[Study of circulating lymphocytes by monoclonal antibodies in myasthenia gravis]. / Estudo dos linfócitos circulantes por anticorpos monoclonais na miastenia grave.

A significant decline of CD3 cell detected by rosettes and a significant increased of B cell populations were observed. The total CD3+, helper CD4+ and suppressor CD8+ T-cell subsets showed no significant variation em relation to sex, age thymectomy and corticotherapy by monoclonal antibodies.

Estudo dos linfócitos circulantes por anticorpos monoclonais na miastenia grave / Circulating lymphocytes by monoclonal antibodies in myasthenia gravis

Os autores avaliam os linfócitos T (CD3, CD4, CD8, CD4/8) por anticorpos monoclonais e rosácea em 20 pacientes e linfócitos B por Fab' por imunofluorescência em 9 pacientes com miastenia grave. Observam elevaçäo significante na populaçäo de linfócito B e reduçäo nos linfócitos T totais CD3 + por rosáceas. Näo foram observadas modificaçöes nas subpopulaçöes celulares com timectomia e corticosteróides

Glucocorticoid receptors in subpopulations of human lymphocytes defined by monoclonal antibodies.

Glucocorticoid receptors (GR) were investigated in subpopulations of lymphocytes identified by monoclonal antibodies. Purified T (OKT3+) and non-T lymphocyte subpopulations were isolated from human peripheral blood using Degalan bead columns coated with rabbit anti-human IgG. Purified subpopulations of OKT4+ and OKT8+ lymphocytes were obtained by coating the nonadherent population (T cells) from the first column with OKT4+ or OKT8+ and pouring it into a second Degalan column, coated with goat anti-mouse IgG. GR content and affinity were analyzed by a whole cell assay with [3H]dexamethasone as tracer. The numbers of GR in lymphocyte subpopulations (OKT3+ cells, non-T cells, OKT4+, and OKT8+ cells) were nearly equal. It is concluded that the differential effects of glucocorticoids on the circulatory kinetics of OKT4+ and OKT8+ cells probably are not related to differences in glucocorticoid receptors of these T-cell subpopulations.

[Long term electrophysiological study on patients with acute myocardial infarction and complete heart block. Is cardiac pacing always necessary? (author's transl)]. / Studio elettrofisiologico a distanza in pazienti con infarto miocardico acuto complicato da blocco atrioventricolare completo parossistico. E sempre indicata l'elettrostimolazione cardiaca permanente?

UNLABELLED: Of 335 consecutive patients (pts) admitted to the coronary care unit (CCU) for acute myocardial infarction (AMI), 34 (10%) evidenced complete heart block (HB). The overall inhospital mortality was 14% (47 pts) versus 39% of the HB group (13 pts). No previous conduction disturbances were documented in 58% of pts before appearance of complete HB. Complete HB was preceded in 52% of pts by first or second degree HB or bundle branch block. Of 21 pts with HB discharged from the hospital, 5 (23%) died between 5 and 24 months (mean 12): no patients had sudden death; 16 pts (76%) are still alive after 13 to 45 months (mean 30). His bundle electrophysiologic (HBE) study was performed in 10 pts of the HB group after 4 to 40 months: 4 pts with anterior versus 6 with inferior AMI. Conduction disturbances were no longer present in all but one pt who had H-V 60 msec. Ajmaline (50 + 50 mg iv) prolonged A-H over 130 msec in 4 pts; H-V was not significantly increased in 8 of the 10 pts, while in two pts was 100 msec. One pt in the acute phase and one pt 12 months later, required pacemaker (PM) implant (both had inferior MI). IN CONCLUSION: no sudden death was documented during the follow-up period. The late HBE study, before and after ajmaline, did not allow to recognize critical conduction abnormalities suggessting prophylactic PM implantation.

["Pericarditis epistenocardica" as as a marker of extensive myocardial infarction. Clinical, electrocardiographic and enzymatic study (author's transl)]. / La pericardite epistenocardica come indice di infarto miocardico esteso. Studio clinico, elettrocardiografico ed enzimatico.

