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Biomedical subjects

C Ribeiro

Publications and source records attributed to C Ribeiro.

At least 55 records · Page 3Linked to original sources
PubMed1993

[The clinical significance of mitral insufficiency detected by Doppler echocardiography in acute myocardial infarct].

OBJECTIVE: To assess the clinical significance of mitral regurgitation (MR) diagnosed by pulsed Echo-Doppler in patients with acute myocardial infarction (AMI). SETTING: Admission in a coronary care unit and a mean follow-up of 12 months. PATIENTS: Seventy nine patients admitted in a coronary care unit, and 66 patients were followed-up for 12 months (mean). METHODS: Pulsed Echo-Doppler were performed within three days after admission and the presence of MR was analyzed by apical four and two chamber views. RESULTS: There were 62 males and 17 females (mean age: 61.4 +/- 10.8 (31-84) years). The location of AMI was: anterior--40, inferior--30, non-Q wave--6, indeterminate--2 and combined--1. Killip classes were: class I--50, class II--20, class III--7 and class IV--2. 17 patients had a previous AMI. The in-hospital mortality was 9 patients (12%) and the post-hospital mortality was 3 patients (4.5%). MR was detected in 24 patients (30%) in whom 14 (58%) had no murmur of MR previously auscultated. MR was considered moderate in 10 patients and mild in the others 14 patients. There were no significant statistical differences in the frequency of MR in relation to AMI location: anterior 57%, inferior 40% (chi 2 = 0.71, NS); to the presence of a previous AMI: 47% vs 26% (chi 2 = 1.93, NS); to age (61 vs 62 years). The patients with MR suffered a more serious degree of heart failure (class III + class IV): 29% vs 4% (chi 2 = 8.41, p < 0.005); higher hospital mortality: 29% vs 4% (chi 2 = 8.41, p < 0.005); and higher one year mortality: 37.5% vs 5.5% (chi 2 = 10.9, p < 0.001). CONCLUSION: The presence of MR had no relationship with AMI location, the presence of a previous AMI or patients age. The patients with MR had a more serious degree of heart failure, higher hospital and one year mortality. The presence of MR detected by pulsed Echo-Doppler is a sign of bad prognosis although being auscultatory silent in a half of patients.

Adult↗
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

[A case of incessant junctional tachycardia in a female patient with aneurysm of the interauricular septum].

A permanent supraventricular tachycardia (SVT) was diagnosed in a 54-year-old hypertensive but cardiologically asymptomatic female patient, admitted to a surgery department for biliary lithiasis and hepatic echinococcosis. Heart rate was about 130 bpm and ECGs showed negative P waves in leads I, II, III, aVF, and precordial leads V2 to V6, being the RP' interval longer than P'R interval. Pharmacological intervention during Holter monitoring (20 hours) was instituted: following i.v. propranolol (4 mg), heart rate progressively decreased (to 112 bpm), mainly due to an increase in SVT RP' interval, and brief, spontaneous SVT interruptions occurred, preceded by P'R interval prolongation; SVT stopped after P' recording, and resumed after 2 sinus beats, (showing enlarged P waves and slightly prolonged PR interval), induced by cycle length shortening; later on, under i.v. amiodarone infusion (100 mg/hour) and coincident with the sleeping period, SVT cycle length progressively increased (to 600 msec), due to equivalent increases in P'R and R'P intervals. Two premature ventricular contractions (PVC) occurred during Holter monitoring at a coupling interval of 80-85% of SVT cycle length (480 msec): one PVC apparently originated in left ventricle lateral wall, captured the atria, which were activated 75 msec earlier than expected; the other PVC, apparently originated in left ventricle septoapical region, did not interfere with SVT cycle length. Before these data, a diagnosis of circus movement tachycardia, incorporating a concealed accessory pathway with slow retrograde conduction and ventricular insertion in the postoroseptal or left posterior paraseptal region, and showing minor impairment of antegrade AV nodal conduction, was made. Invasive electrophysiological study was then discarded. With combined oral antiarrhythmic therapy (amiodarone, 600 mg/d), plus propafenone, 450 mg/d), sinus rhythm was permanently restored, with evidence of intraatrial block, slightly prolonged PR interval and no preexcitation. Transesophageal echocardiography revealed a small atrial septal aneurysm associated with a small atrial septal defect; echocardiographic features were consistent with the hypothesis of incomplete regression of the atrial septal aneurysm after partial closure of the atrial septal defect. Abdominal surgery (cholecystectomy plus partial hepatic pericystectomy) was performed without any complications or SVT recurrences. During a 6-month follow-up period, maintaining amiodarone (200 mg/d) and propafenone (450 mg/d), the patient remained SVT-free, and Holter monitoring performed at 3 and 5 months showed permanent sinus rhythm and 1:1 AV conduction with slightly prolonged PR interval (less than 0.29 sec and shortening at faster heart rates). This case documents Holter monitoring capability for the evaluation of tachycardia mechanisms in patients with permanent SVT.

