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

In this paper demographic characteristics, etiology, pathology and clinical features of infective endocarditis are reviewed simultaneous presentation of the data from our series of 50 cases with infective endocarditis. The peak incidence of infective endocarditis is between 11 and 15 years. Both sexes are equally affected. Patients with congenital or acquired heart disease tend to have hemodynamic trauma to the endocardium and vascular endothelium. These sites form the nidus for circulating bacteria of either spontaneous origin or the result of any oro-dental, genitourinary or other surgery or procedures and produce vegetations characteristic of infective endocarditis. The location of the vegetation is dependent upon the predisposing cardiac lesion. Embolic phenomenon is another cardinal feature of endocarditis and may occur in any organ system. Although a large variety of microbes have been known to cause endocarditis, streptococci and staphylococci remain the most frequent offenders. Clinical diagnosis of infective endocarditis is difficult because of the insidious onset and varied clinical features. A high degree of suspicion is essential for early diagnosis. Any patient with known heart disease and unexplained fever should be suspect for endocarditis. Splenomegaly, petechiae and embolic phenomena support this diagnosis. New or changing murmurs, splinter hemorrhages, Osler's nodes. Janeway's lesions and Roth's spots may be present. Elevated sedimentation rate, microscopic hematuria, leukocytosis with a shift-to-the-left and anemia may further support the diagnosis. Congenital or acquired heart disease and fever are all that will be present in many cases. Only isolation of the causative agent from the blood can confirm the diagnosis.
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PMID:Infective endocarditis: a review. I. Incidence, etiology, pathology and clinical features. 72 71

Retinopathy of prematurity is a disease of developing blood vessels. Although it is seen predominantly in premature infants requiring life support systems to survive, it does occur in full-term infants, infants with hypoxia, cyanotic heart disease and in stillborn infants. Although oxygen has been considered to be the prime aetiologic agent, evidence for this, particularly in recent years, is not compelling. The timing of the occurrence of the disease is closely related to the conceptional age of the infant rather than weeks post birth, birth weight, gestational age at birth. In addition, the case to case similarity of the disease, as well as the diverse cell types produced in unfavourable outcomes (cicatricial ROP), point to the possibility of an in utero insult to the clone of cells giving rise to the vascular endothelium providing blood supply to the neural retina.
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PMID:The premature retina: a model for the in vivo study of molecular genetics? 162 38

These recommendations for secondary prevention of clinical coronary cardiopathy are the result of a symposium attended by 46 experts belonging to the councils on arteriosclerosis, clinical cardiology, epidemiology, and prevention and rehabilitation of the International Society and Federation of Cardiology. Secondary prevention of coronary cardiopathy refers to measures designed to prevent deterioration or death in patients with clinical manifestations of coronary cardiopathy. Such measures in addition to drugs include health actions that may improve the status of various coronary risk factors: the patient's life style should stress maintenance of proper weight, regular physical exercise, reduction of saturated fats and cholesterol in the diet, and elimination of smoking and excessive alcohol consumption. It is considered reasonable to control hypertension through the most innocuous means possible, but findings of the few existing controlled studies of effects of treatment of hypertension in coronary cardiopathy are complex. Drug treatment may be necessary for most patients, but nondrug measures should be added when possible. Various proofs including results of some controlled studies justify the recommendations for reducing elevated levels of serum cholesterol and low density lipoprotein cholesterol through dietary measures. Optimum plasma cholesterol levels are 5.2 mmol/1 or less, and the upper limit is 5.7 mmol/1. The rules for secondary prevention are the same for diabetics as for nondiabetics, but some special precautions are necessary in diabetics. Habitual and vigorous physical activity has been associated with a decline in the incidence of coronary cardiopathy in different population studies, although there has been no demonstration that exercise can alter the progression of atherosclerosis or improve collateral circulation. Stress should be recognized as a risk factor and included in secondary prevention, but the concept that stress is the key risk factor in coronary events is in conflict with a large body of scientific evidence. Oral contraceptives (OCs) tend to increase boood pressure and weight as well as serum triglyceride levels, and to reduce glucose tolerance and high density lipoprotein cholesterol in some formulations. OCs also affect the integrity of the vascular endothelium and alter blood coagulation, fibrinolysis, and platelet function. These thrombogenic changes are intensified with age, especially after 35, and with smoking. OCs are innocuous in women under 35 with no history of venous or arterial disease or pulmonary embolism and who have normal blood pressure and serum cholesterol levels. Patients using OCs should control their blood pressure and weight and be alert to any symptoms of thrombotic episodes. The risk/benefit ratio of longterm estrogen treatment in meno- and postmenopausal women with coronary cardiopathy has not yet been established. Apart from 1 study in primates, there is no evidence that vasectomy should be considered either indicated or contraindicated for coronary patients. Beta blockers, platelet function inhibitors, anticoagulants, and other drugs are under active study for secondary prevention of coronary cardiopathy.
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PMID:[Recommendations for secondary prevention of the clinical coronary cardiopathy]. 285 11

