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

The indices of cardiac performances were compared between 31 continuous ambulatory peritoneal dialysis (CAPD) and 20 long-term hemodialysis (HD) patients. They were subdivided into three groups according to dialysis duration: L-CAPD (n = 16, mean age and CAPD duration were, respectively, 53 +/- 8 [SD] years and 77 +/- 13 months); S-CAPD (n = 15; 52 +/- 12 years, 28 +/- 12 months); HD (n = 20; 51 +/- 10 years, 162 +/- 52 months). The diabetic HD patients (DM-HD; n = 13; 60 +/- 13 years of age, 22 +/- 11 months) were chosen separately. Thirteen normotensive subjects with normal kidney function (mean age, 57 +/- 9 years) were selected as an age-matched control group. There were no significant differences between groups in age, gender, incidence of original kidney disease, or serum biochemical data. The blood pressure and the cardiothoracic ratio in L-CAPD were highest among groups. The indices of left ventricular (LV) hypertrophy as well as LV performance by means of echocardiography or pulsed Doppler were compared. Among nondiabetic dialysis patients, the calculated LV mass index (LVMI) of 166.4 +/- 84.3 g/m2 and the ratio of the peak atrial filling velocity to the peak diastolic flow velocity of 1.25 +/- 0.4 in L-CAPD were greatest, and the left ventricular fractional shortening (%FS) of 34.2 +/- 10.8% in L-CAPD was smallest. LVMI or %FS of L-CAPD was the same as DM-HD of 161.0 +/- 40.7 g/m2 or 31.6 +/- 8.2%. Possibly, poor control of hypervolemia, which is caused by peritoneal problems induced by either peritonitis or chronic exposure to high-glucose dialysate, causes a substantial cardiac preload leading to incipient cardiac failure in L-CAPD. According to the similar results of L-CAPD and DM-HD, it may be that hypertension, hyperlipidemia, or long-term constant glucose loading of CAPD fluids in addition to impaired glucose tolerance by chronic renal failure is more or less related to the progression of LV hypertrophy and latent cardiac dysfunction in long-term CAPD patients. In this context, CAPD of more than 5 years' duration is disadvantageous for preserving cardiac function as compared with HD.
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PMID:Disadvantage of long-term CAPD for preserving cardiac performance: an echocardiographic study. 974 Jan 66

In advanced congestive heart failure with fluid retention, extracorporeal ultrafiltration (UF) causes persistent relief of edema or anasarca through hemodynamic and humoral changes that interrupt refractoriness to diuretics. The intra and extravascular fluid partition in congestive heart failure, as well as changes occurring in the two compartments following fluid withdrawal with UF, are unknown. In 8 congestive heart failure patients with severe fluid retention undergoing UF, we measured total (TBV), intrathoracic (ITBV) and pulmonary blood volumes (PBV), and extravascular lung water (EVLW). The intra and extravascular volumes were evaluated by a fiberoptic thermal dye dilution monitoring system, before, at the end of UF (3697 +/- 699 ml) and 24 hours later. Baseline data were compared with those of 10 subjects without heart failure undergoing coronary bypass surgery. In congestive heart failure patients, as compared with controls, TBV was normal, the intrathoracic blood content (ITBV, PBV and PBV/TBV ratio) was increased and EVLW was normal. UF did not induce significant changes in TBV and in EVLW, and reduced ITBV, PBV and PBV/TBV ratio, suggesting that a shift of fluid from the intra to the extrathoracic intravascular compartment occurred. Because both TBV and EVLW were not affected by the procedure, the largest proportion of fluid removed by UF derived from the systemic extravascular space. Both pulmonary wedge and right atrial pressures significantly decreased after UF, and cardiac output increased. In conclusion, congestive heart failure is associated with normal TBV and EVLW content and with intravascular intrathoracic hypervolemia and extrathoracic hypovolemia. UF induces hemodynamic improvement through a selective fluid removal from the extravascular systemic space without changes in both TBV and EVLW.
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PMID:[Intra- and extravascular volumes in congestive heart failure and their redistribution following extracorporeal ultrafiltration]. 992 85

