310 resultados para Acute myocarditis


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Abstract Hypertension affects 25% of the world's population and is considered a risk factor for cardiovascular disorders and other diseases. The aim of this study was to examine the evidence regarding the acute effect of exercise on blood pressure (BP) using meta-analytic measures. Sixty-five studies were compared using effect sizes (ES), and heterogeneity and Z tests to determine whether the ES were different from zero. The mean corrected global ES for exercise conditions were -0.56 (-4.80 mmHg) for systolic BP (sBP) and -0.44 (-3.19 mmHg) for diastolic BP (dBP; z ≠ 0 for all; p < 0.05). The reduction in BP was significant regardless of the participant's initial BP level, gender, physical activity level, antihypertensive drug intake, type of BP measurement, time of day in which the BP was measured, type of exercise performed, and exercise training program (p < 0.05 for all). ANOVA tests revealed that BP reductions were greater if participants were males, not receiving antihypertensive medication, physically active, and if the exercise performed was jogging. A significant inverse correlation was found between age and BP ES, body mass index (BMI) and sBP ES, duration of the exercise's session and sBP ES, and between the number of sets performed in the resistance exercise program and sBP ES (p < 0.05). Regardless of the characteristics of the participants and exercise, there was a reduction in BP in the hours following an exercise session. However, the hypotensive effect was greater when the exercise was performed as a preventive strategy in those physically active and without antihypertensive medication.

