Cholesterol Embolization

Cholesterol embolization syndrome, also called atheroembolism, occurs when cholesterol crystals break away from an ulcerated atherosclerotic plaque and travel downstream. The usual source is the aorta or the aorto-iliac-femoral arterial system. Unlike a thromboembolus, which commonly blocks a larger named artery, these crystals lodge in arterioles approximately 150–200 micrometres in diameter. The obstruction is only the first injury. The crystals activate the NLRP3 inflammasome, complement pathways and endothelial inflammation; macrophages and giant cells accumulate around the crystal material, while renin–angiotensin–aldosterone system activation worsens local ischaemia. The result is a systemic inflammatory microvascular disease rather than an isolated renal or limb problem. Fever, fatigue, weight loss, raised C-reactive protein and eosinophilia therefore fit the mechanism: this is not simply a silent mechanical blockage. Approximately 80% of cases follow arterial instrumentation, such as cardiac catheterisation, percutaneous coronary intervention, endovascular aortic or peripheral treatment, valve procedures, mechanical thrombectomy or aortic surgery. Anticoagulants and thrombolytic drugs are additional recognised precipitants because destabilisation of thrombus overlying a plaque may release plaque debris. Spontaneous disease is uncommon, occurring in a small minority of cases. The risk...