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)

Endocardial fibroelastosis is an uncommon congenital heart disease in dogs that may be manifested by signs of left-sided congestive heart failure. A three-month-old, male, Fila Brasileiro dog developed signs of generalised heart failure. Physical examination revealed normal temperature, ascites, and pale and cyanotic mucous membranes. The pup died just after radiography which revealed ascites, hepatomegaly, severe cardiac enlargement and pulmonary oedema. At necropsy, serosanguineous fluid in the thorax and abdomen, pulmonary oedema, right ventricular dilatation, hypertrophy and dilatation of the left ventricle, and mitral valve incompetence were observed. The histopathological examination demonstrated that the thickening of the endocardium of the left atrium and left ventricle was due to the presence of elastic and collagen fibres, although there were no signs of an inflammatory process.
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PMID:Endocardial fibroelastosis in a dog. 912 86

Sixteen children, aged 7 months to 12 years, with acute pericarditis, admitted between 1985 and 1993 to a tertiary referral centre were analyzed retrospectively for their presentation, etiology, work-up, management and prognosis. It was found that most of the presenting signs were not specific and were often related to associated diseases such as respiratory tract infections. In 50% of the cases a cause was not found, the others had viral infections (12.5%), tuberculosis (12.5%), Haemophilus influenzae infection (6.25%), Toxocara canis infection (6.25%) and collagen diseases (12.5%). In eight cases non-steroidal anti-inflammatory drugs associated with steroids were given, 7 patients received non-steroidal anti-inflammatory drugs and 1 steroids. The mean follow-up time was 3 years (1 to 5). Six patients had one or more relapses. Five of the 6 patients with relapses were in the group which received steroids. The two patients with tuberculosis underwent pericardiectomy. One child died due to complex heart disease and the remaining 15 were cured. It was concluded that in pericarditis an extensive work-up may not reveal the major etiologies and that long term prognosis is good.
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PMID:[Acute pericarditis in childhood. The 9-year experience of a tertiary referral center]. 923 47

In the acute phase of Chagas' disease, the micropathology of the heart reveals a diffuse focal myocarditis, sometimes of a phlegmonous type and of an intensity not seen in any other inflammatory heart disease. Foci of myocytolytic necrosis and degeneration are seen microscopically with an intense mononuclear infiltrate associated with exudative phenomena and marked parasitism of myofibers. Abnormalities of the coronary microcirculation have been demonstrated in acute chagasic myocarditis as possible cause of transient ischemia consistent with the hypothesis of microvascular factor as a cause of the myocardial changes. Considering that the endothelium plays a key role as controller of the vessel tone regulation and vascular permeability, this investigation was carried out to study the structure of the endothelial lining of the thoracic and abdominal aorta obtained from Trypanosoma cruzi-infected rats in the acute septicemic phase by using scanning and transmission electron microscopy. The findings clearly demonstrate that the infected rats developed changes of the endothelial layer characterized by endothelial cell swelling and a few points of cell cytoplasm discontinuity appearing as holes exposing the subendothelial collagen usually associated with platelet-fibrin aggregates. These changes could disturb the generation of vasoactive substances, impairing the equilibrium between opposing forces. The exposition of the subendothelial collagen due to holes in the endothelial lining would favor platelet-fibrin aggregation. This way, the present results allow speculation that similar endothelial cells changes could be present in the microcirculation, reflecting a reduction in the protective role of the endothelium, participating in the genesis of vasospasm and platelet aggregation within coronary microvessels, and leading to the focal pathology in acute chagasic myocarditis.
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PMID:Aortic endothelial cell changes in the acute septicemic phase of experimental Trypanosoma cruzi infection in rats: scanning and transmission electron microscopic study. 931 44

The CD36 molecule is a multifunctional membrane type receptor glycoprotein that reacts with thrombospondin, collagen, oxidized LDL and long-chain fatty acids (LCFA). LCFA are one of the major cardiac energy substrates, hence LCFA metabolism may have an important role in cardiac diseases. In this study, we analyzed CD36 expression in 200 patients with heart diseases [44 patients with hypertrophic cardiomyopathy (HCM), 16 with dilated cardiomyopathy (DCM), 26 with old myocardial infarction (OMI), 55 with angina pectoris (AP) and 59 with other miscellaneous heart diseases] using a flow cytometer. 123I-beta-methyl-p-iodophenylpentadecanoic acid (BMIPP) myocardial accumulation was also examined in some patients. Eight patients (2 with HCM, 1 with DCM, 2 with OMI, and 3 with AP) were diagnosed as having type I CD36 deficiency (neither platelets nor monocytes expressed CD36). Sixteen patients (3 with HCM, 1 with DCM, 1 with OMI, 8 with AP, and 3 with other heart diseases) showed type II CD36 deficiency (monocytes expressed CD36 but platelets did not). In all 8 patients with type I CD36 deficiency, there was no BMIPP accumulation in the heart. However, in 13 patients with type II CD36 deficiency, focally reduced BMIPP accumulation was observed, but there were no patients without BMIPP accumulation. CD36 deficiency was observed in a higher proportion (12%) of patients with heart disease in this study than in a reported control study. Type I CD36 deficiency is associated with absence of BMIPP accumulation in the heart, hence it may have an important role in LCFA metabolic disorders and some types of cardiac hypertrophy as well as other heart diseases.
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PMID:[Different patterns of 123I-BMIPP myocardial accumulation in patients with type I and II CD36 deficiency]. 949 34

