PubMed Health⌕ Search

Biomedical subjects

M Guarnerio

Publications and source records attributed to M Guarnerio.

36 records · Page 2Linked to original sources
PubMed1985

[Sustained ventricular tachycardia in postinfarct ischemic heart disease: spontaneous polymorphism. Clinical, therapeutic and prognostic aspects].

UNLABELLED: Spontaneous Polymorphism (SP) is present when at least two episodes of Sustained Ventricular Tachycardia (SVT) occur spontaneously in the same patient (pt) with different bundle branch block pattern or with shifting of QRS axis by greater than or equal to 90 in the various episodes. We undertook this study in order to investigate the clinical significance of SP in SVT as well as therapeutic and prognostic implications. MATERIAL AND METHODS. From our global pts populations we chose those with SVT in chronic ischemic heart disease (CIHD) with previous myocardial infarction (PMI), they had to be already studied by electrophysiologic technique (EES). The pts were divided into two groups (Gr.): Gr. I: 13 SP pts (12 M, 1 F, mean age 57.5 +/- 13; mean follow-up 19.2 +/- 11 months); Gr. II: 15 no SP pts (14 M, 1 F, mean age 60 +/- 10; mean follow-up 9.9 +/- 13 months). RESULTS: The two Gr. are comparable in terms of symptoms, exercise tolerance, infarct site, intraventricular conduction disturbances (61.5% and 66.6% respectively), ventricular wells kinetics (38.4% and 26.6% respectively) and time interval between acute myocardial infarction the first episode of SVT (7.58 +/- 6.02 and 8.27 +/- 6.57 years respectively). 8 of the 10 alive Gr. I pts have been treated with Amiodarone (A) (2800-4200 mg/wk). All 9 alive Gr. II pts are on A (1400-4200 mg/wk). A serum level in 7 Gr. I pts was 1.7 +/- 0.65 mcg/ml and 1.61 +/- 0.67 in 5 Gr. II pts. 3/13 Gr. I pts died: 2 for sudden death (15.3%), 6/15 Gr. II pts died: 4 suffered sudden death (26.6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Sustained ventricular tachycardia: low-energy transcatheter internal cardioversion. Efficacy, reliability and tolerance in comparison with ventricular burst].

The aim of this study is to evaluate the efficacy, reliability and patient tolerance of low-energy transcatheter intracardiac cardioversion in the treatment of Sustained Ventricular Tachycardia (VT), and to compare this method to ventricular burst. For this purpose 11 patients (pts) (10 M, 1 F, mean age 50.1 yrs, range 24-72) with 18 different types of VT (17 induced during Endocavitary Electrophysiological Study (EES), 1 "clinical"), who all underwent EES all but 1 with organic heart disease, were first treated by transcatheter intracardiac cardioversion and then, if possible, with ventricular burst at 125%-150% of VT rate. The Medtronic Cardioverter 5350 and the Medtronic catheter 6880 were used. The following results were obtained: transcatheter intracardiac cardioversion terminated 9/18 types of VT (8 types at least 3 times) in 6 pts. Cardioversion threshold was on average 1.31 J (range: 0.14-5). Transcatheter intracardiac cardioversion failed to terminate 9/18 types of VT (in 5 pts); VT acceleration or ventricular fibrillation occurred in 6/9 types. The mean cycle length of successfully cardioverted VT (382 +/- 61 msec.) was significantly longer (p = 0.05) than that of not successfully cardioverted VT (284 +/- 83 msec.) and of the VT in whom an acceleration or a degeneration into ventricular fibrillation was observed (240 +/- 55 msec.). In 4 pts it was necessary to use external DC shock and in 4 supraventricular hyperkinetic arrhythmia was induced. All pts complained of considerable discomfort at shocks greater than or equal to 0.5 J. In all the 7 types of successfully cardioverted VT as well as in 3 out of the 4 types of not successfully cardioverted VT in which it was possible to test ventricular burst, this latter proved to be effective. These results indicate that: the efficacy of transcatheter intracardiac cardioversion is not great at least in our pts (50%); moreover, the transcatheter intracardiac cardioversion is affected by a high incidence of acceleration of VT and degeneration into ventricular fibrillation (33.3%) and by the induction of supraventricular hyperkinetic arrhythmia (22.2%). Patient discomfort appears to be a major limitation to transcatheter intracardiac cardioversion. The VT cycle length is determinant for the success of the transcatheter intracardiac cardioversion and for the induction either of an acceleration of VT or of a degeneration into ventricular fibrillation (which are observed only in VT with cycle length less than or equal to 300 msec.).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

[Clinico-electrophysiologic relations in isolated complete atrioventricular block, congenital or idiopathic].

