Invivo Comprehensive Health Assessment
NMR LipoProfile with Lipids
Comprehensive metabolic panel
MPO is a white blood cell-derived in ammatory enzyme and measures disease activity from the luminal aspect of the arterial wall.
Briefly, when the artery wall is damaged, or inflamed, MPO is released by invading white blood cells where it accumulates. MPO mediates the vascular in ammation that propagates plaque formation and activates protease cascades that are linked to plaque vulnerability. White blood cell activation in the bloodstream, in response to luminal injury of the artery wall including ssures, erosions or a degrading collagen cap, leads to MPO release in the bloodstream. This combination of detrimental effects demonstrates that MPO is actively involved in the progression of atherosclerosis. The Cleveland HeartLab MPO test measures free MPO in the bloodstream.
The MPO test may be performed on individuals with multiple risk factors for cardiovascular disease, or those with established disease.
Lp-PLA2, or lipoprotein-associated phospholipase-A measures disease activity within the artery wall below the collagen or calcified cap due to the activation of macrophages. Lp-PLA2 is not an acute phase reactant. When disease is active in the artery, increased levels of Lp-PLA2 are produced by macrophages and foam cells within the intima of the artery. Lp-PLA2 also interacts with oxidised LDL, which increases inflammation and enhances a pro-atherogenic state, as well as plaque vulnerability. Research suggests that it plays a direct role in the atherosclerotic disease process.
The Lp-PLA2 Activity test may be performed on individuals at intermediate or high risk for developing coronary heart disease
One of the earliest manifestations of endothelial dysfunction is nitric oxide (NO) deficiency, which promotes atherosclerosis. ADMA (asymmetric dimethylarginine) and SDMA (symmetric dimethylarginine), its structural isomer, are metabolites of L-arginine, an amino acid that is catalysed to L-citrulline and NO by nitric oxide synthase (NOS).
Both ADMA and SDMA have distinct pathophysiologies and manifestations. ADMA is a competitive inhibitor of NOS thereby reducing NO production and promoting endothelial dysfunction. SDMA also interferes with NO production, but does so indirectly by reducing the cellular availability of arginine. ADMA is primarily cleared through enzymatic degradation in the bloodstream and identi es subclinical cardiovascular disease. Conversely, SDMA is primarily excreted in the urine and identifies reduced renal function.
ADMA/SDMA may be measured in individuals with multiple risk factors for the development of cardiovascular disease.
Lp(a) is a plasma lipoprotein consisting of a cholesterol- rich LDL particle attached to an additional apolipoprotein called apo(a). Lp(a) levels are genetically determined1and not affected by changes in lifestyle2.
The Lp(a) test may be performed on individuals with a family history of premature coronary heart disease, a genetic predisposition for hypercholesterolemia, established atherosclerosis but with a normal routine lipid pro le, hyperlipidemia refractory to treatment, or a history of recurrent arterial stenosis.
Gut microbes live symbiotically within the human digestive tract and play important roles in host defense, immunity, and nutrient processing and absorption. This diverse community is unique to each person and in uenced by both acute and chronic dietary exposures to various food sources.
Nutrients such as phosphatidylcholine (also known as lecithin),choline,andL-carnitineareabundantinanimal- derived products such as red meat, egg yolk and full-fat dairy products. When consumed, these nutrients are processed by gut bacteria resulting in the release of various metabolites including TMA (trimethylamine) into the blood. TMA is then transported to the liver where it is converted into TMAO (trimethylamine N-oxide) which has been shown to regulate various physiological processes involved in the development of atherosclerosis1,2.
TMAO may be measured in individuals with one or more risk factors for the development of cardiovascular disease and/or individuals whom may bene t from intensive dietary intervention.
CoQ10 is a fat-soluble, vitamin-like substance present in most cells, primarily in the mitochondria. CoQ10 plays an integral role in the generation of cellular energy through aerobic cellular respiration. In addition, CoQ10 is a powerful antioxidant at physiologic concentrations.
The CoQ10 test may be performed on individuals on statin therapy who may or may not be experiencing myalgia symptoms, hypercholesterolemic individuals, and asymptomatic individuals at risk for vascular disease who may have low ApoA1 and/or HDL levels.
Omega-3 and omega-6 fatty acids (FA) are polyunsaturated long chain FA required by the body for proper functioning, normal growth and the formation of neural synapses and cellular membranes. Omega-3 and -6 FA are considered "essential” and obtained primarily from dietary sources.
Three of the most important omega-3 FA are eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA). Omega-3 FA are primarily obtained from oily sh. They have anti-oxidant1, anti-in ammatory2 and anti-thrombotic3 effects, and can help to reduce triglyceride levels4-6. Two of the most important omega-6 FA are arachidonic acid (AA) and linoleic acid (LA). Omega-6 FA are obtained from animal sources and plant oils, and have pro-in ammatory2,7 and pro-thrombotic7 properties at high levels.
OmegaCheckTM may be performed on individuals with hypercholesterolemia, hypertriglyceridemia, hypertension, and/or those at high metabolic or cardiovascular risk.
F2-IsoPs are prostaglandin-like compounds formed from the free radical-mediated oxidation of arachidonic acid1, and are the ‘gold standard’ for measuring oxidative stress in the body. F2-IsoPs also have potent biological effects associated with in ammation and therefore may mediate chronic disease initiation and progression. Additionally, F2-IsoPs may also act as potent vasoconstrictors2 via thromboxane formation in the endothelium, and promote platelet activation resulting in thrombus formation3.
F2-IsoPs may be performed on individuals at risk of future cardiovascular disease due to lifestyle risks, or those with a family history of cardiovascular disease.
Comprehensive Metabolic Profile
Sodium, Potassium, Chloride, Carbon Dioxide, Glucose, BUN, Creatinine, Calcium, Estimated Glomerular Filtration Rate, Albumin, Total Protein, Alkaline Phosphatase, Alanine Aminotransferase, Aspartate Aminotransferase, Total Bilirubin, and Globulin.
References & more info can be found in the Cleveland Heart Lab guide.