In spite of about 300 environmental risk factors of CAD, including lipoprotein(a) high levels, which is  a risk factor, BUT not a cause, of coronary disease, exclusively individuals with CAD Inherited Real Risk can be involved by coronary disease, as I have demonstrated in previous papers (1-19). If physicians do not decide themselves to learn, and thus bedside recognize, such as particular situation of coronary microvessels, characterized by a typical microcirculatory remodelling, CAD will continue to be a growing severe epidemics, unfortunately.

 Sergio Stagnaro MD

Lp(a) appears to be a scavenger for oxPL from oxLDL and apototic cells. Lp(a) binds and transports oxPL and with its high LpPLA2 content mediates their clearance. So when Lp(a) is low it is atheroprotective but when high proatherogenic. Interestingly when I have treated high Lp(a) with niaspan to normal levels I have also seen LpPLA2 normalize. There also appears to be a association between sdLDL subfraction IVb with Lp(a) which improves with niaspan.

Compliment to Woody Johnson for his precise, fascinating and useful comment. He emphasises worthly the importance of free radical scavenger activity of Lp(a). Only if oxidated LDL are dangerous! Interestingly, Woody Johnson refer to the positive effects of niaspan!