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The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosamidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 ± 0.1 to 0.8 ± 0.1 and 1.0 ± 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 ± 18 to 48 ± 20 and 8 ± 4 umol hrVmmol creatinine at 24 and 48 h, respectively (p < 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 ± 0.1 to 0.4 ± 0.1 and 0.8 ± 0.1 ml/min at 24 and 48 h, respectively (p < 0.01). Urinary NAG excretion increased also significantly from 43 ± 9 to 352 ± 79 and 64 ± 23 umol h^_1/mmol creatinine at 24 and 48 h, respectively. Histologic examination of 7 kidneys revealed acute tubular necrosis (n = 4), tubular cytoplasmic vacuolization (n = 2), and no histologic abnormalities (n = 1). Ioxaglate and iopamidol induced no change in serum creatinine and a slight decrease in creatinine clearance comparable to that observed in the control group. Ioxaglate and iopamidol induced a significant increase in urinary NAG excretion at 24 h (ioxaglate: 31 ± 6 to 147 ± 31; iopamidol: 55 ± 20 to 123 ± 31 umol h^_1/mmol creatinine) which was completely reversible at 48 h (ioxaglate: 31 ± 9; iopamidol: 41 ± 8). Histological analysis of 8 kidneys exposed to ioxaglate revealed tubular cytoplasmic vacuolisation (n = 7) and no histologic abnormalities (n = 1). Histological analysis of 10 kidneys exposed to iopamidol revealed tubular cytoplasmic vacuolization (n = 8) and no histologic abnormalities (n = 2). We have described a reproducible and reversible model of contrast-medium-induced acute renal failure in the rat. In this model, ionic and nonionic low-osmolar contrast agents are less nephrotoxic than high-osmolar contrast agents.

This study investigated the impact of ischemic mitral regurgitation (MR) severity and viability on left ventricular (LV) reverse remodeling after cardiac resynchronization therapy (CRT) in patients with ischemic cardiomyopathy. Severe MR and ischemic cardiomyopathy have been associated with lack of LV reverse remodeling after CRT. Fifty-seven consecutive patients with ischemic MR, LV ejection fraction <35%, QRS duration >120 ms, and intraventricular dyssynchrony >50 ms were prospectively included. Stress echocardiography was performed before CRT implantation. Viability in the region of the LV pacing lead was defined as the presence of viability in 2 contiguous segments. Response to CRT at 6 months was defined by evidence of >15% LV decrease in end-systolic volume. Severe MR was defined by an effective regurgitant orifice (ERO) area >20 mm 2 . Thirtythree patients (58%) were responders at follow-up. Baseline ERO area and prevalence of severe MR were not different between responders and nonresponders (19 ؎ 11 vs 21 ؎ 13 mm 2 , p ‫؍‬ 0.67; 52% vs 53%, p ‫؍‬ 0.84). In responders, MR was decreased by 58% (ERO 19 ؎ 12 to 8 ؎ 6 mm 2 ). In the presence of viability in the region of the pacing lead, 74% (n ‫؍‬ 29 patients) were responders (sensitivity 88%, specificity 58%); in the subgroup of patients with viability in the region of the pacing lead and severe MR, 83% (n ‫؍‬ 17 patients) were responders. In conclusion, LV remodeling is frequent and ischemic MR decrease important in patients with viability in the region of the pacing lead without regard to MR severity. © 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;106:31-37) Ischemic heart disease is the most common cause of systolic left ventricular (LV) dysfunction. The prognosis of these patients is particularly modulated by the extent of residual viable myocardium. Cardiac resynchronization therapy (CRT) improves LV function and geometry, exercise capacity, and outcomes of appropriately selected patients with heart failure.1-3 CRT leads to a decrease in mitral regurgitation (MR) severity at rest and during exercise by an increase of LV function and local synchronicity (decrease in mechanical activation delay of papillary muscles). 4 -11 Response to CRT largely depends on extent of LV dyssynchrony, severity of LV remodeling, extent of scar tissue, and possibility offered to the left ventricle to recruit function (contractile reserve). Whether the presence of MR and its severity could modulate the response to CRT is still controversial. Several investigators have suggested that extent of LV reverse remodeling could be lessened in patients with significant MR, particularly in the setting of ischemic cardiomyopathy. [12][13][14] This study investigated the potential impact of MR severity and myocardial contractile reserve on acute and long-term responses to CRT in patients with ischemic cardiomyopathy and significant LV dyssynchrony. MethodsFrom May 2005 to March 2008, 57 patients (mean age 71 Ϯ 8 years, 43 men, (75%) were prospectively enrolled in the Inst...

These data suggest that CSA nephrotoxicity could result from individually determined susceptibility and that hypertriglyceridemia may have a negative impact on renal function and cardiac mortality. The risk of cardiac mortality is increased in heart transplant patients with ESRF. The hypothesis of accelerated atherosclerosis in ESRF patients after heart transplantation leading to higher cardiac mortality incidence needs further study.