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

Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P less than 0.02). Wall thinning with systole was associated with acute infarction or ischemia (P less than 0.0001); decreased thickening (less than normal) commonly occurred in patients with acute myocardial infarction, chronic coronary artery disease, and congestive cardiomyopathy. Patients with atrial septal defect had normal thickening with abnormal motion. Results of this study show that 1) systolic thinning is indicative of an acute event; 2) abnormal changes in systolic wall thickening occur commonly in patients with coronary artery disease or congestive cardiomyopathy; and 3) abnormal wall motion may occur without abnormal wall thickening, as the echoes of patients with atrial septal defect indicate.
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PMID:Systolic thickening and thinning of the septum and posterior wall in patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect. 83 Jan 97

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

Four cases of hypertrophic obstructive cardiomyopathy diagnosed on clinical, phonomechanographic, echocardiographic and haemodynamic criteria progressing to dilated cardiomyopathy are reported. This evolution was observed over a number of years (up to 20 years) and was accompanied by a clinical aggravation in all cases with 2 deaths and atrial fibrillation in 3 of the 4 cases. The signs of intraventricular obstruction [systolic murmur, bulge on the carotid pulse tracing, systolic anterior motion of the mitral valve (SAM) and intraventricular pressure gradient] disappeared as the left heart chambers dilated with a reduction in ventricular wall motion and parietal thinning but no change in myocardial mass.
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PMID:[Progression from hypertrophic obstructive cardiomyopathy to dilated cardiomyopathy. Apropos of 4 cases]. 211 75

Few data are available about cardiac involvement in AIDS. We examined 102 consecutive patients with AIDS diagnosed clinically and serologically (Walter Reed Stage 5 and 6), by means of TM and cross-sectional echocardiography with the aim of detecting cardiac abnormalities. None of the patients had overt clinical signs of heart failure. Fifty-five (54%) patients showed persistent tachycardia, diminished left ventricular (LV) wall thickness (mean 7.6 +/- 0.2 mm) and decreased percentage LV fractional shortening (27 +/- 5). In 42 (41%) there was a globular and poorly contracting LV. Thirty-nine (38%) patients had pericardial effusion which was moderate in 30 and small in nine. In four patients, valvular endocarditic vegetation was shown--on the tricuspid valve in three, on the aortic valve in one: all of them were drug addicts; in three (2.9%) patients a cardiac mass was found which proved to be a localization of Kaposi's sarcoma in two. Twenty-five (24.5%) patients died; necropsy showed cardiac chamber dilation, and thin LV walls in 18. On microscopic examination, myocardial fibrosis and lymphocyte infiltration with cell necrosis were observed. We conclude that cardiac abnormalities are common in AIDS. Impairment in LV contractility as assessed from fractional shortening appears to be the most common echocardiographic finding, followed by LV wall thinning, pericardial effusion and eventually by LV cavity dilation. This evolution is suggestive of myocardial damage and supports the hypothesis that dilated cardiomyopathy may be a cardiac complication of AIDS.
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PMID:Echocardiography detects myocardial damage in AIDS: prospective study in 102 patients. 318 Nov 75

Gated magnetic resonance imaging (MRI) was performed in 6 patients with familial hypertrophic cardiomyopathy associated with abnormal thallium perfusion, and 12 patients with ordinary hypertrophic cardiomyopathy. The patients with ordinary hypertrophic cardiomyopathy and abnormal thickening of the septal wall and normal left ventricular dimensions, while the patients with familial hypertrophic cardiomyopathy had focal wall thinning (usually involving the apical-septal wall) and dilated left ventricle in addition to hypertrophied heart. The quantitative measurement for cardiac dimensions using MRI was similar to that found on echocardiography in all cases. In addition, inhomogeneous signal intensities at left ventricular wall were observed in 3 cases of familial hypertrophic cardiomyopathy, which may suggest the existence of myocardial fibrosis. Gated MRI should be performed for early detection and follow-up of hypertrophic cardiomyopathy, since some patients will progress from hypertrophic cardiomyopathy to dilated cardiomyopathy.
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PMID:Magnetic resonance imaging in familial hypertrophic cardiomyopathy associated with abnormal thallium perfusion and cardiac enzymes. 341 62

A 20-year-old woman whose echocardiograms showed a rare evolution from hypertrophic to dilated cardiomyopathy during a nine year observation period is described. This patient was initially diagnosed as having hypertrophic obstructive cardiomyopathy (HOCM) at the age of 12 years. Her echocardiogram showed marked thickening of the interventricular septum (IVS) and left ventricular posterior wall (LVPW), asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM). Chest radiography revealed a prominent left ventricular border and a cardiothoracic ratio of 0.52. At 18 years of age she experienced onset of palpitation during the 16th week of pregnancy. Her echocardiogram recorded in June 1980 revealed a thickened IVS and LVPW with resolution of the SAM and of the narrow cavity. At 20 years of age she became pregnant again and was admitted to our hospital for the third time at 24 weeks gestation. On admission her blood pressure was 122/60 and her pulse was 56, and moist rales were audible over both lung fields. Peripheral edema was noted. Chest radiography revealed moderate cardiomegaly, a cardiothoracic ratio of 0.66, and congestion of the pulmonary vasculature. An echocardiogram showed thinning of the IVS and LVPW with hypokinesis and dilatation of the cavity compatible with dilated cardiomyopathy (DCM). She delivered a boy on July 15th 1982 at 32 weeks gestation following which she developed marked congestive heart failure. She expired one month later. A chest radiograph made one day before death revealed marked cardiomegaly, a cardiothoracic ratio of 0.76, prominent pulmonary vasculature and a pleural effusion. Autopsy was refused; therefore the terminal DCM-like features were not clarified pathologically. However, the slow progression from HOCM to HCM during eight years and then rapid progression from HCM to DCM during four months was most impressive.
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PMID:[Evolution of dilated cardiomyopathy from hypertrophic obstructive cardiomyopathy: a case report]. 344 76

