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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

Hemofiltration was performed in 15 patients with refractory congestive heart failure. All of these patients had oliguria, although intensive treatment with diuretics, digitalis, vasodilators, and catecholamines was prescribed. Hemofiltration was performed under hemodynamic monitoring in 14 patients. The water removal by hemofiltration decreased pulmonary arterial pressure, pulmonary capillary wedge pressure and right atrial pressure. Despite these hemodynamic improvements, nine patients (60%) died within one month after the start of hemofiltration; the causes were fatal arrhythmia in three, renal failure in two, sepsis in one and irreversible cardiogenic shock in three. Oliguria for over 15 h or a serum creatinine concentration of more than 4.0 mg/dl at the start of hemofiltration related to poor prognosis. In view of these results, hemofiltration for refractory heart failure should be started earlier and performed carefully in order to avoid arrhythmia, cardiogenic shock, and other complications.
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PMID:Hemofiltration as treatment for patients with refractory heart failure. 149 76

Electrolyte abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. Magnesium and potassium deficiencies play an important role in the development of cardiac arrhythmias. Magnesium is essential for the maintenance of intracellular potassium concentration. Although there are conflicting data regarding the prevalence of hypomagnesemia in patients with chronic heart failure (the values range from 7-37%), multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal controls. As magnesium and potassium are mainly intracellular ions, measurements in serum or plasma are of limited value to assess magnesium status. There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for mononuclear cells or erythrocytes or for myocardial and skeletal muscle. Loop diuretics (e.g. furosemide) are supposed to cause a substantial loss of both magnesium and potassium in the plasma and intracellular space. The potassium-sparing diuretics amiloride and triamterene are reported to also exert magnesium-sparing effects. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion. Low magnesium and potassium concentrations increase cardiac glycoside toxicity. In contrast, elevated levels of magnesium decrease the sensitivity of human myocardium to antiarrhythmogenic actions of cardiac glycosides, without affecting maximally developed tension. Moreover, magnesium increases binding affinity of cardiac glycosides to the receptor. The antiarrhythmic action of magnesium is suspected to be mediated by a reduced sensitivity to electrophysiological changes induced by Ca2+, thus indicating Ca2+ antagonistic properties of magnesium. Magnesium deficiency has also been implicated in sudden death, notably in patients with congestive heart failure. Therefore, when treating congestive heart failure, one must consider how to prevent depletion of electrolytes or how to replete potassium and magnesium in deficiency states.
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PMID:Heart failure and electrolyte disturbances. 150 35

A questionnaire on the treatment of congestive heart failure was distributed to physicians in the medical departments of five hospitals in the Oslo area. The 117 (81%) respondents selected first, second and third line therapy in the treatment of mild, moderate and severe heart failure. Diuretics and restrictions on sodium/water dominated as first line therapy for mild heart failure; less than 5% suggested ACE-inhibitors or digitalis. Some differences in priorities were revealed for moderate and severe heart failure. The majority again suggested diuretics and restrictions on sodium/water, but 20% preferred ACE-inhibitors, which were also stated as second or third line therapy by 60% of the physicians. Less than 50% chose digitalis or nitrates as one of the three first therapies.
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PMID:[Treatment of heart failure. A questionnaire among Norwegian hospital physicians]. 141 51

