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

In earlier studies using papillary muscles of the rat left ventricle and highly sensitive thermopiles we demonstrated that the heat liberated per gram of myocardium per unit of developed tension-time integral is decreased when the rats suffered from hypothyroidism or renal hypertension. This increase in economy of force production was shown to be associated with a decrease in myosin-ATPase activity and a change in isomyosin composition. In a recent study we showed an increase in heat per gram of mammalian myocardium per tension-time integral of 70% after application of isoproterenol. In order to study the relationship between energy costs and developed tension-time integral in the human heart, haemodynamics and myocardial oxygen consumption were measured. The data were obtained using a Millar microtip catheter pressure transducer and the argon method. Haemodynamics and myocardial energetics were analysed in 8 patients without significant heart disease before and after application of isoproterenol and in 10 patients with dilative cardiomyopathy (NYHA II-III). During one cardiac cycle, myocardial oxygen consumption per gram of LV myocardium per beat (MVO2/g x beat) is related to LV stress-time integral (integral of sigma xt). The economy of myocardial contraction (EC) was calculated by (formula; see text) EC was 11.3 +/- 3.2 in normal and 14.3 +/- 4.7 dyn x s x g/cm2 x mu cal in dilative cardiomyopathic hearts (NS). Isoproterenol decreased EC from 11.3 +/- 3.2 to 5.5 +/- 1.6 dyn x s x g/cm2 x mu cal in the normal hearts (p less than 0.01). In the rat myocardium, changes in economy of force generation were found due to catecholamines, pressure overload and hypothyroidism. In the human heart, similar energetic changes were observed due to catecholamines. No significant differences in energy of force production were seen between normal and dilative cardiomyopathic hearts. The effect of catecholamines in the mammalian and human myocardium is explained by changes in activation processes and in chemomechanical energy transduction at the level of the contractile proteins.
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PMID:Acute and chronic changes of myocardial energetics in the mammalian and human heart. 366 28

The aim of this study was to describe the aetiology of congestive cardiac failure (CCF) in children with suspected structural abnormalities presenting to a regional hospital in southwestern Uganda. The method used was a prospective descriptive study of successive admissions of children with persistent cardiac signs after routine treatment of CCF. Children with severe anaemia (haemoglobin [Hb]<7 g/dL), pneumonia, sepsis or severe malnutrition were excluded. Chest X-ray, electrocardiogram and echocardiography data were validated by a paediatric cardiologist and radiologist at the Bristol Royal Hospital for Children, UK. A cohort of 58 patients was identified. The aetiology of heart failure in this cohort (n = 58) was due to congenital heart disease (35%), renal hypertensive disease (26%), rheumatic heart disease (17%), cardiomyopathies (12%), endomyocardial fibrosis (7%) and tamponade (3%). In conclusion, this study confirmed the ongoing prevalence of congenital heart disease, rheumatic heart disease and endomyocardial fibrosis in this area. The cardiac effect of renal hypertension was a new and significant finding.
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PMID:Echocardiographic, chest X-ray and electrocardiogram findings in children presenting with heart failure to a Ugandan paediatric ward. 1771 99

Atherosclerosis is a systemic disease responsible for strokes, myocardial infarction, renal hypertension, and intermittent claudication. Acute coronary syndromes (unstable angina, acute myocardial infarction, and sudden cardiac death) are the major causes of morbidity and mortality in developed countries. These acute manifestations of heart disease share a common pathophysiologic phenomenon: coronary thrombosis. Two principal mechanisms are responsible for coronary thrombosis: plaque disruption (75%) and plaque erosion (25%). Disrupted plaques exhibit a large lipid content, increased macrophages, and a thin fibrous cap. Hypercholesterolemia and diabetes are associated with plaque disruption. Eroded plaques are smooth muscle-cell rich with an intact fibrous cap. Cigarette smoking is associated with plaque erosion, most frequently in women with sudden death when they are younger than 50 years of age. Systemic inflammation is a novel, robust marker for future cardiovascular events, not only in patients with established atherosclerotic disease but also in apparently healthy individuals. Local inflammation at the plaque disruption site is documented by increased macrophage infiltration. Macrophages are responsible for plaque disruption, neovascularization, smooth muscle cell apoptosis, and plaque thrombogenicity. Experimental studies have identified the lipid core as the most thrombogenic substrate of the atherosclerotic plaque. Tissue factor, a cell membrane-bound protein, is crucial in thrombus formation. Tissue factor is expressed in apoptotic macrophages, suggesting that macrophages are not only responsible for plaque disruption but also pivotal in thrombus generation, the most important mechanism of acute coronary syndromes.
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PMID:Pathophysiology of plaque disruption and thrombosis in acute ischemic syndromes. 1790 43

Experiments on canine lateral saphenous vein segments have shown that noradrenaline causes potent, flow dependent effects, at a threshold concentration comparable to that of plasma noradrenaline, when it stimulates a segment by diffusion from its microcirculation (vasa vasorum). The effects it causes contrast with those neuronal noradrenaline causes in vivo and that, in the light of the principle that all information is transmitted in patterns that need contrast to be detected - star patterns need darkness, sound patterns, quietness - has generated the hypothesis that plasma noradrenaline provides the obligatory contrast tissues need to detect and respond to the regulatory information encrypted in the diffusion pattern of neuronal noradrenaline. Based on the implications of that hypothesis, the controlled variable of the peripheral noradrenergic system is believed to be the maintenance of a set point balance between the contrasting effects of plasma and neuronal noradrenaline on a tissue. The hypothalamic sympathetic centres are believed to monitor that balance through the level of afferent sympathetic traffic they receive from a tissue and to correct any deviation it detects in the balance by adjusting the level of efferent sympathetic input it projects to the tissue. The failure of the centres to maintain the correct balance is believed to be responsible for inflammatory and genetic disorders. When the failure causes the balance to be polarised in favour of the effect of plasma noradrenaline that is believed to cause inflammatory diseases like dilator cardiac failure, renal hypertension, varicose veins and aneurysms; when it causes it to be polarised in favour of the effect of neuronal noradrenaline that is believed to cause genetic diseases like hypertrophic cardiopathy, pulmonary hypertension and stenoses and when, in pregnancy, a factor causes the polarity to favour plasma noradrenaline in all the maternal tissues except the uterus and conceptus, where it favours neuronal noradrenaline, that is believed to cause preeclampsia. Finally, the shift in the balance caused by the slow physiological increase in plasma noradrenaline concentration in life is believed to be responsible for ageing.
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PMID:The balance between the pro-inflammatory effect of plasma noradrenaline and the anti-inflammatory effect of neuronal noradrenaline determines the peripheral effects of noradrenaline. 2580 43