UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
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The Framingham Study established hypertension as a major cardiovascular risk factor and quantified its atherogenic cardiovascular disease potential. An historical perspective is presented on the epidemiological insights about hypertension derived from 50 years of Framingham Study research into the prevalence, incidence, determinants and hazards of hypertension. Existing misconceptions about the presence of critical levels of blood pressure, the impact of the systolic and diastolic components of blood pressure, the hazard 'mild' hypertension, the impact in advanced age and the hazard of left ventricular hypertrophy. The importance of isolated systolic hypertension and the pulse pressure were demonstrated. It has been demonstrated that hypertension seldom occurs in isolation of other atherogenic risk factors, with which it tends to cluster. This clustering with other metabolically linked risk factors has been shown to reflect insulin resistance promoted by weight gain and abdominal obesity. Obesity was shown to be one of the major determinants of hypertension in the general population. Left ventricular hypertrophy was shown to be an ominous harbinger of cardiovascular disease rather than an incidental compensatory phenomenon. Multivariate risk profiles for coronary disease, stroke, peripheral artery disease and heart failure have been devised to facilitate incorporation of elevated blood pressure in a global, multivariate cardiovascular risk assessment.
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PMID:Fifty years of Framingham Study contributions to understanding hypertension. 1072 12

The debate about the importance of salt in the pathogenesis and treatment of hypertension is still ongoing. The importance of salt is rooted on several factors. First, salt is one of the first factors who has been identified to be of potential importance in blood pressure regulation. Second, during the last decades several other pathogenetic risk factors for essential hypertension have been identified, however, without the identification of one single predominant risk factor. These risk factors include different genetic factors and predispositions as well as modifiable environmental factors. For the development of hypertension usually several of these risk factors have to be present. In miscellaneous disease conditions, such as heart failure, salt induces a sodium and volume retention. Accordingly it is often falsely concluded that salt will lead to a volume retention and hypertension in all subjects and that a salt restriction will lead to a normalization of an elevated blood pressure. Although about 40% of the patients with essential hypertension are salt sensitive, the concept of salt sensitivity is not valid for all subjects of a population. Accordingly one can not conclude that a general salt restriction would be a cure for hypertension. The therapeutic priority in the non-pharmacological prevention and/or therapy of hypertension lies usually in the control of other risk factors than salt intake. These risks include overweight and obesity, alcohol consumption and physical inactivity. These concepts are supported by several recent meta-analysis.
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PMID:[The salt-free diet]. 1075 96

It is well known that the nutritional deficiency possibly causes cardiac dysfunction. Although social hygiene has successfully diminished these cardiac dysfunction in developed countries, patients could be found in certain number under altered clinical profiles than before. Excess intake of carbohydrate drinks and carbohydrates should make beri-beri heart in youth. Not only deficiency but recent dietary habits of excessive nutrition in these developed countries are causing new types of nutritional cardiac dysfunctions such as obesity cardiomyopathy in morbid obese. On the other hand, anorexia nervosa which sometimes shows heart failure and sudden death combines with psychosomatic disorders. In this article, the pathogenesis and treatments are discussed focusing on these three cardiac disorders.
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PMID:[Nutritional myocardial disorders]. 1088 5

Prophylaxis of deep vein thrombosis with standard heparin and low molecular weight heparin has been studied in many clinical trials in surgical patients and in few and various medical conditions in hospitalized subjects. Clinical trials have been conducted in patients with recent myocardial infarction, heart failure, stroke, pulmonary sepsis, cancer, or any acute disease with a high risk factors for deep vein thrombosis (previous thromboembolism, thrombophilia, obesity, recent bedridden, dehydratation.). The combination of a high risk disease with a high risk factor related to the history of the patient might reasonably conduct to a prophylaxis with low molecular weight heparins. The duration of this treatment has to be short and limited to the period of the acute medical condition inducing a high risk for deep vein thrombosis. Prophylaxis has to be offered to patients with ischemic stroke, cardiac failure, recent myocardial infarction, active cancer or any other acute medical disease in patients with a previous thromboembolism or thrombophilia history. Bedridden status and age are not, by themselves, an indication for prophylaxis with heparins. A widespread diffusion of these recommendations is needed to reduce overprescriptions.
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PMID:[Prevention of deep venous thrombosis in medical patients]. 1089 73

