The kidney in heart failure

Renal dysfunction is a constant feature of congestive heart failure and is a stronger predictor of mortality than left ventricular ejection fraction or New York Heart Association classification. In heart failure, a reduction of glomerular filtration rate and renal plasma flow occurs, although the filtration fraction increases. There are many reason for this pattern. A reduction in effective circulating volume stimulates sympathetic activity and the renin-angiotensin-aldosterone system, and it is associated with increased concentrations of atrial natriuretic peptide, brain natriuretic peptide, and tumor necrosis factor alpha. Because in chronic kidney disease heart dysfunction commonly is present, an efficient cardiologist-nephrologist interaction should be promoted.     

延续性护理对慢性心力衰竭患者家庭照顾者照顾负荷的影响

目的探讨延续性护理减轻慢性心力衰竭患者家庭照顾者照顾负荷的效果。方法将109名慢性心力衰竭患者家庭照顾者作为研究对象,实施为期6个月的延续性护理措施,比较干预前后家庭照顾者的负担水平。结果干预后照顾者个人负担、责任负担、负担总分显著低于干预前(均P0.01)。结论延续性护理可减轻慢性心力衰竭患者家庭照顾者的负担水平。     

Surgical alternatives for heart failure.

Heart failure is one of the leading causes of hospitalization in the United States. Congestive heart failure is a chronic, progressive disease and its central element is remodeling of the cardiac chamber associated with ventricular dilation. Secondary mitral regurgitation is a complication of end-stage cardiomyopathy and is associated with poor prognosis. Historically, these patients were not considered operative candidates because of their high morbidity and mortality. Heart transplantation is now considered standard treatment for select patients with end-stage heart disease; however, it is applicable only to a small number of patients. In an effort to address this problem, newer and alternative surgical approaches are evolving, including mitral valve annuloplasty, the Batista procedure, and other left ventricular shape changing technologies. Using these operative techniques to alter the shape of the left ventricle, in combination with optimal medical management for heart failure, improves survival, and patients may avoid or postpone transplantation.     

Acute right heart failure. Etiology--pathophysiology--diagnosis--therapy

Impaired right ventricular (RV) function may be caused by pulmonary hypertension or myocardial ischemia. It is characterized by a dilation of the RV, which is followed by an increase of wall tension and O2-consumption and a decrease of RV ejection fraction (RV 'dysfunction'). If a drop of arterial pressure occurs this my precipitate RV failure and shock (RV 'insufficiency'). Diagnosis of RV failure and monitoring of RV function is difficult. Sometimes, even a severe impairment of RV function goes undetected or is misinterpreted. Patients in the operating room or on intensive care units seem to be especially prone to RV dysfunction and failure. Since a causative therapy often is not readily available, adequate symptomatic therapy is of utmost importance. Four basic principles have to be considered: 1) Optimizing preload: The failing RV requires adequate filling for preservation of stroke volume. On the other hand, overdistension of the RV may result in RV ischemia, thereby further deteriorating RV function Hence, volume loading is important, but requires continuous monitoring. 2) Maintenance of aortic pressure: Vasopressors are indicated if there is a critical drop of coronary perfusion pressure. Norepinephrine presently is the drug of choice for this purpose. 3) Reduction of RV afterload: Whereas intravenous vasodilators are limited in their efficacy in dilating pulmonary vessels due to systemic side effects, inhaled vasodilators result in selective pulmonary vasodilation and may improve RV function. 4) Increase of RV contractility: In RV failure and shock, norepinephrine and epinephrine are the drugs of choice. Inodilators are well suited for reducing pulmonary vascular resistance due to their positive inotropic and vasodilating effects. Since systemic vasodilation may occur, these drugs must only be used in hemodynamically stable patients.     

Primary osteosarcoma of heart with severe congestive heart failure.

We present a case report on a 54-year-old woman with extraskeletal osteosarcoma of the left atrium featuring severe congestive heart failure. We resected the tumor, which occupied the left atrium and had widely infiltrated the atrial wall, but the patients died of the tumor 9 months after surgery. This is to our knowledge the 32nd case of cardiac osteosarcoma ever reported.     

The economic burden of kidney graft failure in the United States

Despite improvements in outcomes for kidney transplant recipients in the past decade, graft failure continues to impose substantial burden on patients. However, the population‐wide economic burden of graft failure has not been quantified. This study aims to fill that gap by comparing outcomes from a simulation model of kidney transplant patients in which patients are at risk for graft failure with an alternative simulation in which the risk of graft failure is assumed to be zero. Transitions through the model were estimated using Scientific Registry of Transplant Recipients data from 1987 to 2017. We estimated lifetime costs, overall survival, and quality‐adjusted life‐years (QALYs) for both scenarios and calculated the difference between them to obtain the burden of graft failure. We find that for the average patient, graft failure will impose additional medical costs of $78 079 (95% confidence interval [CI] $41 074, $112 409) and a loss of 1.66 QALYs (95% CI 1.15, 2.18). Given 17 644 kidney transplants in 2017, the total incremental lifetime medical costs associated with graft failure is $1.38B (95% CI $725M, $1.98B) and the total QALY loss is 29 289 (95% CI 20 291, 38 464). Efforts to reduce the incidence of graft failure or to mitigate its impact are urgently needed.     

