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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indomethacin has been shown to increase virus titers and to worsen cardiac injury in the acute phase of coxsackievirus B4 murine myocarditis. The authors evaluated the effects of indomethacin on the histopathologic changes in a later phase of this disease after virus clearance. Two-day old CD1 mice were infected with coxsackievirus B4. Ten days later, surviving animals were randomized to receive indomethacin or saline intraperitoneally for 10 days. They were then euthanatized, and their hearts were examined for the presence of inflammation, necrosis, scarring, and focal thinning. Mortality was slightly higher among treated animals (7/15 versus 2/12, p = 0.3). The index of inflammation (0.6 +/- 0.5 versus 0.7 +/- 0.5) necrosis and scarring (0.4 +/- 0.5 versus 0.3 +/- 0.5) among treated and control animals, respectively, was not significantly different, but the size of involved myocardium (149742 +/- 201982 versus 35300 +/- 45413 microns2) was remarkably larger (p less than 0.05), and focal ventricular thinning (5/12 versus 0/10, p = 0.03) was encountered among indomethacin recipients exclusively. These findings indicate that indomethacin treatment in the late phase of coxsackievirus B4 myocarditis enhances myocardial damage and increases the incidence of focal ventricular thinning.
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PMID:Focal ventricular thinning caused by indomethacin in the late phase of coxsackievirus B4 murine myocarditis. 131 98

Successive infection of coxsackievirus B3 and encephalomyocarditis virus was investigated as a disease model of chronic myocarditis. Four-week-old C3H/He mice were inoculated with coxsackievirus B3 and then inoculated with encephalomyocarditis virus at 8 weeks old. The hearts were evaluated on histopathological changes compared with those of non-infected mice and mice infected with either virus alone. At 10 weeks old, the hearts of the mice infected successively with both viruses showed co-existence of fibrosis surrounding calcified lesions and marked cellular infiltration with myocardial necrosis. These findings resembled chronic active myocarditis in humans, unlike the lesions due to either virus alone. At 12 weeks old, the hearts of all the infected mice showed fibrosis with scarce cellular infiltration. The successively infected hearts also showed a significantly higher heart weight to body weight ratio than that of the non-infected control mice, and localized wall thinning in the damaged regions. Thus, we conclude that successive infection additively causes myocardial damage that resembles chronic myocarditis and may produce a heart condition similar to dilated cardiomyopathy.
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PMID:Successive infection of coxsackievirus B3 and encephalomyocarditis virus: an animal model of chronic myocarditis. 132 52

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

Twenty-three clinically normal Beagles were inoculated with North American Trypanosoma cruzi isolates from an opossum (Tc-O), an armadillo (Tc-A), or a dog (Tc-D). The dogs were grouped according to the clinical outcome of inoculation. Group 1 consisted of 7 dogs inoculated with Tc-O or Tc-A that died or were euthanatized during acute stages of disease. Group 2 consisted of 5 dogs inoculated with Tc-O or Tc-A, that also developed acute disease, but survived to develop chronic disease. Group 3 consisted of 7 dogs inoculated with Tc-D neither developed acute nor chronic disease. Group 4 consisted of 4 dogs and served as noninoculated controls. In group 1, the gross lesions were diffusely pale myocardiums with right ventricular enlargement, hepatomegaly, and a moderate amount of modified transudate in the abdominal cavity. Severe diffuse granulomatous myocarditis with large numbers of pseudocysts and minimal fibrosis characterized the tissues from all cardiac chambers and septum. The lesions were most severe in the right atrium and ventricle. Mild multifocal myositis and pseudocysts were observed in skeletal muscles and smooth muscles of the urinary bladder and small intestine. Multifocal encephalitis and pseudocysts were in the cerebral cortex, cerebellum, and brain stem. In group 2, the gross lesions were biventricular enlargement and thinning of the ventricular free walls. The right ventricle contained the most severe microscopic changes. There were mild multifocal interstitial lymphohistocytic cellular infiltrates, perivasculitis, and marked fibrosis in all areas of the myocardium. Mild myositis and multifocal encephalitis were seen in the skeletal muscles and brains. Pseudocysts were not observed in any tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathologic features of dogs inoculated with North American Trypanosoma cruzi isolates. 178 18

We report a case of sudden death from hemopericardium consequent to spontaneous rupture of the right ventricle in a 49-year-old chronic chagasic woman. To our knowledge, this is the third reported case of spontaneous cardiac rupture with chagasic cardiomyopathy. In our case we believe that the thinning of the anterior right ventricular wall, its large ray curvature and the increased ventricular pressure were factors favoring the rupture. There was no infarction and the chronic cardiopathy was significant. It caused the thinning of the rupture region through chronic myocarditis.
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PMID:[Sudden death caused by the spontaneous rupture of the right ventricle in a woman with chronic Chagas disease]. 213 89

