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Cardiovascular events (CVE) are the leading cause of mortality in kidney transplant recipients. Increased left ventricular mass (LVM) is a risk factor for CVE. This study investigated the associations of LVM with impaired kidney graft function expressed as lower glomerular filtration rate (GFR) at 1 year after transplantation and future CVE beyond 1 year. The prospective study cohort included 68 nondiabetic recipients of a kidney transplant between January 2004 and December 2005 who underwent a transthoracic echocardiographic investigation at 1 year after transplantation. LVM and left ventricular hypertrophy (LVH) were assessed using 2-dimensional M-mode echocardiography. GFR was estimated (eGFR) by the 4-variable Modification of Diet in Renal Disease formula. Cox proportional hazards analysis was used to estimate cardiac CVE (angina pectoris, acute myocardial infarct, coronary angioplasty or bypass surgery, or sudden cardiac death) hazard ratios (HRs) for patients with LVH versus control subjects with no LVH at 1 year after transplantation. All patients had normal systolic function (ejection fraction >50%) with no symptoms or signs of heart failure. LVH was present in 44 patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR <60 mL/min/1.73 m(2) compared with 40 patients with eGFR ≥60 mL/min/1.73 m(2) (248 ± 61 g and 86% vs 210 ± 46 g and 50%, respectively; P < .01). After a median follow-up of 4.5 years, there were 18 (26.5%) cardiac CVE. The incidence of CVE was higher in patients with LVH than in patients with no LVH at 1 year after transplantation (36.4% vs 8.3%; P = .020). In adjusted analyses, LVH was associated with an increased risk for future CVE (HR, 4.69; 95% confidence interval, 1.02-21.5; P = .037). In kidney transplant recipients, a lower eGFR at 1 year after transplantation was associated with greater LVM and higher incidence of LVH. Presence of LVH was associated with an increased risk for future CVE.

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Ventricular repolarization heterogeneity (VRH) is associated with the risk of arrhythmia and cardiac death. This study investigated the association between VRH and left ventricular mass (LVM) in renal transplant recipients 1 year after transplantation. Echocardiography and 5-min 12-lead electrocardiogram were recorded and GFR was estimated (eGFR) in 68 nondiabetic patients. Beat-to-beat QT interval variability algorithm was used to calculate SDNN-QT and rMSSD-QT indices of VRH. To quantify QT interval variability relative to heart rate fluctuations, QTRR index was calculated. Left ventricular hypertrophy (LVH) was present in 44 patients (65%). LVM and incidence of LVH were increased in 28 patients with eGFR <60 mL/min/1.73 m(2) compared with 40 patients with eGFR > or =60 mL/min/1.73 m(2) (248 +/- 61 g and 86% vs. 210 +/- 46 g and 50%, respectively; p < 0.01). A direct correlation was found between LVM and SDNN-QT (R = 0.47, R(2)= 0.23; p < 0.001), rMSSD-QT (R = 0.27; R(2)= 0.10; p = 0.034), and QTRR (R = 0.55; R(2)= 0.31; p < 0.001) indices. In conclusion, greater LVM is associated with increased VRH in renal transplant recipients, providing a link with the high risk of arrhythmia and cardiac death, specifically in patients with decreased graft function.

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BACKGROUND: It is asumed that the shape and size of the left ventricle could change after successful revascularization and that the shape and size reflect left ventricular function. METHODS: Echocardiography and Simpson's rule were used for evaluating the endocardial surface area of the left ventricle and elongation of the left ventricle as shape index in 13 patients before coronary arterio-venous bypass grafting (CABG) and 1 year after successful CABG. RESULTS: After successful CABG, the left ventricle becomes bigger and less elongated than before CABG. Results show a change from concentric hypertrophy of the left ventricle before CABG to subnormalization after CABG. DISCUSSION: We suppose that the subnormalization of left ventricular size and shape is the result of successful CABG and successful rehabilitation. The change of left ventricular size and shape after CABG might depend more on the original state of the left ventricle before surgery.

