The protective role of PTX3 in CVD is supported by an animal model of acute MI, which showed increased myocardial damage along with increased C3 deposition in PTX3 deficient mice.[26] PTX3 is known to modulate activation of the alternative pathway through Factor H and down-regulate exaggerated inflammation by suppressing leucocyte extravasation through P-selectin.[27–29] Additionally, circulating C3 was positively correlated with IRD duration in our study thus underscoring the potential role of long-term IRD-associated inflammation on cardiovascular health. Here, SELP is linked to myocardial infarction.