Myeloperoxidase is an enzyme that promotes oxidative stress, blood vessel damage, endothelial dysfunction, and unstable atherosclerotic plaque. It converts LDL and HDL lipoproteins to pro-atherosclerotic forms. However, it also has anti-bacterial activity and may support immune defense against pathogens.
Elevated myeloperoxidase levels are associated with more severe atherosclerotic plaque and cardiovascular risk. Low myeloperoxidase may be cardioprotective. Dietary antioxidants can help protect against myeloperoxidase-induced oxidative damage.
Standard Range: 0.00 – 469.00 pmol/L)
The ODX Range: 0.00 – 400.00 pmol/L
Low myeloperoxidase may be associated with MPO deficiency which may be cardioprotective (Tavora 2009).
High levels of myeloperoxidase are associated with oxidative stress, inflammation, endothelial dysfunction, hypertension, increased cardiovascular risk, pulmonary arterial hypertension (Ramachandra 2020), diabetes, smoking, atherosclerotic plaque rupture (Tavora 2009), chronic heart failure (Tang 2006), vascular inflammation (Penn 2013), and increased risk of adverse cardiovascular events (Brennan 2003).
Myeloperoxidase (MPO) is an enzyme produced by activated white blood cells and deployed as part of an inflammatory immune system response. However, MPO generates pathogenic free radicals, including potent hypochlorous acid, and catalyzes the oxidation of low-density lipoprotein, creating a pro-atherogenic form of LDL (Tavora 2009).
Myeloperoxidase also promotes the dysfunction of HDL, further amplifying MPO’s atherogenicity. It is considered a “high-risk” biomarker for individuals with atherosclerosis, hypertension, heart failure, acute coronary syndrome, and stroke (Ramachandra 2020). It contributes to endothelial dysfunction, vasoconstriction, and increased vascular permeability. It is considered a specific marker of vascular inflammation (Penn 2013).
Myeloperoxidase can be found in circulation when fissures, erosions, or a degrading collagen cap is present in plaque. It is considered a marker of the vulnerability of plaque to rupture (Ferrante 2010). Ultimately, the presence of MPO is associated with more severe cardiovascular disease.
Myeloperoxidase levels helped predict the risk of death from coronary artery disease in a prospective study of 885 coronary angiography patients. Those in the highest tertile of MPO had a 2.4-fold greater risk of CVD mortality than those in the lowest. Higher MPO was associated with higher oxidized LDL and CRP, more severe atherosclerotic lesions, and stenosis of 50% or greater (Heslop 2010).
A higher MPO level predicted adverse cardiovascular events in a study of 604 emergency room patients with chest pain, even without myocardial necrosis. MPO was able to predict the early risk of myocardial infarction and future risk of adverse events, whereas troponin T, CK-MB, and C-reactive protein were unable to. The level of MPO associated with the most significant risk was 394.0 pmol/L or higher, representing a 38.4% greater risk. The lowest risk was associated with MPO below 119.4 pmol/L, while controls presented with a median MPO of 120 pmol/L (Brennan 2003). MPO levels are also significantly elevated in chronic heart failure (Tang 2006).
The free radicals generated by MPO oxidize the protein, lipid, and antioxidant components of LDL, an effect that may be mitigated by antioxidants, including vitamins C and E (Carr 2000). Early research indicates that vitamin C scavenges MPO-induced hypochlorous acid, and this action may protect against joint inflammation and damage in rheumatoid arthritis (Halliwell 1987).
Dietary sources of protective antioxidants include fruits, especially berries, vegetables, herbs, spices, onion bulbs, olive oil, cold-pressed seed oils, and other plant-based foods may help prevent myeloperoxidase-induced oxidation (Dimitrios 2006, Yashin 2017). Endogenous antioxidants, including uric acid, bilirubin, albumin, and thiols, also help counteract oxidative stress (Lobo 2010).
Brennan, Marie-Luise et al. “Prognostic value of myeloperoxidase in patients with chest pain.” The New England journal of medicine vol. 349,17 (2003): 1595-604. doi:10.1056/NEJMoa035003
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Heslop, Claire L et al. “Myeloperoxidase and C-reactive protein have combined utility for long-term prediction of cardiovascular mortality after coronary angiography.” Journal of the American College of Cardiology vol. 55,11 (2010): 1102-9. doi:10.1016/j.jacc.2009.11.050
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Ramachandra, Chrishan J A et al. “Myeloperoxidase As a Multifaceted Target for Cardiovascular Protection.” Antioxidants & redox signaling vol. 32,15 (2020): 1135-1149. doi:10.1089/ars.2019.7971
Tang, W H Wilson et al. “Plasma myeloperoxidase levels in patients with chronic heart failure.” The American journal of cardiology vol. 98,6 (2006): 796-9. doi:10.1016/j.amjcard.2006.04.018
Tavora, Fabio R et al. “Monocytes and neutrophils expressing myeloperoxidase occur in fibrous caps and thrombi in unstable coronary plaques.” BMC cardiovascular disorders vol. 9 27. 23 Jun. 2009, doi:10.1186/1471-2261-9-27
Yashin, Alexander et al. “Antioxidant Activity of Spices and Their Impact on Human Health: A Review.” Antioxidants (Basel, Switzerland) vol. 6,3 70. 15 Sep. 2017, doi:10.3390/antiox6030070