Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from patients with heart disease were examined by single sandwich indirect immunofluorescence for the presence of antibodies to human heart muscle. Endocardial biopsy specimens were also examined by direct immunofluorescence for deposition of antibodies in vivo. No consistent or specific abnormality was found in the biopsy specimens or sera of patients with congestive cardiomyopathy. The presence of anti-heart antibodies in cardiac disease appears to reflect damage to cardiac muscle whatever the cause. Immunofluorescence is an insensitive test for anti-heart antibodies.
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PMID:Humoral immunity in cardiomyopathy. 635 29

In 33 puppies 2-4 months of age the model of a congenital heart disease was made as coarctation of the aorta. In 6-12 months 18 animals were taken to study, and in 15 animals the coarctation was removed. The latter animals were observed for other 6-12 months. The hearts of both groups were separately weighed, and the vessels of the coronary system were studied by means of a complex of histological and morphometric methods. Simultaneously, the number of smooth muscle cells, as well as the area and volume of their nuclei in media of small coronary arteries were estimated. At the experimental coarctation of the aorta certain hypertrophic-hyperplastic changes in coronary arteries at all branching levels take place. They are of a compensatory-adaptive character and reflect certain reactions of the vascular wall to an increased coronary hemodynamics under conditions of hyperfunction and hypertrophy of the cardiac muscle. Surgical removal of the coarctation is accompanied with a reduce of the hemodynamic loading of the heart, diminished degree of hypertrophy of the organ and a marked decrease of the hypertrophic-hyperplastic changes in its vessels. At the same time, the cardiac vascular system is adapting to the new conditions of circulation: rearrangement of some coronary arteries and arterioles according to the closed type and reduction of circulation in the vascular branches which have lost their importance in feeding the myocardium.
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PMID:[Morphologic changes in the coronary arteries in experimental coarctation of the aorta and following its correction]. 646 15

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.
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PMID:Hypertropic cardiomyopathy and hyperthyroidism in the cat. 654 Feb 56

Ten patients with myotonic dystrophy have been studied by M-mode and 2-dimensional echocardiography. Six patients had echocardiographic abnormalities: mitral valve prolapse, hypertrophy of the papillary muscles (2 cases); impaired regional left ventricular relaxation, probably due to "cardiac myotonia" (4 patients); and dilatative cardiomyopathy in the sole patient with overt heart disease. There seems to be no relation between involvement of skeletal and cardiac muscle. It is likely, although not proved, that myocardial involvement in myotonic dystrophy occur initially as "myotonia", followed by a "dystrophic" phase with severe dilatative cardiomyopathy, not unlike the skeletal muscle.
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PMID:[Echocardiographic findings in dystrophia myotonica (Steinert's disease)]. 654 38

Taurine is important for the regulation of ionic fluxes in excitable tissues, especially in heart where it is the most abundant amino acid. To investigate a possible role of taurine in uremia, we measured the taurine concentrations in plasma, liver, muscle, heart, and brain tissues of young male Wistar rats. Two groups of rats were studied: (1) rats with acute renal failure (ARF) 12, 24, and 48 hours after bilateral nephrectomy and (2) rats with chronic renal failure (CRF) studied 3 weeks after 5/6 nephrectomy. In ARF animals, taurine increased in plasma and liver two to three times the normal levels, remained unchanged in muscle and brain, but decreased in heart tissue; this decrease (-20%) was significantly correlated with the concomitant increase of BUN and plasma creatinine. In CRF animals, taurine was unchanged in plasma, liver, muscle, and heart, but was increased by 70% in brain accompanied by a high content of gamma-aminoisobutyric acid. The data suggest that in uremia accumulation of taurine is counteracted by increased hepatic elimination and/or decreased synthesis. The depletion of taurine in cardiac muscle might be related to the development of uremic heart disease. The increased concentrations of brain taurine might represent a compensation for the increased neuroexcitability in CRF.
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PMID:Taurine metabolism in experimental renal failure. 658 73

p21ras has been implicated in the hypertrophic response of cultured cardiac myocytes to defined growth stimuli. To determine if activation of ras-dependent intracellular signaling pathways is sufficient to induce in vivo hypertrophy, transgenic mice were created that express oncogenic ras in the cardiac ventricular chamber. Mice homozygous for the transgene displayed morphological, physiological, and genetic markers of marked cardiac muscle hypertrophy. Miniaturized catheterization technology documented a selective prolongation of cardiac relaxation, similar to that seen in early human hypertrophic heart disease. An increase in left atrial mass, in the absence of transgene expression in that chamber, further supported physiologically abnormal left ventricular diastolic function. Histological analysis revealed myofibrillar disarray, indistinguishable from that in hypertrophic cardiomyopathy in man. These studies establish a ras-dependent pathway for hypertrophic heart disease and document the feasibility of mapping in vivo signaling pathways for cardiac hypertrophy and dysfunction by applying in vivo microphysiological assays to genetically manipulated mice. ras-dependent pathways may also be a rational target for developing new approaches to inhibit the genesis of hypertrophy in certain pathological settings.
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PMID:Ventricular expression of a MLC-2v-ras fusion gene induces cardiac hypertrophy and selective diastolic dysfunction in transgenic mice. 755 64

