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Preface: Arterial inflammation is a significant component of atherosclerotic disease process. The inflammatory biomonitor and physical diagnostic tests described provide insight to the influence of atherogenic cofactors such as altered cholesterol metabolism, tobacco use, etc., and their impact on the inflammatory responses in the progression of atherosclerotic lesions. Evidence suggests that the chronic perpetuation of immune mediated vascular inflammation and cholesterol-induced atherosclerosis are key steps in atherogenesis.

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  • MPO is a strong predictor of short term risk for a cardiovascular event.
  • MPO, an enzyme released from white blood cells, accumulates in lesions in the arterial
    wall. MPO diminishes nitric oxide bioavailability and oxidizes LDL, increasing unstable
    lipid deposits in the arterial wall. Lesions can rupture resulting in blockages downstream
    or formation of a thicker endothelial layer.
  • MPO measurements, combined with other inflammatory markers and CIMT, enhance
    cardio- vascular risk prediction especially in patient subgroups associated with low risk.
  • For individuals with increased MPO levels, consider more aggressive lipid lowering and
    antiplatelet drug therapy and lifestyle changes that promote vascular health and reduce
  • Repeat abnormal results every quarter until treatment goal is met, then annually for continuous monitoring of CVD risk.
  • Lp-PLA2 is a strong predictor of short term risk for a heart attack or stroke.
  • Lp-PLA2 is an enzyme released in the plasma as a part of the immune response to vascular injury. Lp-PLA2 hydrolyzes LDL, promoting lipid deposits and rupture prone plaque.
  • High concentrations are found in advanced atherosclerotic lesions.
  • Lp-PLA2 is generally not elevated in systemic inflammatory conditions, and therefore is a good marker of vascular specific inflammation and thrombosis.
  • Lp-PLA2 combined with other test results aids in the decision for lipid lowering or anti-inflammatory therapy and intensified lifestyle changes.
  • For abnormal Lp-PLA2 consider statins, niacin, or fenofibrate therapy. Consider aspirin therapy if not contraindicated. Assess blood pressure. If not at goal, consider anti-hypertensive therapy. Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
  • Repeat abnormal results every quarter until treatment goal is met, then annually to monitor cardiovascular risk.
  • hs-CRP is a protein released during acute phase inflammation.
  • hs-CRP is a well-documented clinical marker of general and cardiac related inflammation,
    even in individuals with normal LDL.
  • Research shows that healthy individuals with elevated hs-CRP are 4 times as likely to
    experience CVD events.
  • Elevated levels, along with other inflammatory bio-monitors and CIMT results, aids in the
    decision for lipid lowering and lifestyle therapy, especially in apparently healthy
    individuals. Rule out and treat other sources of systemic inflammation.
  • For abnormal hsCRP levels consider statins, ezetimibe or combination therapy if not
    contraindicated. Consider aspirin therapy if not contraindicated. Assess blood pressure.
    If not at goal, consider initiating anti-hypertensive therapy. Consider diet/exercise/weight reduction efforts as appropriate.
  • Repeat abnormal results every quarter until treatment goal is met, then annually.
  • F2-IsoPs is a strong predictor of future risk for coronary artery disease.
  • F2-IsoPs are compounds produced by free radical oxidation. They promote platelet activation and aggregation resulting in thrombosis or blood clots.
  • F2-IsoPs levels are reduced with low saturated fat diets, regular exercise and smoking cessation. Consider drug therapy if lipids are not at goal or if other bio monitors are elevated.
  • For abnormal F2-Isoprostane levels consider statins, ezetimibe or combination therapy if not contra- indicated. Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
  • Repeat abnormal results every quarter until treatment goal is met then annually to assess future risk of cardiovascular disease.
  • Microalbumin appearing in the urine reflects glomerular endothelial dysfunction and loss of
    micro- vascular integrity.
  • Individuals with high urinary microalbumin levels are 3 times more likely to develop
  • cardiovascular disease.
  • Patients with inflammation or narrowing of the small arteries in the kidneys are also at risk
    for endo- thelial dysfunction in the rest of their vascular system.
  • Early identification and treatment of lipids, glucose and blood pressure can slow down the
    disease progression. Measure endothelial function to determine vascular compliance.
  • For abnormal Microalbumin/Creatinine levels consider initiating or titrating anti-hypertensive
    therapy. Assess the presence of CAD with imaging techniques such as CIMT and consider aspirin therapy if not contraindicated.
  • Repeat abnormal Microalbumin/Creatinine ratio every 3 - 6 months until controlled, then yearly for high risk individuals with kidney disease, hypertension, and diabetes.
  • Vitamin D deficiency is associated with an increased risk for heart disease.
  • Both forms of Vitamin D are measured; Vitamin D3 is three times as potent as D2.
  • Two-thirds of US population has suboptimal levels of Vitamin D. Consider increasing time in sun, dietary sources, or supplementation.
  • Often patients who have elevated percent body fat concentrations have low Vitamin D levels.
  • When combined with other biomonitors, Vitamin D better defines an individual’s risk for heart disease.
  • For insufficient Vitamin D levels, consider vitamin D-rich foods such as cheese, vitamin D-fortified milk, shitake and button mushrooms, or supplementation with vitamin D3
  • Monitor abnormal Vitamin D measurements quarterly until treatment goal is met, then monitor annually.
  • Oxidized LDL more accurately predicts the progression of heart disease and plaque formation
    in the arteries before symptoms have presented themselves.
  • OxLDL is formed when the ApoB protein on LDL particles becomes oxidized. OxLDL is
    recognized by scavenger receptors on macrophages which engulf OxLDL, leading to foam cell
    formation which in turn initiates artherosclerosis and enhances vascular inflammation.
  • Individuals with high levels of OxLDL are 4 times more likely to develop metabolic syndrome
    in the next 5 years.
  • Increased OxLDL levels are associated with the presence of coronary heart disease, diabetes,
    and acute myocardial infarction. For individuals with elevated OxLDL consider
    cholesterol-lowering medications, CoQ10, Omega-3 fatty acids, vitamin E, and low glycemic foods.
  • Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
  • The OxLDL test can be ordered in conjunction with standard/lipid testing or inflammation testing.

