Prevention of contrast-associated acute kidney injury in an era of increasingly complex interventional procedures.

Radiological and interventional cardiology procedures are in continuous expansion, leading to an important increase in the incidence of contrast-associated acute kidney injury (CA-AKI). Although numerous methods of CA-AKI prevention have been studied, at present, there is no consensus on the definition of this entity or on its prevention. In this paper, we aim to provide a critical analysis of the existing data on the epidemiology, pathophysiology, and clinical significance of CA-AKI. Existing and emergent approaches for CA-AKI prevention are also discussed, with a focus on parenteral fluid administration and on the most recent clinical and experimental data. We also emphasize a number of questions that remain to be answered, and we identify hotspots for future research.

Neutrophil gelatinase-associated lipocalin monitoring reveals persistent subclinical kidney injury following intraarterial administration of iodinated contrast agents.

Clinically overt contrast-induced nephropathy (CIN) is one of the most feared complications in patients exposed to iodinated contrast media and has been extensively studied over the years. Meanwhile, the incidence and evolution of subclinical contrast-induced kidney injury remain elusive. With the continuous increase in the number of patients that are repeatedly exposed to contrast media, elucidating these issues is of critical importance. Accordingly, we aimed to evaluate the incidence and the evolution of clinical and subclinical kidney injury in patients exposed to contrast media. A total of 178 patients who underwent elective percutaneous angioplasty procedures were evaluated prospectively. Serum creatinine and neutrophil gelatinase-associated lipocalin (NGAL) levels were evaluated pre-procedurally, 48 h and 1 month after administration of contrast media. The evolution of creatinine and NGAL levels was analyzed at the three time points, and the potential predictors of contrast-induced clinical and subclinical renal injury were evaluated. Clinically overt CIN occurred in 10 (5.6%) patients. Baseline serum creatinine and the volume of contrast media were the only independent predictors of CIN and in all 10 patients creatinine levels returned to baseline by 1 month (p = 0.32). Subclinical contrast-induced kidney injury was much more common, affecting 32 (17.9%) patients, was only predicted by the baseline serum creatinine, and persisted in 53.1% of patients after 1 month. This study showed that whereas clinically overt CIN is rather rare and regressive, subclinical contrast-induced kidney injury is considerably more frequent, affecting almost 18% of patients that receive intraarterial contrast media. More importantly, subclinical kidney injury persisted after 1 month in more than 50% of the initially affected patients, who may thus be at increased risk for further renal impairment, particularly if exposed to nephrotoxic agents or repeated administration of contrast media.

Prediction of 3-year all-cause and cardiovascular cause mortality in a prospective percutaneous coronary intervention registry: Machine learning model outperforms conventional clinical risk scores.

BACKGROUND AND AIMS: Machine learning (ML) models have been proposed as a prognostic clinical tool and superiority over clinical risk scores is yet to be established. Our aim was to analyse the performance of predicting 3-year all-cause- and cardiovascular cause mortality using ML techniques and compare it with clinical scores in a percutaneous coronary intervention (PCI) population. METHODS: An all-comers patient population treated by PCI in a tertiary cardiovascular centre that have been included prospectively in the local registry between January 2016-December 2017 was analysed. The ML model was trained to predict 3-year mortality and prediction performance was compared with that of GRACE, ACEF, SYNTAX II 2020 and TIMI scores. RESULTS: A total number of 2242 patients were included with 12.1% and 14.9% 3-year cardiovascular and -all-cause mortality, respectively. The area under receiver operator characteristic curve for the ML model was higher than that of GRACE, ACEF, SYNTAX II and TIMI scores: 0.886 vs. 0.797, 0.792, 0.757 and 0.696 for 3-year cardiovascular- and 0.854 vs. 0.762, 0.764, 0.730 and 0.691 for 3-year all-cause mortality prediction, respectively (all p ≤ 0.001). Similarly, the area under precision-recall curve for the ML model was higher than that of GRACE, ACEF, SYNTAX II and TIMI scores: 0.729 vs. 0.474, 0.469, 0.365 and 0.389 for 3-year cardiovascular- and 0.718 vs. 0.483, 0.466, 0.388 and 0.395 for 3-year all-cause mortality prediction, respectively (all p ≤ 0.001). CONCLUSION: The ML model was superior in predicting 3-year cardiovascular- and all-cause mortality when compared to clinical scores in a prospective PCI registry.

Renal dysfunction is associated with lower incidence of positive fractional flow reserve values in patients with severe hypertension.

