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Biomedical subjects

C Perdigão

Publications and source records attributed to C Perdigão.

At least 19 recordsLinked to original sources
PubMed1995

[A challenge].

Explore the source record for details and available documents.

Diagnosis↗
PubMed1995

[Medical instruction].

A study is made of medical education based on the Flenex Reform. The new paths indicated by the Edinburgh Declaration, combining three great models: teaching based on the analysis and solution of problems, the SPICES model and integrated teaching, are presented. Some considerations are made on how the changes declared for the last decade of the century should be implemented, quoting the report from the Interministerial Commission for the Revision of Medical Education.

Education, Medical↗
PubMed1993

[The role of the vascular endothelium and vasospasm in different coronary syndromes. A common physiopathological base for distinct entities?].

A literature review on the endothelial functions and endothelial dysfunction/lesion, as well as the atherosclerosis role in this process is performed. The several physiological explanations of both acute and chronic coronary syndromes are also reviewed, with particular emphasis to the recent studies on vasospasm mechanisms and its role in the physiopathogeny of variant angina and syndrome X. The role of the endothelial dysfunction/lesion as a common physiopathological basis to all coronary syndromes, is discussed.

Angina Pectoris, Variant↗
PubMed1992

[Formation of left ventricular thrombus in acute myocardial infarction: significance of the determination of fibrinogen, of products of fibrinogen degradation, and of plasminogen].

OBJECTIVE: To evaluate the significance of the fibrinogen, the plasminogen and the fibrinogen degradation products levels as marks of left intraventricular thrombosis (LIVT) in acute myocardial infarction (AMI). METHODS: 219 consecutive patients of AMI admitted in a Coronary Care Unit of an University Hospital, were prospectively studied. All protocols included a clinical evaluation, an M-mode and 2D echocardiographic study and blood samples, at day 1, 3, 7 and at hospital discharge. In the intraventricular thrombus evaluation just the 4 Asinger grade was considered. In the laboratory evaluation we used: the Clauss chronometric method for the fibrinogen, the colorimetric method for the plasminogen and the agglutination in plaque for the FDP. The patients with ECO in the 2 or 3 Asinger grades and those in which ECO and laboratory study were not performed in the same day, were excluded. 101 patients remained on the study, and they were divided in two groups: 53 patients with LIVT and 48 patients without it. RESULTS: In both groups the fibrinogen raised along the first six days of the AMI, however in the group with LIVT this level didn't raise as high as in the group without LIVT (p < 0.001). In the FDP evaluation two peaks were found, one at 48 hours and another on the 6 th day, but there were no differences between the two groups. The plasminogen values raised along the first week of AMI, in a similar way in both groups. CONCLUSIONS: a) Fibrinogen levels raises in AMI, but this elevation is significantly smaller in the group with LIVT, which suggests fibrinogen consume in fibrin formation of the thrombus. b) FDP and plasminogen levels raise along the first week of AMI, but in a similar way in the two groups. c) None of these parameters permitted to individualize patients with thrombus formation.

Aged↗
PubMed1992

[Coronary atherosclerosis in acute myocardial infarct. Anatomic profile of diverse causes of death].