Pericarditis may complicate the early phase of myocardial infarction (MI). It occurs when necrosis involves the epicardial surface. To verify if pericarditis may be regarded as a marker of extensive MI, 60 patients with anterior or inferior MI admitted to the Coronary Care Unit within 6 hours from onset of symptoms, were studied by clinical, electrocardiographic and enzymatic parameters. 20 patients developed left ventricular failure (LVF) assessed by clinical, radiologic and hemodynamic indexes (15 mmHg has been considered the upper normal value for mean wedge pulmonary pressure). 9 of the 11 patients with pericarditis (PP) had LVF, versus 11 of the 49 non PP group (P = 0.002). Life threatening arrhythmias (ventricular tachicardia and fibrillation) appeared in 5 of the 11 PP versus 7 of the 49 non PP group (P = 0.04). No significant difference has been found between the two groups concerning the inhospital mortality. In a follow-up of 3 to 18 months, no difference in mortality was observed, while the functional recovery in the PP group was significantly worse (I and II versus III and IV New York Heart Association classes P = 0.003). Higher sigmaST values were found in precordial maps of the PP group, on admission (P = 0.03). After a deep spontaneous fall, sigmaST showed a reelevation which was similar in the two groups. SigmaR showed a greater % decrease however not statistically significant in PP. Creatinekinase enzymatic infarct size was significantly higher in PP group (P = 0.0002). It is concluded that pericarditis is a clinical marker of extensive MI and may be useful in evaluating prognosis and effectiveness of therapeutic interventions in MI.

[CK MB versus total CK in the estimation of myocardial necrosis. Comparative kinetic analysis and evaluation of an immunological method]. / CK MB verso CK totale nella quantificazione della necrosi miocardica. Analisi cinetica comparativa e valutazione di un methodo immunologico.

It has been suggested that the adoption of a relatively specific marker of the myocardial cell, such as creatine kinase MB isoenzyme, can yield improved accuracy in estimating infarct size by serial serum sampling and compartmental analysis. Nevertheless, current methods for the evaluation of isoenzyme activity are cumbersome and unsuitable for clinical use. We have therefore employed a new test for the rapid determination of CK MB activity, based on the immunological inhibition of M subunities. In 19 patients not submitted either to intramuscular injection or to repeated defibrillations, a good correlation was found between indexes of necrosis based on MB and total CK determination (r = 0.94), with the cumulative MB release amounting to 16 +/- 4% of total CK. Significant differences were observed in 3 patients submitted to external cardiac massage (MB = 9 +/- 1% of total CK) thus suggesting a considerable extracardiac source of total CK due to the trauma of the skeletal muscle. The comparative kinetic analysis shows substantial differences between the two isoenzymes, not only concerning the greater disappearance rate of CK MB but, more significantly, related to a faster release of this isoenzyme from the myocardium, which has not been previously reported. The good correlations found between maximal appearance rate and cumulative enzyme release (r = 0.86) suggest that the former may represent an index of the rate of degradation of cellular membranes. Practical implications of these data are discussed.

[Precordial mapping and enzymatic analysis for estimating infarct size in man. A comparative study (author's transl)]. / Mappaggio precordiale ed analisi enzimatica nella valutazione quantitativa della necrosi miocardica

To investigate the relationships between electrocardiographic and enzymatic indexes of infarct size (I.S.), a group of 19 patients with anterior infarction was studied by serial precordial mapping and CPK curves analysis. The time course of ST and QRS changes was examined and a sharp, spontaneous fall of sigmaST was shown to occur within 10-12 hours after onset of symptoms, followed by a gradual rise. sigmaST on admission appears to be a poor predictor of subsequent enzymatic I.S. (r=0.49). Good correlations with I.S. were observed, for sigmaST at 48-96 hours (r=0.82) and, especially, for the percent decrease of sigmaR, with respect to the initial values (deltaR%), (r=0.94).