Vasopasm is a dreadful complication of SAH associated with an important mortality and morbidity. Therapy begins with adequate monitoring and lines, and prevention of secondary brain injuries. 3-H therapy (hypervolemia--hypertension--hemodilution--hyperdynamism) aims to increase perfusion in ischemia areas. 3-H therapy is associated with systemic complication precluding it's prophylactic use. Calcium antagonists, in particular nimodipine, improve outcome and parenteral route is better than oral administration. Tirilazad seems to improve outcome of severe grades. Numerous experiments are performed with drugs interfering with the biochemical cascade leading to vasospasm, but up to today no drug is used in current clinical practice. Intraaortic balloon is still considered as experimental and may have a role in patients presenting with concomitant cardiac failure. Invasive radiology must be considered in vasospasm not improving with standard therapies. Vasopasm is a dire complication after SAH. Support and specific therapies allow a 3-fold reduction in morbidity associated with vasospasm. Vasospasm is a vital emergency, and intervention has to be quick and aggressive.
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PMID:[Vasospasm treatment in intensive care]. 1085 75

Congestive heart failure causes substantial morbidity and mortality. Symptoms and physical findings can help in diagnosis, but have limited sensitivity and specificity. Objective measurement of ventricular function is essential in virtually all patients in whom heart failure is suspected; reversible causes of heart failure must be sought. Out-patient management includes education and counseling, emphasis on and assessment of compliance with diet, and pharmacological treatment. Angiotensin-converting enzyme inhibitors are the mainstay of treatment but are underused, and maximal doses are not given, apparently because of concern about side-effects. Diuretics should be administered only as needed to manage fluid overload. Calcium channel blockers are relatively contraindicated in patients with impaired ventricular function. Patient follow-up should be guided by results of the medical history and physical examination. Routine serial testing of ventricular function and exercise performance is discouraged.
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PMID:[Diagnosis and treatment of heart failure within the community]. 1091 71

Heart failure is an increasingly common and costly chronic disorder, with a rising prevalence of at least 2% in populations over the age of 45 years, mortality rates that are as poor as common solid cancers, and very high health care utilisation costs. Despite increased evidence supporting a range of effective interventions, predominantly therapeutic, there remain significant degrees of physician underperformance in terms of heart failure diagnosis and management. Until the early 1990s, the management of heart failure was largely confined to the symptomatic relief of patients with well established heart failure in fluid overload. The introduction of angiotensin-converting enzyme (ACE) inhibitors provided the first treatments that beneficially altered the prognosis of patients with the most common expression of heart failure, namely established systolic dysfunction, whether symptomatic or asymptomatic. Evidence has now extended these benefits to delaying progression of heart failure and reducing hospitalisation. Much of our understanding of the pathophysiology of heart failure stems from these studies. More recent data has clarified the limited role of digoxin, the important benefits of beta-blockade and aldosterone blockers as adjuvants to ACE inhibition, and the emerging evidence on angiotensin II antagonists. There are, in contrast to these positive findings, reliable data from Europe and North America revealing significant underperformance of primary care and hospital physicians in heart failure diagnosis and management, with evidence of underuse and underdosing of evidence-based therapies. Limited qualitative data suggest the reasons for this underperformance are complex and relate to lack of access to objective testing of ventricular function and exaggerated concerns over treatment risks and side-effects. Heart failure represents a complex cluster of aetiologies and risks that are not easy to correctly identify, even in specialist settings. Since there is now powerful evidence on how heart failure can be modified and improved, explicit guidance is needed for which suspected patients should be referred, for confirmation of diagnosis and advice on appropriate treatment regimes, and for which patients can be handled mainly within primary care but with enhanced access to objective non-invasive tests to improve diagnostic reliability and to stratify patients to evidence-based therapies. Current evidence suggests that in North America and Europe today primary care physicians do underperform in their management of patients with heart failure, often owing to factors outside of their immediate control.
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PMID:Management of heart failure: evidence versus practice. Does current prescribing provide optimal treatment for heart failure patients? 1105 Jul 92

