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

Heart failure (HF) refractory to conventional therapy is a major and increasing public health and financial problem. Refractory HF is associated with hypervolaemia due to sodium and fluid retention, and azotaemia due to renal hypoperfusion. There is extreme renal salt and water retention and marked secondary hyperaldosteronism. In this state, the kidneys are relatively resistant to diuretic therapy, and the use of very high doses of oral or parenteral diuretics only worsens the renal hypoperfusion, making the patient more azotaemic. A logical treatment for this 'cardiorenal syndrome' is the use of dialysis, which is efficient in treating both the hypervolaemia and azotaemia of refractory HF. Peritoneal dialysis (PD), haemodialysis or continuous veno-venous haemofiltration can and have been used, but the simplest long-term treatment is PD. We present several case reports of the successful use of PD in refractory heart failure. In our opinion, chronic PD is a highly effective mode of treatment for refractory HF, and should be more widely used in this condition.
Nephrol Dial Transplant 2005 Jul
PMID:The role of peritoneal dialysis in the treatment of refractory heart failure. 1602 32

While advances in treatment strategies and pharmacotherapy have produced a dramatic reduction in the mortality of patients with heart failure during the past 15 years, there is still a major challenge to improve patient well being, reduce hospitalizations and reduce mortality further. The prevalence of heart failure is not decreasing, and heart failure is currently a cause for hospitalization in >25% of admissions to internal medicine and cardiology departments. It has recently become apparent that anaemia is present in 20-30% of patients with heart failure, and the severity of anaemia has important implications regarding outcome and prognosis. Anaemia may be due to a number of causes, including iron and vitamin deficiency, insidious blood loss, haemodilution, renal impairment and bone marrow depression with resistance to erythropoietin. In the presence of a damaged heart and often coronary artery disease, anaemia may worsen contractile ability and systolic function, while the necessary volume load and ventricular hypertrophy which accompany anaemia contribute to diastolic dysfunction. Preliminary data show that appropriate treatment of anaemia, based on correction of the underlying cause, with, in most patients, the addition of exogenous erythropoietin and iron therapy, improves ventricular function and clinical status. Treatment of anaemia has opened a new frontier in the management of heart failure. We await the results of ongoing clinical trials for more detailed information regarding appropriate haemoglobin targets, choice of medication and dosing and the degree of improvement that may be expected when the issue of anaemia is properly addressed.
Nephrol Dial Transplant 2005 Jul
PMID:Anaemia and heart failure: statement of the problem. 1602 30

Heart failure (HF) is a common disease associated with poor prognosis. Anaemia is commonly associated with HF due to bone marrow depression, reduced availability of iron and haemodilution, and is sometimes aggravated by too frequent blood testing. Low haemoglobin is very detrimental to the haemodynamic state of the patient with decreased cardiac output as it further diminishes the oxygen supply to the tissues. When anaemia is associated with HF. and renal failure, the patient enters a vicious cycle called cardio renal anaemia syndrome. The prognosis of patients with HF is worse as the haemoglobin is lower and even mild anaemia is associated with <1 year survival. Aggressive correction of the anaemia by subcutaneous injections of erythropoeitin and intravenous iron has been shown to improve the functional capacity and quality of life of patients with cardio renal anaemia syndrome and to reduce the need for hospitalization. However, intravenous iron can be detrimental because of increased formation of free radicals, oxidative stress and risk of infection. The level of haemoglobin needed to be achieved is not clear, but it seems indicated to maintain it above 12 g%.
Nephrol Dial Transplant 2005 Jul
PMID:Anaemia and heart failure: aetiology and treatment. 1602 33

