False chordae tendineae in right ventricle of adult human hearts - morphological aspects.

INTRODUCTION: False chordae tendineae are fibrous-muscular bundles which do not interconnect with right atrioventricular valves. The structures have occasionally been described in the right ventricle. There are reports suggesting their influence on electromechanical processes taking place in the heart, in thromboembolic events as well as in the course of cardiac invasive procedures. The objective of the study was to perform a macroscopic evaluation of false chordae tendineae in the right ventricle. MATERIAL AND METHODS: The research specimens consisted of 100 hearts of adult humans, aged from 18 to 59 years, fixed in a solution of 10% formaldehyde and 98% ethanol. The ratio of false chordae tendineae to individual elements of the right ventricle, such as its walls, papillary muscles, septomarginal trabecula and the apex of the ventricle, was examined. RESULTS: During examination, six types of chordae tendineae were described based on the criterion of the type of structures they connected. The most common were false chordae connecting ventricle walls within its apex, while the least common were individual segments of papillary muscles. The research proved that the examined structures are morphologically extremely diverse. Substantial clinical implications of their presence seem very probable. CONCLUSIONS: The present work is the first of a scheduled series devoted to the problem of false chordae tendineae. Further analyses will cover the subject of morphological aspects in a microscopic perspective.

DQA1*03011 allele: protective or an adverse effect on the development of sarcoidosis; preliminary study.

BACKGROUND: Sarcoidosis (SA) is a multisystem granulomatous disorder of unknown etiology. It seems likely that in genetically different predisposed hosts, the same antigen(s) may cause the development of sarcoid Th1 response. The interaction of the T-cell receptor with the human leukocyte antigen-DQA1*03011 peptide-complex can affect T lymphocytes activation in a dose-response manner. OBJECTIVES/METHODS: To test occurrence of DQA1*03011 allele in SA, we compared the distribution of DQA1 alleles in 32 SA patients, 37 TB patients and in 58 healthy volunteers, using a PCR-SSP "high-resolution" method. RESULTS: Our results revealed that after Bonferroni correction DQA1*03011 were less common in SA patients than in the controls (OR 0.16, 95%CI 0.03-0.75). In TB, DQA1*0303 were significantly more frequent and DQA1*0505 less present as compared to the controls (OR 11.03, 95% CI 1.20-95.80, OR 0.29, 95% CI 0.01-0.88). Comparing DQA1 alleles in both patient groups, DQA1*0501, DQA1*0505 alleles were more common and DQA1*03011, DQA1*0302, DQA1*0303 were less common after Bonferroni correction in SA than in TB. CONCLUSION: We revealed that DQA1*03011 allele was less common in SA than in the controls and TB. It seems possible that a low frequency of DQA1*03011 occurrence may be also involved in the etiopathogenesis of SA.

Comparative analysis of mycobacterial heat shock proteins-induced apoptosis of peripheral blood mononuclear cells in sarcoidosis and tuberculosis.

Sarcoidosis (SA) is a granulomatous disorder of an unknown etiology. Mycobacterium tuberculosis heat shock proteins (Mtb-hsp), considered as causative agents, play an important role in apoptosis. A role for apoptosis has been proposed in pathogenesis of SA and tuberculosis (TB) granuloma formation but results remain controversial. Differences in Mtb-hsp-induced apoptosis between SA, TB, and healthy subjects found in this study might put some light on the etiology of SA. Early apoptotic peripheral blood mononuclear cells (PBMC) were determined in 22 SA patients, 20 TB patients, and 20 healthy volunteers by flow cytometry (Annexin-V-FITC). Our results revealed that spontaneous apoptosis of monocytes and CD8+ T-cells was comparable between tested groups. Apoptosis of unstimulated CD4+ T-cells was significantly lower in TB versus controls and insignificantly lower versus SA. Mtb-hsp- and PHA (Phytohemagglutinin)-induced monocytes apoptosis was significantly lower in TB versus controls and SA. Mtb-hsp-induced CD4+ T-cell apoptosis was significantly lower in TB versus controls and SA. There were no differences of PHA-induced CD4+ T-cell and CD8+ T-cell apoptosis between tested groups. Apoptosis of Mtb-hsp-induced CD8+ T-cells was significantly lower in TB and SA versus controls. Analysis of PBMC apoptosis before and after stimulation in each tested group revealed that, in contrast to TB, sarcoid monocytes were resistant to Mtb-hsp- and PHA-induced apoptosis and CD4+ T-cells were resistant to PHA- but not Mtb-hsp-induced apoptosis. CD8+ T-cell apoptosis, before and after Mtb-hsp or PHA stimulation, was significantly increased in all tested groups. It seems likely that dysregulated apoptosis of CD4+ T-cells and resistant apoptosis monocytes may be involved in pathogenesis of SA.

[Apoptosis mononuclear cells in sarcoidosis]. / Apoptoza komórek jednojadrzastych w sarkoidozie.

Sarcoidosis (SA) is a systemic granulomatous disorder of unknown etiology. The diagnosis is firmly established when clinicoradiological findings are supported by histological evidence of noncaseating epithelioid cell granulomas found on tissue biopsy Diagnosis of SA requires exclusion of other causes of granuloma formation, first of all Mycobacterium tuberculosis. Sarcoidosis is a disease known to be associated with various immunological alterations, including depression of cutaneous delayed-type hypersensitivity and an activation of monocytes/macrophages and a heightened helper T cell type 1 immune response at sites of disease but the mechanism leading to the persistent accumulation of inflammatory cells is not understood. In some studies, apoptosis is considered as factor in pathogenesis of sarcoid and tuberculous granuloma. Apoptosis--programmed cell death is a genetically encoded cell elimination program which ensures equilibrium between cell proliferation and cell death and by which crippled, useless or infected cells are eliminated as part of normal physiology. Aberrations in signalling, in receptors or alterations in mechanism of apoptosis are involved in the occurrence of tuberculosis. To date, there are a few of papers concerning alternations of apoptosis of peripheral and alveolar mononuclear cells in sarcoidosis have been published but the results have been controversial.