Table 1 The RAAS acronym: global risk reduction
R | Reductase inhibitors (HMG-CoA). Decreasing modified LDL-cholesterol, i.e. oxidized, acetylated LDL-cholesterol. Decreasing triglycerides and increasing HDL-cholesterol Improving endothelial cell dysfunction. Restoring the abnormal Lipoprotein fractions. Thus, decreasing the redox and oxidative stress to the arterial vessel wall and myocardium. |
|---|---|
Redox stress reduction. | |
A | AngII inhibition or blockade: |
ACEi-prils. ARBS-sartans. Both inhibiting the effect of angiotensin-II locally as well as systemically. Affecting hemodynamic stress through their antihypertensive effect as well as the deleterious effects of angiotensin II on cells at the local level – injurious stimuli -decreasing the stimulus for O2. production. Decreasing the A-FLIGHT toxicities. Plus the direct-indirect antioxidant effect within the arterial vessel wall and capillary. Antioxidant effects. Aspirin antiplatelet, anti-inflammatory effect. Adrenergic (non-selective blockade) in addition to its blockade of Prorenin→Renin Amlodipine with its calcium channel blocking antihypertensive effect, in addition to its direct antioxidant effects. | |
Redox stress reduction. | |
A | Aggressive control of diabetes to HbA1c of less than 7. (This usually requires combination therapy with the use of: Insulin secretagogues, insulin sensitizers (thiazolidinediones), biguanides, alpha-glucosidase inhibitors, and ultimately exogenous insulin.) Decreasing modified LDL cholesterol, i.e. glycated – glycoxidated LDL cholesterol. Improving endothelial cell dysfunction. Also decreasing glucotoxicity and the oxidative – redox stress to the intima and pancreatic islet. Aggressive control of blood pressure, which usually requires combination therapy, including thiazide diuretics to attain JNC 7 guidelines. Aggressive control of dyslipidemias, which frequently requires combination therapy (especially in the metabolic syndrome and T2DM), including TLC, statins, fibrates, selective cholesterol inhibitors such as ezetimibe, and niacin Aggressive control of Hcy with folic acid with its associated additional positive effect on re-coupling the eNOS reaction by restoring the activity of the BH4 cofactor to run the eNOS reaction and once again produce eNO. |
Redox stress reduction. | |
S | Statins. Improving plaque stability (pleiotropic effects) independent of cholesterol lowering. Improving endothelial cell dysfunction. Plus, the direct – indirect antioxidant anti-inflammatory effects within the islet and the arterial vessel wall promoting stabilization of the unstable, vulnerable islet and the arterial vessel wall. Style: Lifestyle modification: lose weight, exercise, and change eating habits. Stop Smoking |
Redox stress reduction | |