The role of the chest X-ray in the evaluation of chronic severe heart failure: things are not always as they appear

The chest x-ray has become a standard clinical test to aid in the evaluation of patients with chronic severe heart failure. To evaluate just how useful this tool is in the routine assessment of pulmonary venous hypertension secondary to heart failure, we compared the radiologist's interpretation of the chest x-ray with hemodynamic data obtained from right heart catheterization in a group of patients undergoing protocol evaluation of an experimental treatment for heart failure. Of 23 patients with pulmonary venous hypertension (pulmonary capillary wedge pressure greater than 20 mmHg) and a complete data base, only 11 had chest x-rays showing evidence of pulmonary venous congestion or interstitial or alveolar edema. The sensitivity of the chest x-ray in selecting patients with a pulmonary capillary wedge pressure over 20 mmHg in this setting was only 48%. In other studies, where the radiologist was aware that his or her reading was being compared to hemodynamic assessments, the sensitivity of the chest film has approached 85%. We feel our analysis more closely parallels routine clinical practice. Clinicians should be aware that the chest x-ray may not be a very sensitive tool for the assessment of pulmonary hemodynamics in patients with severe heart failure.     

Acute Renal Allograft Rejection Following Pegylated IFN-α Treatment for Chronic HCV in a Repeat Allograft Recipient on Hemodialysis: A Case Report

Interferon alpha (IFN-alpha) can be effective therapy for patients with chronic kidney disease who have chronic hepatitis C (HCV). However, acute allograft rejection has been reported in association with IFN-alpha following kidney transplantation, and therefore IFN therapy is recommended prior to, rather than after, kidney transplantation whenever feasible. The special case of repeat allograft recipients who contract HCV after the first transplantation presents special difficulties. This report features the case of a repeat allograft recipient who presented with neutropenic fevers after 5 months of pegylated IFN-alpha therapy, initiated 6 months following the functional loss of his third graft and the reinitiation of hemodialysis (HD). Physical exam, radiographic and laboratory findings led to allograft nephrectomy. The pathologic findings supported a diagnosis of acute-on-chronic rejection. This represents a rare case of IFN-alpha induced rejection following allograft failure and return to HD in a repeat allograft recipient. It also calls attention to the need for a high index of suspicion for the development of allograft rejection, which may require allograft nephrectomy even after allograft 'failure'.     

CRRT治疗老年顽固性心力衰竭的疗效观察

顽固性心力衰竭(CHF)是临床常见而又难治的心脏疾病,其病死率一直居高不下,虽然国内外许多学者采用了多种综合性措施,如主动脉内气囊反搏、植入心脏起搏器等,然而其预后仍较差。近几年来国外学者采用血滤或血透的方法矫治顽固性CHF取得了一些进展。由于研究结果差异较大,已成为     

测定血浆心钠素对小儿心功能不全的诊断意义

采用放射免疫法测定60例心血管病患儿的血浆心钠素,结果,在心功能不全,先天性心脏病、心肌炎者,明显高于正常组;心功能不全组明显高于非心功能不全组。非心功能不全的心血管疾患(如:先天性心脏病、心肌炎)之间无显著差异。说明血浆心钠素测定可作为心功能不全判断指标,并可指导治疗。     

Reduction of Blood Pressure Retards the Progression of Chronic Renal Failure in Man

The effect of blood pressure reduction on the progression rateof chronic renal failure (CRF) was studied in 28 patients withCRF of diverse aetiology entering a prospective study (observationtime 7–24 months, mean 16 months). Endogenous creatinineclearance was 12–66 ml/mm (mean 30±3 ml/mm). Weaimed to keep the blood pressure below 160/90 mmlHg. Dietaryprotein was not restricted. The progression rate of CRF wasassessed from the regression coefficients of the regressionsof creatinine clearance and the inverse of s-creatinine, respectively,on time. Progression rate and the means of all recordings ofmean arterial blood pressure (MAP) and urinary protein excretion,respectively, in each patient during the prospective phase werecompared with retro spective data from the proceeding period(observation time 4–25 months, mean 19 months). The patientsreceived various combinations of antihypertensive drugs includingdiuretics, beta-blockers and vasodilatory drugs. In 19 patientsMAP decreased from 109±2 to 102±2 mmHg (groupI), whereas MAP increased from 105±2 to l08±2mmHgin nine patients (group II). In group I proteinuria was significantlylower (P<0.05) and the progression of CRF was approximately50% slower (P.<0.01) in the prospective phase than in theretrospective phase; no changes were observed in group II. Calculatedfor all patients, significant correlations were observed betweenthe change in MAP and the change in progression rate and proteinexcretion, respectively. These results indicate that loweringof blood pressure results in decreased proteinuria and retardationof the progression of CRF irrespective of the aetiology.     