The ability of magnetic resonance to determine regional left ventricular function was investigated in 18 patients--13 with coronary artery disease (nine with previous infarction), one with congestive cardiomyopathy, one with mitral stenosis, one with an atrial septal defect, and two without detectable cardiac abnormality. Coronal magnetic resonance images were acquired through the aortic valve and sagittal images were acquired in the plane of widest diameter of the left ventricle seen in the coronal image, both at end diastole and end systole. Regional wall motion assessed by magnetic resonance was compared with the results of anteroposterior and left lateral x ray ventriculograms by two independent observers. The left ventricular wall was divided into three segments in each plane and the motion of the segments was classified as normal, hypokinetic, akinetic, or dyskinetic. Muscle thickness was measured in each segment of the magnetic resonance images and was considered to be abnormal if in the systolic images it was less than 75% of that in neighbouring segments or if it failed to increase by at least 25% between diastole and systole. Wall motion assessments by the two methods agreed in 68 of 105 segments analysed, but differed by one class in 32 segments and by two classes in five segments. The differences can be explained by the conditions under which the investigations were performed and by the disparity between a tomographic section and an x ray projection. Magnetic resonance showed 25 segments to have abnormal wall thickness. Only one patient with infarction did not have an area of wall thinning and no patient without infarction had an area of thinning. It is concluded that magnetic resonance allows an accurate non-invasive assessment of left ventricular wall motion and thickness.
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PMID:Assessment of regional left ventricular function by magnetic resonance. 376 12

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

To elucidate the pathophysiology of dilated cardiomyopathy (DCM), the relationship of two-dimensional echocardiographic wall motion abnormalities (asynergy) to histopathological findings was evaluated in autopsied patients including seven with DCM, five with old myocardial infarction (OMI) and three with the normal heart. The DCM cases were classified morphologically in two groups, namely four of type I and II and three of type III, according to Shozawa's classification. Three short-axis views of the left ventricle were divided into 19 segments; the wall motion was assessed visually and classified as normal motion, hypokinesis, akinesis and dyskinesis. The postmortem specimens were immersed in 10% formalin; transverse sections and wall divisions were prepared corresponding to the two-dimensional echocardiographic views, and the area of each segment was determined by a computer planimetry excluding the papillary muscles and trabeculae. Fibrosis (%) was measured histologically by the point counting method with light microscopy. The results were as follows: In DCM, fibrosis (%) increased with increasing severity of asynergy: 17.1% fibrosis in normal motion; 28.7% in hypokinesis; 40.7% in akinesis and dyskinesis. In OMI, fibrosis (%) also increased with increasing severity of asynergy. On comparison of DCM with OMI, no difference was established relating to fibrosis (%) in the asynergic segments; moreover, in both groups, asynergy was detected more frequently in the segments in which fibrosis (%) exceeded 21%. On comparison of type I+II DCM with type III DCM, fibrosis (%) of type III was significantly less than that of type I+II in the same degree of asynergic segments. Moreover, fibrosis (%) of type I+II tended to be greater in the outer layer than in the inner layer, while fibrosis (%) of type III was evenly distributed throughout the myocardium, or greater in the inner layer than in the outer layer. In type I+II, wall thinning was marked with increasing severity of asynergy; in contrast, these correlations were not observed in type III. In type I+II, a higher fibrotic rate was observed in the left ventricular free wall and an abnormal Q wave appeared frequently on ECG. This tendency was not found in type III. These findings indicate that fibrosis is one of the most important factors in decreasing cardiac muscular contractility in DCM, and suggest that there is a different pathogenesis between type I+II and type III fibrosis.
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PMID:[Two-dimensional echocardiographic recognition of dilated cardiomyopathy: comparison with postmortem studies]. 384 89

Five patients with right ventricular dysplasia (RVD) and 28 patients with predominantly left sided dilated cardiomyopathy (DCM) were studied. RVD was characterised by syncope, recurrent sustained ventricular tachycardia, which typically had a left bundle branch block pattern on the surface electrocardiogram, right heart failure, and faint or absence of the right ventricular free wall on the myocardial scintigraphy. Two-dimensional echocardiographic, radionuclide angiographic, and contrast ventriculographic studies were typical of the right ventricular abnormalities in both Uhl's anomaly and arrhythmogenic right ventricular dysplasia. Two of them were died suddenly. Pathologic examinations showed "parchment-like" thinning of portions of the right ventricular free wall and its replacement by adipose tissue, although such degenerations were not found in the septum and the left ventricle. By contrast, DCM was characterised by exertional dyspnea and short run ventricular tachycardia, most of which had a right bundle branch block pattern. Ten of them had left ventricular myocardial defects on the scintigraphy, of whom five died suddenly. Hemodynamic data showed that left ventricular dysfunction was predominant more than right ventricle. Thus we postulate that these two syndromes are manifestations of a congenital, pathophysiologic process - the "involved right or left ventricle" syndrome.
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PMID:[Right ventricular dysplasia: clinical features compared with dilated cardiomyopathy]. 401 15


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