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

Diuretics, together with other drugs and general measures, are of prime importance in the medical treatment of most heart failure patients, namely those with acute pulmonary oedema and overt congestive heart failure. Their beneficial effects result not only from preload and afterload reduction, but also because diuretics are able to improve responses to nitrates and ACE-inhibitors. The appropriate utilisation of diuretics in heart failure therapy frequently involves the use of efficient small doses and drug associations, namely between loop diuretics, thiazides, potassium sparing agents and spirolactone. Physicians must choose the drug carefully, its dosage, time and route of administration, according to the patient's characteristics: heart failure clinical syndrome, age, activity level, systolic or diastolic, left or right ventricular dysfunction, and associated diseases. The role of diuretics in the treatment asymptomatic systolic left ventricular dysfunction and oligosymptomatic diastolic ventricular dysfunction is unclear and should remain under investigation; diuretics may be of benefit in treating those patients with associated diseases, for example arterial hypertension and mild chronic renal failure.
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PMID:[Diuretics in the treatment of heart failure]. 830 46

We report a 70-year-old man who had a sudden onset of right hemiparesis and mutism. The lower extremity was more involved than the upper one. He had a long history of diabetes and chronic renal failure for which hemodialysis was necessary. On August 30, 1990, he had an sudden onset of right hemiparesis and mutism. Neurological examination revealed awake but mute in no acute distress. He could only respond to very simple commands such as opening his mouth or protruding his tongue. He did not appear to understand more difficult questions. In addition, he could not answer verbally. He was totally mute. Cranial nerves appeared intact except for slight right central facial paresis and severe diabetic retinopathy. He had complete paralysis of his right leg and a moderate weakness in his right upper extremity. Deep reflexes were diminished in both upper extremities and absent in the lower limbs. Frotal signs such as grasp and snout reflexes were present. Cranial CT scans revealed an ill-defined low density area in the left parasagittal subcortical area and a part of the anterior cerebral artery territory. The supplementary motor area appeared at least in part to be involved. He was treated with glycerol and other supportive cares, however, his clinical course was complicated by pneumonia, heart failure, septicemia, and he expired two months after his stroke. The patient was discussed in a neurological CPC, and the chief discussant arrived at a conclusion that he had an artery-to-artery embolism at the internal carotid bifurcation resulting in the cerebral infarction mainly in the territory of the anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 70-year-old man with right hemiparesis and mutism]. 836 54

The authors describe their experience with the treatment of nine patients where "essential" mixed cryoglobulinaemia was diagnosed. In addition to extrarenal symptoms all suffered from proliferative glomerulonephritis, most frequently mesangiocapillary. The latter was manifested in most instances during the first examination by nephrotic syndrome and reduced glomerular filtration. Two patients had only asymptomatic proteinuria with erythrocyturia. The majority suffered from arterial hypertension. The patients were treated with prednisone and cyclophosphamide, using initial doses after which the extrarenal symptoms receded promptly. Regression of proteinuria and normalization of glomerular filtration developed more slowly. Only in one patient the glomerulonephritis had a progressive course and terminated by chronic renal failure. One patient died from septicaemia and one from cardiac failure. The authors assume that early diagnosis and effective combined immunosuppression can ensure a favourable course of this rare disease.
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PMID:[Essential mixed cryoglobulinemia and the kidneys]. 837 67

Between 1969 and 1990 six patients (aged 14 to 64 years, mean 43 years) underwent in situ reconstruction for mycotic aneurysm of the ascending aorta. The primary source of infection was endocarditis in three patients (subacute bacterial endocarditis [n = one patient], sepsis with acute endocarditis [n = one patient]), sepsis with sternal osteomyelitis in one, sepsis with purulent pericarditis in one, and generalized febrile illness in one. In five of six patients the treatment consisted of the excision of changed tissue combined with a composite graft (n = one patient), a xenopericardial patch repair (n = one patient), a Dacron graft repair and aortic valve replacement (n = one patient), a Dacron graft repair alone (n = one patient), and a lateral suture combined with double valve replacement (n = one patient). In one patient with perforation of the mycotic aneurysm into the pulmonary artery, the place of rupture was oversewn without excision of the aortic or pulmonary artery tissue. Two patients with local pericardial inflammation were reoperated on during the hospital stay; one of them because of recurrent mycotic aneurysm of the ascending aorta at the other location and the other because of infection of the suture line after the Dacron patch repair. Antibiotic therapy was intravenously administered for 2 to 12 weeks postoperatively and continued orally for 4 to 8 weeks. The mean observation time was 6 years (range 4 months to 16 years). There was no late graft infection, except the chronic infection of the suture line in one patient who died suddenly 4 months after the operation. There was no early death, and there were three late deaths (chronic myocardial failure, one patient, chronic renal failure, one patient, sudden death, one patient). We concluded that in situ reconstruction for mycotic aneurysm of the ascending aorta combined with prolonged antibiotic therapy is an appropriate procedure with satisfactory early and good long-term results.
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PMID:In situ repair of mycotic aneurysm of the ascending aorta. 842 61

