Biomedical subjects
C Ribeiro
Publications and source records attributed to C Ribeiro.
Wall motion abnormalities and late ventricular arrhythmia during the predischarge phase of acute myocardial infarction.
BACKGROUND: Left ventricular wall aneurysm is a complication of acute myocardial infarction which has been considered a precipitating factor of cardiac failure and ventricular arrhythmia. We have evaluated the relation between severe left ventricular wall motion abnormalities and ventricular arrhythmia. METHODS: During a two-year period 146 patients admitted to a coronary care unit with acute myocardial infarction were studied. Radionuclide angiography performed within the second and the fourth weeks was used to analyse phase and wall motility changes, and patients were divided into three groups: 1) Hypokinesia and/or akinesia localized to one segment: with no or slight changes in phase image--102 patients; 2) Aneurysm: left ventricular deformity with well-defined chromatic changes in phase image--19 patients; and 3) Dyskinesia and/or extensive akinesia of two or more segments: phase image with diffuse heterogeneous changes--25 patients. Ventricular arrhythmia was studied using Holter electrocardiography taken during the second week of acute myocardial infarction. Three rhythmic profiles were considered: no premature ventricular contractions--41 patients; with three or more than three premature ventricular contractions per hour--38 patients; repetitive premature ventricular contractions--20 patients. RESULTS: Premature ventricular contractions were absent in 31 (30%) of the patients with hypokinesia/localized akinesia vs 8 (42%) of the patients with aneurysm, and vs 2 (8%) of the patients with dyskinesia/extensive akinesia. Premature ventricular contractions were frequent (> or = 3/h) in 22 (22%) of the patients with hypokinesia/localized akinesia vs 4 (21%) of the patients with aneurysm (p = 0.35; NS), and vs 12 (48%) of the patients with dyskinesia/extensive akinesia (p=0.003). Repetitive premature ventricular contractions were present in 10 (10%) of the patients with hypokinesia/localized akinesia vs 2 (11%) of the patients with aneurysm, and vs 8 (32%) of the patients with dyskinesia/extensive akinesia (p=0.008). CONCLUSIONS: We conclude that the presence of aneurysm was not associated with a higher occurrence of ventricular arrhythmia, but patients with dyskinesia/extensive akinesia had a higher occurrence of ventricular arrhythmia, > or = 3 premature ventricular contractions per hour and repetitive premature ventricular contractions. Our results suggest that ventricular arrhythmia is related to functionally severe wall motion abnormalities, and not to anatomical discriminants. This finding leads us to suggest different electrophysiological mechanisms behind these two entities.
Identification of GTP-binding proteins in turtle urinary bladder epithelial cells.
Water and electrolyte transport in turtle urinary bladder closely resembles that present in the mammalian collecting tubule. Although cAMP is known to participate in the control of mucosal transport processes, the GTP-binding inhibitory Gi and stimulatory Gs proteins which link receptors on the cell surface to the adenylate cyclase system remain to be identified in this urinary epithelium. To this end, individual cells harvested from the mucosal surface of the turtle bladder were isolated using a discontinuous density Ficoll gradient. Examination by electron microscopy of the material from the different layers of the Ficoll gradient confirmed that bands II and III contained carbonic anhydrase-rich cells and granular cells, respectively. Identification of Gi and Gs in carbonic anhydrase-rich and granular cells was accomplished using pertussis (PT) and cholera toxins to promote [32P] ADP ribosylation of the proteins. Separation of Gi and Gs from other cell proteins was accomplished using polyacrylamide gel electrophoresis and autoradiography. Pretreatment of cells with 0.2% triton X-100 substantially magnified the ADP-ribosylation of Gi by PT. A doublet form of Gi was present in the 40-kD region and indicated heterogeneity of the PT substrate in granular and carbonic anhydrase-rich cells. Gs was observed as a single polypeptide at the 42-kD region in both cell types. A distinct 45-kD peptide not present in mammalian collecting tubule was identified by both toxins in granular cells and by cholera toxin in carbonic anhydrase-rich cells. In summary, this investigation identified and characterized Gi and Gs proteins in carbonic anhydrase-rich and granular cells from the mucosa of turtle urinary bladder.(ABSTRACT TRUNCATED AT 250 WORDS)
[Therapeutic application of myocardial cytoprotection].
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The problem of cardiovascular disease in southern Europe.
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Insights into the role of thromboxane A2 and serotonin in the pathogenesis of unstable angina.
New research about platelet and endothelial functions is allowing us to better understand the pathogenesis of myocardial ischemic episodes in patients with unstable angina, creating new perspectives for the rational utilization of therapies. In patients with unstable angina, the episodes of symptomatic and silent ischemia are caused by repeated reductions of coronary blood flow. They are the result of the mechanical effect of the growing thrombus, which causes intermittent episodes of partial obstruction of the arterial lumen, in association with vasoconstriction at the stenotic site and dependent coronary arterial bed, produced by the cyclic release of platelet derived vasoactive products, namely thromboxane A2 and serotonin. Several studies, many of them in animal models of thrombosis, suggest that serotonin and thromboxane A2 are mediators of platelet aggregation, adynamic obstruction and coronary artery thrombosis. Because they cause coronary cyclic flow reductions, they are implicated in the pathogenesis of myocardial ischemic episodes during unstable angina. Drugs that interfere with the arachidonate pathway, and the 5-HT2-receptor antagonists, have been proven to decrease or abolish coronary cyclic flow variations in animal models and man. However, further studies should be done to test the hypothesis that the association of a 5-HT2-receptor antagonist with aspirin may contribute to decrease myocardial ischemia and prevent coronary occlusion in patients with unstable angina. Continuous Holter monitoring during the first week after admission in the hospital should be a good method to evaluate the eventual efficacy of this new class of drugs in abolishing or decreasing the frequency, intensity and duration of myocardial ischemic episodes in patients with unstable angina. The central role of serotonin in the pathogenesis of thrombotic events, and the presumed preventive effect of ketanserin, were the bases of a national multicenter pilot controlled study designed to evaluate the safety and efficacy of ketanserin plus aspirin in the secondary prevention of patients with unstable angina and non-Q wave myocardial infarction (KATUA Trial).
[Acute myocardial infarct in the elderly. Creating scientific bases for its therapy is urgent].
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[The strange lightness of quality...].
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[Medical education].
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[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.
[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.
[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.
[Revista Portuguesa de Cardiologia. Quality and prestige for the use of cardiovascular medicine].
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[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).
[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)
[Revista Portuguesa de Cardiologia. Quality and prestige to the service of cardiovascular medicine].
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[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.
[Angiotensin I converting enzyme inhibitors in ischemic cardiopathy].
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