OBJECTIVE: to study the degree of coronary obstruction by atherosclerotic plaques in a population dying with acute myocardial infarction. We defined subgroups by the degree of the obstructive lesion and compared the severity and distribution of coronary atherosclerotic lesions in different groups according to cause. STUDY DESIGN: systematic prospective study in patients dying in the acute phase of myocardial infarction in a University Hospital Coronary Unit during a four years period. POPULATION AND METHODS: we studied 193 patients corresponding 77% of the patients dead in the same period. 24 patients were excluded by technical reasons related to the preparation of necropsic material. The clinical protocol included 64 parameters and were considered the following causes of death: left ventricular failure (shock or acute pulmonary edema), left ventricular free wall rupture, interventricular septum rupture, primary asystole, pulmonary embolism and ventricular fibrillation. To study of the heart we performed the transverse slices technic after fixation; to study the epicardial coronary arteries we isolated the coronaries after fixation and made 5 mm transverse slices. The slices were macroscopic and microscopic evaluated for the degree of coronary obstruction in every 5 mm segment. We classified the degree of coronary obstruction in five grades: less than or equal to 25%; greater than 25% e less than or equal to 50%; greater than 50% e less than or equal to 75%; greater than 75% e less than 100%; and total obstruction. RESULTS: the degree of coronary obstruction in each epicardial segment were: Right ostium--grade I = 21%, grade II = 46%, grade III = 26%, grade IV = 7%, grade V = 0; Right coronary--grade I = 5%, grade II = 10%, grade III = 19%, grade IV = 28%, grade V = 38%; Left ostium--grade I = 27%, grade II = 50%, grade III = 19%, grade IV = 4%, grade V = 0; Left main--grade I = 16%, grade II = 43%, grade III = 28%, grade IV = 10%, grade V = 2%; Anterior descendent--grade I = 1%, grade II = 5%, grade III = 11%, grade IV = 34%, grade V = 49%; Left circumflex--grade I = 2%, grade II = 14%, grade III = 22%, grade IV = 40%, grade V = 22%. The number of coronary arteries with more than 75% obstruction for each group of one, two or three vessel disease were: 1 vessel--41 cases; 2 vessels--56 cases; 3 vessels--68 cases. The number of vessels with more than 75% obstruction for each cause of death were: Wall rupture--1 vessel = 20, 2 vessels = 18, 3 vessels = 11; Septum rupture--1 vessel = 0, 2 vessels = 2, 3 vessels = 2; Shock--1 vessel = 12, 2 vessels = 21, 3 vessels = 30; Acute pulmonary edema--1 vessel = 1, 2 vessels = 9, 3 vessels = 7; Asystole--1 vessel = 4, 2 vessels = 1, 3 vessels = 8; Pulmonary embolism--1 vessel = 2, 2 vessels = 5, 3 vessels = 8; Ventricular fibrillation--1 vessel = 2, 2 vessels = 0, 3 vessels = 2. CONCLUSION: in most patients dying with acute myocardial infarction, the coronary atherosclerotic lesions were present in two or three epicardial coronary arteries. The left anterior descendent artery was the more frequent artery with major lesion (greater than 75%). Major atherosclerotic lesion in just one vessel were more frequent in patients dying by cardiac rupture.

Autopsy↗
PubMed1992

[Clinical case and review of the subject. Prognosis in acute myocardial infarction].

Aiming to discuss the value of the prognostic indices in the acute myocardial infarction (AMI), we present two cases of AMI, where the predictable prognosis at 48 hours of the onset of symptoms is informed by the outcome of each case. In the first one, a patient in cardiogenic shock had a good evolution because he suffered a biventricular infarction that responsed well to hydric overcharge. The other case, a Killip classe I infarction, was complicated by a late left ventricular free wall rupture. We discuss the several aspects of each case, and finally we do a critical aproach of the most common prognostic indices (Killip and Kimbal classes, Peel prognostic groups and Norris prognostic groups).

Heart Rupture, Post-Infarction↗
PubMed1991

[Intraventricular thrombi in acute myocardial infarct. The Iberian Multicenter Study. Presentation of the study protocol and various preliminary results].

OBJECTIVE: To evaluate the incidence of left intraventricular thrombosis and systemic embolism after acute myocardial infarction, as well as to determine the risk factors of each one of them. To study the morphologic aspects of the thrombus and its relation with systemic embolism. CONCEPTION AND POPULATION: 1505 consecutive patients with acute myocardial infarction from six Iberian Hospital Coronary Care Units--five from Spain and one from Portugal--were studied. All protocols included a clinical evaluation and a M-mode and 2D echocardiographic study at days 1, 3, 7 at hospital discharge, as well as at months 1, 3, 6, 12, and 24 of the follow-up. In the intraventricular thrombus evaluation just the III and IV Asinger grades were considered. RESULTS: From the total studied patients an echocardiographic study of good quality for thrombus evaluation was found in 1360, and 305 (22.3%) of these had a left ventricular thrombus. In anterior infarctions the incidence of thrombus was 39.9%, and in the other localizations was 11.2%. In what concerns the thrombus morphologic aspects, we found a small thrombus (less than 4 cm2) in 71% of the cases, and a big one (greater than or equal to 4 cm2) in 29%; the shape was laminar in 53.6%, protuberant in 41.7% and pediculated in 4.6%; the outline was smooth in 56.7% and irregular in 43.3%; the echodensity was considered homogeneous in 60.1% heterogeneous in 37.6% and cavitated in 3.3%. Of the several parameters evaluated the following were correlated with left intraventricular thrombosis: anterior localization of the infarction, left ventricular failure, ventricular aneurysm, post infarction angina, bundle branche block and no thrombolytic therapy. The incidence of systemic embolism in a mean follow-up of 290 days was 3.96%, being maximum in the first month (3.4%), but an embolic episode still occurred in the following months in 3.02% of the cases. Systemic embolism correlated with left ventricular thrombus, the pediculated shape and the big size of it, as well as with the oldest patients. CONCLUSIONS: A high incidence of left intraventricular thrombosis after acute myocardial infarction correspond to a low incidence of systemic embolism. Some parameters correlated with intraventricular thrombus or with embolism, what allowed us to consider them as risk factors of these clinical entities.

