Living morphogenesis of the ventricles and congenital pathology of their component parts

Living morphogenetic studies show that each definitive ventricle is constructed from different primitive cardiac segments, and each has its specific anatomical features. These ventricular segments are the atrioventricular junction; the primitive inlet segment, part of the primary heart tube, which initially provides the inlets of each ventricle; the primitive outlet segment, which gives rise to both ventricular outlets; and the apical trabeculated regions of the right and left ventricles which grow from the primary heart tube, respectively. In this review, we describe regional pathology based on the relationship of these primitive ventricular components. We propose that the abnormal morphogenesis of one of these segments gives origin to regional ventricular pathology. For example, abnormal embryogenesis of the atrioventricular canal produces malformations of the atrioventricular junctions, such as double inlet ventricle, absence of one atrioventricular connection, and straddling and overriding atrioventricular valves. Similarly, abnormal morphogenesis of the primitive outlet segment gives rise to malformations of the subarterial region of each ventricle, along with the valves guarding these vessels. The principal anatomical features of these malformations of the ventricular inlets and outlets are described, and their possible morphogenesis is discussed. Due to the fact that the apical trabeculated region of each ventricle arises from a separate primitive segment, each ventricle can be identified according to the pattern of its apical trabeculations. This feature is crucial in the elucidation of complex congenital pathology, such as discordant atrioventricular connections.     

Clinical features of idiopathic mitral valve prolapse]

This paper ask a question; is there a generalized defect of the connective tissue among subjects with primary mitral valve prolapse? Based on clinical methods it was found that paired subjects with and without primary mitral valve prolapse, are different in respect of an arbitrary score of joint hypermobility and phenotypic features. This is a statistically significant difference and suggest a possible molecular defect affecting connective tissue in people with primary mitral valve prolapse. Therefore, biochemical and molecular studies should be done to further characterize this abnormality.     

Pulmonary injuries and cytokine levels after the intraperitoneal administration of pancreatic homogenates in rats.

INTRODUCTION: Our objective was to investigate the effects of the administration of pancreatic homogenates, with or without enzymatic activation, to healthy animals regarding cytokine serum levels and the development of pulmonary distress. MATERIAL AND METHODS: 106 male Wistar rats, divided into three groups, were studied: group A, intraperitoneal administration of homogenates activated with enterokinase; group B, homogenates without enterokinase; and group C, control group with administration of physiological saline solution. Each group was divided into 4 subgroups according to the time of sacrifice: 0, 2, 6 and 24 hours. We studied the pulmonary and pancreatic histology, serum parameters of renal and hepatic function, and serum levels of IL-1beta, IL-6 and TNFalpha. RESULTS: There was no mortality in any group. Pancreatic disorders in A and B groups were noted at 24 hours. These two groups had statistically significant higher transaminase serum levels than those of the control group, as well as statistically significant higher creatinine levels in group A. IL-1beta showed a statistically significant higher level at 6 h in both groups, A and B, but was higher in group A, which also exhibited significant pulmonary histologic damage with respect to controls at 6 h. CONCLUSIONS: The higher IL-1beta level in group A may result from production by peritoneal macrophages under the influence of homogenate enzymatic activation. This may be the reason for lung damage.     

The incidence of Trypanosoma cruzi antibodies in patients with dilated myocardiopathy at the Instituto Nacional de Cardiología Ignacio Chávez]

Our objective was to measure the incidence of humoral immune response against Trypanosoma cruzi among patients with a definitive diagnosis of dilated cardiomyopathy at the Instituto Nacional de Cardiología "I. Chávez" over a year. Thirty seven patients were collected, 15 of them (40%) had antibodies against T. cruzi in two different tests, indirect immunofluorescence and ELISA, the presence of IgG antibody was confirmed through Western blot. There was not differences in clinical picture of cardiomyopathy nor on paraclinical studies. However, there was a significant difference in regard socio economical indexes between the group with positive anti T. cruzi antibodies. They had a predominant rural origin, poor housing and were aware of the vector bug. Also they recalled primary infection in their childhood--American trypanosomiasis could be on important etiologic factor for dilated cardiomyopathy in our country.     

Antiphospholipid arterial vasculopathy

We describe 3 relatively young patients who developed arterial occlusions in a limb requiring amputation. All 3 had antiphospholipid antibodies (APLA). In one, these appeared as part of the clinical and serologic spectrum of systemic lupus erythematosus and in the other 2 as a component of a primary antiphospholipid syndrome. Their arterial angiograms showed gradual narrowing of the arterial lumen and the histopathologic study showed striking intimal and medial proliferation as well as some increase in thickness of the adventitia. There was little evidence of thrombosis but in the 2 patients who were amputated early there was mononuclear cell infiltrate of the large arteries and in all 3 there was also leukocytoclastic vasculitis in the skin and/or muscle. We believe this represents a new form of vasculopathy, probably related to the presence of APLA, possibly triggered by the occurrence of vasculitis.     