A RIA for human brain natriuretic peptide (BNP) was developed. Both BNP and atrial natriuretic peptide (ANP) were extracted from human plasma with Vycor glass powder (71% recovery for BNP). The assay had a minimum detection limit of 0.45 fmol/tube and an IC50 of 9 fmol/tube. The within-assay coefficients of variation were 11.4% at 4 pmol/L and 3.2% at 22 pmol/L, and the between-assay coefficient of variation was 11% at 24 pmol/L. There was no significant loss of immunoreactive (IR)-BNP in plasma samples stored at -80 C for 4 weeks. Low rates of labeled BNP and IR-BNP degradation occurred in EDTA plasma incubated at 37 C. The mean venous plasma IR-BNP (6.3 +/- 0.3 pmol/L) in normal subjects (n = 48) was significantly lower than plasma ANP (8.4 +/- 0.6 pmol/L). In contrast to ANP, IR-BNP did not increase when normotensive or hypertensive subjects changed from erect to supine posture. Markedly elevated levels were found in patients with congestive heart failure (mean IR-BNP, 87 +/- 11 pmol/L; ANP, 87 +/- 12 pmol/L; n = 35), recent myocardial infarction (mean IR-BNP, 60 +/- 9 pmol/L; ANP, 33 +/- 6 pmol/L; n = 7), and chronic renal failure. High pressure liquid chromatography of plasma extracts from heart failure subjects revealed both high (mol wt, 10,000) and low (mol wt, 4,000) mol wt IR-BNP. High mol wt BNP was the major component (mean ratio, 1.9:1) and was linearly correlated with low mol wt BNP (r = 0.99). HPLC of plasma extracts from three normal subjects receiving constant infusions of human BNP (2 pmol/kg.min) showed a single major peak eluting in the position of hBNP-32, with no evidence of high mol wt material. These results show that whereas marked elevations in BNP occur in circulatory disorders, a major (> 50%) and consistent contribution to immunoreactivity is due to precursor forms. Further, compared to ANP, there is no IR-BNP response to supine posture in normal and hypertensive subjects.
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PMID:Assay of brain natriuretic peptide (BNP) in human plasma: evidence for high molecular weight BNP as a major plasma component in heart failure. 847 92

A female patient who had open heart surgery for cor triatriatum under hemodialysis, subsequent kidney transplantation and pregnancy is reported. We performed hemodialysis on the patient before, during and after heart surgery to control renal failure. Two years after heart surgery, she received a kidney graft from her mother. The kidney graft showed good function. She was treated with azathioprine and prednisone. Three years after renal transplantation she delivered a healthy male infant by elective Caesarean section at 37 weeks' gestation. Mother and infant did well following delivery. There was lack of hypertension, proteinuria, signs of graft rejection, and recurrence of heart failure during pregnancy. She showed serum creatinine level < 2 mg/dl, a prednisone of < 2 mg/kg/day. Elective Caesarean section has improved hydronephrosis due to the compression of the fetus. The aforementioned good criteria contributed to the successful pregnancy of the renal transplant patient in our experience. We believe early surgical intervention overcomes complicated heart disease even with endstage renal disease, and it gives a chance to receive renal transplantation and have a healthy child. To our knowledge, this is the first report that has described the successful management of open heart surgery under hemodialysis, subsequent renal transplantation and pregnancy in a female patient with chronic renal failure.
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PMID:A case of cor triatriatum with end-stage renal disease: successful management of open heart surgery under hemodialysis, subsequent renal transplantation and pregnancy. 848 11

Primary human hypertension is a polygenic disorder. It is the prevalent cause of cardiovascular disease leading to cardiac failure, stroke, chronic renal failure and, ultimately to death. Several genes are involved in cardiovascular control mechanisms and their genetics are complex. Experimental models which are well defined are needed to clarify the role of individual genes. The generation of the hypertensive transgenic rat line TGR (mREN2)27 bearing the murine Ren-2 gene cloned from the DBA/2J mouse strain provides a monogenic model of hypertension in which the genetic basis (the additional renin gene) is known. These rats develop severe hypertension, which reaches 200 mm Hg and higher at 8 weeks of age in the heterozygous animal. Homozygous rats develop even higher blood pressures than heterozygous animals, which is paralleled by a higher mortality rate in homozygous rats. Animals develop pathomorphologic alterations which are characteristic for systemic hypertension. The transgenic rats are characterized by unchanged or even suppressed concentrations of active renin, angiotensin I (ANG I), ANG II, and angiotensinogen compared to transgene-negative littermates. In contrast, plasma levels of inactive renin (prorenin) are much higher in TGR (mREN)27 rats than in control animals. In the kidneys, renin is suppressed, probably mediated through negative feedback inhibition, in other tissues, especially in the adrenal gland, murine Ren-2 mRNA is expressed at very high levels. The cascade of pathophysiologic events which finally lead to hypertension is not fully understood in this rat model. Treatment with ACE inhibitors or angiotensin II receptor antagonists such as losartan is extremely efficient, which could mean that hypertension in this model is mediated through ANG II. Since the the renin-angiotensin system (RAS) in the kidneys is suppressed, other ANG II generating sites must be considered. This favors the concept of extrarenal RASs in this model.
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PMID:The hypertensive Ren-2 transgenic rat TGR (mREN2)27 in hypertension research. Characteristics and functional aspects. 873 83