Renal plasma flow (RPF), glomerular filtration rate (GFR), renal proximal tubular delivery of sodium and water evaluated by lithium clearance, and hormonal parameters were measured in 12 patients with congestive heart failure NYHA class II-IV before and after captopril treatment for 4 wk and in 13 healthy control subjects. RPF and GFR were significantly decreased in heart failure, whereas the filtration fraction (FF) was increased. Treatment with captopril increased RPF and decreased FF, whereas GFR was unchanged. Total and fractional urinary excretion of sodium were reduced in the patients compared with the controls, but increased after captopril. Fractional excretion of lithium was normal in heart failure and was increased by captopril. Atrial natriuretic peptide, guanosine 3',5'-cyclic monophosphate, and aldosterone in plasma were significantly elevated in heart failure and were reduced by treatment with captopril. Plasma renin activity was increased in patients, correlated inversely with RPF, and increased further after captopril treatment. It is concluded that the reduced sodium excretion in heart failure was caused by a combination of diminished glomerular filtration and enhanced tubular reabsorption beyond the proximal tubule and that treatment with captopril increased urinary sodium excretion partly due to an attenuated sodium reabsorption in the proximal tubule. The present data in patients with congestive heart failure are consistent with an increased intrarenal angiotensin II generation and an elevated plasma level of aldosterone being involved in the pathogenesis of the glomerular hemodynamic changes and the enhanced distal tubular reabsorption, respectively.
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PMID:Mechanisms of sodium retention in heart failure: relation to the renin-angiotensin-aldosterone system. 164 90

We studied the hormonal, renal and hemodynamic effects of prolonged treatment with SCH 39370, a new neutral endopeptidase (NEP) inhibitor, in experimental congestive heart failure (CHF). Coronary-ligated CHF rats and sham-operated controls received vehicle or SCH 39370 30 mg/kg s.c. twice daily for six days. In rats with heart failure, SCH 39370 elevated the high plasma atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) levels 2-fold both initially and at the end of the experiment. Initially, water balance was more negative in SCH 39370-treated CHF rats than in those treated with vehicle. In all SCH 39370-treated rats, ANP, cGMP and electrolyte excretion and diuresis were pronounced for 6 h after injection but attenuated thereafter. Blood pressure and pulse remained unchanged. On reverse phase high performance liquid chromatography (HPLC), ANP-(99-126) appeared to be the only circulating form of ANP in rats with heart failure. Three forms have been discovered in patients with heart failure. HPLC revealed only intact ANP in plasma of rats with heart failure during SCH 39370 treatment. NEP inhibitors may provide a new tool for treating chronic heart failure.
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PMID:Prolonged neutral endopeptidase inhibition in heart failure. 165 77

Recently, major advances have been made in the therapy of chronic congestive heart failure. New vasodilatory and positive inotropic drugs as well as specific antagonists to activated neurohormones have added new therapeutic dimensions. Dopaminergic stimulation, which has been used in acute heart failure for many years has now been introduced with the new substance ibopamine into the therapy of chronic heart failure. The therapeutic efficacy of new drugs in the treatment of chronic congestive heart failure has to be evaluated in terms of their prognostic and therapeutic impact for improvement and symptomatology, which sometimes does not necessarily lead to improvement of prognosis. Ibopamine has potential in improving prognosis by its major effects: vasodilatation, decrease in vasoactive hormones and improvement in renal blood flow and water diuresis. In the long-term therapy of chronic congestive heart failure ibopamine has been useful in mobilization of edema in acute decompensation, improvement of symptoms according to the New York Heart Classification and of exercise tolerance. In addition improvement of hemodynamics with an increase in cardiac output, a decrease in filling pressures and in peripheral resistance has been demonstrated. Efficacy of diuretics is improved and ibopamine has been a valuable adjunct in the pre-operative therapy before cardiac transplantation. Major positive inotropic effects in the usual dose of 100 mg tid, as well as other potentially dangerous effects of beta-receptor-stimulation (such as malignant, ventricular arrhythmias) can be largely excluded. Historically, controls of patients with heart failure of similar severity do not suggest any unfavorable effect of this drug on prognosis.
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PMID:[Ibopamine--clinical results]. 168 95