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1.-Since the parietal endocarditis represents a chapter generally neglected, owing to the relative lack of cases, and somewhat confused because there various terms have been applied to a very same morbid condition, it justifies the work which previously we tried to accomplish, of nosographic classification. Taking into account the functional disturbances and the anatomical changes, all cases of parietal endocarditis referred to in the litterature were distributed by the following groups: A-Group-Valvulo-parietal endocarditis. 1st . type-Valvulo-parietal endocarditis per continuum. 2nd. type-Metastatic valvulo-parietal endocarditis. 3rd. type-Valvulo-parietal endocarditis of the mitral stenosis. B-Group-Genuine parietal endocarditis. a) with primary lesions in the myocardium. b) with primary lesions in the endocardium. 4th type-Fibrous chronic parietal endocarditis (B A Ü M L E R), « endocarditis parietalis simplex». 5th type-Septic acute parietal endocarditis (LESCHKE), «endocarditis parietalis septica». 6th type-Subacute parietal endocarditis (MAGARINOS TORRES), «endocarditis muralis lenta». 2.-Studying a group of 14 cases of fibrous endomyocarditis with formation of thrombi, and carrying together pathological and bacteriological examinations it has been found that some of such cases represent an infectious parietal endocarditis, sometimes post-puerperal, of subacute or slow course, the endocardic vegetations being contamined by pathogenic microörganisms of which the most frequent is the Diplococcus pneumoniae, in most cases of attenuated virulence. Along with the infectious parietal endocarditis, there occur arterial and venous thromboses (abdominal aorta, common illiac and femural arteries and external jugular veins). The case 5,120 is a typical one of this condition which we name subacute parietal endocarditis (endocarditis parietalis s. muralis lenta). 3.-The endocarditis muralis lenta encloses an affection reputed to be of rare occurrence, the «myocardite subaigüe primitive», of which JOSSERAND and GALLAVARDIN published in 1901 the first cases, and ROQUE and LEVY, another, in 1914. The «myocardite subaigüe primitive» was, wrongly, in our opinion, included by WALZER in the syndrome of myocardia of LAUBRY and WALZER, considering that, in the refered cases of JOSSERAND and GALLAVARDIN and in that of ROQUE and LEVY, there are described rather considerable inflammatory changes in the myocardium and endocardium. The designation «myocardia» was however especially created by LAUBRY and WALZER for the cases of heart failure in which the most careful aetiologic inquiries and the most minucious clinical examination were unable to explain, and in which, yet, the post-mortem examination did not reveal any anatomical change at all, it being forcible to admit, then, a primary functional change of the cardiac muscle fibre. This special cardiac condition is thoroughly exemplified in the observation that WALZER reproduces on pages 1 to 7 of his book. 4.-The clinical picture of the subacute parietal endocarditis is that of heart failure with oedemas, effusion in the serous cavities and passive chronic congestion of the lungs, liver, kideys and spleen associated, to that of an infectious disease of subacute course. The fever is rather transient oscillating around 99.5 F., being intersected with apyretic periods of irregular duration; it is not dependent on any evident extracardiac septic infection. In other cases the fever is slight, particularly in the final stage of the disease, when the heart failure is well established. The rule is to observe then, hypothermy. The cardiac-vascular signs consist of enlargement of the cardiac dullness, smoothing of the cardiac sounds, absence of organic murmurs and accentuated and persistent tachycardia up to a certain point independent of fever. The galloprhythm is present, in most cases. The signs of the pulmonary infarct are rather expressed by the aspect of the sputum, which is foamy and blood-streaked than by the classic signs. Cerebral embolism was a terminal accident on various cases. Yet, in some of them, along with the signs of septicemia and of cardiac insufficiency, occurred vascular, arterial (abdominal aorta, common illiac and femurals arteries) and venous (extern jugular veins) thromboses. 5. The autopsy revealed an inflammatory process located on the parietal endocardium, accompanied by abundant formation of ancient and recent thrombi, being the apex of the left ventricle, the junction of the anterior wall of the same ventricle, with the interventricular septum, and the right auricular appendage, the usual seats of the inflammatory changes. The region of the left branch of HIS’ bundle is spared. The other changes found consist of fibrosis of the myocardium (healed infarcts and circumscribed interstitial myocarditis), of recent visceral infarcts chiefly in lungs, spleen and brain, of recent or old infarcts in the kidneys (embolic nephrocirrhosis) and in the spleen, and of vascular thromboses (abdominal aorta, common illiacs and femurals arteries and external jugular veins), aside from hydrothorax, hydroperitoneum, cutaneous oedema, chronic passive congestion of the liver, lungs, spleen and kidneys and slight ictericia. 6. In the subacute parietal endocarditis the primary lesions sometimes locate themselves at the myocardium, depending on the ischemic necrosis associated to the arteriosclerosis of the coronariae arteries, or on an specific myocarditis. Other times, the absence of these conditions is suggestive of a primary attack to the parietal endocardium which is then the primary seat of the lesions. It matters little whatever may be the initial pathogenic mechanism; once injured the parietal endocardium and there being settled the infectious injury, the endocarditis develops with peculiar clinical and anatomical characters of remarkable uniformity, constituting an anatomo-clinical syndrome. 7.-The histologic sections show that recent lesions…