BACKGROUND: Renal dysfunction, an important predictor of cardiovascular mortality, is paradoxically associated with a lower incidence of positive coronary fractional flow reserve (FFR) values, possibly due to renal disease-associated myocardial microvascular dysfunction. It is unknown if this relationship is influenced by arterial hypertension, a condition strongly associated with renal- and microvascular dysfunction. METHODS: The incidence of positive (<0.81) FFR values was retrospectively evaluated in consecutive patients with intermediate severity coronary artery lesions that were either associating or not associating renal dysfunction (creatinine clearance, CrCl <90 mL/min/1.73 m2), and had mild/moderate or severe arterial hypertension (treated by <3 or ≥3 different drugs). RESULTS: Positive FFR values were found in 49.5% of the 109 included patients, with a significantly lower incidence in those with renal dysfunction: 23 vs. 31 cases (39.7% vs. 60.8%, P=0.03). However, uni- and multivariate subpopulation analysis evidenced that renal dysfunction was a significant independent predictor of fewer positive FFR results only in severely hypertensive patients (univariate P values for mild/moderate and severe hypertension: 0.80 and <0.01, respectively; multivariate P in severely hypertensive patients: 0.04). This categorization significantly restricted the number of borderline FFR results (0.75-0.80) where measurement interpretation could be challenging because of renal dysfunction (from 13.8% to 4.6% of the whole study population, P=0.03). CONCLUSIONS: In the current study renal dysfunction was independently associated with a significantly higher incidence of negative FFR results in patients with intermediate severity coronary artery lesions only in the presence of severe arterial hypertension. This observation should be confirmed by large-scale prospective clinical trials.

Atrial electrical remodeling induced by chronic ischemia and inflammation in patients with stable coronary artery disease.

The pathophysiology of coronary artery disease (CAD) includes low-grade chronic inflammation. At its turn, inflammation is known to promote myocardial structural remodeling and to increase vulnerability to atrial arrhythmias. Meanwhile, the impact of chronic inflammation on the electrophysiological properties of the atria remains unknown. We aimed to evaluate the impact of low-grade chronic inflammation on atrial electrophysiology in patients with stable CAD undergoing elective coronary artery bypass grafting (CABG). Circulating levels of several inflammatory, angiogenesis, and endothelial dysfunction markers were determined 1 day before CABG in 30 consecutive CAD patients. Right atrial appendage samples were collected during the CABG procedure; action potential recordings were performed in six study patients using the microelectrode technique. Interleukin (IL)-1b (r = 1.00, P = 0.01), IL-6 (r = 0.98, P < 0.01), vascular endothelial growth factor (VEGF) (r = 0.98, P < 0.01), and hemoglobin (r = 0.98, P < 0.01) levels significantly positively correlated with the duration of atrial depolarization. Consequently, IL-6, VEGF, and hemoglobin (r = -0.86, P = 0.03 for all) levels significantly negatively correlated with the velocity of atrial depolarization. There was no significant correlation between any of the studied markers levels and any of the other parameters of the action potential (all P > 0.05). The present study is the first to demonstrate that in patients with stable CAD, chronic inflammation and ischemia are associated with pro-arrhythmic atrial electrical remodeling. These changes may contribute to the increased propensity to postoperative atrial arrhythmias seen in some of the patients undergoing CABG.

Chronic kidney disease predicts atrial fibrillation in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention.

Background: Atrial fibrillation (AF) often complicates ST-segment elevation myocardial infarction (STEMI). Predictors of AF in this setting include factors related to the acute phase of STEMI and pre-existing conditions. More recently, novel AF predictors have been identified in the general population. We aimed to assess the ability of such novel factors to predict STEMI-related AF.Methods: Data were collected from STEMI patients treated by primary PCI. Factors related to the acute phase of STEMI (Killip class, heart rate, blood pressure on admission, post-PCI TIMI flow), classic (age, hypertension, heart failure, previous myocardial infarction), and more novel (body mass index [BMI], diabetes, chronic kidney disease [CKD], chronic obstructive pulmonary disease [COPD]) AF predictors were evaluated. The ability of these novel factors to predict STEMI-related AF was assessed.Results: Of the 629 studied patients, 10.5% presented STEMI-related AF. AF patients had higher Killip class on admission (p < .0001) and lower post-PCI TIMI flow (p < .01), they were older (p < .0001) and more likely to have a history of heart failure (p = .02) and myocardial infarction (p = .04). BMI, history of diabetes and COPD were similar between patients with and without AF (all p > .05), but CKD was more common in AF patients (p < .0001). In multiple regression analysis, CKD remained a strong independent predictor of STEMI-related AF (p < .0001).Conclusion: Irrespective of other factors, CKD was associated with increased risk of STEMI-related AF. CKD could be used to identify patients who will develop AF in this setting and who would benefit from closer follow-up and more intensive prophylactic strategies.