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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An attempt was made to prove the phenomenon of myocardial collagen breakdown in a norepinephrine (NE) induced model of reversible cardiopathy in anesthetized rabbits. NE (0.3 mg/kg in 90 min) was infused to 22 animals. Histologically it was found that immediately and during the first two days after the catecholamine administration the myocardial collagenous network became disrupted and it partly disappeared. Collagenase and peptidase activities were measured from homogenates of the same hearts. A significant increase of these activities was observed and that could be correlated with the intracellular matrix destruction.
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PMID:Myocardial collagen degradation: morphological and biochemical correlation. 184 16

The Caerphilly Collaborative Heart Disease Study is based on a large cohort of men (2,398) aged 49-66 years at the time of study. Platelet aggregation induced by collagen, thrombin, and ADP was measured in fasting blood samples and was related to prevalent angina, past myocardial infarction, and electrocardiographic evidence of ischemic heart disease. A number of subjects had taken aspirin, other nonsteroidal anti-inflammatory drugs, or other drugs affecting platelet aggregation 7 days before blood sample collection; after the exclusion of these subjects, data were available for 1,811 men. No relations were demonstrated with angina, but significant relations were shown between past myocardial infarctions and electrocardiographic evidence of ischemia and ADP-induced aggregation (both primary and secondary) and between electrocardiographic evidence of ischemia and thrombin-induced aggregation. The strongest relation indicated more than a twofold increase in the odds of a past myocardial infarction in subjects of the highest fifth of ADP-induced primary platelet aggregation compared with the lowest fifth. No significant relations were detected with collagen-induced aggregation. Accounting for a number of possible confounding factors had a relatively small impact on the relations between platelet aggregation and ischemic heart disease. Other evidence, including the well-established effect of aspirin on reducing the incidence of ischemic heart disease, indicates that the relations we describe are unlikely to be simply an effect of IHD on platelets.
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PMID:Ischemic heart disease and platelet aggregation. The Caerphilly Collaborative Heart Disease Study. 198 96

Histochemical and immunohistochemical investigations were performed on tissue obtained from the right heart side in three patients subjected to valve, replacement operations because of severe carcinoid heart disease. Extensive fibrotic changes were present on the endocardium of the right atrium, the papillary muscles of the tricuspid valve and the leaflets of the tricuspid and pulmonic valves of all patients. The main constituent of the lesions was a stroma with abundant acid mucopolysaccharides and collagen but devoid of stainable elastic components. The lesions were in some areas sharply delineated from the normal endocardium, but often also extended into the endocardium and myocardium. Small to medium sized vessels were demonstrated histochemically in the lesions and confirmed by positive immunoreaction against endothelial and smooth muscle cells. The moderate number of mesenchymal cells within the lesions had immunoreactivity consistent with muscle cells which seemed to have a very low proliferating activity. The histochemical and immunohistochemical techniques used confirmed some earlier observations in carcinoid heart disease but also rendered new information contradicting previous findings. The infiltrative nature of the carcinoid plaque gives a new dimension to the carcinoid heart disease. The etiology still remains obscure and well known growth factors for connective tissue such as platelet derived growth factor (PDGF) do not seem to be directly involved in the process.
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PMID:Histochemical and immunohistochemical morphology of carcinoid heart disease. 202 24

Observations are described on the fibrillar nature and structural features of the collagenous interstices of the human myocardium in chronic chagasic cardiomyopathy, comparing them with similar observations in normal hearts, using the picrosirius red technique and polarization microscopy. A total of 28 adult hearts obtained at autopsy were used: 5 control without evidence of cardiac disease, and 23 with chronic Chagas' heart disease. The findings in the myocardium of those without Chagas' disease were in keeping with those reported in the literature. In those with Chagas' disease diffuse interstitial fibrosis could be observed in all cases, albeit to varying degree. The pattern was that of a diffuse increase in the amount of thick collagen fibers surrounding bundles of muscle fibers (perimysial matrix), varying in intensity from one area to another, and around the intramyocardial coronary vessels, combined with a less pronounced increase in the matrix of endomysial collagen. The relationship between the observed myocardial fibrosis and cardiac function, and the potential mechanisms for its production, are discussed. Further research is needed into the patterns and pathogenesis of myocardial fibrosis in order to offer possibilities for prevention and development of corrective forms of therapy for the fibrotic process.
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PMID:The pattern of myocardial fibrosis in chronic Chagas' heart disease. 205 74

