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)

A 15-year-old boy with hypertrophic cardiomyopathy died of congestive heart failure with progressive left ventricular wall thinning with poor systolic function. Microscopic examination revealed patchy fibrosis in the ventricular myocardium with wall thinning, and immunohistochemical evaluation of apoptosis showed apoptotic cells and bodies in the destroyed myocytes along the border between the fibrotic area and myofibril.
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PMID:Apoptosis as a possible cause of wall thinning in end-stage hypertrophic cardiomyopathy. 911 84

Nonuniform hypertrophy of the left ventricle is an important factor in regional diastolic dysfunction in patients with hypertrophic cardiomyopathy (HCM). However, the effect of myocardial perfusion abnormalities on regional diastolic dysfunction has not been established in patients with HCM. We investigated the relationship between regional myocardial perfusion abnormalities and regional early diastolic function in 31 patients with HCM and 8 control patients. Short-axis images of the left ventricle recorded by cine magnetic resonance imaging were divided into ten blocks. The time-to-peak-wall-thickness-thinning rate (TPWR) and the wall thickness were measured in each block. Of the 310 blocks from the patients with HCM, 242 (78%) showed normal thallium-201 uptake (group 1), 40 (13%) showed slightly decreased uptake (group 2), and 28 (9%) showed markedly decreased uptake (group 3). There was no difference in the regional wall thickness among the three groups. The TPWR was longer in patients with HCM than in control patients. It was significantly longer in group 3 (190+/-45ms) than in group 1 (167+/-36 ms) and group 2 (160+/-31 ms). (P < 0.01). The linear regression slope of the relationship between the TPWR and the regional wall thickness was significantly steeper in group 3 than in groups 1 and 2 (P < 0.05). In conclusion, abnormalities in regional myocardial perfusion, in addition to regional hypertrophy, contributed to the regional early diastolic dysfunction in patients with HCM.
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PMID:Effect of regional myocardial perfusion abnormalities on regional myocardial early diastolic function in patients with hypertrophic cardiomyopathy. 955 69

Left ventricular remodeling occurs spontaneously among patients with hypertrophic cardiomyopathy in several ways: (1) wall thickening in children; (2) wall thinning associated with cavity enlargement in midlife; and possibly (3) a very gradual wall thinning process occurring over long periods of time in adulthood.
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PMID:Implications of left ventricular remodeling in hypertrophic cardiomyopathy. 963 72

Heterozygous mice bearing an Arg403Gln missense mutation in the alpha cardiac myosin heavy chain gene (alpha-MHC403/+) exhibit the histopathologic features of human familial hypertrophic cardiomyopathy. Surprisingly, homozygous alpha-MHC403/403 mice die by postnatal day 8. Here we report that neonatal lethality is caused by a fulminant dilated cardiomyopathy characterized by myocyte dysfunction and loss. Heart tissues from neonatal wild-type and alpha-MHC403/403 mice demonstrate equivalent switching of MHC isoforms; alpha isoforms in each increase from 30% at birth to 70% by day 6. Cardiac dimensions and function, studied for the first time in neonatal mice by high frequency (45 MHz) echocardiography, were normal at birth. Between days 4 and 6, alpha-MHC403/403 mice developed a rapidly progressive cardiomyopathy with left ventricular dilation, wall thinning, and reduced systolic contraction. Histopathology revealed myocardial necrosis with dystrophic calcification. Electron microscopy showed normal architecture intermixed with focal myofibrillar disarray. We conclude that 45-MHz echocardiography is an excellent tool for assessing cardiac physiology in neonatal mice and that the concentration of Gln403 alpha cardiac MHC in myocytes influences both cell function and cell viability. We speculate that variable incorporation of mutant and normal MHC into sarcomeres of heterozygotes may account for focal myocyte death in familial hypertrophic cardiomyopathy.
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PMID:Neonatal cardiomyopathy in mice homozygous for the Arg403Gln mutation in the alpha cardiac myosin heavy chain gene. 988 44

We searched the medical literature for articles containing markers of cardiac ischemia and echocardiography in the evaluation of patients presenting to the emergency department to determine their combined clinical use. Several published articles indicate two-dimensional echocardiography is a useful and cost-effective imaging technique for the evaluation of patients with chest pain in the emergency department. New studies are emerging that evaluate ischemic markers in combination with echocardiography to assess patients presenting to the emergency department with chest pain. We searched the MEDLINE Database for English-language articles published from December 1980 to August 1998 using the key words troponin, echocardiography, myocardial infarction, and emergency. These key words were crossed referenced to determine publications in this area. Pertinent trials and reviews were selected from the database. There were six articles evaluating biochemical markers of ischemia and echocardiography to assess patients presenting with acute coronary syndromes in the emergency department. Very few studies combined the information obtained from novel ischemic markers and echocardiogram analysis to help delineate potential cardiac etiologies of acute coronary syndromes. However, the limited studies available indicate that echocardiography is both sensitive and specific for detecting acute myocardial infarction. The presence of regional wall motion abnormalities increases the chance of in-hospital complications and likelihood of developing congestive heart failure after admission for unstable angina. The combined use of troponin T levels and echocardiographic imaging was a more powerful predictor of adverse events than were isolated results. Myocardial scarring with ventricular wall thinning or aneurysm may allow for rapid diagnosis of 'occult' coronary artery disease in a patient presenting with chest pain who does not have a previous history of a cardiovascular event. Echocardiography may also help identify other cardiovascular causes of chest pain, such as aortic dissection, aortic stenosis, cardiac tamponade, pericarditis, and hypertrophic cardiomyopathy. The clinical use of combining ischemic markers of disease with echocardiographic imaging seems justified given their unique clinical advantages. Future clinical trials are needed to determine whether the combination of novel ischemic markers and echocardiography can provide for a more expedient and accurate diagnosis, resulting in improved patient care and a safe reduction in unnecessary hospitalization.
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PMID:Clinical Use of Ischemic Markers and Echocardiography in the Emergency Department. 1117 40