Micronutrient Tests Associated With Vascular Inflammation

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Cofactor to the powerful antioxidant superoxide dismutase that fights inflammation within cells.

Deficiency activates proinflammatory chemicals called cytokines; Deficiency will also kick start a damaging immune response by activating cells called leukocytes and macrophages.

Repairs damage to cells caused by inflammation; Regulates the production of pro-inflammatory cytokines; Recycles vitamins C and E.

Protects organs such as blood vessels, brain and liver from inflammatory damage; Precursor to glutathione production; Supplementation with Nacetyl cysteine raises glutathione.

Vitamin C
Low vitamin C linked to inflammation; Inversely related to C-reactive protein (CRP), a marker for systemic inflammation; Increases glutathione.

Vitamin D
Potent modulator of inflammation; Helps turn off chronic inflammatory responses; Inhibits pro-inflammatory cytokine production.

Vitamin E
Limits destructive cell behavior caused by inflammatory enzymes gone wild; Reduces damage from tumor necrosis factor alpha (TNF-α); Deficiency predisposes a person to inflammationrelated diseases.

Lipoic Acid
Neutralizes free radicals caused by uncontrolled inflammation in both water and lipid phases of the cell; Protects endothelial cells from inflammation; Regenerates other antioxidants such as vitamin E, C and glutathione.
Decreases cytokine production; Invokes an anti-inflammatory response; Precursor to glutathione.

Coenzyme Q10
Decreases several inflammatory markers (CRP and IL-6) in supplementation trials; Affects genes that control response to inflammatory stress.

Vitamin B6
Low B6 status is linked to high levels of CRP and systemic inflammation.

Vitamin B2
Riboflavin (B2) helps minimize pain associated with inflammation; Detoxifies homocysteine, an amino acid that indirectly causes inflammation in various tissues.

Vitamin A
Regulates the cellular immune response to inflammatory signals; Deficiency increases the severity of chronic inflammation; Zinc depletion lowers vitamin A status.

Inflammation raises demand for zinc; Pro-inflammatory chemicals (cytokines) dose dependently decrease in response to zinc repletion.

Deficiency lowers enzyme activity (such as superoxide dismutase) that fights inflammation; Lowers damaging isoprostanes, a byproduct of inflammation.

Subclinical deficiency negatively alters genes that regulate the inflammatory response; Deficiency promotes vascular inflammation.


  • CIMT is a noninvasive way to asses a patient’s cardiovascular health by measuring the thickness of the intima and media layers of the carotid artery.
  • CIMT accurately measures the presence of disease, vascular inflammation, risk of events, and progression or stabilization of the identified disease state.
  • here is a 96% correlation with findings from the CIMT and the presence of plaque in coronary arteries.
  • CIMT characterizes plaque based on the likelihood of predicting events. “Soft” plaque is more vulnerable and more likely to rupture than calcified plaque. Consider
    pharmacological and lifestyle therapy goals to reduce LDL-C and control other factors that promote the vascular inflammation
  • For abnormal CIMT results consider adding or titrating statin therapy, niacin, fenofibrates or aspirin therapy if not contraindicated. Consider clopidogrel if history of CAD. Consider adding Omega 3 or Vitamin D if not contraindicated. Assess blood pressure. If not at goal consider initiating anti-hypertensive therapy. Consider diet/exercise, smoking cessation and weight reduction efforts as appropriate.
  • Repeat CIMT annually to monitor progression, stabilization, or regression of plaque and/or vascular inflammation.
  • Endothelial Function (EF) is a noninvasive test to assess the function of the endothelial lining of the arterial wall.
  • By temporarily occluding the blood flow through arm compression, EF measures the ability of the vasculature to normalize blood flow by a bio-sensor measurement of vascular compliance.
  • Decreased vasodilation shows the initiation of an inflammatory state and endothelial dysfunction which can lead to or accelerate the development of plaque.
  • Endothelial dysfunction is reversible through lifestyle therapy, lipid lowering medications, and disease state control like blood pressure and blood sugar. Repeat EF every six months to monitor changes in arterial endothelial function.