The burden of acute renal failure in nonrenal solid organ transplantation

BACKGROUND: Recipients of nonrenal solid organ transplants are at risk for acute renal failure resulting from cardiac or hepatic failure, prolonged surgery, and nephrotoxic effects of immunosuppression. Single-center studies have suggested a variable incidence of acute renal failure in this population, with an associated increase in mortality. This study examines the incidence of acute renal failure and its associated mortality and morbidity in a modern multicenter cohort. METHODS: All adult liver, heart, and lung transplant recipients from 2002 were identified from the New York Statewide Planning and Research Cooperative System database. The impact of acute renal failure on mortality, length of stay, and charges was analyzed using multivariate regression models. RESULTS: Among 519 liver, heart, and lung transplant recipients, the incidence of acute renal failure was 25%, with 8% of patients requiring renal replacement therapy. Acute renal failure requiring renal replacement therapy was associated with increased mortality among both heart (odds ratio, 9.0; 95% confidence interval, 1.8-45.8) and liver transplant recipients (odds ratio, 12.1; 95% confidence interval, 3.9-37.3). This degree of acute renal failure also increased length of stay by nearly 3 weeks and charges by more than $115,000. Even among patients who did not require renal replacement, acute renal failure was strongly associated with increased mortality, length of stay, and charges. CONCLUSIONS: Acute renal failure remains a common complication of nonrenal solid organ transplantation and is associated with increased mortality, prolonged hospitalization, and significant financial costs.     

Pulmonary function in chronic heart failure. Changes after heart transplantation.

To investigate the impact of chronic heart failure on pulmonary function in heart transplant recipients, pulmonary function was evaluated in 41 consecutive patients (mean age 43 years, range 15-57 years) before and 6 months after successful heart transplantation. The pulmonary function tests included measurements of forced vital capacity [FVC], forced expiratory volume in 1.s [FEV1], FEV1/FVC ratio, total lung capacity [TLC], and diffusion capacity for carbon monoxide [TLCO] and KCO [TLCO per l alveolar volume]. Compared to pretransplant values, spirometry after transplantation revealed modest improvements in FVC (from 77 +/- 16 to 88 +/- 21% of predicted [%pred]; p < 0.001) and FEV1 (from 75 +/- 16 to 85 +/- 22%pred; p < 0.001), whereas the FEV1/FVC ratio was unchanged (81% +/- 11 and 80% +/- 10; p = NS). A slight but statistically significant increase in TLC (from 78 +/- 15 to 86 +/- 18%pred, p < 0.001) was also observed. Prior to transplantation the mean TLCO was 76 +/- 17%pred; 7 of the patients had a TLCO below 60%pred (mean 51% pred). In 33 of the 41 patients a reduction in TLCO was observed after transplantation; for all 41 patients the mean fall in TLCO was 14% of the predicted value (SD 12%pred) (p < 0.0001). Likewise, a significant reduction in KCO was noted (p < 0.0001). Multiple regression analysis revealed that high pretransplant TLCO %pred (p = 0.02) and FVC %pred (p = 0.04) were associated with a less favorable outcome concerning posttransplant TLCO %pred. Although normalization of FEV1, FVC and TLC can be anticipated after correction of severe chronic left ventricular failure by heart transplantation, the pronounced concomitant decline in diffusion capacity observed in this study may be explained by underlying pulmonary disease caused by factors other than long-standing heart failure. Our findings support the notion that pulmonary function abnormalities attributable to chronic heart failure should not preclude consideration for heart transplantation.     

The use of vasodilator agents in the treatment of heart failure.

In cardiac failure unresponsive to digoxin and diuretics, afterload reduction brings about a dramatic increase in cardiac output, renal perfusion and responsiveness to diuretics; furthermore, the decrease in venous pressure relieves the dyspnoea. Intravenous vasodilators should only be used when sophisticated haemodynamic monitoring equipment and experienced physicians are at hand. Indications for the use of these agents are severe cardiac failure, acute myocardial infarction complicated by left ventricular failure, persistent ischaemic pain and limitation of infarct size. A wide variety of oral vasodilator agents is available, all having different sites of action; the choice of vasodilator agents should be tailored to the needs of the patient. Treatment with these agents is indicated in patients in whom cardiac failure becomes refractory to conventional therapy with digoxin and diuretics. The utmost care must be taken to avoid further impairment of cardiac output by excessive reduction of the left ventricular end-diastolic pressure (LVEDP) and hypotension, which will jeopardize myocardial, renal and cerebral perfusion.     

Treatment-seeking delays in heart failure patients.

BACKGROUND: Patients having cardiac symptoms often delay for hours before seeking treatment. Delay time is usually defined as the amount of time between the patient's first awareness of symptoms and arrival at the hospital. Excessive delays in seeking medical care for heart failure (HF) symptoms may influence patient outcomes. However, the treatment-seeking patterns of HF patients are not well understood. METHODS: We obtained data through a retrospective chart audit to describe the treatment-seeking behaviors of 753 HF patients, at a Veterans Administration facility, and to identify predictors of delay in seeking medical care for HF symptoms. Using univariate and multivariate analyses, we assessed relationships among delay time, presenting symptoms, and patient characteristics. RESULTS: The mean delay time was 2.93 +/- 0.68 days. The most common symptoms on admission were dyspnea (76%), edema (66%), fatigue (37%), and angina (25%). Variables negatively affecting delay time included presence of dyspnea and edema (odds ratio [OR], 2.10 and 1.82; confidence interval [CI], 1.38 to 3.19 and 1.17 to 2.82, respectively), care by a primary care physician (OR, 2.04; CI, 1.45 to 2.88), and higher New York Heart Association (NYHA) Class (OR, 1.96; CI, 1.47 to 2.61). Variables positively affecting delay time were the presence of chest pain (OR, 0.42; CI, 0.29 to 0.62) and a history of previous admission for HF (OR, 0.42; CI, 0.28 to 0.62). CONCLUSIONS: Delays in seeking treatment for HF symptoms are significantly high. This study supports the need for interventions that will increase early symptom recognition and management on the part of patients and their families.