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

Hypertension has a high prevalence among elderly patients. Randomised trials have already demonstrated that treating healthy older persons with hypertension is highly efficacious. Nevertheless some questions have arisen. On the one hand the generalizability of these trial results, particularly for older persons with serious medical comorbidities and poor functional status, is not clear. On the other hand different antihypertensive drugs have shown to be effective. Which drug for which patient? Even data from randomised intervention trials showing that the treatment affects cardiovascular morbidity and mortality, were missing, ACE inhibitors have been used for more than a decade to treat high blood pressure. For a younger population the captopril prevention project showed no differences between ACE inhibitors and conventional antihypertensive treatment (diuretics, beta-blocker) concerning the primary endpoints (myocardial infarction, stroke and other cardiovascular death). The STOP-2 study also confirmed these results for elderly patients. When treating elderly patients one must be aware of physiological changes with age and the comorbidities. Of significance among this patient group is declining renal function. Admissions for uraemia that are related to the use of ACE inhibitors are still commonplace, although many cases are preventable by monitoring renal function, but guidelines are still missing. Concerning the comorbidities ACE inhibitors have benefits compared to other antihypertensive drugs, especially in cases of heart failure, diabetes and coronary heart disease.
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PMID:The role of ACE inhibitors in the treatment of hypertensive elderly patients. 1120 Oct 13

Many clinical aspects associated with chronic uraemia and long-term dialysis therapy may determine both the qualification for renal transplantation and post-transplant outcome. These include dialysis access, severe hyperparathyroidism, inadequate or excessive erythropoietin production, heart failure, viral hepatitis, defects of urinary tract and malnutrition. Some of them delay the qualification for transplant, the other on contrary make the need for transplantation very urgent. Selected aspects are discussed in this paper.
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PMID:[Patients on dialysis as renal graft recipients]. 1143 86

Urea transporters have been cloned from kidney medulla (UT-A) and erythrocytes (UT-B). We determined whether UT-A proteins could be detected in heart and whether their abundance was altered by uremia or hypertension or in human heart failure. In normal rat heart, bands were detected at 56, 51, and 39 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa proteins were unchanged. We also detected UT-A2 mRNA in hearts from control and uremic rats. Because uremia is accompanied by hypertension, the effects of hypertension per se were studied in uninephrectomized deoxycorticosterone acetate salt-treated rats, where the abundance of the 56-kDa protein increased 2-fold versus controls, and in angiotensin II-infused rats, where the abundance of the 56 kDa protein increased 1.8-fold versus controls. The 51- and 39-kDa proteins were unchanged in both hypertensive models. In human left ventricle myocardium, UT-A proteins were detected at 97, 56, and 51 kDa. In failing left ventricle (taken at transplant, New York Heart Association class IV), the abundance of the 56-kDa protein increased 1.4-fold, and the 51-kDa protein increased 4.3-fold versus nonfailing left ventricle (donor hearts). We conclude that (1) multiple UT-A proteins are detected in rat and human heart; (2) the 56-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat results can be extended to human heart, where 56- and 51-kDa proteins are increased during heart failure.
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PMID:UT-A urea transporter protein in heart: increased abundance during uremia, hypertension, and heart failure. 1146 20

Patients on maintenance hemodialysis therapy for end-stage renal disease have reduced exercise tolerance. Multiple processes related to uremia and hemodialysis have been implicated in the pathophysiology of this impairment. However, limited data are available to identify the separate and combined effects of clinical factors on the degree of impairment for individuals within this population. For this purpose, data from 193 patients who had undergone exercise testing for two clinical trials were retrospectively analyzed. Univariate and multiple linear regression analyses were used to identify demographic and clinical correlates of peak exercise oxygen uptake (VO2). Peak VO2 averaged 18.5 +/- 6.4 mL/min/kg. On univariate analysis, peak VO2 correlated positively with male sex and hemoglobin, serum albumin, and serum creatinine concentrations and correlated negatively with dialytic age and diagnosis of diabetes or chronic heart failure. In a multiple linear regression model, sex, hemoglobin concentration, age, and diagnosis of diabetes each remained statistically significant. Together, factors included in the model accounted for 41% of the variability in peak VO2 (P = 0.0001). Among factors not correlating significantly with peak VO2 were resting blood pressure, serum carnitine level, and urea clearance assessed by Kt/V. Findings show the range of exercise impairment among clinically stable ambulatory hemodialysis patients, which may be sufficient to interfere with normal daily activities for many of these patients. Although this impairment may be broadly attributable to physiological consequences of uremia, the degree of impairment for individual patients is predicted by demographic factors, coexistent disease, and factors potentially modified by medical therapeutics.
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PMID:Clinical and demographic predictors of exercise capacity in end-stage renal disease. 1177 5