The ascites in the chronic renal failure patient is often difficult to treat and becomes intractable. Continuous ambulatory peritoneal dialysis (CAPD), as a maintenance therapy, is effective in the removal of ascites and may become a good alternative in dialysis therapy. The aim of this study was to evaluate the peritoneal membrane transport characteristics and ultrafiltration rate in CAPD patients who had preexisting ascites. Seven CAPD patients (6 male, 1 female; mean age 43 +/- 11 years) were included. The causes of ascites were liver cirrhosis (n = 4), hemodialysis-associated process (n = 2), and heart failure (n = 1). A peritoneal equilibration test (PET) using 2.5% dialysate was performed by the standard method at ten days after starting CAPD. The solute transport rate [dialysate glucose ratio (D/D6) and dialysate-to-plasma creatinine concentration ratio] showed high (n = 5) or high average (n = 2) transport. In 5 patients with high transport, PET showed a discrepancy between solute transport rate and drain volume. In spite of the high transport rate, the drain volume was greater than expected and corresponded to the area of low average or high average solute transport rate. Considering adequate solute clearance and good ultrafiltration, CAPD is an effective treatment in end-stage renal disease patients with intractable ascites.
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PMID:Discrepancy between solute transport rate and drain volume in CAPD patients with ascites. 886 69

ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease. The renal mechanisms underlying the renal adverse effects of ACE inhibitors--intrarenal efferent vasodilation with a consequent fall in filtration pressure--are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to long term renoprotection. The former is suggested by the positive correlation between the fall in filtration fraction and the reduction in proteinuria found during ACE inhibition. The latter is suggested by the correlation between the (slight) reduction in glomerular filtration rate at onset of therapy and a more favourable course of renal function in the long term. Such a fall in filtration rate at the onset of ACE inhibitor treatment is reversible after withdrawal, and can be considered the trade-off for long term renal protection in patients with diabetic and nondiabetic chronic renal disease. In conditions in which glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibition can induce acute renal failure, which is reversible after withdrawal of the drug. Systemic and renal haemodynamic effects of ACE inhibition, both beneficial and adverse, are potentiated by sodium depletion. Consequently, sodium repletion contributes to the restoration of renal function in patients with ACE inhibitor-induced acute renal failure. Our the other hand, co-treatment with diuretics and sodium restriction can improve therapeutic efficacy in patients in whom the therapeutic response of blood pressure or proteinuria is insufficient. Patients at the greatest risk for renal adverse effects (those with heart failure, diabetes mellitus and/or chronic renal failure) also can expect the greatest benefit. Therefore, ACE inhibitors should not be withheld in these patients, but dosages should be carefully titrated, with monitoring of renal function and serum potassium levels.
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PMID:ACE inhibitors and the kidney. A risk-benefit assessment. 887 74

1. Adrenomedullin is a potent vasodilating peptide first isolated from phaeochromocytoma and adrenal medulla but also found in the heart, lungs and kidneys. It may also be a paracrine factor because endothelial and smooth muscle cells synthesize adrenomedullin as well as express the receptors. Adrenomedullin induces vasorelaxation by activating adenylate cyclase and also by stimulating the release of nitric oxide. 2. We have developed a specific radioimmunoassay and measured the immunoreactivity of human adrenomedullin in the plasma of 58 male subjects: eight with essential hypertension, 12 with heart failure, 10 with ascites due to cirrhosis, 12 with chronic renal failure, four with hypoxia due to chronic obstructive pulmonary disease and 12 control subjects. 3. Plasma levels (mean +/- SEM) in patients with essential hypertension (16.3 +/- 1.9 pmol/l), congestive heart failure (17.5 +/- 2.8 pmol/l) and renal failure (17.7 +/- 2.5 pmol/l) were raised compared with control subjects (7.8 +/- 1.4 pmol/l, P < 0.05), confirming previous reports. 4. In addition, we observed that plasma levels of adrenomedullin were significantly raised in patients with ascites due to liver cirrhosis (15.5 +/- 1.9 pmol/l) and chronic obstructive pulmonary disease with hypoxia (20.0 +/- 1.5 pmol/l). 5. We concluded that the plasma level of adrenomedullin is raised in a variety of diseases.
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PMID:Elevated plasma levels of human adrenomedullin in cardiovascular, respiratory, hepatic and renal disorders. 903 92


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