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

Heart rate monitoring has become a ubiquitous part of fetal and neonatal assessment, and has made detection of bradycardia in the fetal and neonatal periods a frequent occurrence. Evaluation of a fetus or neonate with bradycardia requires an understanding of the mechanisms of bradycardia as well as the cardiac and non-cardiac causes of bradycardia. The mechanisms of bradycardia include sinus bradycardia, abnormalities of sinus node function and abnormalities of atrioventricular conduction. In the instances where sinus bradycardia is pathologic, it usually results from non-cardiac disease. Sinus node dysfunction is rare early in life but can arise from surgical interventions, congenital heart disease, or endovascular manipulations. Abnormalities of atrioventricular conduction have a similar etiology but are more common than sinus node disease. Atrioventricular nodal disease can also result from maternal collagen vascular disease, even in the absence of symptoms in the mother. In these cases, epidemiological issues such as heart block in subsequent pregnancies and the maternal risk of developing symptomatic collagen vascular disease become important. The approach to treatment and long-term prognosis for bradycardia in the neonate is highly dependent on the underlying etiology and on the presence of concurrent factors such as structural heart disease.
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PMID:Neonatal bradycardia. 1082 86

During admission for investigation of dysphagia, an 82-year-old woman suddenly complained of dyspnea, which was followed by cardiogenic shock. Her symptoms, electrocardiogram, echocardiogram and laboratory data were compatible with an extensive acute anterior myocardial infarction. Emergency cardiac catheterization showed no atheromatous narrowing in any coronary artery. However, the contractions of the left and right ventricles were diffusely and severely impaired, except for some hyperkinesis of the basal area. The asynergy, as well as the abnormalities on the ECG, improved almost to normal by the 35th hospital day. An endomyocardial biopsy from the right ventricle during the acute phase showed atypical myocardial damage with proliferation of fine collagen fibers and small round-cell infiltration including polymorphologic leukocytes. This type of transient cardiac disorder has recently been described in Japan, and is called 'Tako-tsubo cardiomyopathy' because of the characteristic appearance of the left ventricular asynergy. In the present case, ventricular asynergy was not limited to the left ventricle, but was also present in the right ventricle.
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PMID:'Tako-Tsubo' transient ventricular dysfunction: a case report. 1098 59

Type XV collagen occurs widely in the basement membrane zones of tissues, but its function is unknown. To understand the biological role of this protein, a null mutation in the Col15a1 gene was introduced into the germ line of mice. Despite the complete lack of type XV collagen, the mutant mice developed and reproduced normally, and they were indistinguishable from their wild-type littermates. However, Col15a1-deficient mice showed progressive histological changes characteristic for muscular diseases after 3 months of age, and they were more vulnerable than controls to exercise-induced muscle injury. Despite the antiangiogenic role of type XV collagen-derived endostatin, the development of the vasculature appeared normal in the null mice. Nevertheless, ultrastructural analyses revealed collapsed capillaries and endothelial cell degeneration in the heart and skeletal muscle. Furthermore, perfused hearts showed a diminished inotropic response, and exercise resulted in cardiac injury, changes that mimic early or mild heart disease. Thus, type XV collagen appears to function as a structural component needed to stabilize skeletal muscle cells and microvessels.
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PMID:Lack of type XV collagen causes a skeletal myopathy and cardiovascular defects in mice. 1115 16

Pictures certainly are worth a thousand words in the case of the structure of the connective tissue skeleton of normal and diseased myocardium. This report reviews the connective tissue matrix of the normal human myocardial tissue and the pathological myocardial fibrosis in left ventricular hypertrophy due to chronic arterial hypertension in humans and in human chronic chagasic myocarditis. The myocardial connective tissue matrix was studied employing a cell-maceration method that removes the myocardial tissue non-fibrous elements, and leaves behind a non-collapsed matrix, thus allowing a better three-dimensional view. Such information extends our knowledge of the expression of interstitial myocardial fibrous tissue in normal hearts and in hypertensive left ventricular hypertrophy and chronic chagasic myocarditis. The progressive accumulation of interstitial collagen fibers in both chronic cardiac diseases may be expected to decrease myocardial compliance and disrupt synchronous contractions 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. In hypertensive heart disease myocardial fibrosis can be also implicated in the genesis of ventricular dysrhythmias, possible causes of sudden death among chronic hypertensive patients. Regarding chronic chagasic myocarditis, myocardial fibrosis is probably implicated in the genesis of malignant ventricular tachyarrhythmias (ventricular tachycardia and ventricular fibrillation), major causes of sudden death among patients with chronic Chagas' heart disease. The collagen distribution could interfere on the electrical properties of the myocardium. Fibrosis can block the cardiac impulse that may recycle (re-entry) through an alternative route and could slow conduction. In addition, the thick collagenous septa encompassing muscle fiber bundles could interfere with lateral impulse conduction, which would favor re-entry. Moreover, the methodology used is a useful tool to study the spatial organization of the collagen fibrils of the myocardium under normal and pathological conditions.
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PMID:Connective tissue skeleton in the normal left ventricle and in hypertensive left ventricular hypertrophy and chronic chagasic myocarditis. 1143 16

