[Activity of serum enzymes in intracoronary thrombolysis: preliminary study].
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Biomedical subjects
Publications and source records attributed to R Chioin.
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One-hundred and eighty-nine patients who underwent cardiac catheterization for suspected ischemic heart disease were assigned to four different groups depending on the number of diseased vessels (0, 1, 2, 3), the dominant artery and the presence of left main coronary stenosis. Among the 45 parameters obtained from history, physical examination, E.C.G., and exercise test multivariate analysis identified (positive stress test, maximal systolic blood pressure, documented myocardial infarction, maximal heart rate, ipercholesterolemia, lateral myocardial infarction, angina during stress test) that were statistically significant. A score system was devised on the basis of the summed-up value of the seven parameters. When the patients were assigned, according to the score, to one of the previously mentioned 4 groups, the classification proved to be correct in 54% of the cases. When we divided the patients in two groups with or without coronary artery disease so that the attribution turned out to be correct in 92% of the cases (sensitivity 94%, specificity 77%), whereas when based on ST segment depression only, the classification was correct in 85% of the cases (sensitivity 84%, specificity 88%).
In a group of coronary patients studies of fibrinolysis were carried out during cardiac bilateral catheterization. The following tests were evaluated: Euglobulin lysis time, fibrinogen, plasminogen, AT III, alpha 1-antitrypsin and alpha 2-macroglobulin. Fibrinolytic activity was reduced in various cardiac chambers. Plasminogen levels were elevated probably because of reduced utilization or consumption. Alpha 1-antitrypsin and alpha 2-macroglobulin levels were greatly reduced both in the arterial and in the venous system. From these results the fibrinolytic system may be concluded to be defective in coronary patients.
The postoperative pathology observed in 17 patients with complete atrioventricular canal, who died following total correction is described. In 3 patients, in whom valve replacement was necessary, the death was due to late prosthetic dysfunction. Out of 14 patients who underwent plastic repair, 4 died from undetected residual cardiac anomalies, which in 2 cases were associated with pulmonary obstructive vascular disease, 3 from unexplained myocardial infarction, 3 from inadequate postoperative care and 4 from pulmonary obstructive vascular disease which presented as an isolated finding. An analysis of the incidence of pulmonary obstructive vascular disease in these patients disclosed that it can develop before one year of age in some patients with Down syndrome.
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Necropsy data on 15 patients, who died after operations for complete atrioventricular defect (CAVD), were reviewed in order to analyze the possible determinants of death. Two infants had undergone a palliative procedure--pulmonary artery banding (Group I); three patients had had prosthetic replacement of one or both atrioventricular (AV) valves (Groups II); and the remaining 10 had had conservative repair with plastic reconstruction of the AV valves (Group III). The most notable pathological findings related to death were as follows: Group I, left ventricular hypoplasia in both infants; Group II, prosthetic dysfunction in all patients; Group III, extracardiac diseases in two-patients and cardiac lesions in six. In Group III severe pulmonary vascular obstructive disease (PVOD) was observed as an isolated finding in two patients and in combination with residual intracardiac anomalies in another two. Analysis of the incidence of PVOD demonstrated that irreversible changes may occur within the first year of life in babies with Down's syndrome, and that these changes well correlate with the calculated pulmonary vascular resistance (PVR) values. From the results of this study we have reached the following conclusions: (1) Prosthetic valve replacement has to be avoided because of a high incidence of prosthesis-related complications and the effectiveness of conservative repair; (2) residual untreated anomalies may affect the outcome of operation and should be accurately recognized and weighted preoperatively; (3) PVOD can occur in CAVD even before the first year of life and can be reliably assessed by the measurement of PVR. High degrees of PVOD frequently interfere with the surgical success, particularly when residual intracardiac anomalies are present. Therefore, we suggest that surgical correction be planned, when indicated, during the first 6 months of life.
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Have been studied 51 patients with aortic incompetency (AI), 46 with mitral insufficiency (MI) and 31 with congestive cardiomyopathy (CM) as example of a primitive myocardial lesion. The mean parametres calculated were: the left ventricular end-diastolic pressure (LVEDP), the ventricular volumes, the ejection fraction (EF), the end-sistolic pressure-volume ratio (Emax) and the eccentricity. In the chronic volume overload, the relationship between the pump performance and the contractility (EF-Emax) is parabolic with an initial plateau (myocardial failure without circulatory failure); the EF-Emax relationship, in the CM, is linear without a plateau. The LVEDP is a limiting factor of the pump-contractility relationship in the AI: for the same value of the contractility, the pump function is greater depressed if the LVEDP is 25 mmHg (loss of the preload modulation); in the MI and CM the depression of the pump performance is a function only of the depressed contractility. The end-systolic eccentricity is correlated with Emax: the changes in the geometrical shape of the left ventricular chamber is due to the depressed contractility.