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Transmission of Chagas disease is realized through contamination of ocular conjunctiva, mucosa or skin with infected dejections eliminated by the insect vectors of Schizotrypanum cruzi (Triatoma infestans, Panstrongylus megistus and Rhodnius prolixus). The triatomid bugs live in holes and craks in the walls, in beds, behind trunks, etc. Found in primitive mud huts covered with thatched roofs, and so the human dwellers have many chances to contract the disease, reinfections being reasonably more to expect than a single inoculation. Experimental work reproducing those natural conditions is welcomed as some important features in the pathologic picture of the disease such as the extensive myocardial fibrosis seen in chronic cases are still incompletely known. Microscopic changes were studied in the heart muscle of seven Cebus monkeys infected by S. cruzi. This animal survives the acute stage of the disease and so is particularly suited to experiments of long duration in which several inoculations of S. cruzi are performed. Three different strains of S. cruzi isolated from acute cases of Chagas' disease were employed. One monkey was injected in the skin with infected blood and necropsied after 252 days. Two monkeys were three times, and one, eight times infected in skin, one of them with contaminated blood, and two with contaminated blood and dejections from infected bugs. The necropsies were performed after 35, 95 and 149 days. One monkey was three times inoculated through the intact ocular conjunctiva (one time with infected blood, two times with dejections from infected bugs), and one time through the wounded buccal mucosa, and necropsied after 134 days. Another monkey was six times inoculated, four times through the intact ocular conjunctiva (one time with contaminated blood, three times with dejections from infected bugs) and two times injected in the skin with infected blood, and necropsied after 157 days. Finally, another monkey was nine times inoculated, four times through the intact ocular conjunctiva (one time with infected blood, and three times with dejections from infected bugs), and five times injected in the skin (four times with contaminated blood, and one time with dejections from infected bugs), and necropsied after 233 days. The microscopic picture was uniform presenting, however, considerable individual variations, and was represented by diffuse interstitial myocarditis, frequently more (marked in the right ventricle base of the heart), accompanied by lymphatic stasis. The infiltration consists of macrophages, plasma cells and lymphocytes, the cellular reaction having sometimes a perivascular distribution, involving the auriculo-ventricular system of conduction, endocardium, epicardium and cardiac sympathetic gangliae. The loss of cardiac muscle fibers was always minimal. Leishmanial forms of S. cruzi in myocardial fibers are scanty and, in two cases, absent. Fatty necrosis in the epicardium was noted in two cases. Obliterative changes of medium-sized branches of coronary arteries (hypersensitivity reaction?) and multiple infarcts of the myocardium was found in one instance. The diffuse myocarditis induced by S. cruzi in several species of monkeys of the genus Cebus observed after 233 days (several inoculations) and 252 days (single inoculation) is not associated with disseminated fibrosis such as is reported in chronic cases of Chagas' disease. Definite capacity of reversion is another characteristic of the interstitial myocarditis observed in the series of Cebus monkeys here studied. The impression was gained that repeated inoculation with S. cruzi may influence the myocardial changes differently according to the period between the reinoculations. A short period after the first inoculation is followed by more marked changes, while long periods are accompanied by slight changes, which suggests an active immunisation produced by the first inoculation. More data are required, however before a definite statement is made on this subject considering that individual variations, the natural capacity of reversion of the interstitial myocarditis and the employement of more than a species of Cebus monkeys probably exerts influence also in the results here reported.

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In search of a suitable vector species for xenodiagnosis of humans and animals with chronic Chagas' disease we first investigated the reactions of different vector species to acute infection with Trypanosoma cruzi. Vector species utilized in this study were: Triatoma infestans, Rhodnius prolixus and Triatoma dimidiata, all well adapted to human habitats; Triatoma rubrovaria and Rhodnius neglectus both considered totally wild species; Panstrongylus megistus, Triatoma sordida, Triatoma pseudomaculata and Triatoma brasiliensis, all essentially sylvatic but some with domiciliary tendencies and others restricted to peridomestic biotopes with incipient colonization of human houses after successful eradication of T. infestans. Results summarized in Table IV suggest the following order of infectivity among the 9 studied vector species: P. megistus with 97.8% of infected bugs, T. rubrovaria with 95% of positive bugs a close second followed by T. Pseudomaculata with 94.3% and R. neglectus with 93.8% of infected bugs, almost identical thirds. R. prolixus, T. infestans and T. dimidiata exhibited low infection rates of 53.1%, 51.6% and 38.2% respectively, coupled with sharp decreases occuring with aging of infection (Fig. 1). The situation was intermediate in T. brasiliensis and T. sordida infection rates being 76.9% and 80% respectively. Results also point to the existence of a close correlation between prevalence and intensity of infection in that, species with high infection rates ranging from 93.8% to 97.8% exhibited relatively large proportions of insects (27.3% - 33.5%) harbouring very dense populations of T. cruzi. In species with low infection rates ranging from 38.2% to 53.1% the proportion of bugs demonstrating comparable parasite densities was at most 6%. No differences attributable to blood-meal size or to greater susceptibility of indigenous vector species to parasites of their own geographical area, as suggested in earlier...