Chronic complications of diabetes are dominated by disorders of the vascular system. They are a much larger burden on both diabetic patients and overall medical costs than diabetes itself. Large vessel problems are far more frequent than microvascular disorders. Loss of arterial elasticity alters arterial flow patterns and increases microcirculatory peak flow rates. Hyperglycemia may directly disrupt elastin formation. Diabetic leg artery disease may be generated by nerve damage, reversing this interactive contribution sequence. The major anatomic feature of microangiopathy in long-term diabetes is an unevenly distributed thickening of the intima of smaller arterioles. The thickening is primarily due to accumulation of type IV (basement membrane) collagen. Arterioles change local vessel diameter to adjust blood distribution to meet current needs. The thickening compromises the maximum local blood flow that may be achieved by this means. Compromise of maximal arteriolar dilatation does not disrupt exercising muscle but in the kidney, retina, and possibly in nerve, local circumstances can generate serious damage. Each of these system's responses has unique features that mediate its vulnerability, but all these organs show arteriolar hyalinization. The increased arteriolar accumulation of type IV collagen appears to be a response to the tangential force generated by flow over local endothelial cells. An increase in peak arteriolar wall force is mediated by a diabetes-specific doubling of erythrocyte membrane curvature change resistance. Red cell aggregation rate determines the rate of damage. The same nonspecific burden may also predispose to heart disease and stroke. Intensive metabolic control improves red cell deformability and protects against arteriolar damage. Therapies that address the rheologic problem more directly may add to the effectiveness of good diabetes control in the future.
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PMID:Development of vascular complications in diabetes. 954 55

The present study deals with both pathologic fibrosis and matrix connective tissue in chronic chagasic myocarditis. A total of 12 hearts were obtained at autopsy. Eight cases of chronic chagasic myocarditis were selected. Four cases without evidence of cardiac disease were used as controls. The diagnosis of chronic Chagas' heart disease was based on previously established criteria. A cell-maceration method was utilized to evaluate the spatial organization of the fibrillar collagen accumulation after removal of the myocardial tissue non-fibrous elements. The relationship between inflammatory cells identified by monoclonal antibodies and interstitial fibrosis stained with picrosirius red was assessed. Striking structural alterations of the collagen matrix in the perimysium were detected: increase in number and thickness of tendon-like structures, and markedly thickened and aggregated collagen strands. Besides, a diffuse increase in the thickness of collagen fibers surrounding individual myocytes, consisting of the endomysial matrix, mainly adjacent to the perimysium, could be observed. The dense-weave endomysial meshwork was composed of fine collagen fibrils, and it was continuous with those of adjacent myocytes, obscuring the lateral struts. Sometimes, thicker struts tethering myocytes to myocytes could be seen. These changes were associated with scattered dense scar-like foci, probably reflecting repair fibrosis associated with myocyte necrosis. Furthermore, the present results clearly showed the colocalization of foci of myocyte necrosis and degeneration and associated fibrosed areas and fibroblasts with T lymphocytes and macrophages. The accumulation of interstitial collagen fibers in chronic chagasic myocarditis may be expected to decrease myocardial compliance and disrupt synchronous contraction of the ventricles during systole, contributing to a spectrum of ventricular dysfunction that involve either the diastolic or systolic phase of the cardiac cycle or both. Myocardial fibrosis can be also implicated in the genesis of malignant ventricular tachyarrhythmias, major causes of sudden death among chronic chagasic patients. The increase in myocardial fibrosis could be directly related to an inflammatory reaction mainly composed of T lymphocytes and macrophages.
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PMID:Fibrosis and inflammatory cells in human chronic chagasic myocarditis: scanning electron microscopy and immunohistochemical observations. 982 33

Occlusive coronary artery disease is an important factor of cardiovascular morbidity and mortality. The rupture of the thin fibrous cap of the atheroma may be one of the causes of acute coronary syndrome, however, the mechanism of formation of fibrous plaque are poorly understood. Elevation of plasma homocysteine, hyperhomocystinemia, H(e), has emerged as an independent risk factor for hypertension and fibrotic heart disease. The extracellular matrix (ECM) components, particularly fibrillar collagen, are elevated in the atherosclerotic lesions and are the essential integral element in holding the oxidized low density lipoproteins (LDL), homocystine, macrophage and foam cells in milieu, constituting the primary atherosclerotic and secondary restenotic lesions. In vivo and in vitro physiological, morphological, cellular, biochemical and molecular experiments have suggested the role of tissue homocystine in cardiovascular fibrosis and adverse ECM remodeling following H(e). The tissue homocystine induces cardiovascular fibrosis and may lead to heart failure via the redox-receptor pathway. The underlying cause and mechanism of cardiovascular fibrosis associated with arteriosclerosis, atherosclerosis, hypertension and coronary heart disease, involve changes in the levels of tissue redox state.
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PMID:Homocyst(e)ine and heart disease: pathophysiology of extracellular matrix. 1022 75

