Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
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.
 ...
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.
 ...
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

A cohort of 432 ESRD (261 hemodialysis and 171 peritoneal dialysis) patients was followed prospectively for an average of 41 months. Baseline and annual demographic, clinical and echocardiographic assessments were performed, as well as serial clinical and laboratory tests measured monthly while on dialysis therapy. The average mean arterial blood pressure level during dialysis therapy was 101 +/- 11 mm Hg. After adjusting for age, diabetes and ischemic heart disease, as well as hemoglobin and serum albumin levels measured serially, each 10 mm Hg rise in mean arterial blood pressure was independently associated with: the presence of concentric LV hypertrophy (OR 1.48, P = 0.02), the change in LV mass index (beta = 5.4 g/m2, P = 0.027) and cavity volume (beta = 4.3 ml/m2, P = 0.048) on follow-up echocardiography, the development of de novo cardiac failure (RR 1.44, P = 0.007), and the development of de novo ischemic heart disease (RR 1.39, P = 0.05). The association with LV dilation was of borderline statistical significance (OR 1.48, P = 0.06). Mean arterial blood pressures greater than 106 mm Hg were associated with both echocardiographic and clinical endpoints. Paradoxically, low mean arterial blood pressure (RR 1.36 per 10 mm Hg fall, P = 0.009) was independently associated with mortality. The association of low blood pressure with mortality was a marker for having had cardiac failure prior to death. We conclude that even moderate hypertension worsens the echocardiographic and clinical outcome in ESRD patients, especially in those without previous clinical cardiac disease.
 ...
PMID:Impact of hypertension on cardiomyopathy, morbidity and mortality in end-stage renal disease. 873 Nov 3

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.
 ...
PMID:The hypertensive Ren-2 transgenic rat TGR (mREN2)27 in hypertension research. Characteristics and functional aspects. 873 83

A cohort of 432 ESRD (261 hemodialysis and 171 peritoneal dialysis) patients was followed up prospectively for an average of 41 months. Baseline and annual demographic, clinical, and echocardiographic assessments were performed, as well as serial clinical and laboratory tests measured monthly while patients were on dialysis therapy. Among hemodialysis patients, after adjustment was made for age, diabetes, and ischemic heart disease, as well as hemoglobin and blood pressure levels measured serially, a 10-g/L fall in mean serum albumin level was independently associated with the the development of de novo (relative risk [RR], 2.22; P = 0.001) and recurrent cardiac failure (RR, 3.84; P = 0.003), de novo (RR, 5.29; P = 0.001) and recurrent ischemic heart disease (RR, 4.24; P = 0.005), cardiac mortality (RR, 5.60; P = 0.001), and overall mortality (RR, 4.33; P < 0.001). Among peritoneal dialysis patients, a 10-g/L fall in mean serum albumin level was independently associated with the progression of left ventricular dilation as seen on follow-up echocardiography (beta, 13.4 mL/m2; P = 0.014), the development of de novo cardiac failure (RR, 4.16; P = 0.003), and overall mortality (RR, 2.06; P < 0.001). Hypoalbuminemia, a major adverse prognostic factor in dialysis patients, is strongly associated with cardiac disease.
 ...
PMID:Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. 873 8

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.
 ...
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.
 ...
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.
 ...
PMID:Elevated plasma levels of human adrenomedullin in cardiovascular, respiratory, hepatic and renal disorders. 903 92

Cardiac abnormalities develop during chronic renal failure. The prevalence of ischemic heart disease, cardiac failure, and left ventricular disorders is high among patients initiating end-stage renal disease (ESRD) therapy, and appears to be getting higher. Age, gender, race, diabetes, and possibly geographic location are predictive of the presence of several cardiac conditions. Cardiac morbidity after the initiation of ESRD therapy is high, and cardiac causes are the most common reported cause of death. Cardiac abnormalities present on starting dialysis contribute to this morbidity and mortality. In epidemiological studies, higher cardiac death rates have also been associated with dialysis rather than transplantation as mode of ESRD therapy, peritoneal rather than hemodialysis, lower dose of dialysis, and unmodified cellulose rather than modified cellulose/synthetic hemodialysis membranes.
 ...
PMID:Cardiac disease in chronic uremia: epidemiology. 923 24


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>