Cardiac surgery associated acute kidney injury (CSA-AKI) is a significant clinical problem. Its pathogenesis is complex and multifactorial. It likely involved at least six major injury pathways: exogenous and endogenous toxins, metabolic factors, ischemia and reperfusion, neurohormonal activation, inflammation and oxidative stress. These mechanisms of injury are likely to be active at different times with different intensity and probably act synergistically. Because of such complexity and the small number of randomised controlled investigations in this field only limited recommendations can be made. Nonetheless, it appears important to avoid nephrotoxic drugs and desirable to avoid hyperglycemia in the peri-operative period. The duration of cardiopulmonary bypass should be limited whenever possible. Off-pump surgery, when indicated, may decrease the risk of AKI. Invasive hemodynamic monitoring focussed on attention to maintaining euvolemia, an adequate cardiac output and an adequate arterial blood pressure is desirable. Echocardiography may be useful in minimizing atheroembolic complications. The administration of N-acetylcysteine to protect the kidney from oxidative stress is not recommended. There is marked lack of randomised controlled trials in this field.

In the large dataset of the SOURCE XT registry, the presence of either pre-existing or NOAF increased all-cause and cardiac mortality and bleeding events. NOAF was associated with increased stroke rates at long-term follow-up.

Concomitant moderate-severe MR was associated with increased early and late mortality following TAVR. A significant improvement in MR severity was detected in half of the patients following TAVR, and the degree of improvement was greater in those patients who had received a BEV.

This preliminary experience showed that, in patients at high risk for conventional surgery, SU-AVR is as safe and effective as TA-TAVI and that it is associated with a lower rate of postprocedural paravalvular leak.

Between 2014 and 2016, the need for ECS remained stable around 0.7%. Left ventricular guidewire perforation and annular rupture were the most frequent causes, accounting for almost half of ECS cases. Half of the patients could be salvaged by ECS-nevertheless, 1 year of all-cause mortality was high even in those ECS patients surviving the in-hospital period.