There is increasing evidence that the membrane-bound thyrotropin receptor (TSHR) may be mediating clinically important direct effects of thyrotropin (TSH) and of TSHR antibodies (TSHRab) in extra-thyroidal tissues. TSHR mRNA has formerly been detected in thyroid, retroorbital muscle and fibroblasts, peripheral lymphocytes and rodent fat. It is well known that thyroid disease may aggravate or induce heart disease, but the pathophysiological role of TSH and TSHRab is not clear. The aim of this study was to investigate if TSHR is present in cardiac muscle. Reverse transcriptase polymerase chain reactions revealed TSHR in human heart and Northern blot on extracted RNA showed a RNA species of 4.4 kb. TSH stimulation of cultured mouse AT-1 cardiomyocytes elevated the levels of intracellular second messenger 3',5'-cyclic AMP. This effect of TSH could be inhibited by TSHR antibodies. In solution hybridization levels of TSHR mRNA in AT-1 cells were 50% of mRNA in crude mouse heart. In conclusion functional TSHR is present in cardiomyocytes.
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PMID:Evidence for the presence of functional thyrotropin receptor in cardiac muscle. 779 53

Heart disease is an entity frequently seen in the fetal alcohol syndrome. This paper describes the effect of in utero ethanol exposure on the postnatal ultrastructural development of rat cardiac muscle. To determine this time-pregnant Sprague-Dawley rats were fed either a nutritionally balanced protein- and vitamin-enriched liquid ethanol diet (with 36% of the calories derived from ethanol) or a liquid diet with maltose-dextrins isocalorically substituted for ethanol. The latter group was designated the pairfed control group. At birth, pups of both the groups were surrogate-fostered by normal dams. Body weights and crown-rump lengths were significantly less in the rat pups exposed to ethanol in utero at 21 days postnatal. Ultrastructural analysis of the cardiac muscle was performed at 7, 14, and 21 days postnatal in ethanol and pairfed groups. Several morphological features of myocyte damage were observed in ethanol-exposed pups, predominantly at 7 days postnatal, with nearly total absence of myocyte damage by 21 days postnatal. The most outstanding changes were observed in the myofibrils, which showed dysplastic changes at 7 days postnatal, a delay in M-band structural development at 14 days postnatal, and a significantly smaller myofibril volume density per tissue volume at 21 days postnatal in the ethanol rat pups compared to the pairfed controls.
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PMID:Fetal alcohol effects on the postnatal development of the rat myocardium: an ultrastructural and morphometric analysis. 795 76

The neonate with circulatory failure and cardiogenic shock is a difficult management problem. However, the initial approach is that of resuscitation with exact diagnosis of secondary concern. Once the infant has been stabilized and septic and hypovolemic shock have been excluded, attention should be directed to the four most likely causes of cardiogenic shock: structural heart disease with left heart obstruction being the most common, cardiac muscle disorders, cardiac dysrhythmias, and cardiac metabolic disorders.
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PMID:Cardiogenic shock in the neonate. 825 87

Doxorubicin (DX)-treated mice represent an animal model for studying new drugs for heart disease. Coincidentally, in the collection of damaged myocardial tissue, thrombosis was detected in the atrium. The incidence reached 75% in mice given 4 mg/kg DX iv 10 times. They were white thrombi consisting of the fibrin, platelets, and neutrophils. Cardiac muscle damage was more prominent in the atria than in the ventricles. Light microscopically, vacuolization and degeneration of atrial myocytes and interstitial inflammatory cell infiltration were observed. Electron microscopy revealed dilatation of the sarcoplasmic reticulum and an increase in number of normal and/or degenerate mitochondria. Inflammation extended from the cardiac muscle to the endocardium. The cause of atrial thrombosis in DX-treated mice is unknown but may relate to endocardial damage and changes of blood flow in the atrium secondary to cardiac muscle damage. DX-treated mice could serve as an experimental animal model for the evaluation of efficacy and toxicity of antithrombotic or antiplatelet drugs.
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PMID:The high incidence of atrial thrombosis in mice given doxorubicin. 829 Aug 67


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