The management of heart failure has evolved in parallel with advances in the understanding of the disease process. Inotropes and diuretics are used to combat pump failure and fluid overload. While no convincing data has emerged regarding the long-term safety of inotropes, new exciting data concerning the role of diuretics, especially aldactone, has led to a renewed interest in this class of drug therapy. Angiotensin converting enzyme inhibitors (ACE inhibitors) were noted to not only affect symptomatology but also decrease mortality by interfering with the renin-angiotensin-aldosterone system. Recent research has focused on more complete blockade of the renin-angiotensin system than that achieved with ACE inhibitors alone with the addition of direct angiotensin II receptor blockers. This new class of drugs may become not only a reasonable alternative to ACE inhibitors in patients intolerant of the drug but also a possible addition to ACE inhibitors in the battle to prevent progression of remodelling and disease. beta-blockers are the most exciting new class of drugs used to combat heart failure. They appear not only to combat the remodelling process that occurs in the progression of disease but also other pathological events such as apoptosis and cellular oxidation. New medical therapies currently being investigated include novel agents such as endothelin antagonists, natriuretic peptides, vasopressin antagonists and anticytokine agents--all part of a new era in drug management of heart failure that has evolved with continued advances in the understanding of chronic heart failure (CHF).
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PMID:New advances in the pharmacological management of chronic heart failure. 1124 47

Fluid imbalance can arise due to hypovolemia, normovolemia with maldistribution of fluid, and hypervolemia. Trauma is among the most frequent causes of hypovolemia, with its often profuse attendant blood loss. Another common cause is dehydration, which primarily entails loss of plasma rather than whole blood. The consequences of hypovolemia include reduction in circulating blood volume, lower venous return and, in profound cases, arterial hypotension. Myocardial failure may result from increased myocardial oxygen demand in conjunction with reduced tissue perfusion. Finally, anaerobic metabolism due to reduced perfusion may produce acidosis and, together with myocardial dysfunction, precipitate multi-organ failure. The splanchnic organs are particularly susceptible to the deleterious effects of hypotension and hypovolemic shock, and these effects, depending upon their duration and severity, may be irreversible despite restoration of normovolemia by fluid administration. Patient monitoring in the intensive care unit typically relies upon central venous pressure devices, whereas the primary focus in the operating theater is blood volume deficit estimated from suction devices. However, estimates of intraoperative blood loss can be inaccurate, potentially leading to inappropriate fluid management. Normovolemia with maldistribution of fluid can be encountered in shock-specific microcirculatory disorders secondary to hypovolemia, as well as pain and stress. Consequent vasoconstriction and reduced tissue driving pressure, as well as leukocyte and platelet adhesion, and liberation of humoral and cellular mediators, may impair or abolish blood flow in certain areas. The localized perfusion deficit may contribute to multi-organ failure. Choice of resuscitation fluid may be important in this context, since some evidence suggests that at least certain colloids might be helpful in diminishing post-ischemic microvascular leukocyte adherence. Excessive volume administration may lead to fluid overload and associated impairment of pulmonary function. However, entry of fluid into the lungs may also be facilitated by increased vascular permeability in certain pathologic conditions, especially sepsis and endotoxemia, even in the absence of substantially rising hydrostatic pressure. Another condition associated with elevated vascular permeability is systemic capillary leak syndrome. The chief goal of fluid management, based upon current understanding of the pathophysiology of fluid imbalance, should be to ensure adequate oxygen delivery by optimizing blood oxygenation, perfusion pressure, and circulating volume.
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PMID:Pathophysiology of fluid imbalance. 1125 92

