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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathophysiological mechanisms are reviewed concerning the onset and the perpetuation of the clinical features of congestive heart failure. This syndrome is a severe condition of poor prognosis and bad life quality which in the last decades has reached, in the western industrial countries, the highest levels of general mortality, mainly due to the high prevalence of hypertensive and ischaemic myocardiopathies in the last years. To the clinical features of heart failure mainly contributes a deregulation of the physiological compensatory mechanisms contemporarily and concurrently activated following the primary deficiency of the heart pump function. In physiological conditions, following the myogenic adapting mechanisms reflex mechanisms intervene, activated by intracardiac and aortic and carotid-sinus mechanoreceptors following the variations in intracardiac and intravascular pressure and generally evoking negative feed-back effects. In patients with heart failure arterial high pressure mechanoreceptors respond to the reduction in effective arterial pressure thus provoking a deactivation of the tonic inhibition on the sympathetic cardiovascular drive. This leads to an activation of peripheral and renal vasoconstrictor tone, to a raised medullary catecholamine incretion, to heart rate and inotropism stimulation, and to an increase in pituitary gland ADH production as well as to an activation of renin-angiotensin-aldosterone system (RAAS). Analogous vasoconstrictive, and sodium and water retentive effects can be elicited by endothelin produced by endothelial cells and found in high plasma levels in CHF. These excitatory effects, leading to a rise in systemic vascular resistance and to hydro-electrolytic retention with volume expansion, are not efficiently counteracted by the opposite effects triggered by cardiopulmonary vagally mediated mechanoreceptors activated by the raised cardiac filling pressure and leading to sympathetic nervous inhibition, peripheral and renal vasodilation, ADH and RAAS inhibition. Analogous effects should be provoked by the raised production, due to enhanced heart wall distension, of atrial natriuretic factor leading to vasodilation, natriuresis and diuresis. Reduced sensitivity of cardiopulmonary baroreceptors and lowered production of ANF due to structural cardiac changes could represent, according to most opinions, the main factors responsible for the prevailing sympathetic activation and hydro-saline retention in CHF. The activation of cardiopulmonary sympathetic positive-feed back afferents, could be also involved in the characteristic alteration of the vago-sympathetic balance in heart failure. The persistent reduction in heart pump function could lead to the instauration of vicious circles among the various regulatory systems and create an overcompensation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The physiopathological aspects and new therapeutic approaches in cardiac-circulatory failure]. 149 59

All hyponatremic states have in common elevation of vasopressin. Without this the loss of salt would be followed by appropriate diuresis and normonatremia. If hyponatremia is triggered by a volume change as in heart failure or portal cirrhosis not only is ADH released but the mechanisms that control salt retention create an essentially sodium free urine, always less than 20 mEq/L. If the initial event is inappropriate ADH secretion whether it be cerebral disease, neoplasm, a pulmonary lesion or a growing list of drugs; there is no related signal for salt retention and urine sodium and tonicity are high, the latter usually higher than that of plasma. If salt loss is due to intrinsic renal disease, diuretics, osmotic or otherwise, or adrenal failure urinary sodium is variable depending upon the magnitude of the response to volume of salt retaining factors. Because hyponatremia is often present with major illness and because more than one factor may be involved in its genesis, the establishment of its origin and appropriate treatment remain a diagnostic and therapeutic challenge.
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PMID:Hyponatremia: manifestations and treatment. 162 51

In contradiction earlier viewpoints, cardiac failure cannot be defined as a purely hemodynamic problem nor as only a cardiac problem. On the other hand decreased cardiac output (Co), increased filling pressure, increased wallstress and myocardial O2-consumption (MVO2) are the cause of many humoral counterregulations. Therefore, it is not always certain if the observed alterations are the causes or consequences of cardiac failure. The systemic counter-regulations will be modulated by desensitized cardiopulmonary mechanoreceptors, followed by decreased inhibition of central vasomotoric stimuli and endothelial and endocardial function, by altered signal transmission, as well as by altered gene expression within the myocytes. Depending on the degree of insufficiency, it may be attempted, by increase of the preload and of the contractility, to restore the hemodynamic basic situation. Such an attempt is based upon increased activity of the sympathetic nervous system, stimulation of the renin-angiotensin-aldosterone-system (RAAS) or the increased level of ADH. The reduced contractility and response of the myocytes, caused by the downregulation of beta 1-receptors and Gs-proteins, as well as by the upregulation of Gi-proteins, and the increased afterload with increased MVO2 and decreased CO all lead to a vicious circle. There are only some mechanisms that are directed against these regulations. The decreased response of the myocardium to endogenous catecholamines, the stimulation of ANP-secretion, as well of the prostaglandin-secretion are among the favorable regulations. They cause increase of natri- and diuresis, improved renal perfusion, vasodilatation, and inhibition of the RAAS and ADH-secretion with reduction of true thirst and craving for salt.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Synopsis of endocrine and hemodynamic changes in heart failure]. 179 35

