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 64-year-old woman was transferred to the intensive care unit with dyspnea and palpitation on effort. Chest x-ray film showed cardiomegaly and pulmonary congestion. We carefully examined for sarcoidosis as a differential diagnosis of heart failure. Serum lysozyme was mildly high, but human atrial natriuretic peptide (HANP) and brain natriuretic peptide (BNP) were strikingly high. Angiotensin converting enzyme was within normal limit. Chest roentgenogram did not reveal bilateral hilar lymphadenopathy. Atrioventricular conduction block was not observed on electrocardiogram. Echocardiographic examination showed left ventricular global hypokinesis with septal thinning and enlargement. Mitral valve regurgitation was recognized by Doppler evaluation. Coronary arteriography showed normal coronary arteries. Endomyocardial biopsy revealed noncaseous epithelioid granulomas containing, Langhans type giant cell accompanied by fibrosis and lymphocyte infiltration. From these data cardiac sarcoidosis was diagnosed. Gallium scintigraphy showed diffuse uptake only in the heart. Treatment with oral prednisolone 20 mg/day was started. Her symptoms improved by several weeks after the medical treatment. In addition, both the value of HANP and BNP were markedly decreased and echocardiogram showed improvement of cardiac systolic function. In Japan, there is a higher incidence of cardiac sarcoidosis than in the West. The prognosis of this condition associated with cardiac dysfunction is reported to be very poor. When progressive heart failure in older patients is seen, cardiac sarcoidosis should also be kept in mind. Endomyocardial biopsy play an important role as the only accurate technique for the diagnosis of cardiac sarcoidosis.
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PMID:[A case of sarcoidosis in which sarocoid granulomas were observed only in the heart]. 1598 67

Chronic ethanol consumption has deleterious effects on the cardiovascular system by directly damaging the myocardial structure and/or by neurohormonal activation. Moreover, nitric oxide (NO) derived from neuronal NO synthase (nNOS) seems to be important to balance the harmful effects of ethanol consumption, because it influences several aspects of cardiac physiology and attenuates pathological cardiac remodeling. However, the impact of chronic ethanol consumption on nNOS expression is unknown. We address this subject in the present study by evaluating whether chronic ethanol consumption induces cardiac remodeling and hypertension, and if these changes are associated with alterations in the expression of nNOS. Male Wistar rats were examined after ingesting a 20% alcohol solution for 6 months. Blood alcohol concentration and brain natriuretic peptide (BNP) levels were measured. The cardiac remodeling was assessed by histomorphometric analysis and the nNOS expression was evaluated by immunofluorescence and western blot analysis. Our results show that chronic ethanol consumption induces cardiac remodeling, namely thinning of left ventricular wall, cardiomyocyte hypertrophy and increased fibrosis, and elevations of arterial blood pressure. They also show that in rats fed with ethanol for 6 months, the circulating BNP levels had decreased as well as the expression of nNOS in left ventricle cardiomyocytes. These findings suggest that the effects of chronic ethanol consumption on BNP levels and/or on nNOS expression in cardiomyocytes may contribute to aggravate the cardiac remodeling and leads to progression of cardiomyopathy.
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PMID:nNOS is involved in cardiac remodeling induced by chronic ethanol consumption. 2559 24

A boy with Duchenne muscular dystrophy was admitted to our hospital due to a transient loss of consciousness. Transthoracic echocardiography revealed left ventricular (LV) dilatation and diffuse hypokinesis of the LV wall. The LV wall was thin, and both non-compaction of the LV wall and marked thinning of the posterior LV wall resulting from a lesion were observed. The plasma B-type natriuretic peptide (BNP) level ultimately increased to 7,795 pg/mL, and the patient died of cardiac arrest following ventricular tachycardia. Severe heart failure, a critical condition, and thinning of the LV wall may have contributed to the markedly high plasma BNP level in this case.
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PMID:Markedly High B-type Natriuretic Peptide Level in a Patient with Duchenne Muscular Dystrophy and Left Ventricular Non-Compaction. 2632 46

Dilated cardiomyopathy (DCM) is the major cause of heart failure affecting both women and men. Limited clinical studies show conflicting data in sex-related differences in the progression of dilated cardiomyopathy and heart failure (HF) outcomes. We examined the comparative sex-related progression of cardiomyopathy and the development of HF (at 4, 7, 13 weeks of age) in a well-established, transgenic mouse model of DCM that recapitulates the progressive stages of human HF. By 13 weeks of age, female mice with DCM had more severe left ventricular systolic dysfunction, left ventricular dilation and wall thinning (P<0.001 for all) than age-matched male mice with DCM. Female mice also had greater lung edema (P<0.001), cardiac fibrosis (P<0.01) and pleural effusions, which were not rescued by ovariectomy. By comparison to DCM male mice at 13 weeks, these pathological changes in female mice with DCM, were associated with significant increases in plasma active renin (P<0.01), angiotensin II (P<0.01) and aldosterone levels (P<0.001). In comparison to DCM male mice, DCM female mice also showed differential expression of the natriuretic peptide system with lower corin and higher ANP, BNP and cGMP levels at 13 weeks of age. We conclude, that female mice with experimental DCM have an accelerated progression of cardiomyopathy and HF, which was not corrected by early ovariectomy. These alterations are associated with early renin activation with increased angiotensin II and aldosterone levels, and altered expression of the natriuretic peptide system.
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PMID:Enhanced heart failure, mortality and renin activation in female mice with experimental dilated cardiomyopathy. 2924 Jul 88