Normal physiological changes in the cardiovascular system in pregnancy such as increase in cardiac output, vasodilatation and hypervolemia are of clinical relevance as they are able to aggravate, mask or even imitate cardiovascular diseases. There is an increase of cardiac size and volume during pregnancy; furthermore hormonal changes lead to diaphragmatic elevation and barrel-shaped thorax followed by a rotation of the cardiac axis to the left (15 degrees-30 degrees). Cardiac topography and size, changes in cardiac functioning and physiology as well as hemodynamic changes lead to auscultatory and ECG changes (i.e. S1-Q3-type, ST-depression, T wave flattening). In addition there is a high incidence of functional systolic and diastolic sounds during pregnancy, which are also able to imitate cardiovascular diseases. The physiological changes in pregnancy are similar to those under heavy exercise. This results in continuous cardiac stress during the whole pregnancy. This stress is specifically high from the 28th to the 34th week of pregnancy and in the post-partum period; the maximum of cardiac stress is reached during labor. Important for the specific cardiac risk during pregnancy is not the type of heart disease but cardiac functioning and the severity of complaints before pregnancy. Principally it has to be expected that preexisting heart diseases will experience an aggravation of one grade according to NYHA during pregnancy. In cases of heart diseases with shunt defects, with shunt defect and injured myocardium, with continuous arrhythmia or atrial fibrillation, patients are at extremely high risk of cardiac death. A termination of pregnancy should be considered in all patients with heart diseases grade III or IV according to NYHA, severe pulmonary hypertension, Eisenmenger's syndrome, severe aortic or pulmonary stenosis, Marfan's syndrome, and severe continuous cardiac insufficiency. The drug therapy of cardiac diseases during pregnancy depends on the specific type of heart disease. Prescription of most drugs is principally possible during pregnancy and breast feeding. However, for most drugs there is only very limited therapeutic experience during this period. Definitively contraindicated during pregnancy and breast feeding are ACE inhibitors, angiotensin I and II blocking agents, vasopeptidase inhibitors and molsidomin, a NO-prodrug. In life-threatening conditions, however, sometimes it will be necessary to administer drugs with only poor experiences in pregnancy.
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PMID:[Risks of pharmacotherapy in heart diseases in pregnancy]. 1137 45

Plasma volume, the intravascular portion of the extracellular fluid volume, can be measured using standard dilution techniques with radiolabeled tracer molecules. In healthy persons, plasma volume remains relatively constant as a result of tight regulation by the complex interaction between neurohormonal systems involved in sodium and water homeostasis. Although chronic heart failure (CHF) is characterized by activation of many of these neurohormonal systems, few studies have evaluated plasma volume in this condition under treatment. Untreated edematous decompensated heart failure (HF) is associated with a significant expansion of plasma volume. Patients with stable CHF, receiving conventional therapy, appear to have a contracted plasma volume, a concept that is in contrast to the widely held belief that CHF is associated with long-term hypervolemia. It is likely that significant changes in plasma volume occur during intensification of medical therapy or during transition from the edematous to the stable state. Clinical assessment of plasma volume may be of particular value during treatment in patients with decompensated HF, in whom the plasma volume is contracted despite an increase in total extracellular fluid volume. Under these circumstances, treatment with inotropes or renal vasodilators may be more appropriate than intravenous diuretics alone. Further studies evaluating plasma volume in HF may help to improve our understanding of the pathophysiologic mechanisms occurring in the development and progression of this complex condition.
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PMID:The regulation and measurement of plasma volume in heart failure. 1208 86

Edema is an adverse event associated with thiazolidinedione therapy The potential for mild-to-moderate peripheral edema with thiazolidinedione is known, especially in patients who have heart failure or use insulin. Our experience reveals that patients who do not have heart failure or do not use insulin also can develop moderate-to-severe edema that necessitates discontinuation of the thiazolidinedione. A 77-year-old man developed ankle, hand, and facial swelling 2 weeks after starting rosiglitazone. After discontinuing the drug, his edema resolved. A 75-year-old man developed bilateral lower leg edema 6 months after switching from troglitazone to pioglitazone. He was hospitalized for 51 days and, after aggressive diuresis and discontinuation of pioglitazone, was discharged with a weight loss of 30 pounds. A 53-year-old man developed lower leg edema 4 weeks after rosiglitazone was increased from 4 mg once/day to 4 mg twice/day. Rosiglitazone was discontinued and the edema resolved. Until the mechanism of action responsible for fluid overload is known, we suggest that thiazolidinediones be administered with caution in all patients.
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PMID:Thiazolidinedione-induced edema. 1212 25


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