Congenital or idiopathic complete A-V block with no detectable heart disease may be complicated by near syncope, syncope or sudden death. The proposed predictive "risk factors" of these events have not proved sufficiently reliable so far. This study was undertaken in order to re-evaluate the correlation between symptoms and clinical and electrophysiological data with particular regard to the junctional recovery time in 10 patients (4 M; 6 F; mean age 24.4 +/- 9.6 at our first observation) with congenital or idiopathic complete A-V block. Patients were divided into 2 groups: group A (3 M; 3 F; mean age 27.8 +/- 10.6 at our first observation) with patients who complained of vertigo, near syncope or syncope before our study; group B (1 M; 3 F; mean age 19.2 +/- 4.1 at first observation) without cardiovascular symptoms before our study. In group A, Holter monitoring revealed periods of asystole longer than 3000 ms in 2, and ectopic ventricular arrhythmias mainly during effort in 2; ergometric stress test performed in 3 patients demonstrated ectopic ventricular arrhythmias in 2 (those who had ectopic ventricular arrhythmias at rest). In all patients the site of the block was suprahisian (demonstrated by electrophysiologic endocavitary study) with a normal H-V interval; mean junctional recovery time was 4.600 +/- 1.620 ms and corrected junctional recovery time was 3.088 +/- 1.500. Four patients had vertigo during the electrophysiologic endocavitary study. After Atropine 0.02 mg/Kg i.v. junctional recovery time and corrected junctional recovery time decreased respectively to 1052 +/- 238 and 166 +/- 38 ms (the measurement was made in 5 patients). In group B Holter monitoring revealed periods of asystole longer than 3000 ms in 1 case. All patients had ectopic ventricular arrhythmias, confirmed by the stress test. In this group too, the block was suprahisian (electrophysiologic endocavitary study) with normal H-V. Mean junctional recovery time was 5162 +/- 2408 ms; and corrected junctional recovery time 3687 +/- 2202. Two patients complained of dizziness during the electrophysiologic endocavitary study. After Atropine 0.02 mg/Kg i.v., junctional recovery time and corrected junctional recovery time decreased respectively to 1300 +/- 356 and 260 +/- 145 ms. Four group A and 1 group B patients received a permanent pacemaker and have remained asymptomatic since.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

[Sustained ventricular tachycardia: induced polymorphism. Clinical and electrophysiological aspects; therapeutic implications].

By induced polymorphism (I.P.) we mean the electrical induction during endocavitary electrophysiologic study (E.E.S.) either of two or more morphologically distinct types of Sustained Ventricular Tachycardia (S.V.T.) (i.e. different bundle branch block patterns or with shifting of QRS by greater than or equal to 90 degrees) or of one type of sustained ventricular tachycardia other than the spontaneous one. Twenty-two patients with clinical sustained ventricular tachycardia, in whom at least one episode of sustained ventricular tachycardia was induced during endocavitary electrophysiologic study, were divided into 2 groups depending on the presence or not of induced polymorphism: Group I consisted of 13 patients with induced polymorphism; Group II consisted of 9 patients without induced polymorphism. All the patients of the Group I had chronic ischemic heart disease (C.I.H.D.); 12/13 previously had myocardial infarction. Only 1 patient of the Group II had chronic ischemic heart disease. Intraventricular conduction defect was present in 9 patients of the Group I and in 2 of the Group II. An overall of 26 sustained ventricular tachycardia episodes were induced in patients of the Group I: 9 with RBBB, 10 with LBBB and 7 with "bizarre" QRS morphology. Sustained ventricular tachycardia reinduction was attempted in 10 patients of the Group I after acute drug testing (Ajmaline, Propafenone, Amiodarone): sustained ventricular tachycardia was no longer inducible in 6, but in 3 of those 4 in whom it was, a marked increase in polymorphism was observed as compared to pre-test pattern. Of the 11 alive patients of Group I, 10 are on Amiodarone alone or in combination with other antiarrhythmic drugs. We conclude as follows: different morphological types of sustained ventricular tachycardia can be quite commonly induced during endocavitary electrophysiologic study; according to our cases induced polymorphism is observed only in patients with chronic ischemic heart disease; patients with induced polymorphism often have intraventricular conduction defect; induced polymorphism furtherly accounts for reentry as the mechanism of sustained ventricular tachycardia in patients with chronic ischemic heart disease; a prevalent morphology of the endocavitary electrophysiologic study induced sustained ventricular tachycardia in patients with chronic ischemic heart disease was not observed at least in our patients; Amiodarone is the drug of choice for the treatment of induced polymorphic sustained ventricular tachycardia patients.

Adult↗
PubMed1984

[Use of transesophageal atrial stimulation in the treatment of atrial flutter. Clinical experience].

Transesophageal atrial pacing with relatively low current output and wide pulse duration has been recently reported. With this method supraventricular tachycardias can be successfully induced and terminated. In this study 23 episodes of spontaneous common atrial flutter (21 patients) were treated by rapid transesophageal atrial pacing (output of 16 Volts and pulse duration of 10 msec). Sinus rhythm resumption was obtained in 18 episodes (78.2%), directly after interruption of stimulation in 7 and following brief periods of atrial fibrillation in 11. All patients tolerated the procedure well with moderate discomfort; no complications were observed. Esophageal pacing offers a useful, rapid, minimally invasive, well tolerated method of terminating atrial flutter in the clinical practice.

