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

Therapy with diuretics and/or digitalis, as well as the compromised cardiac function, contributes to electrolyte alterations (magnesium, potassium) in patients with congestive heart failure. We determined in 29 patients with heart failure (NYHA classes II-IV) the magnesium and potassium content in lymphocytes and in erythrocytes, as well as in 25 healthy subjects. In patients with heart failure, lymphocyte magnesium (4.4 +/- 0.6 fmol/cell) and lymphocyte potassium (50.4 +/- 6.0 fmol/cell) were only slightly (n.s.) lower compared to controls (Mg++: 4.7 +/- 0.6 fmol/cell; K+: 54.6 +/- 6.8 fmol/cell). Only in healthy subjects did we find a positive correlation between magnesium and potassium in lymphocytes (r = 0.83). The electrolyte content in erythrocytes was also not different in patients with heart failure (Mg++: 2.2 +/- 0.1 mmol/l; K+: 96.6 +/- 6.1 mmol/l) and controls (Mg++: 2.2 +/- 0.1 mmol/l; K+: 97.8 +/- 4.0 mmol/l). There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for lymphocytes, or for erythrocytes in both groups. It is concluded that 1) determinations of magnesium and potassium in plasma do not reflect intracellular electrolyte content; 2) the magnesium and potassium content of lymphocytes and erythrocytes were not different in patients suffering from heart failure compared to controls; and 3) in heart failure, the relationship of magnesium and potassium in lymphocytes may be altered.
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PMID:[Magnesium and potassium content in patients with heart failure and in healthy persons. Determination in lymphocytes, erythrocytes and plasma]. 227 65

In 33 patients with heart failure (NYHA II-III) 24-h blood pressure was examined during the titration of two ACE-inhibitors. Blood pressure was measured by the oscillometric method using the blood pressure monitor 90202 from SpaceLabs, Inc. The measurements were taken from 06.00 to 22.00 hours every 20 min, and from 22.00 to 06.00 hours every 1 h. All patients received an additional therapy, either with captopril (group 1, n = 17) or enalapril (group 2, n = 16) in random order. Serum-electrolytes, serum-creatinine, and plasma-renin activity were measured before and during therapy with both ACE-inhibitors. 24-h blood pressure measurements were taken before and on the first and fifth day of the treatment with ACE-inhibitors. The groups did not different in respect to the degree of heart failure, the concomitant medication, or the 24-h profiles of blood pressure and heart rate. The mean initial doses of captopril was 9.2 +/- 1.2 mg. Each patient of group 2 received an initial dose of 2.5 mg enalapril. The maximal decrease of diastolic blood pressure occurred after 1 h in group 1 and after 4 h in group 2 and was similar in both groups (8 vs, 7 mmHg). The 24-h blood pressure values on day 5 were consistently below the pretreatment values (p less than 0.005). Heart rate was not affected by either ACE-inhibitor. The groups did not differ significantly during ACE-inhibition in their 24-h blood pressure and heart rate profiles. Before treatment, serum-sodium, -potassium and -creatinine were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[24-hour blood pressure and renal function in cardiac failure during the titration phase of captopril and enalapril]. 227 66

Before a new drug can be recommended for treatment of chronic heart failure, efficacy and safety have to be fulfilled. In this paper, the safety aspect of ibopamine, a congener of dopamine, is investigated by reviewing the available reports on this drug. A trend towards reduced mortality was found for patients with chronic heart failure during long-term treatment. No change in the potassium serum concentration has been found, whereas the plasma renin activity, plasma norepinephrine levels and the aldosterone secretion were decreased. It is concluded that ibopamine is a safe drug which may become an interesting alternative or additive therapy for patients with chronic heart failure.
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PMID:The safety profile of ibopamine, an alternative substance for treatment of chronic heart failure. 227 51

