Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent observations have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) correlate with cardiac function or prognosis in heart failure patients. However, relatively little is known about changes in their plasma concentration during commonly occurring physiological states such as fatigue. Therefore, this study was designed to examine the physiological changes of plasma ANP and BNP concentrations using a chronic sleep-deprivation model. Bicycle ergometer cardiopulmonary exercise tests were performed in 10 healthy volunteers (mean age: 22.7 years). Blood samples for measuring ANP and BNP were drawn during the resting state and immediately after each exercise test. Cardiac output (CO) was measured during the exercise test by the impedance method. The study conditions were designed as follows: (A) a day following a period of normal sleep (control state) and (B) a day preceded by 1 month during which sleep lasted <60% of normal (chronic sleep-deprived state). Results were as follows. (1) Peak oxygen uptake and peak CO decreased during the sleep-deprived state compared with the control state. (2) There was no difference between peak heart rates measured during exercise under the 2 conditions. (3) Plasma ANP concentration during exercise increased significantly during the control state, whereas only a tendency toward increase was observed during the sleep-deprived state. (4) Plasma BNP concentration during exercise tended to increase in the control state compared with the resting state, whereas there was no difference in plasma BNP between after exercise and resting state in the sleep-deprived state. These results indicate that changes of ANP or BNP induced by exercise tended to be decreased by chronic sleep deprivation.
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PMID:Exercise-induced changes in plasma atrial natriuretic peptide and brain natriuretic peptide concentrations in healthy subjects with chronic sleep deprivation. 1040 84

From the clinical standpoint a cardiomyopathy can be classified as primitive when other causes, i.e. ischemic, infiltrative, systemic diseases, can be ruled out. Initial symptoms usually include a progressive dyspnea and fatigue with tachycardia in a patient previously healthy. Congestive heart failure may be the initial manifestation. Angina is often present, not only because of coronary heart disease. Auscultatory findings usually include a gallop rhythm with a third heart sound, not rarely a four-sound gallop. Blood test to evaluate renal and liver function should be performed. The dosage of troponin I and/or troponin T, plasma renin activity, brain natriuretic peptide or endothelins has recently gained some reputation to indicate prognosis, but there is no reason to believe that these measures are superior to cardiopulmonary stress test.
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PMID:[Dilated cardiomyopathy: role of clinical and laboratory evaluation]. 1202 82

The pharmacotherapy currently recommended by the American College of Cardiology and the American Heart Association for heart failure (HF) is a diuretic, an angiotensin-converting enzyme inhibitor (ACEI), a beta-adrenoceptor antagonist and (usually) digitalis. This current treatment of HF may be improved by optimising the dose of ACEI used, as increasing the dose of lisinopril increases its benefits in HF. Selective angiotensin receptor-1 (AT(1)) antagonists are effective alternatives for those who cannot tolerate ACEIs. AT(1) antagonists may also be used in combination with ACEIs, as some studies have shown cumulative benefits for the combination. In addition to being used in Stage IV HF patients, in whom it has a marked benefit, spironolactone should be studied in less severe HF and in the presence of beta-blockers. The use of carvedilol, extended-release metoprolol and bisoprolol should be extended to severe HF patients as these agents have been shown to decrease mortality in this group. The ancillary properties of carvedilol, particularly antagonism at prejunctional beta -adrenoceptors, may give it additional benefits to selective beta(1)-adrenoceptor antagonists. Celiprolol and bucindolol are not the beta-blockers of choice in HF, as they do not decrease mortality. Although digitalis does not reduce mortality, it remains the only option for a long-term positive inotropic effect, as the long-term use of the phosphodiesterase inhibitors is associated with increased mortality. The calcium sensitising drug levosimendan may be useful in the hospital treatment of decompensated HF to increase cardiac output and improve dyspnoea and fatigue. The antiarrhythmic drug amiodarone should probably be used in patients at high risk of arrhythmic or sudden death, although this treatment may soon be superseded by the more expensive implanted cardioverter defibrillators, which are probably more effective and have fewer side effects. The natriuretic peptide nesiritide has recently been introduced for the hospital treatment of decompensated HF. Novel drugs that may be beneficial in the treatment of HF include the vasopeptidase inhibitors and the selective endothelin-A receptor antagonists but these require much more investigation. However, disappointing results have been obtained in a large clinical trial of the tumour necrosis factor alpha antagonist etanercept, where no likelihood of a difference between placebo and etanercept was observed. Small clinical trials with recombinant growth hormone to thicken ventricles in dilated cardiomyopathy have given variable results.
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PMID:Present and future pharmacotherapy for heart failure. 1208 91