A 10-year-old boy with a medical history of fatigue became nauseous, short of breath and cyanotic within 24 hours after a frightening incident. He was successfully resuscitated after a cardiac arrest. A CT scan revealed a ruptured aneurysm of the ascending aorta. During emergency surgery the ascending aorta and aortic arch were replaced with a 22 mm synthetic graft. No postoperative complications occurred. There was no associated trauma, syphilis, collagen diseases (Marfan's syndrome, Ehlers-Danlos syndrome), congenital heart disease or autoimmune disease. The cause of the aneurysm and rupture remain unclear.
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PMID:[Rupture of thoracic aneurysm in a 10-year old boy]. 1177 Feb 68

Using polarization microscopy and morphometrical methods, the influence of hypertension on the collagenous structures in the Lamina fibrosa of bicuspid valves of 14 middle-aged persons (30 to 50 years) were examined. The measurements were performed on histological sections. A group of 14 middle-aged subjects free from heart disease served as the control group. Furthermore, the results were compared to earlier findings on the histological biomorphosis of the atrioventricular valves. The following changes were observed and quantitatively determined: a) an enhancement of the percentage of the mechanically more resistant collagenous fibers (unsilvered, type I collagen), b) a stronger lateral aggregation of the collagenous fibrils of both types I and III collagen, c) a significant decrease of the total numbers of collagenous fibers per measuring area, and d) a significant decrease of the portion of silvered fibers (type III collagen) per measuring area for both sexes. The fiber density distributions confirm the observed changes: in the hypertension group the collagenous fibers are less densely distributed than in the control group. The observed regression of the content of collagenous fibers in the hypertension group is probably due to the anti-hypertensive treatment. Following the findings the turn-over of type III collagen is stronger influenced than that of type I collagen. The initial results determined in human heart valves confirm findings in animal models and characterize them with regard to the collagen types mentioned.
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PMID:[Changes in the collagen structures of human heart valves in relation to age and hypertension]. 1182 87

Estradiol inhibits cardiac fibroblast growth and may protect against cardiac remodeling associated with heart disease. However, the mechanisms by which estradiol attenuates cardiac fibroblast growth remain unclear. Because cardiac fibroblasts express cytochrome P450s (CYP450s) and catechol-O-methyltransferase (COMT) capable of converting estradiol to hydroxyestradiols and methoxyestradiols, respectively, and because hydroxyestradiols and methoxyestradiols (estradiol metabolites with little affinity for estrogen receptors) are potent inhibitors of cardiac fibroblast growth, we hypothesized that the antimitogenic effects of estradiol are mediated via hydroxyestradiols and/or methoxyestradiols. The inhibitory effects of estradiol (1 to 100 nmol/L) on serum-stimulated (3)H-thymidine incorporation (DNA synthesis), (3)H-proline incorporation (collagen synthesis), and cell number (proliferation) were enhanced (P<0.005) by CYP450 inducers 3-methylcholanthrene (10 micromol/L) and phenobarbital (10 micromol/L). Moreover, the inhibitory effects of estradiol were blocked by the CYP450 inhibitor 1-aminobenzotriazole (10 micromol/L) and the COMT inhibitors quercetin (10 micromol/L) and OR486 (10 micromol/L). In contrast to estradiol, the modulators of CYP450 and COMT were poor ligands for estrogen receptors (binding affinity less-than-or-equal 0.0001% versus estradiol). In cardiac fibroblasts, both quercetin and OR486 inhibited the metabolism of hydroxyestradiol to methoxyestradiol and blocked the inhibitory effects of hydroxyestradiol on cardiac fibroblast proliferation and DNA and collagen synthesis. The abrogating effects of quercetin and OR486 on the metabolism and antimitogenic effects of 2-hydroxyestradiol were mimicked by 20 micromol/L norepinephrine and isoproterenol, substrates for COMT. Our findings provide evidence that estradiol can inhibit cardiac fibroblast growth via an estrogen receptor--independent pathway that involves the local metabolism of estradiol to methoxyestradiols.
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PMID:Methoxyestradiols mediate the antimitogenic effects of locally applied estradiol on cardiac fibroblast growth. 1188 82

