35 episodes) and 32 did not. All pts were given amiodarone empirically (mean dose: 390 mg) and followed-up for a mean period of 29.5 months (range 1-137). Two pts (3.8%) died of non cardiac causes, 5 (9.6%) of non sudden cardiac death and 7 (13.4%) of sudden death. Fifteen pts (28.8%) experienced non fatal arrhythmic recurrences. Four out of 7 pts who died suddenly experienced non fatal arrhythmic recurrence before death. The actuarial incidence of cardiac death was 10.8, 22.7, 31.5, 31.5% at 1, 2, 3 and 5 years; the actuarial incidence of sudden death was 8.9, 12, 22.1, 22.1% at 1, 2, 3 and 5 years; the actuarial incidence of non fatal arrhythmic recurrences was 17.4, 26.3, 26.3, 26.3, 44.7% at 1, 2, 3, 4 and 5 years. Univariate analysis identified recent myocardial infarction, NYHA functional class, detection of frequent and/or repetitive premature ventricular contractions on Holter monitoring and non fatal arrhythmic recurrences as predictors of cardiac death (p less than 0.05), while only non fatal arrhythmic recurrences were associated with sudden death (p less than 0.05). Twenty-two pts (42.3%) developed side effects. Nine (17.3%) discontinued amiodarone: 6 pts (11.5%) because of side effects and 3 inadvertently.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Idionodal reciprocal tachycardia irresponsive to pharmacological prophylaxis. Description of a case successfully treated with radio frequency].

The case of a 63-year old female suffering from recurrent paroxysmal supraventricular tachycardia for 30 years is reported. In the past she was treated unsuccessfully with multiple drugs. Electrophysiological study showed dual nodal pathways and the inducibility of a junctional reciprocating tachycardia with RR and V-A intervals respectively 360-410 and 40 msec. Radiofrequency was applied for 30" in the nodal region during induced reciprocating tachycardia. The arrhythmia was interrupted after a few seconds and a 1st degree A-V block persisted for a few minutes. Repeated electrophysiological studies were performed 30 minutes and 20 days after the ablating procedure. They showed a slight increase in AH interval from 55 msec to 90 and 65 msec respectively, as well as the persistence of anterograde dual nodal pathways and the disappearance of retrograde conduction of the A-V node. No reentry arrhythmia could be induced. After six months the patient is asymptomatic and drug free.

Electrocardiography↗
PubMed1990

[Clinical and prognostic value of evaluation of atrial vulnerability in an electrophysiological endocavitary and transesophageal study].

UNLABELLED: Atrial fibrillation or flutter is frequently inducible during endocavitary or transesophageal electrophysiologic study. However, its clinic and prognostic significance has not yet been clarified. We studied 443 patients: 276 underwent endocavitary electrophysiologic study, 228 underwent transesophageal electrophysiologic study and 61 underwent both methods. In 343 of them a satisfactory echocardiogram was obtained. Patients were divided in three groups: gr. I, 93 patients with documented episodes of paroxysmal atrial fibrillation or flutter; gr. II, 257 patients with or without heart disease without clinical atrial fibrillation or flutter; gr. III, 93 symptomatic or asymptomatic Wolff-Parkinson-White patients without clinical atrial fibrillation or flutter. Gr. I included patients without overt heart disease (20), with WPW (11), mitral valve prolapse (4), and miscellaneous (58). Gr. II included patients without overt heart disease (49), with concealed Kent bundles (7), Mahaim (1) or James fibers (1) mitral valve prolapse (6), sick sinus syndrome (40), miscellaneous (91), or syncope of an unknown origin (62). Atrial vulnerability was evaluated both by endocavitary and transesophageal electrophysiologic study using two different protocols; the first protocol was moderately aggressive (prot. A), while the second was aggressive (prot. B). Endocavitary electrophysiologic study. Prot. A: single and double extrastimuli at the three heart rates (sinus, 100 and 150/m'), 10/m' incremental atrial pacing from 160 to 250/m; prot. B: prot. A + incremental atrial pacing from 260/m' up to 2:1 St-A block. Transesophageal electrophysiologic study. Prot. A: 10" atrial burst at 100-600/m' prot. B: prot. A + 6-9" increasing rate bursts from 200 to 800/m'. End point of all protocols: initiation of greater than 1' atrial fibrillation or atrial flutter. RESULTS: Endocavitary electrophysiologic study. A greater than 1' atrial fibrillation or atrial flutter was induced with the two protocols respectively in 67% (52/78) and 85% (51/60) of gr. I, in 17% (26/150) and 36% (38/105) of gr. II and in 35% (17/48) and 44% (21/48) of gr. III (gr. I vs gr. II p less than 0.001 for prot. A and p less than 0.01 for prot. B; gr. II vs gr. III p less than 0.001 for prot. A and NS for prot. B). Induced atrial fibrillation or atrial flutter using the two protocols had a greater than 5' duration respectively in 83 and 78% of gr. I, 62 and 42% of gr. II and in 41 and 38% of gr. III.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1989