The body's vasculature plays a critical role in the development of functional and structural alterations responsible for tissue and organ damage in laboratory animals and human subjects during illness and senescence, and in response to stress. Components of the vasculature, namely, major arteries such as the aorta, smaller arteries, arterioles, capillaries, post-capillary venules, and collecting central veins, all serve as conduits through which vital substrates are delivered to cellular masses and/or waste products are removed. A number of physical and neurohumoral agents known to be responsive to stress stimuli exert functional control over the vasculature. Both physical and emotional stress have been found to cause significant hemodynamic alterations. Large artery rigidity, for instance, develops rapidly following stress-induced activation of the autonomic nervous system. Associated with this process is increased release into the circulation of catecholamines and angiotensin-II. At the same time, insulin resistance develops, accompanied by nitric oxide release and changes in the immune system. The response of large arterial conduits to stress is characterized by increased pulse pressure, which in turn affects the endothelium of the arterial vessels responsible for determining total peripheral resistance. Microcirculation networks, where a large fraction of the blood volume is contained, are affected as well, and the blood in them is subject to redistribution into adjacent interstitial fluid compartments. Changes in endothelial permeability, secondary to variations in pulse pressure, can lead to interstitial edema and changes in the physicochemical properties of interstitial compartments. These changes give rise to alterations in the traffic of substrates and waste products between blood and cells. This sequence of events also takes place in the vasa vasorum microcirculation that nourishes large arteries, and likely contributes to remodeling of the vascular wall and to atherogenesis. The contribution of large artery rigidity to the morbidity and mortality associated with arterial hypertension, diabetes mellitus, heart failure, and terminal uremia, is relatively well established in human populations. In addition, it appears that aortic rigidity precedes the development of arterial hypertension in the spontaneously hypertensive rat (SHR) model, as well as in individuals with borderline hypertension. The fact that some of the functional and structural vascular alterations produced by stress are reversible reinforces the importance of developing behavioral techniques and pharmacologic agents that can successfully interrupt this pathological sequence of events.
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PMID:Vascular response to stress in health and disease. 1204 May 37

Among the uremia-associated risk factor, which can be influenced today, anemia is considered most relevant because it induces functional and organic alterations of cardiac/circulatory function. Research concerning influence of the anemia on the pulmonary hemodynamic and cardiac output (CO) in pre-uremic patients are not available up to now. Cardiac and circulatory function of 52 patients were examined before initiation of dialysis therapy using a Swan-Ganz thermodilution catheter. After excluding patients with impaired cardiac pump function the results of 31 of the 52 patients could be analyzed. They were divided into two groups (Hb > resp. < 7.0 g/dl): in patients with severe anemia (Hb 5.7 +/- 0.6 g/dl; n = 7) cardiac index was higher (4.8 +/- 0.4 1/min/m2 < 0.01) compared with the other group (Hb 9.8 +/- 1.7 g/dl; n = 24; CI 3.9 +/- 1.1 1min/m2). The increase of cardiac index caused by anemia correlated with increased stroke volume and heart rate and lowered pulmonary and peripheral resistance. Patients with severe anemia showed a tendency to an impaired cardiac index below Hb < 5-6 g/dl. The hypercirculation did not cause an increase of the pulmonary arterial and pulmonary wedge pressure. Particularly in the case of already existing myocardial damage and coronary arteriosclerosis the presence of anemia and renal insufficiency leads to a highly increased morbidity and mortality. This "cardio-renal anemia-syndrom" is responsible for frequent refractory heart failure. Disturbances of cardiac/circulatory function are observed in pre-uremic patients three times more frequently than in patients after myocardial infarction. Early correction of anemia seems to reduce the risk of fatal cardial complications and to improve the quality of life and the prognosis of pre-uremic patients.
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PMID:Renal anemia and its hemodynamic response--findings invasively determined over a period of 20 years. 1222 27

Cardiovascular disease is virtually a sine qua non of chronic kidney disease, as is poor quality of life. Dialysis patient for example, have cardiovascular death rates 10 - 20 times those of the general population. Recent estimates indicate that at least half of all patients starting dialysis therapy will have an admission for a major cardiovascular event within 5 years, of which cardiac failure is the most common. Both experimental and clinical studies suggest that the cardiovascular system in uremia is in a state of premature senescence, one which is poorly suited to the supraphysiological hemodynamic demands to which it is subjected. Most patients develop cardiomyopathy, which clearly predisposes to cardiac decompensation. Anemia and hypertension are the most obvious modifiable overload parameters in uremic patients. Several prospective observational studies have demonstrated anemia to be an independent risk factor for each step in the process leading from hemodynamic overload, through maladpative left ventricular enlargement to left ventricular failure and death. This process starts with declining renal function, long before end-stage renal disease, the traditional time at which intervention has started to be seriously considered. The case for normal hemoglobin in patients with chronic kidney disease is still greatly disputed. Observational studies, which examine left ventricular size, quality of life, functional status, hospitalization and survival, are overwhelmingly supportive. Intervention trials, to date, suggest clear benefits of a physiological approach to anemia management in terms of quality of life, and likely benefits in terms of left ventricular stress minimisation and associated remodelling. Whether these translate into a reduction in outcomes like cardiac failure or death remains an unanswered question.
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PMID:Should hemoglobin be normalized in uremic patients? 1222 28