Platelets are small cells, 1/14th the volume of erythrocytes, and about 1000 billion circulate in human blood as smooth anucleate disks. Their job is to survey the lining of our blood vessels, the endothelium. In acute damage and extravasation, platelets are activated by contact with exposed collagen and aggregate together at the wound sites to initiate clotting and stop bleeding. Forming a physical plug to seal a hemorrhaging vessel is the key role of blood platelets. However, milder injury to the endothelium, perhaps a result of high blood pressure, raised plasma cholesterol, or smoking, also causes platelets to adhere to the internal walls of arteries. Such precipitate adhesion and activation of platelets initiates an inflammatory response of the vessel wall and predisposes to vascular complications, including thrombosis, premature heart disease, myocardial infarcts or strokes, and diabetes. It is essential, therefore, that during normal vascular hemostasis platelet activation is tightly controlled. Indeed, both platelets and endothelial cells produce and secrete chemicals that directly inhibit platelet aggregation. A key agent is the free radical gas nitric oxide (NO). Here, we review how this 30-Da molecular messenger is synthesized by a catalytic cassette 10,000 times larger and how it functions to suppress platelet "stickiness." We also present new evidence that directly links plasma lipoproteins with platelet activation: we describe at the molecular level how apoE, a protein with a prominent role in cholesterol transport, interacts with the platelet surface to stimulate NO production and hence attenuate platelet activation.
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PMID:Nitric oxide and platelet aggregation. 1023 45

The primary cause of cardiac morbidity and mortality in developed countries is ischemic (coronary) heart disease. The incidence of this disease is virtually all due to atherosclerosis, and ischemic heart disease is also the most prevalent disease in the industrialized world, causing over 40% of all deaths in the United States and Western Europe. In Japan, the incidence of ischemic heart disease due to coronary atherosclerosis is gradually increasing as well. Compared with the classical nomenclature of atherosclerosis; that is, fatty streak, fibrous plaque and complicated lesions, the term Stary's classification has been universally accepted because it reflects the more recently acquired knowledge about the morphological and biochemical details of the processes in coronary atherosclerosis, which have been obtained by new strategies such as angioscopy, intravascular ultrasound and molecular biological methods. The term Stary's classification has been applied for the coronary atherosclerosis of patients with acute coronary syndrome at the National Cardiovascular Center, for the analysis of predisposing atherosclerosis of these patients. The recent findings regarding acute coronary syndrome resulting from a rupture of coronary atherosclerotic plaques indicate that this syndrome is probably the most important mechanism underlying the sudden onset. It has been found that the risk of plaque rupture may depend more on plaque composition than on plaque size. Plaques rich in soft extracellular lipids and macrophages are possibly more vulnerable to plaque rupture. Two of the goals of the present review are to clarify how plaque disruption occurs and to elucidate the relationship between plaque disruption and coronary risk factors in elderly Japanese patients with acute coronary syndrome. Coronary stents have been shown to be efficacious in the treatment of acute and threatened closure complicating percutaneous transluminal coronary angioplasty (PTCA) and have produced encouraging initial results in the prevention of restenosis. In the autopsy study of restenosis after PTCA, it was observed that dense caps of collagen fibers in the adventitia in the vicinity of the disrupted internal elastic laminae were present in all of the remodeling lesions. It is suggested that remodeling, which resulted in adventitial scarring, is one of the major causative factors of restenosis after PTCA. The long-term success of stenting, however, remains limited by the occurrence of late in-stent restenosis, with an incidence of 20-42% depending on the stent design and the patient population studied. Another aim of the present review is to describe the pathological mechanism of restenosis after PTCA and/or stent replacement and, consequently, the vascular remodeling that occurs around adventitial tissue after PTCA and intimal hyperplasia that is chronically irritated by a foreign body granulomatous reaction after stenting. Finally, the results of the investigation of the effect of a tissue factor pathway inhibitor on the prevention of interventional restenosis is described.
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PMID:Coronary atherosclerosis and interventions: pathological sequences and restenosis. 1036 46

Adequate control of survival or programmed cell death (apoptosis) of cardiovascular cells appears as an important drug target. While prevention of apoptotic death of cardiomyocytes has been assessed in detail, selective induction of apoptosis of vascular smooth muscle cells or fibroblasts could also be of relevance. Thus, induction of apoptosis of vascular smooth muscle cells by p65 NF-kappa B and Bcl-xL antisense oligonucleotides or p53 overexpression could be useful for limiting vascular lesions associated with restenosis. Although fibroblasts represent the majority of cardiac cells, few attempts were made to induce fibroblast apoptosis in disorders associated with excessive collagen deposition and fibrosis. It is hypothesized that early interference with fibroblast proliferation after myocardial infarction or inflammatory heart disease limits fibrosis which further impairs cardiac performance. A candidate approach could involve growth factor analogues which are known to induce fibroblast apoptosis when an incomplete growth stimulus persists.
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PMID:Control of apoptosis of cardiovascular fibroblasts: a novel drug target. 1041 46


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