Cardiac involvement in collagen diseases was studied in 917 patients representing all the cases of collagen diseases diagnosed in the "N. Gh. Lupu" Institute of Internal Medicine between 1985 and 1987. The prevalence of the various cardiac disorders was studied within every disease or group of diseases diagnosed according to clinical, ECG, radiologic and when necessary echocardiographic data. Collagen heart disease was diagnosed in 38.2% of the patients. In the case of systemic lupus erythematosus, of polyarteritis nodosa and of progressive systemic sclerosis this proportion exceeds 50%. The most frequent cardiac disorders were the rhythm and conduction disturbances, detected in 112 patients (12.2%). The cardiomyopathies and myocarditis, not infrequent (7.4%) represented an element of severity influencing the evolution and prognosis of disease. Myocardial ischemia secondary to coronary vasculitis syndromes has proved to be an important pathogenic mechanism of cardiac disorders. By their frequency and severity, the cardiac involvements in collagen diseases have proved important, becoming sometimes a central diagnostic, therapeutic and prognostic problem.
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PMID:Is cardiac involvement in collagen diseases important? A clinical study in 917 patients. 209 92

Myocyte hypertrophy and myocardial fibrosis have been observed in transplanted human hearts, and both could potentially have an adverse effect on long-term cardiac function. There has been some concern that distant donor heart procurement and cyclosporine treatment increase the risk of these changes, but their incidence and severity have not been documented quantitatively in large numbers of cardiac transplant recipients. We used light microscopic morphometric methods to estimate myocardial collagen volume fraction and myocyte width in right ventricular endomyocardial biopsies from 95 recipients at 3 years posttransplantation, and electron microscopic stereology to estimate myocardial vascularity and myocyte myofibril content in 40 recipients, also at 3 years posttransplantation. We compared those with locally and distantly procured donor hearts (mean ischemic time 160 minutes) and cyclosporine versus noncyclosporine immunosuppression. Controls were pretransplant right ventricular biopsies from 20 donor hearts which were free of heart disease. We found no significant differences in myocardial collagen volume fractions. Myocyte hypertrophy was typical of all the transplant biopsies (mean myocyte width 20.2 microns, SD 3.0 in all transplants versus 11.8 microns, SD 2.2 in controls, P less than 0.001), but distant donor procurement and cyclosporine had no significant effect. There were significant reductions of myofibril volume fraction in the transplants, which raises the possibility of gradual decompensation in some patients. There were no significant differences in myocardial vascularity, although a few patients were well below the control range. We conclude that distant donor heart procurement, with ischemic times averaging less than 3 hours, and cyclosporine treatment are not responsible for significant hypertrophy or fibrosis in most transplants. Hypertrophy is typical of the transplanted heart, and it is possible that associated abnormalities might have an effect on cardiac function in some long-term survivors.
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PMID:Pathologic changes in the long-term transplanted heart: a morphometric study of myocardial hypertrophy, vascularity, and fibrosis. 214 25

The extracellular matrix of the myocardium contains an elaborate structural matrix composed mainly of fibrillar types I and III collagen. This matrix is responsible for the support and alignment of myocytes and capillaries. Because of its alignment, location, configuration and tensile strength, relative to cardiac myocytes, the collagen matrix represents a major determinant of myocardial stiffness. Cardiac fibroblasts, not myocytes, contain the mRNA for these fibrillar collagens. In the hypertrophic remodeling of the myocardium that accompanies arterial hypertension, a progressive structural and biochemical remodeling of the matrix follows enhanced collagen gene expression. The resultant significant accumulation of collagen in the interstitium and around intramyocardial coronary arteries, or interstitial and perivascular fibrosis, represents a pathologic remodeling of the myocardium that compromises this normally efficient pump. This report reviews the structural nature, biosynthesis and degradation of collagen in the normal and hypertrophied myocardium. It suggests that interstitial heart disease, or the disproportionate growth of the extracellular matrix relative to myocyte hypertrophy, is an entity that merits greater understanding, particularly the factors regulating types I and III collagen gene expression and their degradation.
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PMID:Collagen and the myocardium: fibrillar structure, biosynthesis and degradation in relation to hypertrophy and its regression. 214 89