Immunoadsorption (IA) represents an additional therapeutic approach in patients with severe heart failure due to dilated cardiomyopathy (DCM). nt-BNP and nt-ANP plasma levels are prognostic markers in patients with heart failure. The effect of IA on nt-BNP and nt-ANP plasma levels is unknown. In this case control study, 30 patients suffering from severe heart failure (LVEF < 35%) due to DCM were included. In 15 patients, IA was carried out in four courses of monthly intervals until month 3. For analysis of the acute and prolonged effects, the plasma levels of nt-BNP and nt-ANP were determined before and after each IA course. In 15 comparable DCM patients (controls), plasma levels of nt-BNP and nt-ANP were determined at baseline and after 3 months. LVEF remained stable during this study in the control group. In contrast, in the IA group after 3 months, LVEF increased from 29.7 +/- 1 to 38.6 +/- 2%, P < 0.001. In the control group, the nt-BNP and nt-ANP plasma levels remained stable during the 3 months of the study. In the IA group after the first IA course, the level of nt-BNP was acutely reduced from 1501 +/- 328 to 925 +/- 151 fmol/mL, P < 0.01. In addition, the nt-ANP level was reduced from 4439 +/- 1271 to 2897 +/- 825 fmol/mL, P < 0.01. In the IA group, the reduction of these two parameters remained detectable after 3 months before the last course: nt-BNP: 714 +/- 119 fmol/mL, nt-ANP: 2227 +/- 427 fmol/mL, P < 0.05. The improvement of left ventricular function during IA is accompanied by a reduction of nt-BNP and nt-ANP plasma levels in patients with DCM.
Ther Apher Dial 2006 Feb
PMID:Effects of immunoadsorption on the nt-BNP and nt-ANP plasma levels of patients suffering from dilated cardiomyopathy. 1655 35

L-carnitine plays an essential role in the beta-oxidation of fatty acids by catalyzing their transport into the mitochondrial matrix. The kidney maintains plasma free L-carnitine levels in the homeostatic range by selective saturable tubular reabsorption. The preferential retention of free L-carnitine over acyl-L-carnitines by the kidney is lost in patients with end-stage renal disease (ESRD). Loss of renal parenchyma as a site of carnitine synthesis, as well as nonselective clearance of L-carnitine by the dialysis procedure lead to dialysis-related carnitine deficiency. Numerous studies investigating whether L-carnitine supplementation will alleviate several dialysis-related symptoms, such as intradialytic hypotension, heart failure, muscle weakness, low exercise capacity, and anemia, have reported conflicting results. Many of these studies suffer from a lack of randomization and control groups, heterogeneity in the administration of L-carnitine, and nonstandardized measures of symptom improvement. More data exist to support the use of L-carnitine in selected anemic dialysis patients with very large erythropoietin requirements in whom extensive examination for reversible causes of anemia was unrevealing.
Semin Dial
PMID:Dialysis-related carnitine disorder. 1689 11

The current understanding of dialysis-related amyloidosis has evolved over the past two decades. In the early 1980s, several researchers found amyloid deposits in the synovia of carpal tunnel syndrome (CTS), which have been recognized as a complication of chronic hemodialysis. The enigma was resolved in 1985, when beta2-microglobulin (beta2-m) with a molecular weight of 12,000 Da was identified as the major constitutional protein of this amyloid. Amyloid fibrils of this type that contain the sub-unit protein of human leukocyte antigens (HLA), beta2-m, deposit predominantly in osteoarticular tissues, inducing musculoskeletal symptoms such as CTS, polyarthralgia, bone cyst showing radiolucency at X-ray examination and destructive spondyloarthropathy. In addition, extra articular symptoms such as ischemic colitis, megaloglossia, and heart failure, that is, systemic involvement occasionally occur. We confirmed that the prevalence of CTS increases with duration of dialysis. Most patients with CTS associated with beta2-m amyloid deposits have undergone hemodialysis for 10 years or more. Up to 50% of patients had developed this complication after 20 years and the percentage was even higher after 25 years. General categories of therapeutic approaches for amyloidosis include prevention of onset or progression, symptomatic therapy (conservative treatment, orthopedic procedures, and physiotherapy), and renal transplantation. It is critical to elucidate the detail mechanisms of the amyloid fibril formation, and establish its radical treatment. It is also important to develop novel therapies such as cell implantation to compensate for normal kidney functions of uremic toxin protein metabolism.
Ther Apher Dial 2006 Aug
PMID:Current clinical aspects of dialysis-related amyloidosis in chronic dialysis patients. 1691 Nov 83

