Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven inbred mouse strains were examined for the presence of chronic Chagas' cardiomyopathy in postacute Trypanosoma cruzi infection. DBA/1, DBA/2, BALB/c, B10.T (6R), B10.Q, B10.D2, and B6 mice were infected for 100 days with the Brazil strain of T. cruzi. Standard histologic examination of cardiac tissue from these mice revealed the following relationship among the different strains based on the severity of observed inflammation (myocarditis): BALB/c, DBA/1, and DBA/2 were the most inflamed; B10.T (6R) and B10.Q were intermediate; and B6 and B10.D2 showed the least inflammation. Examination of these tissues for characteristics of myocardiopathy such as cell swelling, edema, vacuolization, necrosis, myocytolysis, connective tissue infiltration, and thinning of the right ventricular wall indicated a relative relationship among the different strains relative to the severity of cardiomyopathy as follows: BALB/c, DBA/2, and DBA/1 showed the most cardiopathy (pathopermissive); B10.T (6R) and B10.Q showed intermediate pathology; and B6 and B10.D2 showed the least involvement (pathoresistant). Anti-heart antibody present in the sera of all these mice showed specific reactivity in western blots to a 43-kDa glycoprotein from normal heart tissue. Also, anti-heart antibody enzyme-linked immunosorbent assay titers for all mouse strains were similar and showed no correlation with the severity of tissue damage. The fact that different inbred strains show various degrees of myocarditis and cardiomyopathy may be useful in the study of pathogenesis of chronic Chagas' disease. Results from this limited list of inbred strains suggest that background genes, rather than the major histocompatibility complex, play the major role in the expression of cardiac pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential cardiac histopathology in inbred mouse strains chronically infected with Trypanosoma cruzi. 149 Dec 99

A previous study showed that the vas deferens of mice in the acute phase of Chagas' disease had a slight increase in the muscle layer area associated with a small decrease in the luminal area. The vas deferens of chronic chagasic mice, investigated in the present experiment, presented a marked increase in the luminal area in addition to a significant thinning of the muscle and epithelium layers. The structural alterations of the vas deferens observed in the acute and chronic phases of Chagas' disease were compared with the evolution of chagasic esophagopathy.
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PMID:The male reproductive organs in experimental Chagas' disease. II. Morphometric study of the vas deferens in the chronic phase of the disease. 150 80

A previous study showed amastigote forms of Trypanosoma cruzi in the sex organs of male mice 15 days after inoculation. The purpose of the present work was to investigate the sequelae occurring in the male reproductive system during a later phase of Chagas' disease. Depleted germinal epithelium and release of immature germ cells into the tubular lumen were observed in the testis of chronic chagasic mice. The relative weights of the epididymis, vas deferens and seminal vesicle were significantly increased. Histological examination revealed a sharp thinning of the ductal and acinar walls. The results are discussed in terms of a neuromotor disturbance leading to sperm retention.
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PMID:The male reproductive organs in the chronic phase of experimental Chagas' disease. 159 May 93

To study left ventricular diastolic function in Chagas's disease, simultaneous echocardiograms, phonocardiograms, and apexcardiograms were recorded in 20 asymptomatic patients with positive Chagas's serology and no signs of heart disease (group 1), 12 with Chagas's heart disease and symptoms of ventricular arrhythmia but no heart failure (group 2), 20 normal subjects (group 3), and 12 patients with left ventricular hypertrophy (group 4). The recordings were digitised to determine left ventricular isovolumic relaxation time and the rate and duration of left ventricular cavity dimension increase and wall thinning. In groups 1 and 2 (a) aortic valve closure (A2) and mitral valve opening were significantly delayed relative to minimum dimension and were associated with prolonged isovolumic relaxation, (b) left ventricular cavity size was abnormally increased during isovolumic relaxation and abnormally reduced during isovolumic contraction, and (c) peak rate of posterior wall thinning and dimension increase were significantly reduced and duration of posterior wall thinning was significantly prolonged; both of these abnormalities occurred at the onset of diastolic filling. These abnormalities were more pronounced in group 2 and were accompanied by an increase in the height of the apexcardiogram "a" wave, an indication of pronounced atrial systole secondary to end diastolic filling impairment due to reduced left ventricular distensibility. Group 4, which had an established pattern of diastolic abnormalities, showed changes similar to those in group 2; however, the delay in aortic valve closure (A2) and in mitral valve opening and the degree of dimension change were greater in the latter group. Thus early isovolumic relaxation and left ventricular abnormalities were pronounced in the patients with Chagas's heart disease and may precede systolic compromise, which may become apparent in later stages of the disease. The digitised method is valuable in the early detection of myocardial damage.
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PMID:Echocardiographic features of impaired left ventricular diastolic function in Chagas's heart disease. 315 54

