Warfarin has been utilized for decades as an effective anticoagulant in patients with a history of strong risk factors for venous thromboembolism (VTE). Established adverse effects include bleeding, skin necrosis, teratogenicity during pregnancy, cholesterol embolization, and nephropathy. One of the lesser-known long-term side effects of warfarin is an increase in systemic arterial calcification. This is significant due to the association between vascular calcification and cardiovascular morbidity and mortality. Direct oral anticoagulants (DOACs) have gained prominence in recent years, as they require less frequent monitoring and have a superior side effect profile to warfarin, specifically in relation to major bleeding. The cost and lack of data for DOACs in some disease processes have precluded universal use. Within the last four years, retrospective cohort studies, observational studies, and randomized trials have shown, through different imaging modalities, that multiple DOACs are associated with slower progression of vascular calcification than warfarin. This review highlights the pathophysiology and mechanisms behind vascular calcification due to warfarin and compares the effect of warfarin and DOACs on systemic vasculature.

Cardiogenic shock (CS) remains a significant clinical challenge with persistently high mortality rates. Defined by impaired cardiac output resulting in end-organ hypoperfusion, CS commonly arises from acute myocardial infarction (AMI-CS) or acute exacerbations of heart failure (HF-CS). The severity of CS is classified by the Society for Cardiovascular Angiography and Interventions (SCAI) into stages A (at risk) through E (extremis), which informs treatment strategies, including pharmacotherapy and mechanical circulatory support (MCS). Recent advancements in percutaneous mechanical circulatory support devices, including intra-aortic balloon pumps (IABPs), Impella devices, TandemHeart, Protek-Duo, and veno-arterial extracorporeal membrane oxygenation (VA-ECMO), have transformed management paradigms by offering targeted hemodynamic support. While DanGer-SHOCK, a pivotal randomized trial, demonstrated improved outcomes with early Impella use in anterior STEMI-associated CS, the trial’s focus population and center expertise suggest that its findings should be interpreted in the context of broader AMI-CS and HF-CS presentations. Device selection is guided by shock severity, anatomical considerations, comorbidities, and institutional capabilities. This review synthesizes current evidence, evaluates the clinical utility and efficacy of existing and emerging percutaneous MCS technologies, and highlights ongoing clinical trials and future directions in optimizing CS management. Emphasis is placed on individualized patient selection, evidence-based deployment of MCS devices, and multidisciplinary team collaboration, which collectively represent a critical transition towards improving clinical outcomes in CS.

Chronic kidney disease (CKD) is a globally recognized public health concern. Multiple studies have shown the association of CKD with cardiovascular mortality that persists after adjustment for traditional cardiovascular disease (CVD) risk factors. CKD causes accelerated coronary artery disease (CAD). In this chapter, we discuss the pathophysiological mechanisms that play a role in increasing CVD risk in patients with CKD. Further we delve into some commonly encountered challenges related to CVD in patients with CKD. These include revascularization challenges, contrasted induced nephropathy and alterations in traditional risk factors for CVD in renal transplant patients.