Amiodarone↗
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↗
PubMed1992

[Ethics in researcher-research promotor relations].

The performance of Clinical Trials can give rise to ethical problems especially between the researchers and the promotors but sometimes also with those who are in charge of the publication of results. Medicine and the Pharmaceutical Industry must face up to the need to try and save a marriage that is not only one of convenience but most of all lifesaving. The Industry supports the major slice of Postgraduate and Continuous Medical Education with its main goal being the promotion of its products. The Educational component we doctors are interested in is usually secondary for the Industry. A Clinical Trial comprises several steps beginning with the design of its protocol, its discussion by promotors and scientists and its performance where researchers, monitors, and official auditors have the main role. The analysis of the results should be handled by official boards unrelated to either promotors or researchers and their publication should be undertaken by a reliable Medical Journal whose editorial board would authenticate the accomplished scientific work. Ethical Commissions, both national and institutional, have a unique role in the analysis and authorization of Clinical Trials. Before any drug is put onto the pharmaceutical market, it is obligatory that the four successive phases of Clinical Pharmacological Studies be accomplished. A common problem we usually face is to differentiate a Phase IV from just a Promotional Trial. When a Promotional Trial is done, all the clinical goals of investigation have already been reached. The objectives of Promotional Trials are merely related to the Marketing Department and disregard any scientific purposes. Promotional Trials should not involve Universities, Hospitals and other official Institutions.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1991

[Antithrombin III. Physiologic, physiopathologic and laboratory aspects].

Hemostatic control is based in a delicate balance between the activities of activator enzymes and their inhibitors, each one depending on a large number of proteins. Plasma Antithrombin III (ATIII) is one of the most important coagulation inhibitors and the fundamental enzyme for the therapeutical action of heparin. In the last years it was well established that ATIII deficiency accounts for a thrombotic state and inefficiency of heparin therapy. In this work, the authors review the biology of ATIII including its biochemical nature, its physiology, physiopathology and mechanism of action, analysing the implications of its deficiency. The authors draw the attention on clinical and laboratory studies that analyse the prevalence and importance of congenital and acquired deficiency of ATIII, in relation to the prevalence of venous thrombosis. Finally, the laboratory methods applied to the study of ATIII and to the biological control of heparin therapy are described with emphasis on the importance of the ATIII concentrates on this type of treatment. Also the fundamental aspects of heparin resistance are specially mentioned.

Antithrombin III↗
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

[Rhythmic profiles of the late phase of acute myocardial infarction as a function of age].

OBJECTIVES: To evaluate the incidence of ventricular arrhythmias in the late phase of acute myocardial infarction (AMI) and to compare it with the following clinical parameters: age, sex, AMI localization, ventricular function (Killip classes), maximal creatinokinase (CK max) and the presence of sinus tachycardia. DESIGN: Prospective study, during a period of 31 months, of a non-selected group of patients with AMI. SETTING: Coronary Care Unit (UTIC-Arsénio Cordiero). PATIENTS: Non-selected group of 153 patients with acute myocardial infarction who survived the second week of disease. MATERIAL AND METHODS: 24-hour Holter ECG performed between the 4th and the 25th day of AMI. The patients were divided into two groups according to the hourly frequency of premature ventricular beats (PVB): less than 3 per hour (PVB less than 3/h) and 3 or more per hour (PVB greater than or equal to 3/h). RESULTS: PVB greater than or equal to 3/h occurred in 36 patients (24%). There was no differences in the occurrence of ventricular arrhythmias between sex, AMI localization, AMI size evaluated by CK max, and the presence of sinus tachycardia. Patients in Killip class III had more ventricular arrhythmias (67%) than patients in Killip class I (23%) (p less than 0.005), in Killip class II (18%) (p = 0.007), and in Killip IV (0%) (p = 0.017). In patients with serious left ventricular failure (classes III + IV) the ventricular arrhythmias were not significantly higher (40%) than in patients without serious left ventricular failure (classes I + II) (22%) (chi 2 = 2.5; p less than 0.25 NS). Patients with less than 41 years old had less PVB greater than or equal to 3/h (4%) than patients between ages 41-69 (24%) (p less than 0.05), and than patients over 70 years old (47%) (p = 0.00075). CONCLUSIONS: The majority of patients (76%) showed a low risk rithmic profile (PVB less than 3/h) in the late phase of AMI. Among all parameters the age of the patients was the one best related to the occurrence of ventricular arrhythmias. Sex, AMI localization, AMI size, and the presence of sinus tachycardia were not related to the presence of PVB. A slight tendency was found in patients with heart failure to have more PVB. On the other hand the elder group carried a statistically significant risk factor for a higher occurrence of ventricular premature beats.

Adult↗