[Lymphomatous development of Sjögren's syndrome].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Bettini.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The most suitable approach to the athletes with WPW is controversial. Therefore 66 symptom-free athletes with WPW and without heart disease (53 M, 13 F, mean age 21.98 yrs, min 12--max 44) underwent a study protocol whose end-point was the induction of supraventricular tachyarrhythmia, i.e. atrial fibrillation or, if not possible, atrial flutter or atrial tachycardia at rest and during ergometric stress test. The athletes with shortest R-R interval between preexcited beats less than or equal to 240 ms at rest and/or less than or equal to 210 ms during exercise were judged as being at risk i.e. no fit for sport activity. The end-point was reached in 64/66 athletes (in 62 atrial fibrillation). In 4 athletes with life threatening arrhythmia induced at rest the evaluation during exercise was not performed. According to the evaluation at rest we were able to identify only 18 athletes (28.1%) as being at risk, while according to the complete study protocol 26 athletes (40.6%) were judged as such. In 23/64 athletes (36%) this judgement was discordant with the usual non invasive evaluation (i.e. Holter monitoring, ergometric stress test, ajmaline test). During induced atrial fibrillation no significant difference, was found between the percentage of preexcited beats at rest and during exercise. On the average, 40 min. are required for performance of this study protocol (if the induced arrhythmia lasts less than 5 min.). According to our results we conclude: a) the non invasive assessment of the WPW athletes is unsatisfactory; b) the induction of atrial fibrillation during exercise gives a remarkable increase of the diagnostic power with respect to the assessment only at rest; c) since it is simple to perform and not expensive (in time, staff and cost) and because of its high diagnostic yield, we regard this protocol as fundamental for the electrophysiological evaluation of WPW athletes and also suitable for systematic study of WPW patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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)
Explore the source record for details and available documents.
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)
The widespread use of antiarrhythmic agents to control severe life-threatening arrhythmias evidenced the possibility of a worsening of arrhythmias induced by the same drugs. We performed a retrospective analysis studying the worsening phenomenon in patients who underwent pharmacological invasive and non invasive antiarrhythmic tests to choose the drug to be administered in the chronic treatment. Particularly we reviewed: 101 acute pharmacologic non invasive tests for "stable" ventricular ectopic beats using computerized automatic continuous recording system which allows quantitative and qualitative evaluation of arrhythmias. The drugs tested were: Propafenone (25 patients), Disopiramide (25 patients), Tocainide (11 patients), Lorcainide (8 patients), Lorajmine (13 patients), Nadolol (9 patients). In accordance with Vallebit et al., we considered arrhythmias worsening criteria: the onset of non sustained or sustained ventricular tachycardia; an increase of four fold the number of ventricular ectopic beats and/or ten fold the repetitive forms. A worsening of arrhythmias was observed in 4/101 (3.9% patients); 1/9 treated with Nadolol, 1/25 with Propafenone, 1/35 with Disopiramide, 1/13 with Lorajmine. For one young patient the worsening phenomenon could be considered a toxic picture, because of the very high drug plasmatic levels (Lorajmine) observed for the whole duration of the sustained VT induced from the drug. For the remaining 3 patients the response resambles a paradox effect. 34 pharmacologic invasive tests in 30 patients with common recurrent ventricular tachycardia, during electrophysiologic endocavitary study. The drugs tested were: Propafenone (12 patients), Amiodarone (11 patients), Ajmaline (4 patients), Tocainide (3 patients), Lorcainide (2 patients), Lorajmine (1 patient), Disopiramide (1 patient).(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
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.
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.
We have reviewed a series of 90 consecutive patients with multiple myeloma (MM) diagnosed in the period 1.1.1971-31.12.1980 and subsequently treated with an intermittent administration of melphalan and prednisone (62 IgG MM, 20 IgA MM and 8 Bence-Jones (BJ) MM). Unfavorable prognostic factors were: presence of micromolecular M component (K or lambda), serum creatinine greater than or equal to 2 mg/dl, serum calcium greater than or equal to 12 mg/dl, presence of BJ proteinuria, Hb less than 10 g/dl, diffuse osteolytic lesions, bone marrow plasma cell percentage greater than or equal to 30%. In particular, according to the recent staging system proposed by Merlini et al. [Blood 55: 1011, 1980], the most important prognostic parameters for IgG and BJ MM were: serum creatinine, BMPC % and serum calcium; for IgA MM the most important were: serum hemoglobin, calcium and M component levels. We have compared the survival curve of 45 patients who died, with the predicted survival curve according to the multivariate regression analysis of Merlini and co-workers; the prediction was equally precise for all the three types of MM considered, thus showing the high sensibility of this new staging system.
Explore the source record for details and available documents.
Although Lown grading system of ventricular premature complexes (VPCs) has important conceptual shortcomings and has shown severe limitations in either cross-sectional or longitudinal studies, this classification is still the most well-known and used method to characterize the arrhythmologic ventricular pattern of the individual patient. We have looked at a modification of VPCs Lown grading scheme to correct the defects and to make the use of the classification more accurate. Our proposal is based on maintenance of 5 classes--similar to those of Lown original classification--to which we have assigned a score from 0 to 60. We have also introduced many sub-classes, each with a definite score, to better characterize the type of arrhythmic event. The sum of the score of the highest class and the score of every subclass furnishes the final score. This score is a direct index of the importance of the ventricular arrhythmias and seems to be useful for statistical evaluation of the anti-arrhythmic therapy and for follow-up studies, as confirmed by preliminary clinical results obtained through the use of this new VPCs classification.
Explore the source record for details and available documents.