umor shrinkage or progression, time to tumor progression, and progression-free survival are surrogate imaging end points that are frequently used to rate the efficacy of anticancer treatment. The Response Evaluation Criteria in Solid Tumors (RECIST) guidelines have been introduced to standardize such measurements and to provide cutoff values for response classification (1-3).Since the introduction of RECIST guidelines (1-3), a multitude of studies have been performed to assess withinand between-reader agreement of analyses with RECIST versions 1.0 and 1.1. The focus of these published studies was on the effect of manual versus automated size measurements and of uni-versus bidimensional or volumetric measurements of target lesions (4-16). To avoid between-reader variability from these causes, the RECIST consortium recommends using dedicated oncology software tools that help automatize and thus standardize the measurement of target lesion diameters (2).However, with or without use of these software systems, RECIST requires readers to select target lesions. Depending on the type of response classification system used (ie, the maximum number of reportable target lesions), readers must base their response analysis on a more or less small sample of the overall tumor load. It is the implicit assumption of all current response assessment systems that size changes of these target lesions are sufficiently representative of size changes of the entire bodily tumor load. Under the World Health Organization, readers were free to select and measure as many target lesions as deemed appropriate; under the first version of RECIST (RECIST 1.0), readers could select up to
Background
Epicardial adipose tissue (EAT) exerts cardiopathogenic effects, but the independent association between EAT and cardiovascular (CV) calcification in patients with chronic kidney disease (CKD) remains controversial. We therefore assessed the association between EAT, CV risk factors and CV calcifications.
Methods
257 patients with CKD Stage 3 and/or overt proteinuria underwent quantification of EAT, coronary artery calcification and aortic valve calcification by computed tomography. Framingham and American College of Cardiology and American Heart Association (ACC-AHA) 10-year CV event risk scores were calculated for each patient.
Results
Using multivariable regression analysis, higher EAT was significantly associated with the majority of investigated risk factors {higher age: odds ratio [OR] 1.05/year [95% confidence interval (CI) 1.02–1.08]; male sex: OR 4.03 [95% CI 2.22–7.31]; higher BMI: OR 1.28/kg/m2 [95% CI 1.20–1.37]; former smoking: OR 1.84 [95% CI 1.07–3.17]; lower high-density lipoprotein cholesterol: OR 0.98/mg/dL [95% CI 0.96–1.00] and lower estimated glomerular filtration rate: OR 0.98/mL/min/1.73 m2 [95% CI 0.97–0.99]; all P < 0.05} and was not associated with diabetes mellitus, hypertensive nephropathy, total cholesterol and albuminuria. EAT was positively associated with higher ACC-AHA and Framingham risk scores. EAT correlated with coronary artery calcification and aortic valve calcification [Spearman ρ = 0.388 (95% CI 0.287–0.532) and rrb = 0.409 (95% CI 0.310–0.556), respectively], but these correlations were dependent on CV risk factors.
Conclusions
The increase of EAT can be explained by individual CV risk factors and kidney function and correlates with 10-year risk for CV event scores, suggesting that EAT is a modifiable risk factor in patients with CKD. Although EAT correlates with CV calcifications, these relations depend on CV risk factors.
Background Aortic stenosis (AS) may lead to diastolic dysfunction and later on heart failure (HF) with preserved left ventricular ejection fraction (HFpEF) via increased afterload and left-ventricular (LV) hypertrophy. Since epicardial adipose tissue (EAT) is a metabolically active fat depot that is adjacent to the myocardium and can influence cardiomyocytes and LV function via secretion of proinflammatory cytokines, we hypothesized that high amounts of EAT, as assessed by computed tomography (CT), may aggravate the development and severity of LV hypertrophy and diastolic dysfunction in the context of AS. Methods We studied 50 patients (mean age 71 ± 9 years; 9 women) in this preliminary study with mild or moderate AS and mild to severe LV diastolic dysfunction (LVDD), diagnosed by echocardiography, who underwent non-contrast cardiac CT and echocardiography. EAT parameters were measured on 2nd generation dual source CT. Conventional two-dimensional echocardiography and Tissue Doppler Imaging (TDI) was performed to assess LV function and to derive myocardial straining parameter. All patients had a preserved LV ejection fraction > 50%. Data was analysed using Pearson's correlation. Results Only weak correlation was found between EAT volume or density and E/é ratio as LVDD marker (r =-.113 p = .433 and r = .260, p = .068 respectively). Also, EAT volume or density were independent from Global Strain Parameters (r = 0.058 p = .688 and r =-0.207 p = .239). E/é ratio was strongly associated with LVDD (r = .761 p�0.0001) and Strain Parameters were moderately associated with LV Ejection Fraction (r =-.669 p�0.001 and r =-.454 P�0.005).
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