Prolonged use of the food dye tartrazine (FD&C yellow no 5) and its effects on the gastric mucosa of Wistar rats.

Tartrazine is one of the most widely used artificial foods, drugs and cosmetic dyes. It is a nitrous derivative and is known to cause allergic reactions such as asthma and urticaria, as well as having been the focus of studies on mutagenesis and carcinogenesis due to its transformation into aromatic amine sulfanilic acid after being metabolized by the gastrointestinal microflora. 45 male Wistar rats were assigned to a control group (A) or a treatment one (B). The treatment group received 7.5 mg x kg(-1) x day(-1) of tartrazine daily in drinking water offered ad libitum for ten months from weaning to the age of twelve months. There was a significant increase in the number of lymphocytes and eosinophils of the gastric antrum mucosa. No carcinogenetic changes in any gastric area were observed during the study. As tartrazine belongs to the azo class, it is still a possible food carcinogen. Other studies with different doses and schedules, observing their effects associated to other carcinogens should be carried out if their safe use is to be recommended.

Perioperative acute myocardial infarction after valve replacement.

The incidence of fatal acute myocardial infarction (AMI) after valve replacement has decreased with use of cold potassium-induced cardioplegia. Despite this method of myocardial preservation, 12 of 662 consecutive patients submitted to valve replacement had this complication. This study retrospectively analyzes, in those 12 patients, the etiologic profile of fatal perioperative AMI, together with its morphologic aspects. The clinical picture in 11 patients was a refractory low cardiac output state. In only 3 cases was AMI diagnosis confirmed during life. Six patients either had a technical complication or a coronary embolus; in these patients AMI was localized in the vascular bed of a single occluded coronary artery, and its morphologic picture resembled that of usual AMI. The 6 other patients did not have a defined cause for AMI and coronary occlusion was not present. In 4 such patients, there was massive circumferential necrosis, mainly in the subendocardium; comparatively, there was a greater prevalence of hemorrhage, contraction bands and necrosis of the layer of subendocardial cells adjacent to the left ventricular cavity. The findings for this group suggest myocardial necrosis due to cell damage during cardiopulmonary bypass; no predisposing factor for perioperative AMI was identified.

Inferior epigastric artery as a free graft for myocardial revascularization.

The inferior epigastric artery was used as a free graft for direct myocardial revascularization in 22 patients from October 1987 to July 1988. The artery was used either alone or along with internal mammary artery or saphenous vein grafts. The inferior epigastric artery was dissected through an infraumbilical incision without entrance into the peritoneal cavity. The results depend on the technique used for the aortoepigastric anastomosis. When a segment of saphenous vein or a patch of bovine pericardium was sutured to a large aortic orifice with the inferior epigastric artery previously anastomosed to these patches, the patency rate of the free grafts in the early postoperative period was 100%. Histologic examination showed identical structure of the inferior epigastric artery and the internal mammary artery. Application of the inferior epigastric artery is an attempt to increase the use of arterial grafts for myocardial revascularization.

Usefulness of T-cell phenotype characterization in endomyocardial biopsy fragments from human cardiac allografts.

The mean numbers of cytotoxic/suppressor (CD8+) and helper/inducer (CD4+) T cells were determined in 111 successive endomyocardial biopsy fragments from eight cardiac allograft patients in an attempt to define their significance in the rejection process. Endomyocardial fragments from autopsy or donor hearts without myocarditis were evaluated as controls. The mean numbers of CD8+ and CD4+ T cells in the control group were 0.8 and 0.5 cells/field at x400 magnification, respectively. The mean numbers of CD8+ T cells per field in the cardiac allograft biopsies were 2.4, no rejection group; 5.4 mild rejection group; 11.1, moderate rejection group; and 4.9, resolving rejection group. The mean numbers of CD4+ T cells per field for the same groups were slightly lower than those of the CD8+ T cells. The number of CD8+ T cells per field reliably indicated the severity of rejection. Patients with normal numbers of CD8+ T cells and no evidence of rejection had better long-term outcomes (two or fewer moderate rejection episodes) than those with higher numbers. Analysis of the data suggests that the presence of two or fewer CD8+ T cells/field may be considered normal in the myocardial interstitium. The diagnosis of no evidence of rejection should be coupled to the presence of a normal number of CD8+ T cells. High numbers (greater than 10) of CD8+ T cells, even in absence of myocytolysis, should be treated more assertively, including the use of high doses of prednisone, because all our cases with high numbers showed a worse histologic picture at the subsequent biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute myocardial infarction with diffuse endarteritis, contraction bands, and distal thrombosis of the coronary arteries in a heart transplant patient.

