Frequency of metastatic tumors in the heart

Introduction. Secondary or metastatic tumors in the heart occur more frequently than primary ones, and, according to the published series, their frequency found in autopsic material ranges from 1.6% to 20.6%. Metastatic tumors in the heart are rarely clinically symptomatic, and, therefore, they are rarely diagnosed within the lifetime. They are mostly diagnosed at autopsy. The aim of this study was to analyze the frequency of metastatic tumors of the heart, their primary localization, as well as the localization of the metastases found in the autopsic material within the period 1972−2004. Metods. During the autopsy of the patients died of metastatic tumors, we microscopically and macroscopically analyzed all the organs and tissues to determine the metastases of primary tumors in other organs, especially in the heart and pericardium. Results. Within the period from 1972−2004, 11 403 autopsies were performed. In 2 928 (25.6%) out of 11 403 autopsies, the presence of malignant tumor was diagnosed, and in 79 (2.7%) of these cases, metastasis of the heart was found out. Only in 5 of the cases, the presence of metastasis in the heart was diagnosed during the lifetime. The most frequent metastases in the heart were caused by pulmonary carcinoma (18 cases), leukemia and malignant lymphoma (8 cases, each), then pancreatic and breast carcinoma, while the metastases of other carcinomas were rather rare. In 40 (60.76%) cases, the metastasis was localized in the myocardium, but more often in the left ventricle, in 24 (30.38%) cases in the pericardium, in 4 cases in the epicardium and in the 3 of them in the mitral and tricuspid valve. Only in one case of renal carcionoma, metastasis was found in the right atrium and it occurred by spreading (dissemination) through the lumen of the inferior vena cava. Conclusion. Metastatic tumors of the heart are rather rare, and rarely clinically symptomatic, and, thus, rarely diagnosed during life. The methods of choice for the diagnosis of the metastasis in the heart are echocardiography, computerized tomography, magnetic resonance imaging, cytological analysis of the pericardial effusion and biopsy. The treatment includes surgery, chemotherapy and radiotherapy

Changes of calcium in blood and urine during different salt intake regimens in hypertensive subjects

The findings of this study support the opinion of altered calcium metabolism in hypertensive subjects sensitive to salt intake. By demonstrated results we tried to define clinically different pathophysologic and potentially different therapeutic subgroups in hypertensive population and to point to clinical and biochemical heterogeneity of primary hypertension

Importance of inflammation in arteriosclerotic plaque destabilization and rupture

Introduction. Although Rudolf Virchow considered arteriosclerosis an inflammatory disease in his book Cellular Pathology published in 1858, the opinion that it was a degenerative arterial disease as a civilization disease prevailed. Nowadays, a great attention has been paid to the inflammatory process in the pathogenesis of arteriosclerosis and particularly in the destabilization and rupture of plaque. Aim. To find out whether T and B lymphocytes, lipid macrophages, vascular smooth muscle and mast cells as well as plaque destabilization and rupture are present in ruptured arteriosclerotic plaque in the coronary arteries. Methods. Histochemical and immunochemical analyses of 68 ruptured arteriosclerotic plaques from the coronary arteries were performed. Microscopic examination revealed the presence of inflammation elements in all of them. The following histochemical and immunochemical methods were applied: Masson's trichrome, actins, vimentin, CD3, CD43, CD68, CD20, CD45 and chlorine acetyl esterase. The control group included 10 arteriosclerotic plaques from the coronary arteries with fibrous cap, but without inflammation cells. Results. Rupture of the arteriosclerotic plaque fibrous cap, with thinned and torn collagen fibers, was found in all of the 68 arteriosclerotic plaques. In 57 out of 68 analysed plaques, the increased number of T-lymphocytes, lipid macrophages, vascular smooth muscle and mast cells particularly on the plaque rupture site were found. In the remaining 11 specimens, mast cells were present in a somewhat smaller number. In the control group with the stable plaque, inflammation cells were not observed. Conclusion. Our results pointed out that the inflammatory elements, which might exert an effect upon the arteriosclerotic plaque destabilization, and rupture had been present in the ruptured arteriosclerotic plaque

Morphological changes in aorto-coronary vein graft: The analysis of autopsy and biopsy material

Background. Patients with implanted aortic coronary grafts have different survival time, which raises the question why the efficacy of graft implants is so poor. The aim of this study was to present the results of the analysis of morphological changes in the vein grafts taken after the death of patients who died after surgery in different time intervals, as well to present the analysis of the grafts obtained after surgical reintervention. Methods. The total number of 656 grafts of 308 dead patients was analyzed, as well as 76 grafts from 40 patients who underwent surgical reintervention. According to the duration of the graft since surgical intervention until death, all the analyzed changes were divided into two groups: a) early changes and complications, and b) late changes and complications in aorto-coronary vein grafts. Results. After the autopsy, 518 vein grafts from the first group were evaluated histopathologically. Changes were found in the form of small or large areas with peeled endothelium in 266 grafts, with the insudation of fibrin and thrombocytes in such places, subendothelial edema, and occlusive thrombosis of the graft lumen. Significant stenosis, which occurred distally from the anastomoses, was present in 118 grafts without changes in the walls of the graft, and there was significant narrowing of the graft lumen in 134 vein grafts due to intimal hyperplasia. In the second group, 138 grafts were histopathologically analyzed after autopsy. Significant hyperplasia was present in 117 grafts with the migration of smooth muscle cells from media into intima, and in 21 grafts there were atheromatous plaques. In 120 veins analyzed before the graft implantation, the lesion or the lack of endothelium was found, as well as the penetration of fibrin and blood elements and intimal hyperplasia. In 46 veins analyzed before the graft implantation, significant intimal hyperplasia with the elevated number of smooth muscle cells was found. Conclusion. The most frequent lesions in the grafts were the lesions of the endothelium, which caused thrombosis formation and lumen occlusion. Intimal hyperplasia in patients with longer survival time occurred due to the migration of smooth muscle cells from the media, or due to the formation of atherosclerotic plaques, which caused graft lumen stenosis or thrombosis