Young rabbits (1-2 months of age) inoculated with trypomastigote forms of the Colombia strain of Trypanosoma cruzi have been shown to develop cardiac pathological changes (together with parasitological and immunological alterations) which are very similar to those observed in the acute and chronic phases of Chagas' disease in man. The cardiac alterations in the acute phase are characterized grossly by slight cardiomegaly with dilatation of the right-sided chambers. Microscopically they are characterized by mild focal myocarditis. The chronic phase is characterized by moderate to marked cardiomegaly with hypertrophy and dilatation of both ventricular chambers. There is thinning of the apical region (apical aneurysm), particularly of the left ventricle. Focal myocarditis is seen microscopically with areas of myocytolytic necrosis, atrophic and hypertrophic myofibers, an inflammatory response predominantly composed of mononuclear cells and interstitial fibrosis. Cineventriculography in the left ventricle of rabbits during the chronic phase disclosed regional myocardial dysfunction, with typical apical systolic bulging. The pathogenesis of Chagasic cardiomyopathy is briefly discussed in the light of these findings. Our investigation has further shown that this animal model is particularly suitable for studies on on the mechanisms, pathology and treatment of Chagas' heart disease.
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PMID:The evolution of experimental Trypanosoma cruzi cardiomyopathy in rabbits: further parasitological, morphological and functional studies. 351 79

In male BALB/c mice aged 5-6 weeks inoculated three times at intervals of 15 days with 1 X 10(7) epimastigote forms of the PF strain of Trypanosoma cruzi and challenged 30 days after the last inoculation with 2 X 10(4) trypomastigote forms of the Colombia strain of T cruzi (the mice were sacrificed 80-100 days after the challenge) a cardiomyopathy very similar to that observed in the chronic phase of Chagas' disease in man develops. The cardiac syndrome is characterized grossly by cardiomegaly with hypertrophy, dilatation of ventricular chambers, and thinning of the apex of the left ventricle (apical aneurysm) and microscopically by focal areas of myocytolytic necrosis and myocardial degeneration with an inflammatory response composed of mononuclear cells (predominantly macrophages and a few lymphocytes) with concurrent interstitial fibrosis and occasional myofibers containing pseudocysts. In addition, aggregated platelets and occlusive thrombi were found in small epicardial and intramyocardial vessels of infected mice as compared with controls. The potential role of intravascular platelet aggregation in the causation of focal myocardial necrosis and degeneration and apical aneurysm in experimental T cruzi cardiomyopathy in BALB/c mice is discussed.
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PMID:Experimental Trypanosoma cruzi cardiomyopathy in BALB/c mice. The potential role of intravascular platelet aggregation in its genesis. 623 12

The effect of early chronic Chagas's disease on the timing and extent of regional left ventricular wall motion was studied with a frame by frame analysis of left ventriculograms in nine patients and compared with those in 19 normal subjects. In all the patients there was hypokinesis or akinesis in the anteroapical region together with delay in the onset of inward movement. Hypokinesis of the proximal inferior segment was also present, but the time of onset of inward motion here was normal. These differences can be explained on the basis of regional asynchrony within the normal left ventricle, where anteroapical wall motion is delayed with respect to that elsewhere. Thus contraction of the diseased anteroapical segment starts against an appreciable pressure and so may be isometric, whereas the affected proximal inferior segment starts contracting earlier against a lower pressure and so is able to shorten. No abnormalities of wall motion were seen during isovolumic relaxation despite segmental involvement, which is a distinctly different finding from that in patients with coronary artery disease. This may be due partly to the absence of incoordinate relaxation in Chagas's disease and partly to myocardial involvement by Chagas's disease in the mid-anterior segment. This is the site of rapid early diastolic wall thinning, which has been put forward as a major mechanism of normal rapid ventricular filling and whose premature activity causes disturbances in regional wall motion before mitral valve opening when relaxation is incoordinate. Thus quantitative analysis of both the timing and amplitude of wall motion indicates fundamental differences between Chagas's disease and coronary artery disease, when a less complex analysis would have shown a similar pattern of segmental dysfunction in both. Since the effect of the same pathological process on wall motion varies with the site of ventricular involvement, the importance of the disturbances seen in Chagas's disease becomes apparent only when the non-uniformity of normal left ventricular structure and function is taken into account.
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PMID:Left ventricular wall motion in patients with Chagas's disease. 668 24