End-stage hypertrophic cardiomyopathy (ES-HCM), affecting 5-10% of human hypertrophic cardiomyopathy (HCM) patients, is characterized by relative thinning of the ventricular walls and septum with dilation of the ventricular lumen, decreased fractional shortening, and progression to heart failure. C. J. Baty and others recently documented similar progressive changes to ES-HCM in a family of four cats through serial echocardiograms. At the time of heart failure, these cats exhibited changes similar to those exhibited by human ES-HCM patients. Our objectives were to describe the pathologic alterations associated with ES-HCM and investigate the pathogenesis in three of the four cats. Grossly, there was left atrial dilation with relative thinning of the interventricular septum (IVS) and left ventricular free wall (LVFW). The left atrium contained large thrombi in two of the three cats, and all three cats died following thromboembolization of the aortic bifurcation. Histologically, all three cats had subendocardial and myocardial fibrosis, predominantly of the IVS and LVFW, and one cat had acute, multifocal, myocardial infarcts with mononuclear inflammatory cell infiltrates. The pathogenesis of ES-HCM is uncertain, but theories implicate occlusion of the coronary blood flow by thickening of the coronary vessels, coronary vascular thromboembolism or coronary vessel spasm, apoptosis of myocytes, and myocardial hypertrophy beyond the ability of the vasculature to supply blood. Apoptosis assays did not reveal any apoptotic myocytes. Considering the hypercoagulative state of these cats, coronary vascular thromboembolism could be a major contributing factor. We cannot exclude apoptosis or coronary vessel spasm on the basis of the data presented.
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PMID:Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy. 1600 5

We present the case of a 70-year-old man admitted in congestive heart failure. The patient was diagnosed 22 years ago of hypertrophic cardiomyopathy (HC). ECG showed a very peculiar and pathological form of left bundle branch block (LBBB). 2D-echocardiogram revealed a dilated left ventricle (LV) and ejection fraction of 25%. LV remodeling represents an important component of the pathophysiology of HC and, paradoxically, some patients develop LV wall thinning, systolic dysfunction, and congestive heart failure (in the absence of coronary artery disease). This evolution is designated as "end-stage" or "burned-out"phase. We present this rare LBBB and his pathological evolution along the time as unique manifestation of this "burned-out" phase. The mechanism of this wall thinning remains unclear but changes in ECG may alert us about it.
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PMID:Atypical left bundle branch block in dilative "burned-out" phase of hypertrophic cardiomyopathy. 1640 70

Hypertrophic cardiomyopathy patients rarely have left ventricular apical aneurysms without coronary artery disease and the pathophysiological processes responsible for apical wall thinning and aneurysm formation are not known exactly today. Here we present a rare nonobstructive hypertrophic cardiomyopathy case with an apical thrombotic aneurysm.
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PMID:Rare clinical presentation of nonobstructive hypertrophic cardiomyopathy: apical aneurysm with thrombus. 1708 37

The authors report the case of a patient with hypertrophic cardiomyopathy who developed progressive and severe left ventricular wall thinning, as assessed by two-dimensional echocardiography, despite a preserved supranormal ejection fraction and an absence of cardiac symptoms. Extensive fibrosis was identified on cardiovascular magnetic resonance.
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PMID:Severe left ventricular wall thinning and extensive fibrosis without evolution to end stage disease in a patient with hypertrophic cardiomyopathy. 1980 10

Infiltrative cardiomyopathies are characterized by the deposition of abnormal substances that cause the ventricular walls to become progressively rigid, thereby impeding ventricular filling. Some infiltrative cardiac diseases increase ventricular wall thickness, while others cause chamber enlargement with secondary wall thinning. Increased wall thickness, small ventricular volume, and occasional dynamic left ventricular outflow obstruction (e.g., amyloidosis) can outwardly appear similar to conditions with true myocyte hypertrophy (e.g., hypertrophic cardiomyopathy, hypertensive heart disease). Likewise, infiltrative disease that presents with a dilated left ventricle with global or regional wall motion abnormalities and aneurysm formation (e.g., sarcoidosis) may mimic ischemic cardiomyopathy. Low-voltage QRS complex was the sine qua non of infiltrative cardiomyopathy (i.e., cardiac amyloid). However, low-voltage QRS complex is not a uniform finding with the infiltrative cardiomyopathies. The clinical presentation, along with functional and morphologic features, often provides enough insight to establish a working diagnosis. In most circumstances, however, tissue or serologic evaluation is needed to validate or clarify the cardiac diagnosis and institute appropriate therapy.
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PMID:Infiltrative cardiovascular diseases: cardiomyopathies that look alike. 2041 25


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