Long-term follow-up of patients with unexplained syncope and negative electrophysiologic study.

Fifty-eight patients (29 M, 29 F, mean age 60.8 +/- 16 years) with unexplained syncope at the end of a complete clinical and electrophysiological evaluation, were followed for a mean period of 36.6 +/- 20.5 months (median: 30.5 months). Structural heart disease was present in 32 patients (55.2%). The standard ECG was normal in 24 (41.4%) and showed sinus bradycardia (greater than 40 m-1) and/or first degree AV block and/or intraventricular conduction disturbances in 29 patients (50%). During follow-up, recurrences of syncope were observed in 11 of 43 untreated patients (25.6%), three of seven electrically treated patients (42.9%) and two of eight pharmacologically treated patients (25%). The cause of these recurrences was cardiac in one (1.7%), non-cardiac in 10 (17.2%) and remained undetermined in five (8.6%). Sudden death occurred in only one patient (1.7%), who was receiving chronic amiodarone therapy. These results indicate that (1) syncopal recurrences may occur in an appreciable percentage of patients with unexplained syncope and a negative electrophysiologic study during a relatively long-term follow-up, (2) syncopal recurrences, when they occur, are generally due to a non-cardiac cause, (3) sudden death is an occasional and rare event in this patient population and (4) empirical prophylactic treatment with a permanent pacemaker or antiarrhythmic drugs does not usually prevent complications during the follow-up.

Adult↗
PubMed1989

[Usefulness of transesophageal electrophysiological study during the ergometric test in the evaluation of supraventricular paroxysmal tachycardia occurring during exertion].

Transesophageal electrophysiologic study has recently been proposed for the evaluation of supraventricular arrhythmias. In this report we present 13 cases, with palpitations occurring only during effort, due to a suspected supraventricular tachycardia, in which the usefulness of the transesophageal electrophysiologic study performed during stress test was evaluated. Of these 13 patients, nine were male and four were female, mean age was 29 yrs. Twelve cases had no heart disease, one had a moderate mitral valve insufficiency. Nine cases had a normal ECG, four had a WPW pattern. In 9/13 cases no significant arrhythmia was ever documented, in 1/13 ventricular premature beats were present in the basal ECG, in 1/13 a atrial fibrillation and in 2/13 a supraventricular reciprocating tachycardia was recorded. In all cases a maximal exercise test and a 24-hour Holter monitoring were performed. In all pts a transesophageal electrophysiologic study was performed both at rest and during extra-stimuli and incremental atrial pacing. The end point of transesophageal study was the induction of a sustained (greater than 30") supraventricular tachycardia. RESULTS. Maximal exercise test was negative in 11/13 cases; it showed ventricular premature beats in one case and initiated a supraventricular tachycardia in one. The 24 hour Holter monitoring was negative in 12/13 cases while it showed frequent ventricular premature beats in one. Resting transesophageal electrophysiologic study revealed dual A-V nodal pathways in six pts: in one of them a junctional re-entry was induced; in two a single echo beat was observed, while in three no reentry was observed. In three cases a supraventricular tachycardia was induced which was sustained in one and unsustained (7" and 24") in two cases. In 4 cases transesophageal electrophysiologic study gave no information. Transesophageal stimulation during exercise induced a greater than 30" reciprocating tachycardia in all patients, at work loads of 30-180 watts. Six pts had an intranodal tachycardia (V-A less than 70 msec) a further six pts had a atrioventricular tachycardia involving a Kent bundle (V-A greater than or equal to 70 msec), which was concealed in two, and one had a atrial tachycardia. In four cases (3 with intranodal and 1 with atrioventricular tachycardia), exercise transesophageal study was repeated after chronic therapy with betablockers (sotalol 240 mg/die or metoprolol 200 mg/die). In all cases, after therapy, the induced tachycardia had a longer cycle and in two cases it was induced at a higher work load. In a further two cases flecainide (200 mg/die) was tested. In one case (with atrial tachycardia), the arrhythmia was no longer inducible after therapy, in another case (with intranodal tachycardia) the drug had no effect. CONCLUSIONS. In patients with paroxysmal supraventricular tachyarrhythmias occurring during effort the basal ECG is normal or shows a WPW pattern. The maximal exercise test and 24 hour Holter monitoring give no information in over 90% of cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1988