A retrospective study of Chagas's heart disease was carried out by a review of necropsy reports with special reference to the lesion known as the apical aneurysm. It was concluded that this lesion was more frequent in men, was unrelated to age, and was unrelated to heart weight. Patients dying of the cardiac consequences of Chagas's cardiomyopathy were more likely to have an apical aneurysm than those whose death was unrelated to the disease but the mode of death (sudden, or with heart failure) was unconnected with its presence. Transillumination from within the ventricle at necropsy was not only useful in demonstrating the aneurysm but also showed areas of myocardial thinning elsewhere. Thrombosis within the lesion was frequent. The aetiology of the apical aneurysm is discussed and it is concluded that while ischaemia, inflammation, thrombosis, and mechanical factors may produce and localise this lesion, the underlying cause is the basic pathogenetic process-parasympathetic nerve cell destruction.
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PMID:Apical aneurysm of Chagas's heart disease. 729 39

A 50-year-old South American Indian woman, a native of Brazil and now a resident of Shiga Prefecture, was admitted to our hospital because of dyspnea on exertion. We initially suspected dilated cardiomyopathy due to an enlarged and diffusely hypokinetic left ventricle (LV) on echocardiogram. Coronary arteriograms were normal, and histological examination of right ventricular endomyocardial biopsy specimens showed findings compatible with chronic myocarditis. Magnetic resonance imaging revealed localized thinning and a small apical aneurysm at the LV. Since she had previously lived in a high-risk region for Chagas' disease, two immunological examinations for Trypanosoma cruzi were performed. The results of both tests were compatible with the disease. Recently, an increasing number of patients with Chagas' disease have been found in the United States among immigrants from South American countries, and the risk of transmission of the disease through contaminated blood transfusion is becoming a national problem. We report this case with reference to the present state of the problem in the United States and the potential problems it presents in Japan because of the marked increase in the number of immigrants from the affected area.
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PMID:A highly suspected case of chronic Chagas' heart disease diagnosed in Japan. 765 15

Verapamil has been shown to attenuate the extent of myocardial injury in murine models of chronic Trypanosoma cruzi infection. Infected mice treated with verapamil have significantly lower myocardial expression of inducible nitric oxide synthase and cytokines and substantially less inflammatory infiltrate and myocyte necrosis at necropsy. In the present study, we examined the cardiac structural and functional correlates of verapamil treatment in CD1 mice infected with the Brazil strain of T. cruzi using serial transthoracic echocardiography. There were four groups: uninfected- untreated control, uninfected-verapamil-treated, infected-untreated control, and infected-verapamil-treated. Verapamil was given in drinking water (1 gm/l) continuously from the day of infection for a total of 120 days. Mice were evaluated at baseline, 40 and 150 days p.i. Mice in the untreated-infected group compared with the mice in the infected-verapamil-treated group showed thinning of the left ventricular wall (0.84 +/- 0.02-vs-0.92 +/- 0.04, P<0.05 mm), increase in the left ventricular end-diastolic diameter (3.27 +/- 0.15-vs-2.74 +/- 0.05 mm, P<0.05) and reduction in percent fractional shortening (37 +/- 2-vs-53 +/- 4%, P<0.05). No differences in these parameters were noted among mice in the uninfected-untreated and uninfected-verapamil-treated groups. Furthermore, right ventricular dilation was more severe in mice from the infected-untreated group as compared with those in the infected- verapamil-treated group (visual grade 1.9 +/- 0.4-vs-1.0 +/- 0.2, P<0.05). At necropsy, the extent of myocardial injury, as determined histologically, was significantly greater in the infected-untreated mice. These data provide cardiac structural and functional correlates for the previously observed cardioprotective effects of verapamil in chronic chagasic cardiomyopathy.
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PMID:Cardioprotective effects of verapamil on myocardial structure and function in a murine model of chronic Trypanosoma cruzi infection (Brazil Strain): an echocardiographic study. 1181 98


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