血液透析对慢性肾功能衰竭患者血浆心钠素水平的影响

本文观察了15例慢性肾功能衰竭病人透析前后的血浆心钠素浓度改变.患者透析前血浆心钠素浓度较正常人明显增高(P相似文献   

Partially Reversible Chronic Renal Failure Due to Long-term Use of Non-steroidal Anti-inflammatory Drugs

A case of partially reversible chronic renal failure due tolong-term NSAID use is discussed. An analysis of this and similarcases recently reported indicates many similarities betweenchronic NSAID nephropathy and analgesic nephropathy.     

High β-adrenoceptor density on peripheral blood mononuclear cells in progressive multiple sclerosis: a manifestation of autonomic dysfunction?

In multiple sclerosis (MS) up-regulation of β-adrenoceptors on peripheral blood mononuclear cells (PBMCs) has been attributed to either autonomic dysfunction, inflammation or a combination of the two. We have compared secondary progressive MS patients with normal subjects (NS) and two models of autonomic dysfunction; pure autonomic failure (PAF) and multiple system atrophy (MSA, Shy-Drager syndrome). There was up-regulation of β-adrenoceptors on PBMCs in MS and PAF patients but not in MSA patients. Only in PAF patients β-adrenoceptor up-regulation was correlated with low plasma levels of noradrenaline (NA) and adrenaline (Ad). In addition to studies in the basal state, measurements also were made after the centrally acting sympatholytic agent clonidine. These were combined with haemodynamic and neurohormonal measurements. After clonidine, there was a fall in blood pressure in NS and MSA patients but not in MS and PAF patients; a rise in growth hormone (GH) in NS and PAF patients but not in MS and MSA patients; and an up-regulation in PBMCs β-adrenoceptors in NS but not in MS, MSA and PAF patients. Up-regulation of β-adrenoceptors on PBMCs in MS could be attributed to autonomic dysfunction but the disparity between MS and PAF patients when considering their plasma levels of NA and Ad argue against. Although the neurohormonal responses to clonidine and the physiological assessment of autonomic function in progressive MS patients, demonstrate central autonomic dysfunction resembling that of the MSA patients, the normal basal β-adrenoceptor densities in the latter, suggests that the up-regulation of these receptors is independent of the central autonomic dysfunction in MS.     

Nodular hyperplasia surrounding fibrolamellar carcinoma

We report a case of acetaminophen-induced liver necrosis in a 14-year-old girl. At autopsy, a 9 cm subcapsular nodule was present in the right lobe of the liver which showed distinct zonation: a central greyish white area of fibrolamellar carcinoma with a peripheral fleshy, tan-coloured rim ranging from 1 to 2 cm in thickness. This peripheral zone consisted of nodular, hyperplastic parenchyma resembling the changes seen in focal nodular hyperplasia, and stood out from the adjacent necrotic parenchyma. The sparing of this zone from the deleterious effects of acetaminophen provides indirect evidence of a predominantly arterial rather than portal blood supply to this region. The arterial supply was most probably derived from the tumour vasculature and may explain the parenchymal hyperplasia sometimes reported adjacent to a fibrolamellar carcinoma. Awareness of this phenomenon is essential when evaluating a needle biopsy, as sampling of this region may lead to a false negative diagnosis.     

Acute heart failure and acute renal failure in Kawasaki disease

Acute renal failure and acute heart failure are rare in Kawasaki disease. We experienced two patients with Kawasaki disease who presented acute renal failure and acute heart failure. These two patients gave us an important insight into the understanding of water balance and fluid therapy in Kawasaki disease. One patient showed acute prerenal failure due to fluid exudation from the intravascular to the extravascular space, and subsequent acute heart failure. The other patient showed acute heart failure caused by fluid infusion for the treatment of dehydration. It is suggested that acute renal failure could be caused by a fluid shift from the intravascular to the extravascular space in Kawasaki disease. It is also demonstrated that the reserve of cardiac function could be decreased in patients with Kawasaki disease due to myocarditis even with normal echocardiography and chest X-rays.