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Biomedical subjects

C Perdigão

Publications and source records attributed to C Perdigão.

At least 19 recordsLinked to original sources

[A challenge].

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Diagnosis

[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

[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

[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.

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[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

[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

[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

[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

[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

[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

[2 cases of acute myocardial infarct complicated by fatal pulmonary embolism].

Two cases of pulmonary embolism with lethal course in the setting of acute myocardial infarction are presented. Both cases are clinically characterized by a late pulmonary embolism occurrence (2nd and 3rd week, respectively), and the presence of a large infarct, heart failure during acute myocardial infarction evolution and the interruption of anticoagulant therapy due to a complication. From the anatomic point of view, both cases had large hearts and very large biventricular infarctions. On the other hand, deep venous plexus constituted the pulmonary embolism origin in one case, and right ventricular thrombosis in the other.

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[Intraventricular thrombi in acute myocardial infarct. Clinicoanatomic study carried out in 193 consecutive cases].

AIMS: To determine the incidence of intraventricular thrombi in patients who died of acute myocardial infarction, as well as to define the clinico-anatomical parameters of the population with thrombi. CONCEPT OF THE STUDY: To apply a clinical as well as an anatomical protocol of prospective study, in patients who died of acute myocardial infarction. The clinical protocol contemplates 64 parameters and the anatomical protocol contemplates 34. in the anatomical study were used very discriminative technics, already presented in previous papers. PLACE OF THE STUDY: The study took place in a CCU and pathological department of an University Hospital. MATERIAL AND METHODS: 193 patients who died successively of acute myocardial infarction in a CCU between 1983 and 1986. The only criteria for the inclusion in the study was the possibility of doing a necropsy study, which was done in 77% of the patients who died in that period. The study was a prospective one, being excluded only the patients in whom the anatomical study didnt confirm recent myocardial infarction. The clinical data were observed during the stay in the CCU using a protocol developed for this study. In the anatomical study a protocol developed by the authors was applied, using very discriminative anatomical quantification technics of the infarct size as well as of the coronary obstruction degree by atherosclerotic plaques. All data were stored and treated in a computer program developed for this study. RESULTS: From the 193 cases that have been studied, 88 (43%) presented thrombus in at least one of the ventricular cavities, 38 (26%) only in left ventricle, 15 (8%) only in right ventricle and 35 (18%) in both ventricles. The set with thrombus has presented a few characteristics which granted it some individuality. Thus, this group presented: a higher delay between the beginning of acute myocardial infarction and the admission in the CCU (and so in the beginning of the anticoagulant therapy), lower prevalence of diabetes, higher prevalence of left ventricular failure (Killip class III or IV), higher prevalence of cardiogenic shock and so a higher need of inotropic therapy, higher heart weight, higher prevalence of auricular thrombi and bigger infarct size when evaluated by a QRS score. In the group with left ventricular thrombi, the anterior infarct was more frequent and in the group with right ventricular thrombi the right ventricular infarct was also more frequent. The systemic embolism was uncommon in this group (1 case in 193 patients). CONCLUSIONS: 1. The intraventricular thrombi occurs in about half of the patients who died of acute myocardial infarction. 2. The group with thrombi has presented some characteristics which makes it different from the group with no thrombi. 3. The delay in the beginning of the anticoagulant therapy seems to be a risk factor of intraventricular thrombosis.

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[Incidence and forms of clinical presentation of the various morphologic types of myocardial laceration in the acute phase of infarct. A 4 years' caseload at a coronary unit. A clinico-anatomic study of 193 successive cases].

AIMS: To determine the incidence of different morphological type of myocardial laceration (wall rupture) in patients who died of acute myocardial infarction, as well as to study the several clinical forms of presentation of different types of myocardial laceration. CONCEPT OF THE STUDY: To apply a protocol of prospective study, that includes 64 clinical and 34 anatomical parameters, using very discriminative technics in the anatomical study, already presented in previous papers. PLACE OF THE STUDY: The study took place in a CCU and pathological department of a University Hospital. POPULATION: Of 1308 patients successively admitted in a CCU with acute myocardial infarction between 1983-1986, 252 have died. It was possible to perform a necropsy study in 193. The only criterion for inclusion was the family agreement. METHODS: The study was a prospective one, being excluded only the patients in whom the anatomical study didn't confirm recent myocardial infarction. The clinical data were observed during the stay in the CCU, using a protocol developed for this study. In the anatomical study a protocol developed by the authors was applied, using very discriminative anatomical quantification technics of the infarct size as well as of the coronary obstruction degree by atherosclerotic plaques. In the study of the myocardial laceration a fourteen septal perpendicular cuts technic was applied, with a laceration development macroscopic study, and microscopic study of the more interesting cuts. All data were stored and treated in a computer program developed for this study. RESULTS: From the 193 cases that have been studied, 49 presented a complete free wall rupture (25%) and in two others there were an interventricular septal rupture and free wall rupture. The amount of free wall rupture was then 51 cases (26%), with a corrected incidence for the population with AMI of 5.1%. In 7 cases we found an interventricular septal rupture (in two cases associated with complete free wall rupture and in other two cases with an incomplete left ventricular rupture), what represents an incidence in necropsy of 3.6%. Since that in this period five patients with septal rupture have been operated and in three others the hemodynamic diagnosis was made, dying this patients without being performed necropsic study, the amount of septal ruptures was of 15 cases, what represents a corrected incidence of 1.1% in the population with AMI. The clinical forms of presentation of free wall rupture were the following: syncope followed by death (60%), shock (21%), transitory syncope (4%), psycho-motor troubling (4%). Pain persistence or recurrence associated with other clinical symptoms occurred in 63% of the patients. Hypotension, not always evoluting to shock, occurred in 33%, and pericarditis in 21% of the cases. When the different anatomical types of free wall rupture were considered (type I-direct rupture; type II-multicanalicular rupture; type III-rupture covered by an interventricular thrombus), we observed that in type I there was prevalence of syncope (71% and only 50% showed pain persistence or recurrence, when in type II syncope occurred in 67% and shock in 22%, with pain in 56%, and in type III the occurrence of syncope and shock were similar (44% vs 38%), with pain in 81% of the cases. Hypotension was verified in 56% in type III, 21% in type I and 22% in type II. Pericarditis never occurred in type I, happened in 33% in type II and 25% in type III. The terminal accident took an average 44 minutes long in type I, 3.8 hours in type II and 9.2 hours in type III. The delay in admission was nine hours in type I, 19 in type II and 30 in type III, and the time between the onset of symptoms and death was 2.9, 2.7 and 5.4 days respectively in types I, II and III. In what concerns the interventricular septal rupture shock occurred in all cases but one, in which association with free wall rupture determined cardiac tamponade with syncope.(ABSTRACT TRUNCATED AT 400 WORDS)

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