Fatigue and mainly dyspnea are symptoms the most often found in patients with diastolic heart failure. Flash pulmonary oedema is one of the most often found mode of clinical presentation. The heart has a normal size at chest X ray. Hemodynamic evaluation, the gold standard, shows increase in filling pressure but is not routinely performed. Doppler echocardiography has become the reference exam. It allows demonstrating: 1. the normal systolic function of the left ventricle (normal ejection fraction); 2. existence of a structural abnormality of the diastolic dysfunction; 3. calculating the level of pulmonary pressures. In the next years, it is likely that an increased plasma level of brain natriuretic peptide (BNP) becomes mandatory for a positive diagnosis.
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PMID:[Diagnosis of diastolic heart failure]. 1243 93

The aim of this prospective study was to evaluate the association of peripheral B-type natriuretic peptide (BNP) levels with clinical symptoms and central hemodynamic and echocardiographic measures in cardiac transplantation. BNP reflects ventricular wall stress and correlates with severity of heart failure. No previous investigation has comprehensively assessed the rapid bedside BNP assay for predicting hemodynamic measures of cardiac allograft function in heart transplantation. We evaluated BNP levels using a rapid point-of-care assay in 87 stable cardiac transplant recipients who had 237 consecutive measurements along with endomyocardial biopsy, right-sided cardiac catheterization, and echocardiography. Using median tendencies, 2 groups were identified: the low BNP group (n = 116, BNP <150 pg/ml) and the high BNP group (n = 121, BNP >/=150 pg/ml). The high BNP group had increased right atrial pressures, higher pulmonary artery systolic pressures, pulmonary capillary wedge pressures, and lower cardiac index. Besides hemodynamic variables, the presence of right ventricular dysfunction (p = 0.05) and significant tricuspid regurgitation (p = 0.003) were associated with higher BNP levels. Independent predictors of BNP levels on multivariate analysis included elevated pulmonary capillary wedge pressure, lower cardiac index, and symptoms of dyspnea and fatigue. This initial investigation establishes the accuracy of a point-of-care BNP assay in predicting cardiopulmonary hemodynamic aberrations despite preserved left ventricular systolic function in heart transplant recipients. Rapid bedside BNP analysis may provide a noninvasive surrogate method for the comprehensive assessment of cardiac allograft function and hemodynamics in heart transplantation.
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PMID:Usefulness of B-type natriuretic peptide levels in predicting hemodynamic perturbations after heart transplantation despite preserved left ventricular systolic function. 1248 42

Many patients in our nephrology department who have anaemia and chronic kidney insufficiency (CKI) show evidence of congestive heart failure (CHF). This triad of anaemia, CKI and CHF is known as the cardio-renal anaemia syndrome. The three conditions form a vicious circle, in which each condition is capable of causing or being caused by another. Anaemia can increase the severity of CHF and is associated with a rise in mortality, hospitalization and malnutrition. Anaemia can also further worsen renal function and cause a more rapid progression to dialysis than is found in patients without anaemia. Uncontrolled CHF can cause rapid deterioration of renal function and anaemia. CKI can also cause anaemia, as well as worsen the severity of CHF, and is associated with increased mortality and hospitalization in patients with CHF. Aggressive therapy against CHF with all the conventional medications at the accepted doses often fails to improve the CHF if anaemia is also present but is not treated. In studies in which the anaemia was corrected with s.c. erythropoietin and, in some cases, with i.v. iron, however, the cardiac function improved, as assessed by measurement of the left ventricular ejection fraction and oxygen utilization during maximal exercise. Symptomatic patient functioning improved, as monitored by shortness of breath and fatigue on exertion, and the need for hospitalization and oral and i.v. diuretics markedly decreased. The quality of life, as judged by different criteria, also improved. The glomerular filtration rate, which fell rapidly when the anaemia was untreated, stabilized in patients when their anaemia was treated. Nephrologists need to assess the cardiac status of all patients with CKI carefully, and this includes an echocardiogram along with possibly measuring the levels of B-type natriuretic peptide. Nephrologists also need to use the indicated agents for CHF at the recommended doses, while cardiologists and internists need to be more aware of the importance and lethal effects of even mild anaemia and the benefits of its treatment in CHF and CKI. Cooperation between these specialists will allow better and much earlier treatment of the anaemia, CHF and CKI, and prevent the deterioration of all three conditions.
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PMID:The cardio-renal anaemia syndrome: does it exist? 1460 93

Left ventricular diastolic dysfunction plays an important role in congestive heart failure. Although once thought to be lower, the mortality of diastolic heart failure may be as high as that of systolic heart failure. Diastolic heart failure is a clinical syndrome characterized by signs and symptoms of heart failure with preserved ejection fraction (0.50) and abnormal diastolic function. One of the earliest indications of diastolic heart failure is exercise intolerance followed by fatigue and, possibly, chest pain. Other clinical signs may include distended neck veins, atrial arrhythmias, and the presence of third and fourth heart sounds. Diastolic dysfunction is difficult to differentiate from systolic dysfunction on the basis of history, physical examination, and electrocardiographic and chest radiographic findings. Therefore, objective diagnostic testing with cardiac catheterization, Doppler echocardiography, and possibly measurement of serum levels of B-type natriuretic peptide is often required. Three stages of diastolic dysfunction are recognized. Stage I is characterized by reduced left ventricular filling in early diastole with normal left ventricular and left atrial pressures and normal compliance. Stage II or pseudonormalization is characterized by a normal Doppler echocardiographic transmitral flow pattern because of an opposing increase in left atrial pressures. This normalization pattern is a concern because marked diastolic dysfunction can easily be missed. Stage III, the final, most severe stage, is characterized by severe restrictive diastolic filling with a marked decrease in left ventricular compliance. Pharmacological therapy is tailored to the cause and type of diastolic dysfunction.
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PMID:Role of diastole in left ventricular function, II: diagnosis and treatment. 1556 51