The obese ZDFxSHHF-fa/fa(cp) model was developed by crossing lean female Zucker Diabetic Fatty (ZDF +/fa) and lean male Spontaneously Hypertensive Heart Failure (SHHF/Mcc-fa(cp), +/fa) rats. The purpose of the present study was to determine renal function and morphology, hemodynamics, and metabolic status in ZDFxSHHF rats. Two sets of experiments were conducted. First, we evaluated heart and kidney function and metabolic status in aged (46 weeks old) male obese ZDFxSHHF and age matched obese SHHF rats, lean Spontaneously Hypertensive (SHR) and lean normotensive Wistar Kyoto (WKY) rats. In the second set of experiments, renal function and structure as well as metabolic and lipid status were determined in lean (LN) and obese (OB) adult (29-weeks of age) ZDFxSHHF rats. At 46 weeks of age ZDFxSHHF rats are hypertensive expressing marked cardiac hypertrophy associated with diastolic dysfunction and preserved contractile function. Fasted hyperglycemia and hyperinsulinemia are accompanied by moderate hypercholesterolemia and hypertriglyceridemia. Obese aged ZDFxSHHF have marked renal hypertrophy, a 3-8 fold decrease in creatinine clearance (compared with SHHF, SHR and WKY), a high percent of segmental + global glomerulosclerosis (59.8%+/-10.8), and severe tubulointerstitial and vascular changes. Obese ZDFxSHHF rats die at an early age (approximately 12 months) from end-stage renal failure. Studies conducted in 29-week animals showed that, although both LN and OB 29-week old animals are hypertensive, OB animals have more severely compromised renal function and structure as compared with lean litter-mates (kidney weight: 2.56+/-0.16 vs. 1.61+/-0.12 g; creatinine clearance: 0.42+/-0.04 vs. 1.24+/-0.13 L/g kid/day; renal vascular resistance 12.39+/-1.4 vs. 6.14+/-0.42 mmHg/mL/min/g kid; protein excretion: 556+/-16 vs. 159+/-9mg/day/g kid, p < 0.05, OB vs. LN, respectively). Obesity is also associated with hyperglycemia (424+/-37 vs. 115+/-11 mg/dL), hyperinsulinemia (117.2+/-8.8 vs. 42.3+/-3.5 microU/mL), hypertriglyceridemia (5200+/-702 vs. 194+/-23 mg/dL), hypercholesterolemia (632+/-39 vs. 109+/-4mg/dL), and presence of segmental + global glomerulosclerosis (20.1+/-3.2% vs. 0.1+/-0.1%) with prominent tubular and interstitial changes (p < 0.05, OB vs. LN, respectively). In summary, the present study indicates that the crossing of rat strains of nephropathy produces hybrids that carry a high risk for severe renal dysfunction. The ZDFxSHHF rats express insulin resistance, hypertension, dislipidemia and obesity and develop severe renal dysfunction. In addition, the hybrids do not develop some of the complications (hydronephrosis or congestive heart failure) common for the parental strains that may compromise studies of renal function and structure. Therefore, the ZDFxSHHF rat may be a useful model fore valuating risk factors and pharmacological interventions in chronic renal failure.
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PMID:Renal function and structure in diabetic, hypertensive, obese ZDFxSHHF-hybrid rats. 1090 Nov 78

Measurement of regional sympathetic activity in lean essential hypertension patients using electrophysiologic (sympathetic nerve recording) and neurochemical (measurement of norepinephrine spillover) techniques demonstrates activation of sympathetic outflow to the heart, kidneys, and skeletal muscle vasculature in younger (< 45 years) patients. The increase in sympathetic activity is a mechanism for both initiating and sustaining the blood pressure elevation. Sympathetic nervous activation also confers specific cardiovascular risk. Stimulation of the sympathetic nerves to the heart promotes the development of left ventricular hypertrophy and contributes to the genesis of ventricular arrhythmias and sudden death. Sympathetically mediated vasoconstriction in skeletal muscle vascular beds reduces the uptake of glucose by muscle, and is thus a basis for insulin resistance and consequent hyperinsulinemia. Understanding the neural pathophysiology of obesity-related hypertension has been more difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac norepinephrine spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal norepinephrine spillover, but without suppression of cardiac sympathetics, as here cardiac norepinephrine spillover is more than double that of normotensive obese and 25% higher than in healthy volunteers. Increased renal sympathetic activity in obesity may be a necessary cause for the development of hypertension (predisposing to hypertension development), but apparently is not a sufficient cause. The discriminating feature of the obese who develop hypertension is the absence of the presumably adaptive suppression of cardiac sympathetic outflow seen in the normotensive obese. The sympathetic nervous system has moved towards center stage in cardiovascular medicine. The importance of sympathetic activation in heart failure progression and mortality and in the generation of ventricular arrhythmias is now well established. In essential hypertension also, although the mechanism differs somewhat between the lean and obese, the sympathetic nervous system is a key factor in the genesis of the disorder, and additionally promotes the development of complications. Through their central inhibition of sympathetic nervous activity, I1 agents such as rilmenidine powerfully reduce sympathetic nervous activity in essential hypertension patients, lowering blood pressure, and carrying the potential for specific cardiovascular protection.
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PMID:The sympathetic system and hypertension. 1092 28

