Plaque Stabilization and Decreased Plaque Thrombogenicity
Experiments have demonstrated that cholesterol reduction is accompanied by favorable alterations in a number of mediators of plaque stability.[39,40]Studies have shown that statins decrease macrophage number, reduce expression of tissue factor, adhesion molecules, and matrix metalloproteinases within plaque.[39] The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors also reduce the oxidation of LDL, macrophage uptake of LDL,[24,25] and reduce monocyte adhesion to endothelium.[25] Lipid lowering with statins results in increased smooth-muscle cell content (a surrogate of plaque stability) and decreased collagen degradation (which may further enhance plaque stability).[39] Clinical studies support these experimental observations and provide further evidence that statin therapy may be associated with plaque stabilization. Statins may also inhibit atherogenesis through the inhibition of vascular smooth-muscle cell proliferation and migration, and thus attenuate plaque growth and new lesion formation.[41]
"While plaque stabilization mainly focuses on repairing the endothelial cap and strengthening collagen content, plaque regression mainly focuses on aggressive lipid management to remove necrotic components and restore normal endothelial function of the arterial wall. Plaque stabilization has already been proven to reduce clinical events and studies with statins, HDL-C increasing agents, anti-thrombotic agents, ACE inhibitors, calcium antagonists, oral anti-oxidants, and diet modifications have shown that reduction in clinical events need not be reflected by reduced plaque volume. The major studies supporting plaque stabilization included MIRACL, PACT, CURE, HOPE, and Lyon Diet Heart Study."
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If using exercise though, care must be taken:
"Sudden rupture of a vulnerable plaque may occur spontaneously without obvious triggers. By contrast, it may follow a particular event, such as extreme physical activity (especially in someone unaccustomed to regular exercise), severe emotional trauma, sexual activity, exposure to illicit drugs (cocaine, marijuana, amphetamines), exposure to cold, or acute infection (106–114)."
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Another factor which may contribute toward decreased risk for stroke with statin therapy is the effect of statins on platelets and the endogenous balance of thrombosis/thrombolysis.[40] Statin therapy decreases platelet activation and aggregation, and thereby may decrease the propensity toward thrombosis.[10,23,42,43]
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This can definitely be reduced through diet
Also:
"Diets such as Mediterranean diet, high in omega-3 polyunsaturated fatty acids (PUFA), and vegetarian diets have inverse relationships with CVD. Dark chocolate, foods with low glycemic index, garlic, ginger, omega-3 PUFA, onion, purple grape juice, tomato, and wine all reduce platelet aggregation. Dark chocolate and omega-3 PUFA also reduce P-selectin expression. In addition, dark chocolate reduces PAC-1 binding and platelet microparticle formation. Berries inhibit platelet function (PFA-100)."
"Coffee drinking decreases platelet aggregation, and induces a significant increase in phenolic acid platelet concentration. The antiplatelet effect of coffee is independent from caffeine and could be a result of the interaction of coffee phenolic acids with the intracellular signalling network leading to platelet aggregation."
https://www.ncbi.nlm.nih.gov/pubmed/18439332
Statin therapy inhibits tissue factor expression by macrophages, which plays an integral role in blood coagulation and is an important determinant of plaque thrombogenicity.[23,25] There also may be a reduction in plasminogen activator inhibitor activity, which would facilitate fibrinolysis.[23] All of these factors may contribute toward decreased risk for stroke seen in the statin studies. These statin effects may lead to decreased thrombus formation and thereby influence the development of clinical activity related to atherosclerotic plaque.
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