Acute heart failure has recently become a very common syndrome. Therefore, even if you are not a cardiologist, you should know how to diagnose and treat it. A basic technique is here summarized. Diagnosis of heart failure can be performed from a simple criteria including coarse crackles, an extra-sound (S3), a distention of the cervical vein, cardiomegaly, pulmonary edema, and serum levels of B-type natriuretic peptide (100 pg/ml<). After diagnosis, the severity should be assessed by the degrees of both pulmonary edema and cardiac output. For these evaluations, a Swan-Ganz catheter might not be needed, since we can evaluate them clinically, i.e., physical examinations and auscultation. We can then treat the patient with heart failure with a vasodilator and/or diuretics. If the blood pressure is low, we can administer a low dose of an inotropic agent. But an inotropic agent should be withdrawn as early as possible, because they can occasionally have deleterious effects. Finally, please bear in mind that the elimination of several triggers, e.g., infection, transient cessation of medication, and physical or metal stress, and also the detection of early symptoms of heart failure, e.g., shortness of breath on exertion, fatigue, increase in body weight, and appetite loss, are very important for the prevention of acute heart failure.
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PMID:[Diagnostic and therapeutic technique for acute heart failure]. 1567 66

For a further depiction of exercise-induced cardiac dysfunction, N-terminal pro-brain natriuretic peptide (NT-pro-BNP) and cardiac troponin T (cTnT) were measured in recreational cyclists (n = 29) during the Otztal Radmarathon 2004. In all subjects, NT-pro-BNP significantly increased from 28 +/- 21 to 278 +/- 152 ng/L immediately after the race (p <0.001), decreased again on the following day, and returned to baseline values 1 week later. The mean percentage increase in NT-pro-BNP was 1,128 +/- 803%. CTnT, negative in all subjects before the race, increased transiently in 13 athletes (45%), with levels ranging from 0.043 to 0.224 mug/L in 8 of them (28%). One day after competition, cTnT had normalized in all athletes. Because of the typical release of kinetics, the deflection of NT-pro-BNP is considered to be the adequate volume regulatory response of a hemodynamically stressed heart to prolonged strenuous exercise. The observed kinetics of cTnT substantiate a release from the free cytoplasmatic pool due to the half-life of cytosolic cTnT. In healthy cyclists, transient increases in NT-pro-BNP and cTnT are more likely to reflect cardiac fatigue than injury.
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PMID:Effect of competitive marathon cycling on plasma N-terminal pro-brain natriuretic peptide and cardiac troponin T in healthy recreational cyclists. 1612 5

B-type natriuretic peptide (BNP) is an endogenous cardiac neurohormone, produced in the ventricles in response to pressure and volume elevation. Nesiritide is identical to endogenous BNP and is synthesized using recombinant DNA technology. It is currently used in the treatment of acute decompensated heart failure. In clinical trials, nesiritide has been shown to decrease pulmonary capillary wedge pressure, pulmonary artery pressure, right atrial pressure, and systemic vascular resistance, as well as increase cardiac index and stroke volume index. Infusions of nesiritide have led to increased diuresis and natriuresis. Patients treated with nesiritide have reported improvements in global clinical status, dyspnea, and fatigue. Therapy with nesiritide has resulted in decreased plasma renin, aldosterone, norepinephrine, and endothelin-1 levels, as well as reduced ventricular ectopy and ventricular tachycardia. Heart rate variability also improved with nesiritide. Patients with acute coronary syndromes, serious arrhythmia, renal disease, diastolic dysfunction, or vasopressor dependence have been safely managed with nesiritide. Early treatment with nesiritide in the emergency department may lead to decreased length of hospital stay and reduced readmission rates compared to standard care. Outpatient serial infusions of nesiritide in severe heart failure patients on optimal medical therapy may result in improved clinical status, increased ejection fraction, reduced aldosterone and endothelin-1 levels, and decreased hospitalizations. Potential future uses of nesiritide include treatment of acute coronary syndromes, pulmonary hypertension, bronchospasm in chronic lung disease, and as antifibrotic/anti-remodeling therapy or bridge to cardiac transplant. The possibility of subcutaneous injections of nesiritide has been studied in both animals and humans.
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PMID:Nesiritide: past, present, and future. 1633 35


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