On epidemiological basis EMF behaves like a vector transmitted disease. The cardiac pathologies of EMF and HES are identical. In some cases of HES, hypereosinophilia may return to normal, leaving residual heart disease that is exactly like EMF. Most temporary residents from Europe and North America who developed EMF while resident in the endemic areas of Africa had hypereosinophilia that was induced by helminths. In our case studies from the EMF endemic areas of Nigeria, most children with acute idiopathic myocarditis associated with helminth induced hypereosinophilia, developed clinical EMF on follow up. We showed also that the rate of decline in the incidence of hypereosinophilia in EMF cases was significantly related to the duration of symptoms. Our studies and other observations show that EMF, like HES is a multiple system disease with similar organ damage. The morphologic evolution of cardiac damage in EMF appears similar to that reported for HES; with a stage of myocarditis/pericarditis, followed by a stage of cardiac necrosis, a stage of thrombosis and by the chronic fibrotic stage. Also during larval migration, all the helminths associated with EMF induce the same spectrum of damage in the central and peripheral nervous system, in the lungs, kidneys and skin, as are reported for HES. The cardiovascular damage reported for these worms (which include hypersensitivity vasculitis, acute myocarditis/ pericarditis) are also similar to what is reported for HES. Acute endomyocardial necrosis and thrombosis that are similar to what is found in HES, have been documented in Trichinella Spiralis and in filariasis. Increased cerium concentrations have been documented in the endocardium of EMF cases from South India. It remains to be established whether cerium excess, which is known to stimulate collagen synthesis does accelerate the process of endomyocardial fibrosis, following cardiac necrosis (which may have been triggered by helminths and the associated hypereosinophilia).
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PMID:Aetiology of endomyocardial fibrosis (EMF). 1192 51

In the heart, collagens are the major extracellular matrix (ECM) protein. The fibrillar collagens of the heart surround and interconnect myocytes and muscle fibers to provide for muscle fiber and myocyte alignment which imparts mechanical support to the myocardium and governs tissue stiffness. Loss of collagen fibrils and struts are said to lead to myocyte slippage, ventricular dilation, and progressive contractile dysfunction. Failed human hearts examined either at autopsy or explantation invariably exhibit alterations of the ECM primarily due to changes in collagen. Modulation of the balance between matrix synthesis and degradation is important in the process of ventricular remodeling and in the pathophysiology of chronic heart failure. Support for the importance of the ECM and activity of matrix metalloproteinases (MMP) in the development of chronic heart failure has been demonstrated both in animal models of heart disease and in humans. A causative role for the ECM in this process was recently revealed in experiments using a transgenic mouse model that expresses the specific collagen-degrading enzyme, MMP-1, in the heart. These studies demonstrated that chronic expression of MMP-1 leads to dynamic changes in the heart and ultimately results in systolic dysfunction. Multiple studies in animal models have also shown that inhibition of MMP activity in animal models of heart failure have attenuated the onset of left ventricular dilatation. Future studies will determine whether inhibition of MMP activity improves morbidity and mortality in patients with heart failure.
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PMID:Matrix metalloproteinase disruption of the extracellular matrix and cardiac dysfunction. 1200 33

The syndrome of heart failure is still imperfectly understood. It is defined as effort intolerance caused by heart disease, often with a neuroendocrine response that leads to fluid retention and promotes an adverse vicious circle. The cause of this response is generally thought to be a low blood pressure, leading to adrenergic and rennin-angiotensin activation. The result is increased peripheral vasoconstriction, which maintains the blood pressure while punishing the already failing myocardium by demanding more work against the increased afterload. The evolution of heart failure is traced out from an initial pressure or volume overload that initiates a series of growth signals to cause myocardial growth. Why the apparently well-compensated LV should degenerate into failure is not clear, but impaired coronary flow reserve and excess angiotensin II activity with fibrosis and apoptosis all probably play a role. The collagen matrix normally limits cardiac chamber expansion so that matrix remodeling under the influence of matrix metalloproteinases is required for the LV to enlarge in volume. Regarding the neuroendocrine responses, excess adrenergic activity promotes failure by myocardial membrane damage and calcium overload, and by increasing the myocardial oxygen demand and the afterload. Beta2- adrenergic stimulation may (unexpectedly) be anti-apoptotic and cardioprotective. Activation of the rennin-angiotensin system (RAS) is clearly very harmful, as shown by numerous studies in which inhibiting agents have reduced human mortality. Specific adverse consequences of RAS activation include (1) excessive peripheral vasoconstriction; (2) aldosterone-mediated sodium retention and myocardial fibrosis; (3) increased endothelial damage; and (4) excessive angiotensin II effects at intracellular sites. Other neuroendocrine changes are increased levels of endothelin and of cytokines such as tumour necrosis factor-alpha. Ergoreflexes from the ailing skeletal muscle may further promote adrenergic and RAS activation. Conversely, increased release of natriuretic peptides from the left heart is cardioprotective by limiting fluid retention and promoting vasodilation. Current therapies of heart failure are largely based on inhibition of the neuroendocrine response.
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PMID:The neuroendocrinology of congestive heart failure. 1238 58


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