The diaphragm as a striated muscle is characterized by the repetition of a single element arranged in series: the sarcomere containing two kinds of myofilaments: a thick one constituted by the myosin, and a thin one primarily composed of actin. The myosin molecule consists of two heads where two myosin heavy chains (MHC) are fixed, a flexible hinge with two light (MLC) chains, and long rod-shaped tails. The diaphragm contains 4 MHC isoforms (MHC-slow, MHC-2A, MHC-2B, MHC-2X) and 6 MLC isoforms (MLC-1f, MLC-3f, MLC-1sa, MLC-1sb, MLC-2f, MLC-2s/v). In humans, the diaphragm contains mainly fibers expressing the isoforms MHC-slow, MHC-2A, and MLC-2f, MLC-2s et MLC-1f. For the mechanical properties of the different isoforms, there is a gradient from the MHC-slow to the MHC-2A, MHC-2B and MHC-2X/2B. According to the circumstances, the diaphragm will adapt towards a slow profile (COPD, cardiac failure and in animals: Duchenne muscular dystrophy, denervation-1 week, age-female, corticosteroids, chronic stimulation), or a fast profile (in animals: chronic hypoxia, denervation-2 weeks, age-males) or a more oxidative profile (in animals: cachexia, obesity). The reasons why the diaphragm adapts towards a slower or a faster muscle are not known. In fact, for a given pathological situation, several factors are able to influence the fiber composition of the diaphragm. Therefore, the net result of the influence of these different factors in terms of MHC and MLC diaphragm adaptation is difficult to predict.
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PMID:[Clinical relevance of myosin isoforms in the diaphragm]. 1093 18

In 1996 and 1997, 52 patients were admitted to the Princess Margaret Hospital, Nassau, Bahamas, with a confirmed diagnosis of acute myocardial infarction (AMI). The average time to presentation after the onset of symptoms was 18 hours, with 56% of patients presenting within 12 hours. Risk factors identified for ischaemic heart disease were hypertension (77%), obesity (62%), diabetes mellitus (35%), tobacco smoking (25%), a family history of coronary artery disease (17%) and hypercholesterolaemia (8%). Medications administered in the treatment of AMI included oral nitrates (96%), intravenous heparin (90%), beta-blockers (65%), morphine (15%), thrombolytic agents (8%) and lignocaine (4%). In hospital post myocardial infarction complications were angina (23%), arrhythmias (12%) and cardiac failure (10%). The average hospital stay was eight days, with a mortality rate of 19%. These results show that there is considerable room for improvement, particularly in the use of thrombolytic therapy, to ensure that all patients receive optimal acute and post myocardial infarction care.
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PMID:Management of acute myocardial infarction in the public sector in the Bahamas. 1094 48

The left ventricular hypertrophy is a risk marker of the cardiovascular morbidity and mortality in hypertensive patients--it contributes to sudden death, myocardial infarction, myocardial ischemia, heart failure, arrhythmias, left ventricular diastolic dysfunction, stroke and renal failure. The mechanisms by which the heart hypertrophy increases the risk of cardiovascular morbidity and mortality, however, is not completely clear yet. Pressure overload (resulting in the concentric hypertrophy) and volume overload (resulting in the eccentric hypertrophy) of the left ventricle play a significant role in the development of the hypertrophy of the left ventricle. Other risk factors, stimulating left ventricular hypertrophy, include growth factors, genetic predisposition, age, obesity, hyperinsulinemia and anemia. The hypertrophy of left ventricle most often occurs with hypertension, cardiomyopathy and aortic stenosis. Several clinical studies evaluated functional consequences of the reduction of the ventricular hypertrophy and found out that the function of the left ventricle to be improved in hypertensive patients who had undergone an effective and long-term antihypertensive treatment. However, these studies did not differentiate whether for the improvement in the function of left ventricle was the matter of the reduction of the left ventricular mass or whether it was because of the decrease of the arterial pressure during the period of anti-hypertensive treatment. On the basis of the literature studied we can emphasize that the reduction of myocardial hypertrophy resulting from a specific antihypertensive treatment appears to be more favourable than harmful for the heart's pump performance.
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PMID:[Hypertrophy of the left ventricle--etiopathogenesis, clinical consequences and prognosis]. 1104 62

L-Arginine (Arg) is the substrate for the synthesis of nitric oxide (NO), the endothelium-derived relaxing factor essential for regulating vascular tone and hemodynamics. NO stimulates angiogenesis, but inhibits endothelin-1 release, leukocyte adhesion, platelet aggregation, superoxide generation, the expression of vascular cell adhesion molecules and monocyte chemotactic peptides, and smooth muscle cell proliferation. Arg exerts its vascular actions also through NO-independent effects, including membrane depolarization, syntheses of creatine, proline and polyamines, secretion of insulin, growth hormone, glucagon and prolactin, plasmin generation and fibrinogenolysis, superoxide scavenging and inhibition of leukocyte adhesion to nonendothelial matrix. Compelling evidence shows that enteral or parenteral administration of Arg reverses endothelial dysfunction associated with major cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes, obesity/insulin resistance and aging) and ameliorates many common cardiovascular disorders (coronary and peripheral arterial disease, ischemia/reperfusion injury, and heart failure). Dietary Arg supplementation may represent a potentially novel nutritional strategy for preventing and treating cardiovascular disease.
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PMID:Arginine nutrition and cardiovascular function. 1105 97

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