Adult↗
PubMed1983

Familial endemic persistent atrial standstill in a small mountain community: review of eight cases.

Familial persistent atrial standstill (PAS) has been rarely documented. Five patients, three male and two female (mean age 46 years at first observation), with familial 'complete' PAS, all from a small mountain community (900 residents) have been studied. Diagnostic criteria were: absence of P wave in any lead of the standard electrocardiogram; no electrical activity of the atria with extremely slow junctional escape rhythm on the endocavitary recordings; lack of atrial excitability; absence of atrial wall movement at fluoroscopy; no mitral A wave on the echocardiogram. All patients had marked cardiac enlargement primarily due to atrial enlargement and all had impaired functional class. Some had bradycardia for many years but none had syncope. Permanent cardiac pacing was carried out in all. Two had cerebral embolism. In the same community there were three patients, one male and two female (mean age 34 years at first observation), with 'partial' atrial standstill characterized by absence of P waves in any lead of the standard electrocardiogram and by endocavitary recording of electrical activity limited to a localized region of the atrium. These three patients also had cardiac enlargement primarily due to atrial enlargement but to a lesser degree than the patients with complete PAS. One patient had cerebral embolism. The familial and endemic character of the disease is stressed. Cardiac enlargement due primarily to atrial enlargement seems to be a common feature of both the complete and partial form of the PAS syndrome.

Adult↗
PubMed1983

Evidence of a reentry circuit in the common type of atrial flutter in man.

To investigate the mechanism of atrial flutter (AF) in humans, we studied 13 patients during episodes of spontaneous common AF, with simultaneous multiple atrial endocavitary recordings and atrial programmed stimulation. In all patients, low paraseptal atrial activation preceded high right atrial activation, and the latter preceded mid- or low lateral right atrial activation (recorded in five patients). Programmed atrial stimulation resulted in early reset of the AF cycle, with an unchanged poststimulation AF activation pattern. The poststimulation cycle recorded from an even potential to the site of stimulation was always shorter than the basic flutter cycle length. The poststimulation cycle recorded at the site of stimulation was always equal to or longer than the flutter cycle length. These results strongly favor the existence of a reentry circuit to which the extrastimulus has access.

Adult↗
PubMed1983

Clinical evaluation of new antiarrhythmic agents: experiences with propafenone.

The authors propose a general design for the clinical evaluation of new antiarrhythmic agents with special reference to their experience with propafenone, a new Class 1 agent. The drug was studied in 61 patients affected by PSRT, VEBs or RVT often unresponsive to other drugs. Both acute i.v. sensitivity tests and evaluation of chronic oral treatment were carried out. The results indicate that propafenone is a highly effective drug and that its oral activity may be predicted in individual patients by an acute i.v. administration. The most frequent adverse reaction was a widening of QRS complex. However the drug had to be withdrawn due to impaired intraventricular conduction in one patient only. More frequently (four cases) its withdrawal was due to adverse extracardiac reactions.

Adolescent↗
PubMed1983

[Validity and limits of invasive pharmacological tests in the treatment of malignant ventricular hyperkinetic arrhythmias].

Programmed stimulation can now be safely performed for the evaluation of therapy for recurrent ventricular tachyarrhythmia. The initiation of ventricular tachycardia appears closely related to its actual spontaneous clinical occurrence. Serial electrophysiologic studies can be performed and are effective in prospectively evaluating the response to antiarrhythmic drugs. The efficacy of therapy based on the results of programmed stimulation appears to be good. On the other hand, Amiodarone can be effective in the chronic treatment as well as in patients with ineffective acute drug test.

Adult↗
PubMed1981

[Another type of interaction between blood levels of digitalis and anti-arrhythmic drugs: digoxin and amiodarone. Experience with long-term therapy].

In clinical Arrhythmology it is often necessary to associate digitalis and antiarrhythmic agents. This calls for study of possible interaction between the employed drugs. We found a statistically significant correlation between digitalis and amiodarone plasma level in patients on long term treatment with both drugs. A statistically significant linear correlation between plasma amiodarone level and digoxin (0.25 mg/day) or beta-methyldigoxin (0.20 mg/day) was documented in 33 patients. 23 patients had been treated with these drugs for paraxysmal reciprocating supraventricular tachycardia since an average of 52 months (computerized follow-up). (Amiodarone average weekly dose was 1078 +/- 168 mg after a loading dose of 12 gm given over one month). 10 patients were on chronic treatment with higher weekly doses of amiodarone (average dose 2380 +/- 731 mg per week). Thyroid function tests (T4; T3; T3UP; TSH; rT3) were checked in every patients. Further studies are warranted to understand the mechanism of the interaction between amiodarone and digitalis. As a clinical implication we point out that amiodarone-digoxin (or betamethyldigoxin) interaction in our patients has neither resulted in over-therapeutic plasma level nor in signs of digitalis toxicity.

Aged↗