Reverse atherosclerosis diet
Calcification at the outer base of older or more advanced lesions. The remnants eventually include calcium and other crystallized materials within the outermost and oldest plaque. This is promoted by low-density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides ) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDL). One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). Upon formation, intraluminal thrombi can occlude arteries outright (e. , coronary occlusion), but more often they detach, move into the circulation, and eventually occlude smaller downstream branches causing thromboembolism.
Most commonly, soft plaque suddenly ruptures (see vulnerable plaque ), causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately five minutes. Chronically expanding lesions are often asymptomatic until lumen stenosis is so severe (usually over 80%) that blood supply to downstream tissue(s) is insufficient, resulting in ischemia. Atherosclerosis is therefore a syndrome affecting arterial blood vessels due to a chronic inflammatory response of WBCs in the walls of arteries. Apart from thromboembolism, chronically expanding atherosclerotic lesions can cause complete closure of the lumen. The plaque is divided into three distinct components. g. These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. These accumulations contain both living, active WBCs (producing inflammation ) and remnants of dead cells, including cholesterol and triglycerides.