Age Factors↗
PubMed1990

[A case of rupture of the left ventricle free wall with papillary muscle dysfunction following acute myocardial infarction, operated on successfully].

The authors present a case of left ventricular free wall rupture post acute myocardial infarction, associated with mitral papillary posterior muscle necrosis, operated by infartectomy and mitral valvular protesis replacement. They refer the various complications occurred during the hospital staying, and discuss its medical and surgical approach. The patient was discharged alive and six months after the infarction keeps a moderate activity.

Female↗
PubMed1989

[Clinical methods for evaluating infarct size and its anatomic correlations. A study conducted with 193 cases. II. Evaluation of infarct size by determining maximal creatine phosphokinase in serum. Enzimatico-anatomic correlations].

AIMS: To compare the infarct size calculated by the peak serum CK method with the anatomic infarct size in a population dying of acute myocardial infarction. CONCEPT AND PLACE OF THE STUDY: To use the method of peak serum CK in the assessment of infarct size, calculated by a method developed by the authors, in a population dying of acute myocardial infarction in a coronary care unit. METHODS: 193 patients who successively died with acute myocardial infarction entered the study. After establishing the exclusion criteria the anatomical infarct size was measured using the method developed by the authors of myocardial slices after fixation of the heart and by the peak CK method. The two methods were correlated using linear regression curves. RESULTS AND CONCLUSIONS: A global correlation between the two methods was found although wide scattered values were found. After dividing the population in several subgroups, the analysis showed that survival below 48 hours, death in left ventricular failure, inferior infarcts and reinfarction influenced negatively this correlation. The anatomical method showed its value for this kind of evaluation having always in mind its known limitations. The enzyme method looked less discriminating as peak CK, obtained by 12 h sampling will seldom reflect the peaks of CK liberation curve. As the study was applied to a population of patients dying of acute myocardial infarction its results cannot be applied without caution to a population of survivors. We anticipate that in such a population peak CK will have a better correlation with real CK peaks even with 12 hours sampling and therefore reflecting more accurately infarct size.

Autopsy↗
PubMed1989

[Clinical methods for evaluating infarct size and its anatomic correlations. Study carried out in 193 cases. III. Comparison of data on the evaluation of the infarct size using the QRS score and a method of maximal creatine kinase determination in the serum].

AIMS: To compare two methods concerning the clinical evaluation of infarct size--one using a QRS score, the other based on peak Ck values--applied to the same population. CONCEPT AND PLACE OF THE STUDY: to determine--based on previously established correlations between a QRS score and the anatomic total infarct size on one hand, and between the peak CK values and the anatomic recent infarct size on the other hand--which myocardial infarction subgroup constitutes the best indication for each method. The study took place in a Coronary Care Unit of a Central Hospital. MATERIAL AND METHODS: 193 patients who died successively of acute myocardial infarction through out 4 years were studied. After establishing the exclusion critéria, the QRS score was calculated according to the method of Selvester modified by Wagner, and peak CK values were evaluated. Infarct size, either recent or old, was determined by means of an anatomical method developed by the authors and based on Hackel's and Alonso's previous works. Correlations were established between data from each clinical method and those from the anatomical method. Several myocardial infarction subgroups were considered for comparison of the correlations found in each subset. RESULTS AND CONCLUSIONS: As long as QRS score was regarded, significant correlations were found between the evaluation by QRS score and anatomical infarct size in the subgroups of patients with severe pump failure, prior myocardial infarction, or total loss of ventricular muscle mass of at least 20 percent; however, a significant correlation was missing when the whole myocardial infarction group was taken into consideration. When peak CK value were considered, a weak significant correlation was found between the evaluation by enzyme determination and anatomical infarct size in the whole group of patients, but a stronger correlation was present in the subgroups of patients with survival longer than 24 hours, anterior wall myocardial infarction, free wall cardiac rupture, or first acute myocardial infarction. In conclusion the choice of the method to be used in the clinical evaluation of infarct size should take into account the type of population beeing studied, and follow the results obtained in different myocardial infarction subgroups as mentioned above.

Creatine Kinase↗