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Death Independent (death + independent)
Selected AbstractsDoes Left Atrial Size Predict Mortality in Asymptomatic Patients with Severe Aortic Stenosis?ECHOCARDIOGRAPHY, Issue 2 2010Grace Casaclang-Verzosa M.D. Background: We assessed the hypothesis that diastolic function represented by left atrial size determines the rate of development of symptoms and the risk of all-cause mortality in asymptomatic patients with severe aortic stenosis (AS). Methods: From a database of 622 asymptomatic patients with isolated severe AS (velocity by Doppler , 4 m/sec) followed for 5.4 ± 4 years, we reviewed the echocardiograms and evaluated Doppler echocardiographic indices of diastolic function. Prediction of symptom development and mortality by left atrial diameter with and without adjusting for clinical and echocardiographic parameters was performed using Cox proportional-hazards regression analysis. Results: The age was 71 ± 11 years and 317 (62%) patients were males. The aortic valve mean gradient was 46 ± 11 mmHg, and the Doppler-derived aortic valve area was 0.9 ± 0.2 cm2. During follow-up, symptoms developed in 233 (45%), valve surgery was performed in 290 (57%) and 138 (27%) died. Left atrial enlargement was significantly correlated with symptom development (P < 0.05) but the association diminished after adjusting for aortic valve area and peak velocity (P = 0.2). However, atrial diameter predicted death independent of age and gender (P = 0.007), comorbid conditions (P = 0.03), and AS severity and Doppler parameters of diastolic function (P = 0.002). Conclusion: Diastolic function, represented as left atrial diameter, is related to mortality in asymptomatic patients with severe AS. (ECHOCARDIOGRAPHY 2010;27:105-109) [source] The Relation Between Mitral Annular Calcification and Mortality in Patients Undergoing Diagnostic Coronary AngiographyECHOCARDIOGRAPHY, Issue 9 2006Howard J. Willens M.D. To determine whether the observed association between mitral annular calcification (MAC) and mortality is independent of the severity of coronary artery disease (CAD), we analyzed data from 134 male veterans (age 63 ± 10 years) followed for 5 years who had undergone diagnostic coronary angiography and transthoracic echocardiography within 6 months of each other. Echocardiograms were retrospectively reviewed for the presence of MAC. The relation of MAC to all-cause mortality was analyzed using logistic regression, and odds ratios (OR) were calculated. MAC was present in 49 (37%) subjects. Over the 5-year follow-up period, 38 (28%) patients expired. Five-year survival was 80% for subjects without MAC and 56% for subjects with MAC (P = 0.003). MAC (OR = 3.16, 95% confidence interval [CI]= 1.43,6.96, P = 0.003), ejection fraction (OR = 0.76, 95% CI = 0.59,0.97, P = 0.02), and left main CAD (OR = 2.70, 95% CI = 1.11,6.57, P = 0.02) were significantly associated with mortality in univariate analysis. After adjusting for left ventricular ejection fraction, number of obstructed coronary arteries and the presence of left main coronary artery stenosis, MAC significantly predicted death (OR = 2.48, 95% CI = 1.09,5.68, P = 0.03). Similarly, after adjusting for predictors of MAC, including ejection fraction, age, diabetes, peripheral vascular disease, and heart failure, MAC remained a significant predictor of death (OR = 2.38, 95% CI = 1.02,5.58, P = 0.04). MAC also predicted death independent of smoking status, hypertension, serum creatinine, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and C-reactive protein levels (OR = 3.98, 95% CI = 1.68,9.40, P = 0.001). MAC detected by two-dimensional echocardiography independently predicts mortality and may provide an easy-to-perform and inexpensive way to improve risk stratification. [source] Early nuclear exclusion of the transcription factor max is associated with retinal ganglion cell death independent of caspase activityJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2004Hilda Petrs-Silva We examined the behavior of the transcription factor Max during retrograde neuronal degeneration of retinal ganglion cells. Using immunohistochemistry, we found a progressive redistribution of full-length Max from the nucleus to the cytoplasm and dendrites of the ganglion cells following axon damage. Then, the axotomized cells lose all their content of Max, while undergoing nuclear pyknosis and apoptotic cell death. After treatment of retinal explants with either anisomycin or thapsigargin, the rate of nuclear exclusion of Max accompanied the rate of cell death as modulated by either drug. Treatment with a pan-caspase inhibitor abolished both TUNEL staining and immunoreactivity for activated caspase-3, but did not affect the subcellular redistribution of Max immunoreactivity after axotomy. The data show that nuclear exclusion of the transcription factor Max is an early event, which precedes and is independent of the activation of caspases, during apoptotic cell death in the central nervous system. J. Cell. Physiol. 198: 179,187, 2004© 2003 Wiley-Liss, Inc. [source] Original Article: A prospective study of uric acid by glucose tolerance status and survival: the Rancho Bernardo StudyJOURNAL OF INTERNAL MEDICINE, Issue 6 2010C. K. Kramer Abstract., Kramer CK, von Mühlen D, Jassal SK, Barrett-Connor E (University of California, La Jolla, CA; and Hospital de Clinicas de Porto Alegre, RS, Brazil). A prospective study of uric acid by glucose tolerance status and survival: the Rancho Bernardo Study. J Intern Med 2010. Objectives., Little is known about uric acid (UA) levels and mortality in the context of glycaemia. We examined whether serum UA levels predict all-cause and cardiovascular disease (CVD) mortality differentially in older adults by glucose tolerance status. Design and methods., Between 1984 and 1987, 2342 community-dwelling men and women had an oral glucose tolerance test, UA measurement, and assessment of traditional CVD risk factors. We defined glucose tolerance status as normoglycaemia (NG), pre-diabetes (pre-DM), and type 2 diabetes mellitus (T2DM). Ninety per cent were followed for vital status up to 23 years. Death certificates were coded using the Ninth International Classification of Diseases. Results., Baseline age was 69.5 years; 44.4% were men. At baseline 939 had NG, 957 pre-DM, and 446 T2DM. The mean UA by glucose tolerance status was 327.1, 362.8, and 374.7 ,mol L,1. During follow-up, there were 1318 deaths 46.8% attributed to CVD. In Cox-regression analysis, each 119 ,mol L,1 (2 mg dL,1) increment in UA levels predicted an increased hazard ratio (HR) for all-cause deaths independent of age, smoking, body mass index, alcohol, physical activity, diuretic use and estimated glomerular filtration rate in all groups (NG: HR 1.25 95% CI 1.06,1.47, P =0.005; pre-DM: HR 1.20 95% CI 1.06,1.37, P = 0.04; T2DM: HR 1.20 95% CI 1.01,1.47, P = 0.04). After adjusting for CVD risk factors, the UA association with CVD mortality was significant only in the pre-DM and T2DM groups. Conclusion., All-cause mortality was independently associated with UA in all groups, but UA predicted CVD mortality only in those with abnormal glucose tolerance. [source] | ||||||||||