[Validity of the study of the electrophysiological effects of anti-arrhythmia drugs in man prior to modern antiarrhythmic therapy. Multicenter study].
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Biomedical subjects
Publications and source records attributed to A Lotto.
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Myoglobin, total CK and MB CK isoenzyme were determined in the sera of 6 patients admitted with arrhythmias and treated with D.C. countershock and also in 37 patients with acute myocardial infarction or anginal syndrome. All the three tests were increased in patients with myocardial infarction. Serum myoglobin seems sufficiently sensitive and specific but the time required for the assay is a limiting factor for practical use in emergencies. After electrical cardioversion, myoglobin and CPK remain normal, although MB isoenzyme was increased in two of six patients. These results suggest that electrical cardioversion in itself does not influence serum levels of myoglobin. The occasional increase of MB CK observed after cardioversion seems to be the consequence of an easier release of the enzyme due to a myocardial injury.
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Echocardiography is a non invasive technique particularly useful to assess both hemodynamics and left ventricular performances; different methods have been proposed to evaluate echocardiographically the cardiac output. The aim of this work is to suggest a new method (planimetry of the area enclosed by echoes from the mitral valve) stating its advantages and limits and to test three already known methods (cubes method, method of Lalani and Lee, method of Rasmussen and coll.) comparing them to thermodilution. In 24 patients admitted in our Coronary Care Unit for acute myocardial infarction 30 measurements have been performed simultaneously with echocardiography and thermodilution. Statistical analysis (correlation coefficient with the method of the square minimums and Student's 't') of the results has shown that the cubes method is unprecise (P = NS) and unbiased (d = 0.97 +/- 15.46); Lalani-Lee method is unprecise (P = NS) and biased (d = 9.64 +/- 21.36) by a systematic underestimate error concealed by the poor precision; Rasmussen and coll. method is precise (P < 0.01) but biased (d = --3.03 +/- 5.5), the systematic mistake being entirely due to the group of patients with abnormal hemodynamics. Our method is precise (P < 0.01) and unbiased (d = --0.04 +/- 9.62) in patients both with normal and abnormal hemodynamics. Therefore this method offers the following advantages: 1) it is unbiased, even in the presence of abnormal left ventricular performance; 2) it is sufficiently precise, having a correlation coefficient with thermodilution of r = 0.80; 3) it measures directly the amount of flow due to the atrial systole; 4) the measurement is rapid and hardly biased by the reader.
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In 49 patients with sick sinus syndrome the following electrophysiological parameters were studied: sinus node recovery time and conduction time, atrial and AV nodal refractory periods, atrioventricular and intraventricular conduction. Moreover, pharmacological, vagal and sympathicomimetic stimulation were performed. These data were related to the clinical picture to establish any possible correlation leading to a more specific therapeutical choice. Patients were divided in two groups: group 1, with a prevalence of tachyarrhythmic symptoms and a lesser incidence of syncope, in which cases the sinus node function appeared to be only slightly affected. In group 2 small incidence of tachyarrhythmias and a clear prevalence of syncope with severe impairment of sinusal automaticity and/or sinoatrial conduction were present; AV and IV conduction disturbances were equally distributed in both groups. In more than 1/3 of the cases of the group I arrhythmias were succesfully treated with pharmacological therapy only, with Group 1 A antiarrhythmic agents in most cases. In the other cases of this Group and in all cases of Group II permanent electrical stimulation alone or together with drug therapy was necessary. Long term results with different therapeutical choices and, specifically, with the type of stimulation chosen in individual cases (sequential, rate-programmable ventricular, demand ventricular) are presented.
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A case of urinary malakoplakia involving both ureters and the bladder is presented. Ultrastructural data relating to the ureteric lesion are illustrated. Pale, dark and intermediate cells were involved in the pathological process. Features common and specific for these three types of cell are described. Dark cells are thought to be of a histiocytic nature, while the others are of either histiocyte or urothelial origin. Cytoplasmic inclusions were abundant in all three types in the form of single-or multicentred multilamellar bodies. It was not clear whether these were the product of secretion or phagocytosis. Michaelis-Gutmann bodies, on the other hand, were found to be due to the deposition of needle-like crystals inside pre-existing multicentred multilamellar bodies. Pathogens could not be demonstrated for certain. It is felt, therefore, that the aetiology of malakoplakia must be considered as debatable. Biochemical and immunological research directed to the detection of a possible enzyme deficiency is suggested, along with further ultrastructural investigation of the histogenesis of the pale and intermediate cells.
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Atrail programmed stimulation (APS) and His bundle recordings were performed in 24 patients with assessed sick sinus syndrome, 14 of whom had previously suffered from bouts of spontaneous paroxysmal tachycardias (Group I) and 10 with no history of previous similar complication (Group II). APS reproduced re-entry arrhythmias in 13 cases of Group I (92%). In 6 cases, junctional reciprocating tachycardia was elicited and the atrioventricular node function curve showed a typical steplike profile, consistent with longitudinal dissociation of the node itself as a cause of reciprocation. In 7 cases with previous paroxysmal atrial tachycardias, APS elicited intra-atrial re-entry arrhythmias. Absolutely no arrhythmia was elicited by APS in the 10 cases of Group II. High incidence of basal prolongation of conduction intervals was observed in both Groups (11 cases in Group I, 6 cases in Group II). Intra-atrial and/or atrio-nodel conduction delays were recognized in all the cases with intra-atrial re-entry arrhythmias. These results suggest that so called bradycardia-tachycardia syndrome should be regarded as an independent clinical form from the sick sinus syndrome, sharing with the latter the sinusal disfunction only. Re-entry mechanisms seems to be mainly responsible for the inititation of paroxysmal tachyarrhythmias: re-entry in the atrium, based on stable conduction delays, is probably correlated with scattered lesions of the same degenerative process affecting the sinus node. On the contrary, the frequent association of sick sinus syndrome with junctional paroxysmal tachycardia and its comples dissociation mechanism of the a-v node, raises the suspicion that, in such cases, two completely different processes are merely coexisting: a degenerative lesion of the sinus node and an anatomical or functional anomaly of a separate portion of the conduction system.
Hemodynamic and hemogasanalytic comparative study was performed in 46 patients admitted to our Coronary Care Unit because of myocardial infarction. The values of pH; PO2; PCO2; HbaO2; HbvO2; SBP; CVP; PAP; WP; Q; and CI were recorded simultaneously in every patient one or more times during the first 72 hours of the disease. The patients were divided into four classes according to the severity of hemodynamic impairment. Statistical analysis of the obtained results was then performed. In all patients more or less severe hypoxemia was found, but it was not statistically related to the severity of hemodynamic impairment. Instead, the values of PvO2 and HbvO2 showed a very significant correlation with Q and CI. Moreover, in 11 patients the venous admixture (QVA/Q) was measured several times in order to study the cause of the arterial hypoxemia thoroughly. It showed a very significant direct correlation with Q and CI. The interpretation of this phenomenon is then discussed and it is suggested that, in such patients, an increase of cardiac output causes an increased flow through poorly ventilated areas.
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