Case presentation
Past Medical History
Family History
Social History
Laboratory Values
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
|
Comment
Discussion
DRUG | PERCENT INCRESE |
---|---|
Nicotinic acid (niacin) | 15% – 35% |
Fibrates | 10% – 15% |
Estrogens | 10% – 15% |
Statins Coupled Dual Effect Associated with potent LDL-C reduction, which make the statins "shine" | 5% – 10% |
Alpha blockers | 10% – 20% |
Alcohol (in moderation) | 10% |
Ezetimibe | 3% |
Isolated low HDL-C
1. | Elevated triglycerides. | (Component of metS) |
---|---|---|
End stage renal disease | ||
Hypothyroidism [also increased total Chol/HDL-C ratio. | ||
2. | Obesity and Overweight. – [waist measurement] – | (Component of metS) |
[Visceral obesity in particular] | ||
For every 3 kg. (7 lbs.) weight loss HDL-C increased 1 mg/dL. | ||
3. | Prediabetes and overt Type 2 Diabetes Mellitus. | (Component of metS) |
4. | Physical inactivity | (lifestyle choice). |
5. | Smoking | (lifestyle choice). |
6. | Very high carbohydrate intakes > 50–60% of energy | (lifestyle choice). |
[Especially Fructose Containing Soft Drinks.] | ||
7. | Metabolic Syndrome: As potent a risk factor as smoking. | |
8. | Drugs, such as beta-blockers, anabolic steroids, and progestational agents. |
REVERSE CHOLESTEROL TRANSPORT |
---|
Accepts cholesterol from the macrophage and tissues and transports it back to the liver for disposal in the bile (figure 1). |
Acts a an apoprotein donor to the other lipoproteins |
ANTIOXIDANT
|
Antioxidant activity (through intimal paraoxonase, and redox -sensitive methionine residues of apo A-1) |
Increases eNOS and endothelial nitric oxide |
ANTIINFLAMMATORY
|
Downregulates adhesion molecule expression on endothelium: (I-CAM, V-CAM and MCP-1) |
Inhibits neutrophil degranulation |
ANTITHROMBOTIC
|
Antithrombotic activity via its ability to block TxA2 and potentiates activity of proteins: C and S. |
Stimulates prostacyclin production (antithrombotic and vasodilitory). |
ENDOTHELIAL PROTECTION PROTERTIES
|
Acts as an endothelial mitogen and inhibits endothelial cell apoptosis: This would help to decrease the incidence of plaque erosion and promote plaque stabilization |
Stimulates endothelial nitric oxide (eNO and its enzyme eNOS) and prostacyclin production with vasodilatation, antioxidant, and anti-inflammatory properties. |
Emerging novel risk markers of atherosclerosis
The Atherosclerotic Kitchen Sink
RISK FACTOR | ODDS RATIO |
---|---|
Abnormal lipids: ApoB/ApoA-1 | 3.25 |
Smoking | 2.87 |
Diabetes | 2.37 |
Hypertension | 1.91 |
Abdominal obesity Reason for such a high OR: This could aggravate smoking, diabetes, hypertension, obesity, alcohol abuse and even nutrition (eating aggressively) | 1.12 |
Psychosocial Factors | 2.67 |
Alcohol use | 0.91 |
Physical Activity | 0.86 |
Consumption of fruits and vegetables | 0.70 |