The effects of Ticlopidine on platelet function at rest and after exercise test in 12 patients with a history of myocardial infarction but no risk factors and/or residual angina, were investigated. The patients were treated with 500 mg per diem Ticlopidine or placebo for 15 days in a crossover double-blind study. Blood samples were taken before and 3 minutes after maximum effort exercise cycle tests. Blood samples from 25 healthy volunteers of comparable age and sex were used for control purposes. The parameters examined were: platelet aggregation induced by ADP (1 and 3 mumol/l), Arachidonic Acid (AA) (1.3 mmol/l) and collagen (2 micrograms/ml); the presence of circulating platelet aggregates and plasmatic fibrinogen levels. When compared with the controls, the patients showed higher levels of aggregation caused by ADP, AA and collagen as well as circulating aggregates. Exercise produced a statistically significant increase in platelet activation, while Ticlopidine significantly inhibited the platelet aggregation induced by ADP, AA and collagen as well as circulating aggregates both at rest and after the exercise test. Fibrinogen levels were higher in the heart attack patients than the controls especially after exercise, but not to a statistically significant degree. Treatment with Ticlopidine did not influence plasma fibrinogen levels. It is not known whether the patients with signs of effort-induced platelet aggregation run a higher risk of ischaemic cardiopathy or whether drug treatment could prevent this eventuality.
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PMID:[Effects of ticlopidine on platelet function at rest and after exercise in patients with previous myocardial infarct. An acute crossover double-blind study]. 217 69

Doppler flow velocity waveform analysis (FVWFA), recorded from the dorsalis pedis artery (DPA) and the radial artery (RA), was performed on 36 women in attempting to detect an initial diabetic microangiopathy (DM). The study comprised two groups of women affected by non-insulin-dependent diabetes mellitus, 6 patients (pts) of reproductive age (1), 12 pts in menopause (II), and two groups of age-matched healthy controls (C) (III and IV). Clinical signs of initial DM were present in group I. All the examined pts were nonsmokers and normotensive and without cardiopathy, signs of diabetic macroangiopathy, collagen vascular disease and/or Raynaud's phenomenon, and renal failure. Four waveform dimensions capable of separating different degrees of peripheral obstructive arteriolar disease were determined on velocity tracing and the results used in a single best discriminant equation. The resultant discriminant score (DS), derived by FVWFA on DPA, showed a highly accurate rate of separating the young pts with DM from both C and the pts in menopause without DM. Furthermore, the resultant DS was statistically not different in groups II, III, and IV. In conclusion, FVWFA on DPA, in this experience, has proved to be an accurate and sensitive method in the detection of initial DM.
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PMID:Use of Doppler flow velocity waveform analysis in detection of initial diabetic microangiopathy. 222 66

The hearts obtained at autopsy of 67 patients with hypertension, diabetes mellitus, or both were examined microscopically and histochemically, and the amount of fibrosis was determined. Significant differences in heart weight, interstitial fibrosis, replacement fibrosis, and perivascular fibrosis were found among the groups. The mean heart weight of the hypertensive-diabetic patients was significantly greater than that of the hypertensive patients and the diabetic patients. The amount of microscopic fibrosis increased between the groups, the lowest in hypertensive hearts, midrange in diabetic hearts, and highest in hypertensive-diabetic hearts. Total fibrosis correlated with heart weight among diabetic and hypertensive-diabetic patients and was significantly greater among patients with congestive heart failure, most of whom had histories of both hypertension and diabetes. The microscopic grade of fibrosis correlated significantly (p less than 0.01) with a quantitative, histochemical determination of the amount of collagen per milligram of total noncollagenous protein in the heart tissue. Myocardial fibrosis may contribute to the diastolic dysfunction typical of hypertensive-diabetic cardiomyopathy, in which congestive heart failure is a common sequela. The importance of hypertension in the pathogenesis of severe diabetic heart disease is discussed.
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PMID:A comparison of the pathological spectrum of hypertensive, diabetic, and hypertensive-diabetic heart disease. 202 37


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