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The study was based on 462 patients who underwent kidney transplantation from 1986 through 2004. Cyclosporine (CsA)-related thrombotic microangiopathy (TMA) was observed in 15 (3.3%) patients. The donor ages ranged from 9 to 51 years and cold ischemia times from 12 to 31 hours. Hemolytic-uremic syndrome (HUS) developed 2 weeks after transplantation in 14 patients and later in 1 subject. Histopathologic examination demonstrated glomerular-type TMA in 3 patients, a mixed type (glomerular and vascular) in 11 patients, and a nonspecific mesangial widening with tubulointerstitial lesions in 1 patient. Follow-up biopsies revealed resolution of TMA in 4 patients and chronic vascular TMA in 1 patient. Six patients with mixed-type TMA needed transient hemodialysis. No patient with the glomerular-type TMA needed dialysis (P = .103), and 14 of 15 had good resolution of graft function after CsA dose reduction or temporary discontinuation or continuation of optimal dose. Only 1 graft with mixed-type TMA was lost due to irreversible HUS. The mean glomerular filtration rate (GFR), predicted by the Nankivell equation, was 76 +/- 13 mL/min and 80 +/- 27 mL/min at 1 month after discharge for glomerular- and mixed-type TMA, respectively (P > .05). GFRs 1 year after HUS were 82 +/- 12 and 87 +/- 21 mL/min for the glomerular and the mixed types, respectively (P > .05). We concluded that the mixed-type TMA was associated with a more severe early clinical course than the glomerular-type TMA. The 1-year prognosis was good in the majority of patients, with no significant differences between those with the glomerular- and mixed-type TMA.

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A simple computer program was made to draw different left ventricle shapes in order to support the theory of elongation and to get a visual presentation of the shape of the left ventricle. Experimental data, obtained from echocardiography and Simpson's rule, were used for this program. The results yielded different shapes under different physiological circumstances, indicating the sensitivity of the method. It was concluded that these figures (shapes) support the use of elongation as a shape index.

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OBJECTIVES: This study was done to quantify the shape of the left ventricle (LV). It was proposed that the shape of the LV is intimately related to its performance and that its elongation (ELO) is a sensitive measure of this performance. The performance was tested against classical cardiovascular parameters. METHODS: Using echocardiography and Simpson's rule, the endocardial surface area of the LV was calculated noninvasively with a simple experimental-mathematical model at enddiastole and endsystole. ELO as shape index was derived from the endocardial surface area of the LV with a simple formula. The endocardial surface area of the LV and ELO were determined in volunteers, in patients with mild heart failure and in patients with severe heart failure. RESULTS: The normal value of endocardial surface area of LV at enddiastole is 138.3 cm2 while the normal value at endsystole is 99 cm2. The endocardial surface area of the LV is significantly bigger in patients with mild heart failure than in volunteers (p < 0.01) while the parameters ELO, ejection fraction and Doppler measurements are similar. The normal values of ELO at diastole and systole are 12 and 25 respectively. The value of ELO at endsystole is lower only in patients with severe heart failure. This means a more spherical shape and poor systolic function of the LV. CONCLUSION: ELO is usefull as quantitative and qualitative index of left ventricular shape. ELO could be integrated and applied with new diagnostic tools such three-dimensional and contrast echocardiography.

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To check whether in vivo EDTA prevents complement activation resulting from blood contact with the dialyzer membrane, sham hemodialysis (HD) was performed in seven healthy volunteers using Cuprophan hollow-fiber dialyzers. Blood samples were drawn from the arterial and venous blood lines of the dialyzer before and after EDTA was infused into the arterial line. Venous line plasma C3a concentrations before EDTA infusion were significantly higher than after EDTA. Also, venous line plasma C3a concentrations before and after EDTA infusion were significantly higher than in the arterial line. These results indicate that complement activation can be attenuated by EDTA during sham HD. Technical improvements in the procedure may permit complete inhibition of complement activation.

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