The case history of a heart transplant patient who died of an acute myocardial infarction 6 months after the procedure is described. The finding of contraction bands and thrombosis associated with endarteritis suggests that coronary vasospasm may have contributed to the acute myocardial infarction during an episode of vascular rejection.

[Mitral valve insufficiency caused by endomyocardial fibrosis of the left ventricle. A case report]. / Insuficiência da valva mitral por endomiocardiofibrose do ventrículo esquerdo. Relato de caso.

A 38-year old female patient, who had asymptomatic heart disease for seven years, developed progressive and fatal heart failure in eight months. The diagnosis of mitral valve insufficiency was made five months before death. The necropsy revealed that the etiology of mitral insufficiency was isolated left ventricle endomyocardial fibrosis with unusual involvement of the posterior cusp of the mitral valve.

[Fatal active rheumatic disease. Study of 13 necropsy cases]. / Doença reumática ativa fatal. Estudo de 13 casos de necrópsia.

PURPOSE: To study the clinical features of a group of patients with fatal acute rheumatic fever (ARF). PATIENTS AND METHODS: Thirteen patients with ARF, the ages ranged between 4.5 and 25 (mean 14) years. Eight patients were male. Patients were studied in two groups: group A of those 14 year-old or younger (8 cases), and group B of those older than 15 years (5 cases). RESULTS: Clinical presentation was fever and severe heart failure in all patients. In group A, it was the first attack of ARF in 5 patients. The time elapsed between beginning of symptoms and hospital admission ranged between 10 and 90 (mean 40) days. Mitral insufficiency occurred in all patients. The blood leukocyte count was greater than 10000 per mm3 in six cases. Atrioventricular block occurred in one case. Valvular vegetations were detected on echocardiogram in 4 cases. Two patients received antibiotic therapy. Surgical treatment of the valvular heart disease was carried on in one patient. In group B, it was the first ARF attack in 2 cases, the time elapsed between beginning of the symptoms and hospital admission ranged between 4 and 60 (mean 21) days. Leukocyte count greater than 10000 por mm3 occurred in 4 cases. Atrioventricular block was diagnosed in one case. Valvular vegetations on echocardiogram were detected in 2 patients. In two cases, the treatment was antibiotic therapy. Three patients were operated on. CONCLUSION: ARF may still be fatal, even in the first attack or in patients in the third decade of life. Other diagnoses are frequently considered, due to the intense clinical and laboratorial manifestations.

Mitral restenosis in the early postoperative period of a patient with systemic lupus erythematosus.

A forty-eight year old woman, who had undergone mitral comissurotomy and subsequently developed early restenosis, presented with major comissural fusion and verrucous lesions on the cuspid edges of the mitral valve, with normal subvalvar apparatus. Patient did well for the first six months after surgery when she began to present dyspnea on light exertion. A clinical diagnosis of restenosis was made, which was confirmed by an echocardiogram and cardiac catheterization. She underwent surgery, and a stenotic mitral valve with verrucous lesions suggesting Libman-Sacks' endocarditis was found. Because the diagnosis of systemic lupus erythematosus (SLE) had not been confirmed at that time, a bovine pericardium bioprosthesis (FISICS-INCOR) was implanted. The patient did well in the late follow-up and is now in NYHA Class I.

[Fatal cardiac tamponade in systemic lupus erythematosus associated with vasculitis similar to polyarteritis nodosa]. / Tamponamento cardíaco fatal em portadora de lupus eritematoso sistêmico associado com vasculite semelhante a poliarterite nodosa.

We report the case of a 21 year-old woman who developed systemic lupus erythematosus and fatal cardiac tamponade. Necropsy examination revealed cardiac tamponade as well as other findings of SLE and an unsuspected vasculitis similar to polyarteritis nodosa.