Not uncommonly, hemodialysis patients with normal results in myocardial perfusion tests can still have a cardiac event within 2 years of evaluation. We examined possible risk factors for progression of coronary atherosclerosis in hemodialysis patients. We prospectively evaluated ability of myocardial perfusion imaging carried out under pharmacologic stress to predict 2-year outcomes in 77 hemodialysis patients, specifically thallium-201 single-photon emission computed tomography (SPECT) using high-dose adenosine triphosphate as the stressor. The primary end-point was a cardiac event (cardiac death, non-fatal acute coronary syndrome, or hospitalization for acute ischemic heart failure). Factors independently influencing duration until a cardiac event in hemodialysis patients were identified using stepwise multiple regression analysis. Myocardial perfusion defects were shown in 36 patients. Patients with a perfusion defect were more likely to have cardiac events than those with normal perfusion (78% vs. 15%, P < 0.001). Time until occurrence of a cardiac event in hemodialysis patients showed a significant, independent association with known coronary artery disease [regression coefficient (RC) = -3.391, P = 0.046], elevated C-reactive protein (RC = -5.813, P = 0.005), and a reversible myocardial perfusion defect (RC = -7.386, P < 0.001). An analysis based on the 'best cut-off' of CRP as identified on the basis of the ROC curve augmented the positive and negative predict value of CRP for the prediction of coronary events to 65 and 74%, respectively. Myocardial perfusion SPECT and measuring the plasma concentration of CRP might be useful for the prediction of hemodialysis patients with progression of coronary atherosclerosis.
Ther Apher Dial 2006 Aug
PMID:Independent risk factors for progression of coronary atherosclerosis in hemodialysis patients. 1749 9

Arteriovenous fistulas (AVFs) are the preferred type of vascular access, but relatively little is known regarding their effects on cardiovascular remodeling and cardiac function. The following is a review regarding the immediate and long-term complications associated with AVF creation, including the development of left ventricular hypertrophy, high-output cardiac failure, exacerbation of coronary ischemia, and the possible contribution to the development of central vein stenosis.
Semin Dial
PMID:The cardiovascular effects of arteriovenous fistulas in chronic kidney disease: a cause for concern? 1697 Jul 29

Although the use of continuous ambulatory peritoneal dialysis (CAPD) to treat refractory heart failure is not new, in combination with current medical treatment it improves patients'symptoms as well as their cardiac function. We started 16 patients (13 men with a mean age of 66.3 +/- 2.8 years, and 3 women with a mean age of 72 +/- 4.2 years) on CAPD. All patients were symptomatic with congestive heart failure. Mean left ventricular ejection fraction (LVEF) before the start of CAPD was 31% +/- 3%. Introduction to CAPD was associated with a significant improvement in LVEF (to 44% +/- 6%, p < 0.05) and in blood pressure control at 1 year. Also at 1 year, 87% of patients were classified as New York Heart Association grade I or II (maximum possible grade is grade III). These results suggest that CAPD is a treatment of choice for patients suffering from a combination of congestive heart failure and chronic renal insufficiency.
Adv Perit Dial 2006
PMID:Continuous ambulatory peritoneal dialysis is effective for patients with severe congestive heart failure. 1698 58

Premature cardiovascular disease is the leading cause of morbidity and mortality in patients with end-stage renal failure. Natriuretic peptides, specifically brain natriuretic peptide, are released from the heart in response to chamber distension and thus increased in the presence of volume expansion and cardiac overload. Their physiological role is to cause vasodilatation and promote natriuresis to maintain volume homeostasis. Increasingly serum levels of brain natriuretic peptide are used to both diagnose and manage cardiovascular disorders. Furthermore, augmenting the beneficial hemodynamic actions of brain natriuretic peptide may have a therapeutic role in decompensated heart failure. However, the diagnostic role of serum brain natriuretic peptide levels in patients with advanced renal dysfunction remains to be defined. These patients have a high prevalence of left ventricular disorders, specifically left ventricular hypertrophy, which may reduce the diagnostic utility of brain natriuretic peptide. In addition, ventricular stretch may be determined by intravascular volume status rather than by cardiac dysfunction. Nonetheless, as the prognosis of patients with end-stage renal failure and co-existing heart failure is so poor, the availability of a further marker of cardiac ''distress'' may in the future become a useful diagnostic tool and in due course may become a primary goal for titration and tailoring of therapy.
Semin Dial
PMID:Diagnostic, prognostic, and therapeutic implications of brain natriuretic peptide in dialysis and nondialysis-dependent chronic renal failure. 1724 21


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