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In an attempt to define the mouse-model for chronic Chagas' disease, a serological, histopathological and ultrastructural study as well as immunotyping of myocardium collagenic matrix were performed on Swiss mice, chronically infected with Trypanosoma cruzi strains: 21 SF and mambaí (Type II); PMN and Bolivia (Type III), spontaneously surviving after 154 to 468 days of infection. Haemagglutination and indirect immunofluorescence tests showed high titres of specific antibodies. The ultrastructural study disclosed the cellular constitution of the inflammatory infiltrate showing the predominance of monocytes, macrophages with intense phagocytic activity, fibroblasts, myofibroblasts and abundant collagen matrix suggesting the association of the inflammatory process with fibrogenesis in chronic chagasic cardiomyopathy. Artertolar and blood capillary alterations together with dissociation of cardiac cells from the capillary wall by edema and inflammation were related to ultrastructural lesions of myocardial cells. Rupture of parasitized cardiac myocells contribute to intensify the inflammatory process in focal areas. Collagen immunotyping showed the predominance of Types III and IV collagen. Collagen degradation and phagocytosis were present suggesting a reversibility of the fibrous process. The mouse model seems to be valuable in the study of the pathogenetic mechanisms in Chagas cardiomyopathy, providing that T. cruzi strains of low virulence and high pathogenecity are used.

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In an attempt to establish an experimental model of acute schistosomiasis, sequential histological changes were investigated in the skin, lung, liver and spleen of mice infected with 30 or 100 cercariae of Schistosoma mansoni according to four sets of experiments: single infection, repeated infections, unisexual infection and infection in mice born from infected mothers. Animals were killed every other day from exposure up to 50 days after infection. Only mild, isolated, focal inflammatory changes were found before the appearance of mature eggs in the liver, even when repeated infections were made. Severe changes of reactive hepatitis and splenitis appeared suddenly when the first mature eggs were deposited, around the 37th to 42nd day after infection. The mature eggs induced lytic and coagulative necrosis of hepatocytes around them which was soon followed by dense infiltration of eosinophils. So, mature egg-induced lesions appeared as the major factors in the pathogenesis of acute schistosomiasis in mice. Mice born from infected mothers were apparently able to rapidly modulate the egg-lesions, forming early fibrotic granulomas. The murine model of acute schistosomiasis appeared adequate for the study of pathology and pathogenesis of acute schistosomiasis.

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A model of acute schistosomiasis of the mouse was used to observe whether curative treatment would be followed by an enhancement of the hepatic and splenic lesions, as a consequence of the massive destruction of worms and eggs within the portal system. Mice infected with 50 cercariae of Schistosoma mansoni were treated with both oxamniquine and praziquantel on the 50th day of infection and submitted to a sequential histologic examination from the 2nd to the 45th day after treatment. Although severe focal lesions due to dead and disintegranting worms were present in the livers of the treated animals, no aggravation of the general changes (reative hepatitis and splenitis, or periovular granulomas) was seen in comparison with a control non-treated group. Of 50 animals treated during the acute phase of schistosomiasis only one died espontaneously, while 16 ou of 30 infected controls died before the end of the experiment. The present investigation indicates that curative treatment during the acute phase of schistosomiasis does not enhance previous lesions at first and results in progressive disappearance of the lesions starting six days following chemotherapy.

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Tissue parasitism, inflammatory process (histologic methods) and sympathetic denervation (glyoxylic acid-induced histofluorescence for demonstration of catecholamines) were studied in the heart (atrium and verntricle) and the submandibular gland of rats infected with the Y strain of Trypanosoma cruzi. In the heart paralleling intense parasitism and inflammatory process, the sympathetic denervation started at day 6 of infection and at the end of the acute phase (day 20) practically no varicose nerve terminals were found in both myocardium and vessels. In the submandibular gland, in spite of the rarity of anastigote pseudocysts and the scarcity of inflammatory foci, slight to moderate (days 13-15 of infection) or moderate to severe denervation (day 20) was found. At day 120 of infection both organs exhibited normal pattern of sympathetic innervation and only the heart showed some inflammatory foci and rare psudocysts (ventricle). Our data suggest the involvement of circulating factors in the sympathetic denervation phenomena but indicate that local inflammatory process is, at least, an aggravating factor.