[Mitral valve aneurysm associated with mitral insufficiency in absence of aortic insufficiency]. / Aneurisma de valva mitral associado a insuficiência mitral, em ausência de insuficiência aórtica.

Two 31 year old patients were interned with cardiac insufficiency (functional class III). Case number one infective endocarditis with mitral valve 8 months before. Case number two had previous rheumatic disease. Both had severe mitral insufficiency and were submitted to replacement of mitral valve. Surgical findings included the presence of aneurysm mitral leaflet (posterior in case one and both in case two). The pathologic study showed mitral valve prolapse and signs of previous endocarditis in case one and rheumatic lesion in the other case.

Human heart-infiltrating T-cell clones from rheumatic heart disease patients recognize both streptococcal and cardiac proteins.

BACKGROUND: beta-Hemolytic streptococcal infection in developing countries still causes thousands of causes of rheumatic heart disease, demanding surgical valve correction. Antigenic mimicry between self and streptococcal components has been proposed as the triggering factor leading to autoimmunity in individuals with genetic susceptibility. Although heart streptococcal-M protein cross-reactive antibodies have been demonstrated, heart tissue damage seems to be T lymphocyte-dependent. We studied the infiltrating T lymphocytes in rheumatic heart lesions with the aim of understanding the role of cellular immune response at the site of the lesions. METHODS AND RESULTS: We obtained 107 T-cell clones from surgical fragments of cardiac tissue from four rheumatic heart disease patients. We tested their capacity to recognize streptococcal M protein-derived synthetic peptides and heart proteins. We found eight infiltrating T-cell clones from all four patients that simultaneously recognize streptococcal M and heart proteins. Among the M-protein sequences tested, only synthetic peptides corresponding to regions 1 through 25, 81 through 103, and 163 through 177 were simultaneously recognized with heart protein fractions. Interestingly, regions 81 through 103 and 163 through 177 have been known to bear heart cross-reactive epitopes at the antibody level. Five of these clones are CD4+, and one is CD8+. CONCLUSIONS: The presence of heart-M protein cross-reactive T-cell clones in rheumatic heart lesions suggests their direct involvement in the pathogenesis of this disease. The dissection of protective and pathogenic epitopes of streptococcal M protein is an important step in allowing the development of a safe anti-streptococcal synthetic vaccine.

Ductus arteriosus rupture as a balloon catheter atrioseptostomy complication.

A newborn with transposition of the great arteries presented with rupture of the ductus arteriosus after balloon catheter atrioseptostomy. The necropsy study demonstrated persistent ductus patency, and a 0.5-cm-long horizontal fissure could be observed. On microscopy, there was laceration of the intimal layer, with wall dissection and focal hemorrhage extending to the adventitia. Ductus rupture was attributed to the wall weakness, as a consequence of prostaglandin E1 administration.

Molecular evidence for antigen-driven immune responses in cardiac lesions of rheumatic heart disease patients.

Rheumatic heart disease (RHD) is a sequel of post-streptococcal throat infection. Molecular mimicry between streptococcal and heart components has been proposed as the triggering factor of the disease, and CD4(+) T cells have been found predominantly at pathological sites in the heart of RHD patients. These infiltrating T cells are able to recognize streptococcal M protein peptides, involving mainly 1-25, 81-103 and 163-177 N-terminal amino acids residues. In the present work we focused on the TCR beta chain family (TCR BV) usage and the degree of clonality assessed by beta chain complementarity-determining region (CDR)-3 length analysis. We have shown that in chronic RHD patients, TCR BV usage in peripheral blood mononuclear cells (PBMC) paired with heart-infiltrating T cell lines (HIL) is not suggestive of a superantigen effect. Oligoclonal T cell expansions were more frequently observed in HIL than in PBMC. Some major BV expansions were shared between the mitral valve (Miv) and left atrium (LA) T cell lines, but an in-depth analysis of BJ segments usage in these shared expansions as well as nucleotide sequencing of the CDR3 regions suggested that different antigenic peptides could be predominantly recognized in the Miv and the myocardium. Since different antigenic proteins probably are constitutively represented in myocardium and valvular tissue, these findings could suggest a differential epitope recognition at the two lesional heart sites after a common initial bacterial challenge.