Trypanosoma cruzi was believed responsible for causing chronic dilatative myocarditis in 2 female hunting dogs. Clinical signs included ascites, respiratory distress, thoracic effusion, cyanosis, and weak pulse with ventricular arrhythmias. Electrocardiography indicated first-degree heart block, chamber enlargement, and ventricular-based arrhythmias unresponsive to treatment. M-mode echocardiography of 1 dog confirmed bilateral cardiac enlargement and septal and left ventricular free wall thinning. Multifocal infiltrates of plasma cells, lymphocytes, and histiocytes, cardiocyte degeneration, and multifocal fibrosis were the predominant histologic lesions. Trypanosoma cruzi pseudocysts were infrequently found.
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PMID:Chronic dilatative myocarditis caused by Trypanosoma cruzi in two dogs. 258 22

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

We encountered two children with chronic idiopathic myocarditis accompanied by marked right ventricular dilatation, who died of progressive right heart failure. A definitive diagnosis was made by histological examination of the myocardium at autopsy. The patients were both boys, aged 7 years and 1 year and 4 months, and a number of identical features were evident upon physical and laboratory examinations. No heart murmur was heard, and gallop rhythm was noted in distant heart sounds. Electrocardiogram revealed intraventricular block, low voltage QRS complex, and ST-T abnormality. Two-dimensional Doppler echocardiogram and right ventriculogram showed marked dilatation and decreased contractility of the right ventricle as well as tricuspid regurgitation. Thinning of the wall and marked dilatation of the right ventricle were confirmed at autopsy. Our observations showed that chronic myocarditis associated with tricuspid regurgitation may readily lead to marked right ventricular dilatation even exceeding the degree of left ventricular dilatation. Idiopathic myocarditis associated with such unusual features is relatively rare, and may present problems in differentiation from other congenital heart diseases causing dilatation and dysfunction of the right ventricle.
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PMID:Idiopathic myocarditis characterized by marked right ventricular dilatation. Report of two autopsy cases. 358 7

Echocardiographic findings of 11 patients with dilated cardiomyopathy (DCM) were compared with those of 11 patient with coronary triple vessel disease, who showed extensive left ventricular (LV) wall motion abnormalities (abnormal LV regional wall motion observed in more than six of seven segments as classified by AHA) and a dilated LV cavity (LVEDVI: 120 ml/m2 or greater), consistent with so-called ischemic cardiomyopathy (ICM). Short-axis two-dimensional echocardiograms of the left ventricle at the mitral valve, papillary muscle, and apical levels were divided equally into eight segments starting from the posterior aspect of the right side of the interventricular septum. Non-uniformity of LV regional wall motion abnormalities was demonstrated in seven patients (64%) with DCM and 11 patients (100%) with ICM, and that of LV regional wall motion abnormalities of more than two degrees was observed in one patient (9%) with DCM and nine patients (82%) with ICM. LV regional wall thinning was observed in two patients (18%) with DCM and 11 patients (100%) with ICM. Increased echo intensity of the LV regional wall was observed in only four patients with ICM. Two patients (18%) with DCM and 11 patients (100%) with ICM had episodes of chest pain and the former two had LV regional wall thinning, suggesting the possibility of post-myocarditis cardiomegaly. Abnormal Q waves in the electrocardiograms were observed in 10 patients (91%) with ICM and in two (18%) with DCM. Exercise ECG tests were positive in nine of 11 patients with ICM, but in none of the five DCM examined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of echocardiographic findings in patients with coronary triple vessel disease and dilated cardiomyopathy]. 383 56

Segmental wall motion abnormalities are common in patients with myocarditis. Left ventricular (LV) regional wall motion was assessed in six patients with myocarditis by two-dimensional echocardiography. Some of our patients demonstrated regional thinning of the wall, similar to myocardial infarction. Therefore, segmental wall motion abnormalities with or without regional wall thinning detected by two-dimensional echocardiography cannot be used to differentiate myocarditis from coronary artery disease. Nevertheless, echocardiography can be performed repeatedly and is useful for evaluating the severity of myocarditis by assessing LV regional wall motion abnormalities, changes in LV wall thickness and cardiac pump function during the course of the disease.
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PMID:Echocardiographic assessment of left ventricular wall motion in myocarditis. 384 73


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