Ibopamine is a novel oral dopamine analogue with vasodilatory, positive inotropic and diuretic effects. In a double-blind, randomized study, the drug was investigated in 12 patients (mean age 49 +/- 10 years, 8 male, 4 female) with mild or moderate heart failure (NYHA classes II:8 patients, III:4 patients). Effects of single oral doses of 200 mg ibopamine, of 40 mg furosemide and of 200 mg ibopamine + 40 mg furosemide were compared in each patient at 3-day intervals. 1 h after administration, systolic and diastolic blood pressure increased from 120 +/- 11 to 124 +/- 9 and from 76 +/- 5 to 81 +/- 6 mm Hg in the ibopamine group. During 4 h after drug ingestion, urinary flow was significantly raised from 124 +/- 81 to 228 +/- 166 ml/2 h in the ibopamine group (p less than 0.05), while the administration of furosemide (with or without ibopamine) resulted in several folds increases of urinary flow. After ibopamine, the 2-h creatinine clearance rose from 123 +/- 73 to 131 +/- 85 ml/min (not significant). Sodium and potassium excretion remained essentially unchanged by ibopamine, while effects of furosemide were several folds of those of ibopamine. Plasma renin activity was lowered to 65% by ibopamine (p less than 0.01). No additive effects of ibopamine in the presence of furosemide were observed for all parameters tested. These results indicate that ibopamine has smaller renal effects than furosemide with regard to water diuresis and kaliuresis. These effects of ibopamine could reflect direct changes of renal function or secondary effects of neurohumoral origin. Ibopamine does not produce undesirable renal side effects, but affects the neurohumoral status favourably. This drug, thus, could be useful as an adjuvant therapy in mild heart failure.
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PMID:Extracardial effects of oral ibopamine versus furosemide in patients with mild or moderate heart failure. A double-blind, randomized trial. 227 57

The results of the European Working Party for Hypertension in the Elderly Study showed that treatment of high blood pressure reduced the morbidity and mortality from strokes and myocardial infarction and reduced the incidence of heart failure in elderly patients. The largest number of hypertensive patients are elderly, and it is in this group of patients that the maximum benefit of treatment might be expected. The present study was designed to study in detail the efficacy and tolerability of ketanserin in an elderly population. Seventeen elderly (greater than 70 years) patients with a lying systolic blood pressure of 160 mmHg and/or a diastolic blood pressure of greater than or equal to 90 mmHg were included in the study. For the 12 patients who completed the study, the mean blood pressure was significantly reduced on ketanserin compared with placebo (p less than 0.001) in the supine and erect positions. The mean net changes in blood pressure after 8 weeks were 21/17 mmHg and 23/16 mmHg erect. Heart rate was also significantly reduced (p less than 0.001) by a mean of 8 beats/min lying and 9 beats/min erect. Analysis of ambulatory 24-hour ECG tapes showed no significant effect of ketanserin on heart rhythms. Ketanserin therapy had no significant effect on routine hematology, plasma electrolytes, biochemistry, or urinalysis. Total exchangeable sodium and potassium and body weight were also unchanged. On ketanserin treatment, the overall quality of life score was significantly improved (p = 0.002; analysis of variance on log transformed data) compared with the placebo phase.
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PMID:A placebo-controlled crossover study of ketanserin in elderly hypertensive patients. 228 40

The article reports the efficacy and tolerability of a new slow-release formulation of furosemide (Lasix Retard) given to an elderly (mean: 72 years, range 48-92) population (n = 115, 77 females) suffering from hypertension or heart failure. In 34 of 52 patients with heart failure the clinical condition improved. Lasix Retard reduced blood pressure significantly from 187/99 to 166/93 after one year on 30 mg/day (n = 19). It was found that Lasix Retard replaces thiazide diuretics without causing any significant change in blood pressure. There were no significant changes in metabolic indicators (S-potassium, S-urate, S-glucose). Side effects were in the same range as reported for thiazide diuretics. There were 33 (29%) drop-outs.
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PMID:[Furosemide capsules in the treatment of hypertension or heart failure in the elderly in general practice]. 233 10