Cardiopulmonary bypass in children with congenital heart disease is associated with significant morbidity manifested by increased complement degradation products, heightened pulmonary vascular activity, and coagulopathy. In adults with cardiac disease, the prostaglandins (eicosanoids) have been shown to contribute to the pathophysiologic response to extracorporeal circulation. This study assessed the effect of cardiopulmonary bypass in infants and children on two potent eicosanoids: thromboxane, a vasoconstrictor and platelet aggregating agent, and prostacyclin, a vasodilator and platelet disaggregating agent. The biochemical profiles of thromboxane and prostacyclin were evaluated in temporal relationship to selected parameters of platelet loss and pulmonary vascular hemodynamics during and after cardiopulmonary bypass. Twenty-one children, aged 3 days to 9 years, with congenital heart defects who were undergoing repair with cardiopulmonary bypass were studied. Nine pediatric patients undergoing palliative heart operations with no cardiopulmonary bypass served as the control group. In the group having cardiopulmonary bypass, the thromboxane concentration significantly increased during bypass (195 +/- 10 to 910 +/- 240 pg/ml, +/- standard error of the mean, p less than 0.005), whereas the control group demonstrated no significant change in thromboxane concentration. The highest thromboxane values were seen in the youngest patients (p less than 0.002). There was no significant correlation between thromboxane changes with alterations in pulmonary vascular resistance, platelet loss, duration of cardiopulmonary bypass or aortic cross-clamping. Prostacyclin levels rose significantly in both the bypass group (100 +/- 20 to 570 +/- 80 pg/ml, p less than 0.01) and in the control group (109 +/- 44 to 589 +/- 222 pg/ml, p less than 0.01), which apparently is due to surgical manipulation of vascular endothelium. These data show that eicosanoid production is significantly altered in children during cardiopulmonary bypass. Although thromboxane, a potent vasoconstrictor, is produced in significant amounts during and after cardiopulmonary bypass, our data show that thromboxane does not directly mediate changes in pulmonary artery hypertension and is not quantitatively related to platelet loss during pediatric cardiovascular operations.
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PMID:Effects of cardiopulmonary bypass on eicosanoid metabolism during pediatric cardiovascular surgery. 328 61

Since infective endocarditis may affect individuals without pre-existing valvar heart disease, and Staphylococcus aureus is the organism most commonly involved, the binding characteristics of S aureus to several components of normal vascular endothelium and subendothelium were studied. S aureus adhered specifically to endothelial monolayers (6.08(1.10)%; p less than 0.005), fibronectin (5.43(0.81)%; p less than 0.001), fibrinogen (7.13(1.43)%; p less than 0.001), and acid soluble calf skin collagen (2.38(0.90)%; p less than 0.001). S aureus also adhered specifically to Von Willebrand factor (1.62(0.28)%, p less than 0.001). Protein A containing (Cowan I) and deficient (Wood) strains of S aureus adhered similarly to all surfaces and substrates (NS). Escherichia coli adhered poorly. Immunofluorescence microscopy of preconfluent endothelial cells identified an extensive pericellular fibronectin network at regions of cell to cell contact. Light microscopy showed S aureus binding solely within these regions. Therefore, the ability of S aureus to infect valvar endothelium may be dependent on the presence of a fibronectin receptor. The existence of specific receptor for S aureus on the endothelial cell surface itself remains undetermined.
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PMID:Bacterial tissue tropism: an in vitro model for infective endocarditis. 328 1

Recent developments in basic vascular biology have provided new insights into mechanisms contributing to pulmonary hypertension and novel approaches to its treatment. Although it has long been recognized that normal vascular endothelium produces endogenous vasodilators, identification of the so-called endothelium-derived relaxing factor as a gas, nitric oxide, led to extensive studies in several experimental models of pulmonary hypertension and in various clinical settings. Endogenous nitric oxide production modulates vascular tone in the fetal and postnatal lung, and contributes to the normal decline in pulmonary vascular resistance at birth. Exogenous (inhaled) nitric oxide therapy causes potent and selective pulmonary vasodilation in neonates with severe pulmonary hypertension (ie, persistent pulmonary hypertension of the newborn), as well as in patients with pulmonary hypertension due to congenital heart disease, acute hypoxemic respiratory failure, primary or unexplained pulmonary hypertension, and other diseases. The safety and efficacy of inhaled nitric oxide therapy is currently being examined in multicenter trials. Other endothelium-derived products, such as the potent vasoconstrictor peptide endothelin, may contribute to abnormal vascular tone, reactivity, and structure in the pulmonary circulation. Basic studies of mechanisms to altered vessel growth and remodeling may lead to further therapeutic strategies for chronic pulmonary hypertension.
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PMID:Pathogenesis and treatment of neonatal and postnatal pulmonary hypertension. 806 32

