Invivo Health Assessment
NMR LipoProfile with Lipids
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.
References & more info can be found in the Cleveland Heart Lab guide.