Mitral peak Doppler E-wave to peak mitral annulus velocity ratio is an accurate estimate of left ventricular filling pressure and predicts mortality in end-stage renal disease
ABSTRACT The study aimed to assess whether the mitral peak Doppler E-wave to peak mitral annulus velocity ratio (E/Ea) estimates left ventricular (LV) filling pressure (LVFP) and predicts mortality in end-stage renal disease.
In all, 125 candidates for renal transplant were prospectively studied. LV end-diastolic pressure of 15 mm Hg or greater at cardiac catheterization was defined as elevated LVFP.
Severe coronary artery disease, N- terminal pro-B-type natriuretic peptide level, left atrial size, flow propagation velocity, mitral E/Ea ratio, pulmonary atrial reversal velocity, and pulmonary-mitral atrial wave duration predicted an increased LVFP. However, the mitral E/Ea ratio (odds ratio 8.1, 95% confidence interval 5.1-9.6, P = .003) was the only independent predictor. An E/Ea of 15 or more, seen in 31 (25%) patients, predicted increased LVFP with sensitivity of 82% and specificity of 88%, and was associated with increased mortality (P = .005).
In end-stage renal disease, mitral E/Ea ratio 15 or higher accurately predicts increased LVFP and mortality.
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ABSTRACT: Heart failure (HF) is very common in the general population, and risk factors for HF, such as coronary artery disease, diabetes, obesity, and hypertension, are frequently present in patients with CKD. Therefore, HF is also an important cause of morbidity and mortality in this population. Diastolic heart failure (DHF), also called HF with preserved ejection fraction, refers to a clinical syndrome in which patients have symptoms and signs of HF, normal or near normal left ventricular (LV) systolic function, and evidence of diastolic dysfunction (e.g., abnormal LV filling and elevated filling pressure). Recent data suggest that HF with normal ejection fraction is even more common in patients than HF with low ejection fraction, including those on hemodialysis. Not surprisingly, DHF is a strong predictor of death in CKD patients. In this article, we review the information available on the mechanisms, clinical presentation, impact, and potential interventions in DHF based on evidence from CKD patients, as well as evidence from the general population potentially applicable to the CKD population.Seminars in Dialysis 01/2012; 25(1):35-41. DOI:10.1111/j.1525-139X.2011.01011.x · 2.07 Impact Factor
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ABSTRACT: Patients can have diastolic dysfunction with or without a depressed ejection fraction. The measurements used as the gold standard for diagnosing diastolic dysfunction are obtained by cardiac catheterization, which is not practical. Echocardiography has emerged among the noninvasive imaging modalities as the most versatile method for day-to-day use in clinical laboratories. This article summarizes the available techniques, with emphasis on the clinical application of each method.Journal of the American College of Cardiology 05/1989; 13(5):1027-9. DOI:10.1016/0735-1097(89)90255-6 · 15.34 Impact Factor
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ABSTRACT: Solid-pseudopapillary tumors (SPTs) are unusual pancreatic neoplasms of low malignant potential that most frequently affect young women. Genetic events contributing to the development of SPTs are unknown. Whereas the more common ductal adenocarcinomas of the pancreas essentially never harbor β-catenin or APC gene mutations, we have recently identified alterations of the APC/β-catenin pathway in other nonductal pancreatic neoplasms including pancreatoblastomas and acinar cell carcinomas. We analyzed a series of 20 SPTs for somatic alterations of the APC/β-catenin pathway using immunohistochemistry for β-catenin protein accumulation, direct DNA sequencing of β-catenin exon 3, and direct DNA sequencing of the mutation cluster region in exon 15 of the APC gene in those SPTs that did not harbor β-catenin mutations. Immunohistochemical labeling for cyclin D1 was performed to evaluate the overexpression of this cell-cycle protein as one of the putative downstream effectors of β-catenin dysregulation. In addition, we analyzed the SPTs for genetic alterations commonly found in pancreatic ductal adenocarcinomas, including mutations in the K-ras oncogene and p53 and Dpc4 tumor suppressor genes, using direct DNA sequencing of K-ras and immunostaining for p53 and DPC4. Almost all SPTs harbored alterations in the APC/β-catenin pathway. Nuclear accumulation of β-catenin protein was present in 95% (19 of 20), and activating β-catenin oncogene mutations were identified in 90% (18 of 20) of the SPTs. Seventy-four percent (14 of 19) showed overexpression of cyclin D1, ranging from 10 to 70% of tumor nuclei. In contrast, no K-ras mutations were present in any of the 20 SPTs, and Dpc4 expression was intact in all 16 SPTs for which immunohistochemical labeling was successful. Overexpression of p53 was limited to only 3 of 19 (15.8%) SPTs. These results emphasize the two distinct, divergent genetic pathways of neoplastic progression in pancreatic ductal and nonductal neoplasms.American Journal Of Pathology 05/2002; 160(4):1361-9. DOI:10.1016/S0002-9440(10)62563-1 · 4.60 Impact Factor