Infectious endocarditis caused by Candida. Presentation of 3 cases and review of the literature

We present 3 patients with infective endocarditis due to Candida sp. They were not immunodeficient subjects, but they had major surgery, longterm antimicrobial therapy and prosthetic implants. Candida endocarditis is a difficult diagnosis for biological and technical. There is also poor results with and therapeutic reasons. The combined treatment with amphotericin B and 5-fluorocytosine, plus surgical removal of the infected tissue is recommended widely in the literature.     

Substrate for endothelial prostacyclin production in the presence of platelets exposed to collagen is derived from the platelets rather than the endothelium

Interactions between vascular endothelial cells and blood platelets have been investigated using a model microcirculation consisting of microcarrier beads colonized with human umbilical vein endothelial cells (HUVECs) and perfused with washed platelet suspensions. To simulate the effects of endothelial desquamation and exposure of subendothelium, fibrillar collagen in suspension was coinjected with the platelets. In this model, neither the passage of platelets alone nor collagen alone stimulated prostacyclin (PGI2) production by the HUVECs. Platelets activated by coinjection with collagen released thromboxane A2 (TXA2), and this was associated with the simultaneous production of PGI2 by the HUVECs. By means of double-isotope experiments with [3H]arachidonic acid (AA) incorporated into platelets and [14C]-AA into HUVECs, it was shown that all the PGI2 generated was derived from platelet AA and/or endoperoxides. This interpretation was strengthened by the finding that PGI2 production was not prevented by treatment of HUVECs with indomethacin followed by perfusion with collagen-stimulated platelets. AA metabolites in double-isotope label experiments were further characterized by reverse-phase chromatography, and it was shown that both cyclooxygenase and lipoxygenase products of the HUVECs were derived from platelet membrane lipid. Thrombin regularly produced transient PGI2 release, but showed rapid tachyphylaxis. Platelet-derived compounds including ADP, ATP, and platelet-activating factor (PAF) did not produce PGI2 release by HUVECs in this system. Thus, the transfer of AA and metabolites from collagen- stimulated platelets is likely to be the mechanism for PGI2 production in the context of minor degrees of endothelial desquamation.     

Endoscopic management of variceal bleeding

For the primary prophilaxis of the variceal bleeding, non selective beta-blockers (propanolol, nadolol) are still the mainstay of treatment but endoscopic ligation are becoming more popular Thanks to modern control procedures the acute bleeding mortality has been reduced. Endoscopic ligation is the prefered method for esophageal varices and the cyanoacrylate injection is the better method for fundic varices. Pharmacological therapy with octreotide or terlipresine seems to be effective, specially if endoscopic treatment is not available. TIPS is a good salvage option in case of endoscopic or pharmacologic failure. Endoscopic ligation seems to be the prefered method for secondary prophylaxis, specially compared with sclerotherapy. Some drugs that reduce portal hypertension are a good alternative. It is still very necessary to define technique and criteria of endoscopic variceal eradication to reduce the great variability reported in published trials.     

Histopathological lesions of the liver in hairy cell leukemia: a report of 14 cases

Pathological lesions of the liver were studied in 14 cases of hairy cell leukemia, a rare hematologic neoplasm involving numerous organs. Tumor infiltration of hepatic parenchyma was observed in all cases. Tumor cells were easily recognized by their cytological features, namely their "halo" appearance consisting of a clear rim of abundant cytoplasm surrounding uniform round or slightly indented nuclei. Portal infiltration was observed in all cases, associated with sinusoidal infiltration in 12 cases. A peculiar change of the sinusoids, i.e., the angiomatous lesions, was noted in 9 of 14 patients. Angiomatous lesions consisted of intralobular cavities without zonal predominance which were lined by tumor cells which replaced the normal sinusoidal wall and were filled with red blood cells and tumor cells. This pattern of involvement is different from hepatic localization of other blood malignancies and is highly suggestive of hairy, cell leukemia. It might reflect the unique phenotype of the tumor cells, which express lymphocytic and monocytic features. The angiomatous lesion strongly mimics peliosis hepatis and could be, as well as in peliosis, the consequence of modification of the sinusoidal barrier. In hairy cell leukemia, sinusoidal wall abnormalities might be secondary to infiltration of the sinusoids by tumor cells.