Diuretics, together with digitalis glycosides and vasodilators are of prime importance in the medical treatment of patients with congestive heart failure (CHF). Diuretics provide quick symptomatic relief in these patients. Their beneficial effect is related to the promotion of sodium and water excretion via the kidney, thus reducing extracellular fluid volume expansion and mitigating the increase in preload and afterload caused by sodium and water retention. Loop diuretics administered intravenously are indispensable in the management of pulmonary oedema; thiazides and loop diuretics in low doses are effectively used in the oral treatment of mild to moderate heart failure. Torasemide is a new loop diuretic which differs from furosemide (frusemide) and related loop diuretics by virtue of its longer elimination half-life and longer duration of action, with almost complete bioavailability. The efficacy and tolerability of torasemide have been compared with furosemide in several studies. Once daily oral administration of torasemide (starting with 5mg) or furosemide 40mg reduce bodyweight, oedema and symptoms of heart failure to a similar extent. Mean New York Heart Association class is consistently reduced by 0.5 to 0.7. Intravenous administration attenuates the increase in intracardiac pressures during exercise in patients with CHF, and produces acute improvements in cardiac haemodynamics in patients with high grade left heart failure. A beneficial effect on both pulmonary and cardiac haemodynamics has been demonstrated during chronic oral treatment of patients with previously untreated CHF. Torasemide was well tolerated with only mild and transient adverse effects reported in a small number of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute and long term effects of loop diuretics in heart failure. 171 15

After large myocardial infarction, compromised left ventricular (LV) function and changes in the peripheral circulation result in the syndrome of chronic congestive heart failure. Although treatment with angiotensin-converting enzyme inhibitors improve cardiovascular function, it is difficult to determine whether this benefit is due to changes in organ versus muscle function. The rat model of heart failure, created by ligating the left coronary artery, results in pathophysiology that is similar to that seen in patients, i.e., increased LV end-diastolic pressure and volume, hypertrophy of the noninfarcted myocardium, prolongation of the time constant of LV relaxation, decreased venous compliance, and increased total blood volume. In noninfarcted papillary muscles, isolated from rats with heart failure, maximal developed tension and peak rate of tension rise (+dT/dt) are decreased, time to peak tension is prolonged, and myocardial stiffness is increased. Morphologic changes include an increase in papillary muscle myocyte cross-sectional area and an increase in myocardial hydroxyproline content. Captopril (2 g/liter drinking water) alters LV loading by decreasing arterial pressure, increasing venous compliance, and decreasing blood volume. This results in a decrease in LV end-diastolic pressure and volume. In the noninfarcted myocardium, time to peak tension is shortened, whereas developed tension, +dT/dt, and muscle stiffness remain abnormal. Captopril decreases myocyte cross-sectional area, but collagen content remains elevated. Thus, in the rat infarct model of heart failure, treatment with captopril alters LV remodeling and hypertrophy but produces only modest improvement in muscle function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of captopril on contractility after myocardial infarction: experimental observations. 174 17

In heart failure, neurohumoral factors are important determinants of left-ventricular function, not only by direct mechanisms on the myocardium, but also by indirect effects through modulation of pre- and afterload. In experimental models of heart failure, as well as in patients with cardiac dysfunction, it has been demonstrated in the early phase of the disease that the sympathetic activity and the secretion of atrial natriuretic peptide are stimulated. This is associated with an increased synthesis of vasodilator prostaglandins in the kidney, predominately prostaglandin E2. Prostaglandin E2 plays an important role by its vasodilator and natriuretic properties in preserving renal blood flow, natriuresis and diuresis. The stimulation of the secretion of atrial natriuretic peptide in relatively moderate heart failure leads to a suppression of the activation of the renin-angiotensin-aldosterone system. In more severe heart failure vasoconstrictor, sodium and water-retaining mechanisms like the renin-angiotensin-aldosterone system are activated with the consequence of an increase of systemic vascular resistance, a reduction of renal blood flow, and an increased fluid retention. The inhibition of cyclooxygenase, leading to a blockade of the synthesis of prostaglandins, leads in early heart failure to a dramatic change in renal blood flow with an increase of renal vascular resistance and a decrease of renal perfusion which causes renal functional impairment.
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PMID:[Renin, aldosterone and prostaglandins in heart failure]. 179 34


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