coronary calcifications and the paradoxes of statins and endurance exercise

Coronary artery calcification is by definition coronary artery disease

Calcification can occur in the intima and in the media with possible different pathological implications.

All coronary artery calcifications (CAC) are not created equally. Dense calcification can occur in fibrous,stable plaques which carry little risk of rupture but can narrow the coronary arteries causing angina and ischemia on exercise. Spotty calcification can occur on unstable plaques which can rupture causing an acute coronary events and yet not be detectable on stress testing.

The is more than adequate epidemiologic evidence that statins can decrease the risk of coronary artery events- certainty when used in secondary prevention.So it seems paradoxical that more intense statin therapy as with the more potent statins  and for longer periods of time is associated with more CAC.The standard answer to this apparent paradox is that statins are able to stabilize plaques making them less at risk of rupture and that in part the putative stabilization involves dense calcification.

There is also more than adequate epidemiologic evidence that endurance exercise decreases the risk of coronary artery disease and cardiac vascular mortality.so it seems paradoxical that studies (at least some) have shown increase coronary artery calcifications with increasing levels of exercise. Might a reasonable answer to this paradox be that endurance exercise helps stabilize plaques by calcifying them. In fact some of the authors who have reported increased CAC with increased exercise have suggest that mechanism.

Merghani et al (1)reported on a study of  152 men who had logged an average of 31 years of endurance exercise type activities. All had echocardiograms,24 hour Holter, stress ECG,CT coronary angiograms (CAC) and cardiac MRs with gadolinium as did 92 age matched controls with similar Framingham Risk scores.

15  athletes and none of the controls had late gadolinium enhancement (LGE) on the MRs, 7 of which had a coronary artery pattern.(The LGE issue will need to be written about at a later date.,for now  the focus is on the  calcification.)

60% of the athletes and 63% of controls had a normal CAC score but only athletes (11.3%) has a CAC score of 300 or greater. So the incidence of any calcification was about the same in athletes and controls but the athletes had more calcium and more demonstrable luminal stenosis ( greater than 50%) in 7.5% of the athletes and in none of the controls.

So does this mean that long time endurance exercise increased the risk of coronary artery disease?
Maybe an answer to that is related to another question-does the increase in calcium scores noted in patients taking statins mean that statins increase the risk of coronary artery disease which is , of course, a conclusion contrary to realms of clinical trial results demonstrating the value of statins, at least in secondary prevention.

In regard to the second question there is a great deal of data regarding what could be called the statin plaque paradox-statins increase coronary artery calcium even as they shrike the plaques.A person's calcium score could increase even as the plaques regress because of the increased density of calcification bought about by the statins.

For long term endurance athletes who might be worrying that their ill spent youth and/or middle age and /or early old age was in fact ill spent might get some sense of relief from these comments from Dr  Benjamin Levine.


1)Merghani,A Prevalence of subclinical Coronary artery Disease in Masters endurance theleres with a low atherosclerotic risk profile. Circ. 2017, 136, p 137