Anis Ahmad
To cure coronary artery disease, complete removal of atheroma from coronary arteries is necessary and may be achieved using pharmacological intervention. This hypothesis requires verification by a trial. The conditions that lead to the formation of atheroma are as follows: Insulin resistance and vascular endothelial dysfunction, Atherogenic dyslipidemia, Risk factors for coronary artery disease, Inflammation of coronary arteries, Drugs that increase insulin resistance. Atheroma formation begins with the formation of fatty streaks on the endothelium, which progress into stable or unstable atheromatous plaques. The unstable plaque has a thin fibrous cap that is prone to rupture. Unstable plaques contain a large lipid pool consisting of oxidized low-density lipoprotein (LDL), apoB and cholesterol that can grow; they are also have heavy inflammatory cell infiltration, including monocytes, macrophages and T cell lymphocytes. Moreover, debris from ruptured macrophages that were overloaded with lipids attracts more macrophages. The plaque can grow and protrude into the coronary artery lumen. Plaques exhibit overgrowth of vasa vasorum and they can rupture, leading to the formation of a large thrombus that may severely or completely obstruct the coronary artery. Hemorrhage may also occur in the plaque. Carvedilol and metformin promote plaque stability. The supply of lipids to the lipid pool in the plaque is reduced by statins and evolocumab, and lipids are removed from the lipid pool by apoA-1 and high-density lipoprotein (HDL) as their levels in the blood are increased. Severe inflammation is treated with carvedilol, metformin, statins and apoA. Growth of vasa vasorum is attributed to insulin resistance and can be reversed by carvedilol and metformin, thereby preventing hemorrhage. The size of the thrombus on a ruptured plaque can also be reduced by carvedilol, metformin and apoA-1, as these three agents prevent platelet aggregation. Thrombi are removed by endothelial thrombolysis. A thrombus may also form in the plaque from intraplaque hemorrhage; if present, the size of this type of thrombus will be small, as vasa vasorum are atrophic. In both cases, thrombi are removed by endothelial thrombolysis. Subsequently, healthy macrophages infiltrate and remove debris, after which the plaque changes to a fibrous nodule that can be removed by endothelial fibrinolysis. The plaque is then completely removed.