Regression of left ventricular hypertrophy in hemodialysis patients is possible. Left ventricular hypertrophy represents the major risk factor for cardiac morbidity and mortality. Therefore, their regression is mandatory. Since the causes of uremia-associated left ventricular hypertrophy are multifactorial, various therapeutic options can be considered: optimal control of arterial hypertension and volume status, optimal correction of metabolic acidosis, best possible correction of hypoalbuminemia and severe secondary hyperparathyroidism, modern pharmacotherapeutic strategy for the treatment of heart failure (use of angiotensin-converting enzyme inhibitors in combination with angiotensin II receptor blockers and beta-blockers) and total correction of renal anemia. Following the proposed therapeutic strategies we could, by using echocardiography, distinguish in 100 hemodialysis patients the following 3 groups (on the average after 1.5 years): 36 patients with initially normal left ventricular mass index (LVMI (g/m2), F < 110; M < 130) maintained normal (group 1); in 31 patients with moderately increased LVMI full regression resulted (group 2); 33 patients with severely increased LVMI (group 3) had to be further divided into 2 sub-groups: 22 patients with significant improvement of LVMI, 11 patients with no, regression. For the first time we were able to show that it is possible to maintain initially normal LVMI during long-term treatment and to achieve complete regression and significant improvement of LVMI in our patients. However, since LVMI requires a long time to develop, a similarly long time must be estimated for its regression. However, 11 patients remained therapeutically resistant. In this group, severe heart diseases were often combined and highly prevalent, including ischemic heart and valve diseases and end-stage dilatative cardiomyopathy. These patients had to be transferred to cardiac surgery. Anemia is considered to be one of the most important factors for the development of left ventricular hypertrophy. Therefore, total correction of renal anemia has to be strongly recommended in addition to other measures of our therapeutic strategy to maintain full or significant regression of left ventricular hypertrophy.
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PMID:Regression of left ventricular hypertrophy in hemodialysis patients is possible. 1222 31

Without intervention, premature cardiovascular disease is virtually certain in progressive chronic kidney disease (CKD). Whatever age the patient, the cardiovascular system in uraemia is senescent and poorly suited to dealing with supraphysiological haemodynamic demands. Anaemia and hypertension are the principal haemodynamic risk factors that can be treated. Many observational studies have shown that anaemia is a risk factor for haemodynamic overload, maladaptive left ventricular growth, left ventricular failure and death. The justification for normal target haemoglobin (Hb) in patients with CKD is still debated. Observational studies of left ventricular size, quality of life, functional status, hospital admission, and survival support higher Hb concentrations (> or =12 g/dl). Intervention trials to date suggest that a physiological approach to anaemia management benefits quality of life, and possibly left ventricular hypertrophy and dilatation. Obviously, avoiding anaemia is the only way to minimize time-averaged, anaemia-related haemodynamic load. Whether this strategy, involving efficient surveillance, early detection, early intervention, and high Hb targets that are independent of the phase of CKD, actually reduces cardiac failure or death remains to be seen.
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PMID:Anaemia: cardiovascular adaptations and maladaptive responses in chronic kidney disease. 1238 55

Though sudden cardiac death accounts for as much as 15% of all cause mortality in uremia, reports concerning advanced A-V block, requiring permanent cardiac pacing in end-stage renal disease (ESRD) hemodialysed (HD) patients are very few. This is the first long term prospective study reporting on systematic permanent pacemaker implantation, in a cohort of ESRD patients from a single HD unit. Between 01/06/1997 and 30/12/2001, 396 pacemakers were inserted for advanced, symptomatic A-V block in our institution, including 5 in ESRD, HD patients (M/F--4/1, age 47-73, M +/- SD--61 +/- 12 years) from a single dialysis center, treating 137 patients during the study period. Thus, the incidence and prevalence of A-V defects treated by permanent pacing in uremic patients was 0.81% and 3.65% respectively. Conversely, the incidence and prevalence of ESRD treated by hemodialysis, among patients with advanced A-V conduction disturbances, requiring permanent pacing were 0.28% and 1.26%. Mitral valve calcifications were present in all patients; 3 subjects also had extensive aortic valve calcifications. Left ventricular hypertrophy (echocardiographic Framingham criteria) was present in 4 patients, but the systolic function (ejection fraction and fractional shortening index) was normal in all cases, although a clinical picture of chronic heart failure was seen in 3 subjects preoperatively. A-V conduction defects were attributed to extensive metastatic calcifications, involving the cardiac squeleton, consecutive to severe hyperparathyroidism and inadvertent use of calcitriol and calcium carbonate as phosphate binders. No technical difficulties, short or long-term complications related to pacemaker implantation (4 VVI and 1 VVD devices) were encountered. Acute threshold and sensing values were similar with those of non-uremic patients. During follow-up, one patients died from a non cardiac death. If optimal hemodialysis is provided, benefits of permanent pacing are equal in uremic or non uremic patients and pacemaker implantation should be instituted as a prompt life-saving method in all dialysis patients with chronic symptomatic advanced A-V blocks.
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PMID:[Permanent cardiac pacing for chronic symptomatic atrioventricular block in uremic hemodialysed patients. A prospective study]. 1263 71


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