Ventricular remodeling is a repair process. It can follow myocardial infarction, mechanical overload (for example, in hypertension or valvular heart disease), and also occurs in inflammation and dilated cardiomyopathy. Remodeling can be an (early) adaptive process followed by a maladaptive (late) phase and involves all cells that are present in the myocardium - the myocyte, the interstitial cells, the vascular endothelium, and the immune cells. Despite the varying etiopathology that these different aspects of heart disease share, a similar sequence of molecular, biochemical and mechanical events that can lead to heart failure, myocyte hypertrophy, extensive extracellular matrix production and fibrosis, even in patients who were previously unaffected by the original disease process (for example, inflammation or infarction). Heart failure can be influenced by treatment of the underlying disease and by modification of the remodeling process, for example, by ACE inhibitors (cardioreparation). In experimental animals it has been clearly demonstrated that ACE inhibitors may even prevent a genetically predetermined left ventricular hypertrophy (cardioprevention).
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PMID:Ventricular remodeling. 868 17

Estrogens prevent heart disease in women and have also been shown to retard atherogenesis in animal models. Estrogens may act at several steps in the atherogenic process to prevent cardiovascular disease. Some of the benefits of estrogens can be ascribed to their ability to favorably alter the lipoprotein profile, i.e. increase high-density lipoprotein and decrease low-density lipoprotein, and also to their ability to prevent oxidative modification of low-density lipoprotein. Other beneficial effects of estrogens include direct actions on the vascular endothelium and vascular smooth muscle, leading to a decrease in the expression of adhesion molecules involved in monocyte adhesion to endothelial cells, and to a decrease in certain chemokines involved in monocyte migration into the subendothelial space. Estrogens may also affect the later stages of atherogenesis. Finally, estrogens may modify the behavior of atherosclerotic vessels by altering their reactivity and thereby promoting vasodilation, and this may also partly account for their ability to prevent clinical events due to cardiovascular disease.
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PMID:Estrogens and atherosclerosis. 913 Dec 62

Twenty-four adults (average age 28 years) patients with congenital heart disease were examined; infective endocarditis was diagnosed in all of them by Duke criteria and was confirmed in 18 by surgery and/or pathology. Patients were divided into 2 groups. Group A was made up of 13 patients with left ventricular outflow obstruction, including ten with bicuspid aorta. Group B was made up of 11 patients with shunts (PDA or VSD), either isolated or associated with other abnormalities. The principal alterations associated with the infectious processes were trauma to the endocardium or vascular endothelium from accelerated turbulent flow (jet lesion) and valvular deformities. The principally transesophageal echocardiographic recordings showed infective vegetations on the four cardiac valves, mural endocarditis in both ventricles and right atrium, perivalvular abscesses and fistulae. The echocardiographic information aided in selecting the type of treatment in this group of patients with high intrahospital mortality (25%).
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PMID:[Transthoracic and transesophageal echocardiography in the study of adults with congenital cardiopathy and infectious endocarditis]. 981 Mar 66

Congenital heart disease with increased pulmonary blood flow commonly leads to the development of pulmonary hypertension and increased vascular reactivity. These serious sequelae are associated with the following two major categories of congenital heart defects: those resulting in increased pulmonary blood flow and increased pulmonary arterial pressure and those resulting in increased pulmonary venous pressure. Recent evidence that the pulmonary vascular endothelium is an important determinant of vascular tone has led to the hypothesis that endothelial injury, secondary to congenital heart disease with increased pulmonary blood flow, disrupts these regulatory mechanisms and thereby plays a role in the development of pulmonary hypertension and its associated increased vascular reactivity. In many animal models, endothelial dysfunction is a precursor for smooth muscle dysfunction, and there is an apparent progression from endothelial dysfunction to smooth muscle dysfunction as vascular changes progress. We established a chronic model of pulmonary hypertension with increased pulmonary blood flow in young lambs by placing a systemic-to-pulmonary shunt in utero. In this model, we found significant physiologic and molecular alternations of both the nitric oxide (NO) and endothelin signaling pathways, two important mechanisms by which the endothelium regulates pulmonary vascular tone. These alterations occur extremely early and precede severe anatomic changes. Early endothelial damage may contribute to the development of pulmonary hypertension and its associated enhanced pulmonary vascular reactivity.
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PMID:The pathophysiology of pulmonary hypertension in congenital heart disease. 1056 99


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