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.
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PMID:[ADH (anti-diuretic hormone), aldosterone (PA) and renin activity (PRA) in patients with respiratory failure]. 269 88

An inappropriate antidiuretic hormone secretion (SIADH) has been recognized as the cause of hypotonic hyponatremia, and the occurrence of this syndrome, accompanied by an ADH-producing adenocarcinoma in the nasal cavity, is reported. In February, 1987, a 50-year-old male, showing sights of delirium, disorientation, and irritability was admitted to the hospital. The patient was observed to be healthy, except for a neck lymphnode metastasis that was present up to the time of his hospitalization. The hyponatremia was incidentally found, although dehydration or intravascular volume depletion were not noted. These neuropsychiatric symptoms were considered to be associated with hyponatremia due to SIADH. He had had a partial maxillectomy, a neck dissection, and irradiation to the nose and nasal cavity 32 months earlier, and then underwent a surgical resection of the neck metastasis; he had a total of 10 other operations before the onset of the symptoms. Upon initial inspection, since neither an intracranial invasion nor a brain metastasis was found, we diagnosed that his symptoms were due to an autonomic disturbance caused by surgical and mental "stress". When he died of cardiac failure due to a mediastinal invasion 8 months after the onset of SIADH, tumor tissues was extirpated in an autopsy and was then cultured. In this manner, it was proved that the tumor cells had been producing ADH. This procedure clarified that the syndrome had resulted from an ADH-producing tumor of the nasal cavity.
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PMID:[A case of adenocarcinoma of the nasal cavity associated with syndrome of inappropriate secretion of antidiuretic hormone(SIADH)]. 277 60

A course of hemosorption combined with chemotherapy resulted in much less frequent attacks of angina pectoris and in compensation of cardiac insufficiency in 27 coronary heart disease patients resistant to chemotherapy. There was an increase in the drugs efficacy. Sensitivity of the lymphocytes to chemotherapeutic agents administered rose as shown by rosette test due to specific unlocking of the receptors. The underlying mechanism of hemosorption-related compensation of cardiac insufficiency implies correction of secondary hyperaldosteronism and a decrease in the level of ADH leading to enhanced diuresis, natriuresis, inhibited kaliuresis and to normal values of blood electrolytes.
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PMID:[Hemosorption in the treatment of patients with ischemic heart disease and drug-resistant stenocardia]. 281 Dec 47

The effects of polyunsaturated fatty acids (phosphatidylcholine) on renal function in healthy subjects and in patients with chronic renal failure, with liver cirrhosis, and with heart failure were studied. The drug was administered at 3.5 mg/kg i.v. (Linoleic acid 1.24 mg/kg). In all cases, the administration of the drug caused an increased excretion of sodium and especially of water with a reduction in basal urinary hypertonicity. The polyuria was caused by the higher glomerular filtration rate not being counterbalanced by an increase in tubular water reabsorption. The water reabsorption was mostly anisosmotic. The presence of urinary hypertonicity excluded an inhibition of ADH secretion by this drug. The sodium excretion was probably caused by an increase of the glomerular filtration rate whereas no significant changes in the tubular reabsorption of sodium were seen. We found a significant (p 0.05) increase in PGE2 urinary excretion after phosphatidylcholine administration. Lysine - acetylsalicylate injection after phosphatidylcholine, in other trials in the same patients, prevented the effects previously reported. Therefore we suggest that the effects of this drug are mediated by an increased availability of renal prostaglandins.
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PMID:Effects of polyunsaturated fatty acids and prostaglandin synthesis on renal function. 308 1

