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: Atherosclerosis and its fearsome complications represent the first cause of morbidity and mortality worldwide. Over the last two decades, several evidences have been accumulated, suggesting a central role for inflammation in atheroma development. High sensitivity C-reactive protein (hsCRP) is a well-established marker of cardiovascular (CV) disease; high levels of hsCRP have been associated with adverse CV outcome after acute coronary syndrome (ACS) and, despite some controversy, an active role for hsCRP in initiation and development of the atherosclerotic plaque has been also proposed. Randomized clinical trials focusing on hsCRP have been crucial in elucidating the anti-inflammatory effects of statin therapy. Thus, hsCRP has been progressively considered a real CV risk factor likewise to low-density lipoprotein cholesterol (LDL-C), rising the concept of residual CV inflammatory risk. Subsequent research has been designed to investigate potential new targets of atherothrombotic protection. Despite clinical usefulness of hsCRP is widely recognized, hsCRP may not represent the ideal target of specific anti-inflammatory therapies. Clinical investigations, therefore, have focused also on other inflammatory mediators, restricting hsCRP to an indicator rather than a therapeutic target. The aim of the present review is to provide an illustrative overview on the current knowledge of atherosclerosis and inflammation, highlighting the most representative clinical studies of lipid lowering- and antiinflammatory therapies focused on hsCRP in CV diseases.

Background: Acute kidney injury (AKI) after transcatheter aortic valve implantation (TAVI) has been associated with worse outcomes. However, the impact on outcome of AKI in TAVI-patients is not well established. Methods: Inoperable patients with severe aortic stenosis (AS) undergoing TAVI in 2010-2018 were enrolled in this study. AKI and chronic kidney disease (CKD) were defined according to KDIGO guidelines. Patients were divided in two groups according to post-procedural AKI development. The primary endpoint was 30-day allcause mortality across the two groups. Results: A total of 373 patients (mean age 82.3 ± 6) were analyzed. Compared to non-AKI patients, those who developed AKI, were treated more frequently with trans-apical TAVI (66% vs 35%, p<0.01), with greater amount of contrast medium (200.6 vs 170.4 ml, p=0.02) and in presence of clinically significant peripheral artery disease (PAD, 33% vs 21%, p=0.04). Trans-apical access (OR 3.24, 95% CI 1.76-5.60, p<0.01) was associated with a 3-fold risk of AKI. After adjustment for age, Society of Thoracic Surgery risk score (STS), PAD, access type, EF and contrast medium amount, patients with AKI presented an increased risk of 30-day all-cause mortality (HR=1.25, 95%CI 1.09-1.69, p=0.008). Patients with CKD IV and V, who developed AKI, presented a 9-fold 30-day mortality risk (HR=9.71, 95% CI 2.40-39.2, p=0.001). Conclusion:In our analysis, AKI was a strong predictor of 30-day all-cause mortality. Particularly, patients with severe CKD with AKI showed the highest 30-day mortality risk. Thus, this group of patients might benefit from closer monitoring and specific kidney protection therapies.