Comparison of acute kidney injury classifications in patients undergoing transcatheter aortic valve implantation: Predictors and long-term outcomes.

BACKGROUND: Acute kidney injury (AKI) was demonstrated to adversely affect outcome in patients undergoing transcatheter aortic valve implantation (TAVI). We compared predictors for AKI and associated outcomes according to various definitions among patients undergoing TAVI in a tertiary medical center. METHODS: Two-hundred and seventeen TAVI patients were evaluated for the occurrence of AKI according to Kidney Disease Improving Global Outcomes (KDIGO)/Valve Academic Research Consortium (VARC-2) and Risk Injury Failure Loss End-Stage (RIFLE) definitions. Multivariate analysis was conducted to assess predictors of AKI. Cox hazard ratio was used to evaluate long-term mortality in this patient population. RESULTS: AKI occurred in 23 and 21% of patients (n = 49, n = 46) according to KDIGO/VARC-2 and RIFLE definitions, respectively, with an approximate 10% of disagreement between both systems. Predictors of AKI according to KDIGO/VARC-2 were chronic obstructive pulmonary disease (COPD; OR = 2.66, P = 0.01), PVD (OR = 3.45, P = 0.02) and a lower baseline eGFR (OR = 1.03 per 1 mL/min/1.73 m(2) decrease, P = 0.02). While BMI (OR = 1.12, P = 0.01), prior ischemic heart disease (OR = 2.35, P = 0.04) and COPD (OR = 2.18, P = 0.04) were associated with AKI as defined by the RIFLE definition. AKI defined by either classification was independently associated with long-term mortality (HR = 1.63, for the KDIGO/VARC-2 definition and HR = 1.60 for RIFLE definition, P = 0.04 for both models), with borderline superiority of the KDIGO/VARC-2 classification. CONCLUSIONS: Different clinical characteristics predict the occurrence of AKI after TAVI when RIFLE and KDIGO/VARC-2 classifications are used. Both classification systems of AKI identify patients with increased risk for long-term mortality, with superiority of the KDIGO/VARC-2 definition, which should be used for AKI grading.

Age-dependent effect of left ventricular ejection fraction on long-term mortality in patients with heart failure (from the Heart Failure Survey in ISrael).

Contemporary heart failure (HF) therapies have not resulted in improved outcomes among patients with HF and preserved left ventricular ejection fraction (LVEF). We sought to evaluate the differential effect of LVEF on long-term mortality after hospitalization for acute decompensated HF in a real-world setting. All-cause mortality at 4 years after hospitalization for HF was assessed by LVEF (categorized as preserved [≥50%], mildly [40% to 49%], moderately [30% to 39%], and severely [<30%] reduced) among 1,620 patients enrolled in the Heart Failure Survey in ISrael. Among the study patients, 30% had preserved LVEF and 20%, 25%, and 25%, had mild, moderate, and severe reductions in LVEF, respectively. Multivariate analysis showed that patients with preserved LVEF had a similar risk of long-term mortality as patients with mild or moderate reduction in LVEF (hazard ratio [HR] 0.92 [p = 0.40] and 1.01 [p = 0.90], respectively) while severely reduced LVEF conferred increased increase rate compared with preserved LVEF (HR 1.20, p = 0.04). Interaction term analysis showed that the risk associated with severely reduced LVEF was evident only among patients ≤75 years (HR 1.49, p = 0.003), whereas among older patients, there was no difference in the risk of long-term mortality between those with preserved versus severely reduced LVEF (HR 1.02 [p = 0.86]; p value for age-by-LVEF interaction = 0.03). In conclusion, patients hospitalized for HF who have preserved LVEF experience similar long-term mortality as patients with mild or moderate reductions in LVEF, whereas severely reduced LVEF remains an independent predictor of long-term mortality in this population. The differential effect of LVEF on long-term mortality is significantly attenuated in the older age group.

Regulatory T cells and IL-10 levels are reduced in patients with vulnerable coronary plaques.

BACKGROUND: Despite having a similar large extent of atherosclerotic coronary affliction, some patients suffer of recurrent cardiac events, whereas others remain asymptomatic. HYPOTHESIS: We hypothesized the existence of a systemic "signature" that could distinguish "vulnerable" patients with preexisting coronary atherosclerosis from those having similar risk factors and atheromatous burden, but no history of clinically evident plaque rupture/erosion. METHODS: Twenty three patients who had at least two prior myocardial infarctions ("vulnerable group") were matched in respect to their background and coronary atherosclerosis extent with twenty one patients without a history of previous myocardial infarction who underwent routine coronary angiography before valvular surgery. We studied a panel of cytokines, antibodies and hormones including IL-6, IL-10, IL-12, antibodies to ß2 glycoprotein I (ß2GPI), antibodies to oxidized-LDL, adiponectin and resistin, along with levels of circulating EPCs and Tregs. RESULTS: A significantly higher level of Treg cells was present in the control (73.4%±4) than in the "vulnerable patient" group (62.2%±10.7), p<0.001. IL-10 level was also significantly higher in the control than in the vulnerable patients (2.6±1.2 pg/ml versus 0.9±0.1 pg/ml respectively, p=0.03). There was no significant difference in the circulating levels of the other cytokines, hormones or EPCs between the two groups. CONCLUSION: Regulatory T cells and serum IL-10 may discriminate "vulnerable" versus stable patients and may have a protective role against plaque rupture in patients with coronary atherosclerosis.