Congestive heart failure is associated with ventricular hypertrophy and dilatation, increased circulating catecholamines, and peripheral vasoconstriction. The extent to which these changes occur, whether they are a favorable "compensatory mechanism" or contribute to cardiocirculatory dysfunction, depends on the cause and severity of the heart failure. The addition of new sarcomeres through ventricular hypertrophy distributes the excess workload of the failing ventricle over more contractile units. In ventricular pressure overload, hypertrophy primarily increases wall thickness and ventricular volume is not usually increased; the converse is true with ventricular volume overload. Hypertrophy can result in enhanced or depressed contractile performance, depending on the stimulus for hypertrophy and method by which contractility is evaluated. The "ventricular function curve," which relates stroke volume to ventricular filling pressure or volume, overestimates the role played by the "Starling principle" as a compensatory mechanism and underestimates how well contractile performance is preserved. The evaluation of end systolic pressure-volume relationships under conditions of variable afterload closely reflects the isometric length-tension relationship and is therefore a more accurate way to quantitate cardiac muscle performance. Pressure overload hypertrophy usually leads to a depression in contractility whereas volume overload may not. An exaggerated sympathoadrenal response is another hallmark of severe heart failure that enhances contractility, helps initiate hypertrophy, and maintains arterial perfusion pressure. A generalized increase in peripheral vascular resistance occurs and is most prominent in those circulations most susceptible to neurohumoral control (renal, splanchnic, cutaneous). This favors perfusion of the cerebral and coronary circulations. Vasoconstriction is further enhanced by the activation of the renin-angiotensin-aldosterone system and secretion of ADH. This results in sodium retention and plasma volume expansion. In early mild heart failure, vasomotor tone may be normal at rest; however, the sympathoadrenal response to exercise may be intense. Moderate alpha receptor stimulation reduces skeletal muscle blood supply and favors the intramuscular redistribution of blood flow from inactive to active muscle fibers, thereby maintaining a normal oxygen consumption. During the later stages of heart failure, increased vascular stiffness due to increased sodium content and excessive norepinephrine appears to restrict nutritional blood flow to exercising muscle at the conductance-vessel level. Vasodilator drugs may reduce aortic impedance and improve cardiac output, may lower ventricular filling pressure, and relieve congestive symptoms, and may result in complex but favorable changes in the distribution of blood flow to the regional circulations.
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PMID:Cardiocirculatory dynamics in the normal and failing heart. 645 90

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.
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PMID:[Hyponatremia--with comments on hypernatremia]. 1089 27

Sympathetic overdrive in acute low cardiac output syndrome, diverts blood from cutaneous and visceral circulation centripetally. Microcirculation in general, and renal circulation in particular, deteriorates during these circulatory adjustments leading to multi-organ failure (MOF). Decreased afferent glomerular arteriolar blood flow, increased renal sympathetic nerve discharge and a resultant decreased sodium chloride delivery around macula densa stimulates the Juxta-glomerular apparatus (JGA) and triggers renin-angiotensin-aldosterone mechanism. This, along with increased ADH production results in a state of vasoconstriction, increased after-load, and continued fluid retention, further compromising the visceral microcirculation. Initially the fluid retention under the effect of aldosterone and ADH is iso-osmotic, but later under inappropriate ADH action more water than salt is retained, as evidenced by the presence of hyponatraemia and 'water-logging' in the endstage of this condition.The author hypothesizes that: although physiological, the persistent stimulation of the JGA during the low cardiac output state plays an important role in perpetuating a negative cardiovascular vicious cycle and further aggravating it into MOF. Furthermore, by infusing hypertonic saline and hence increasing the sodium chloride delivery to the distal tubules and the macula densa, the JGA could be inhibited. This strategy should work like angiotensin-converting-enzyme-inhibitor drugs in chronic cardiac failure, except by acting at the root cause and inhibiting Renin production at its source. It should further help by stimulating atrial natriuretic peptide secretion.
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PMID:Possible role of juxtaglomerular apparatus in low cardiac output syndrome and multiple organ failure: modulation by high sodium load. 1142 43


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