Diuretic drugs have been the mainstay of treatment for heart failure. Specific elucidation of the effects of diuretics on electrolytes, however, has been difficult, since the heart failure state itself may alter the electrolyte balance. Nevertheless, it is noteworthy that the natriuretic effect of loop diuretics is greater in edematous patients than in healthy volunteers; yet, the initial kaliuresis is minimal--perhaps because aldosterone levels are low. With continued treatment (or after the edema has been cleared), however, the natriuretic action of loop diuretics is less than that seen in controls, but loss of potassium occurs. The addition of a thiazide to a loop diuretic enhances its natriuretic effect. Both loop and thiazide diuretics can induce depletion of magnesium. Potassium-sparing diuretic drugs augment the natriuresis induced by loop or thiazide diuretics but limit or prevent the loss of potassium or magnesium in the urine, at least in the short term. However, potassium-sparing diuretics can exacerbate the development of hyponatremia.
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PMID:Interaction of diuretics and electrolytes in congestive heart failure. 230 24

Congestive heart failure is characterized by both disturbances in electrolyte homeostasis and neuro-hormonal regulation. Total body potassium is reduced, and this reduction bears a modest relation to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Patients with decompensated heart failure show increases in both plasma epinephrine and plasma norepinephrine, whereas patients with chronic stable heart failure usually have an increase only in plasma norepinephrine. High levels of circulating epinephrine may contribute to the development of hypokalemia by activating skeletal muscle and liver membrane beta 2-adrenergic receptors, which in turn stimulate intracellular cyclic adenosine monophosphate to activate the membrane-bound Na+K(+)-adenosine triphosphatase pump. The net result is that potassium flux across the cell membrane from the extracellular to the intracellular space increases, setting the stage for hypokalemia and possibly serious ventricular arrhythmias. Other mechanisms that may contribute to the development of hypokalemia in heart failure include the kaliuresis brought on by excessive levels of aldosterone. Moreover, it is likely that the activity of facilitated by concomitant activation of the renin-angiotensin system. Increased sympathetic nerve activity may then release additional renin from the kidney (by way of a beta 2-adrenergic mechanism). Therefore, both the sympathetic nervous system and the adrenal medulla may interact to cause hypokalemia in patients with heart failure. Because hypokalemia is known to predispose patients to ventricular arrhythmias, it may be prudent to aggressively maintain serum potassium levels in patients with heart failure in the range of 4 to 5 mEq/liter.
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PMID:Interaction of the sympathetic nervous system and electrolytes in congestive heart failure. 230 25

Angiotensin-converting enzyme (ACE) inhibitors and diuretics are known to cause hyperkalaemia. We undertook a prospective analysis over a period of six months of patients admitted under our care. Of 217 patients, 39 (18 per cent) were admitted with congestive cardiac failure/left ventricular failure. Of these 39 patients, 21 (54 per cent) were prescribed ACE inhibitors. Seven of these 21 patients subsequently developed hypokalaemia. This was irrespective of the type or dose of the diuretic but seemed to be related to the dose of the ACE inhibitor. In three cases the hypokalaemia was corrected by the addition of a potassium-sparing diuretic; in two cases a potassium supplement was added; and in the other three an increase in the dose of the ACE inhibitor for the resistant heart failure corrected the potassium deficit. This study shows that one should be alert to both hyperkalaemia and hypokalaemia when using a combination of ACE inhibitors and diuretics.
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PMID:ACE inhibitors and diuretics causing hypokalaemia. 231 35

This study tested the hypothesis that membrane transport is the major biochemical system of the myocardium altered in furazolidone-induced cardiomyopathy (round heart disease), before the development of myocardial failure, and that metabolic enzymes and contractile proteins are less affected. Compared with controls, maximal percentage depression of activities of myocardium from furazolidone-treated birds were 40 for creatine kinase, 30 for glycolysis, 30 for glycogen, 20 for myofibrils, 20 for Krebs's cycle enzymes, 15 for fatty acid oxidation and 10 for total soluble protein. Sodium and potassium transport, antioxidant system activity, myosin, myosin isoenzyme patterns and amino acid aminotransferases were unaffected. In marked contrast, the calcium-transport ATPase activity of the sarcoplasmic reticulum had undergone a 60 per cent compensatory increase in activity. The pattern of biochemical changes observed is consistent with a role of ischaemia in the pathogenesis of round heart disease and indicates that calcium transport by the sarcoplasmic reticulum is the major biochemical system affected.
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PMID:Myocardial biochemical changes in furazolidone-induced cardiomyopathy of turkeys. 232 37


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