Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases. CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h. More sensitive markers of renal injury are desired, therefore, several biomarkers of tubular injury are under evaluation. Multiple risk factors may contribute to the development of CIN; these factors are divided into patient- and procedure-related factors. Treatment of CIN is mainly supportive, consisting mainly of careful fluid and electrolyte management, although dialysis may be required in some cases. The available treatment option makes prevention the corner stone of management. This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications.

The clinical, genetic, and molecular paradigm of arrhythmogenic right ventricular cardiomyopathy (ARVC) has markedly progressed through the last three decades, shifting from the classical ARVC as a progressive condition characterized by fibrofatty replacement of the right ventricle,2,3,4 into a wider spectrum of arrhythmogenic cardiomyopathy (AC),5 which covers ARVC with its various clinical phases (occult, electric, right heart failure and late stage biventricular heart failure), biventricular arrhythmic cardiomyopathy, left dominant arrhythmic cardiomyopathy, Naxos and Carvajal syndromes. Epidemiologically, the disease was first associated with the Mediterranean basin (mainly Italy and France), however further studies have reported AC in many races and ethnic backgrounds6,7,8. Moreover, with regard to the pathoitiology of the disease, dysplasia was originally assumed as the disease mechanism. Other mechanisms were later postulated, such as inflammation and transdifferentiation. However, more recent animal models have established that dystrophy, either by myocyte necrosis or apoptosis, is the founding pathological process of AC

Cardiogenic shock (CS) in the setting of acute coronary syndrome carries detrimental consequences and high levels of mortality and morbidity if not managed promptly. Acute mitral regurgitation (MR) as a complication of the myocardial infarction might superimpose refractory CS that warrants mitral valve repair. There has been growing use of Transcatheter edge-to-edge mitral valve repair (TEER) as a therapy for CS secondary to acute MR. In this cohort, we describe two cases of CS secondary to acute ischemic MR managed with a Mitraclip.

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