Atrial electrophysiologic properties of patients with asymptomatic Wolff-Parkinson-White syndrome.

To evaluate the existence of a peculiar atrial electrophysiologic substrate, we studied 18 patients with asymptomatic Wolff-Parkinson-White (WPW) syndrome. These patients were compared with 10 age-matched normal subjects (N). Effective and functional refractory periods were determined at two right atrial sites (high and low in the lateral wall), during atrial pacing (100 min-1) and at twice diastolic threshold. Disperson (D) of effective (ERP) and functional (FRP) refractoriness was evaluated as the difference between refractory periods at the two atrial sites. WPW patients showed significantly lower mean values of effective and functional refractoriness at both atrial sites and significantly higher mean values of D-ERP and D-FRP. Moreover, in calculating the highest normal values of D-ERP and D-FRP (as mean values of N plus 2SD) it was observed that WPW with abnormal values of D showed a statistically (chi 2 test) higher incidence (100%) of induced atrial fibrillation (AF). These findings indicate the existence of both an abnormal atrial electrophysiologic substrate and of a higher vulnerability in WPW. Finally, AF was induced generally at the site with the lower refractoriness (i.e. low lateral site). This should be taken into account when considering how atrial fibrillation can be induced more easily.

Adolescent↗
PubMed1987

[The Italian Group for the Study of Streptokinase in Myocardial Infarct: Study of electrocardiographic changes].

The twofold purpose of the ECG sub-group study of G.I.S.S.I. (Gruppo Italiano per lo Studio della Streptokinasi nell'Infarto miocardico) is to evaluate whether exist different ECG evolution in pts with AMI treated with streptokinase (SK YES) and/or with coronary reperfusion (early CK peak) with respect to pts non treated with streptokinase (SK NO) and/or without coronary reperfusion (late CK peak) and to establish whether the ECG is useful to recognize the patients in which reperfusion occurs. Among 365 pts randomized for G.I.S.S.I., 209 pts with first myocardial infarction, admitted within 6 hours from the onset of pain, alive for at least 24 hours, were included. 98 were SK YES and 111 SK NO: 48 cases (group A) had the CK peak before 15th hour; 59 cases (group B) had the CK peak between 15th and 21th hour: 102 cases (group C) had the CK peak after 21th hour. In all the patients ECG was analyzed on admission and thereafter at 3rd, 6th, 9th, 12th, 24th hours and on 2nd, 3rd, 7th and 14th days. RESULTS--Anterior myocardial infarction--SK YES pts had in respected to SK NO pts a significantly lower sum of ST elevation on anterior leads (sigma ST increases V1-V6) at all times after admission starting from 6th hour. A similar behaviour was observed in groups A and B in respect to group C. SK YES pts when compared to SK NO pts had an earlier loss of the sum of R wave in anterior leads (sigma RV1-V6), although the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