The skeptical cardiologist did not get to travel to Munich to attend the recent European Society of Cardiology meetings but the electrophysiologist, John Mandrola did. He summarized two big trials which showed no benefit of aspirin in the primary prevention of cardiac disease, one in patients with diabetes and one in patients with moderate risk in Ten Things I Learned About Aspirin at ESC
Of note, the lack of benefit in these studies is partially related to a much lower rate of events than predicted from standard risk models.
Why? Mandrola notes:
“societal efforts, such as lower rates of smoking and removal of trans-fats from the food supply, have led to a heart-healthier environment. In addition, greater use of preventive therapies—statins and antihypertensive meds, for instance—have also contributed to lower rates of cardiac disease. These developments increase the difficulty of running trials for primary prevention but are decidedly good news for patients.”
Similar to the ASPREE study, aspirin did not show any benefit in reducing GI cancer in these two large studies.
So aspirin may be less effective than it was decades ago because we have done a good job overall of reducing the risk of heart attack and stroke.
acetylsalicylic ally Yours,
h/t Reader Francis
1 thought on “What John Mandrola Learned About Aspirin in Munich”
Something that always confuses me is what is the threshold of primary vs secondary prevention? In the ASCEND trial it specifically eliminates the patient subset that has had a MI, angina pectoris, revascularization or angioplast. This leads me to conclude that their definition of secondary prevention relies on having one of the CV events above. What about other diagnostic tests like CAC or CIMT? If one has calcification revealed by either test (>50% for age under 65) than would they be considered secondary prevention or primary prevention? Would you still recommend someone with a higher CAC or CIMT (>50% for age under 65) to still use aspirin therapy? Do you feel that CAC or CIMT is a definitive diagnostic tool to determine existing occlusive vascular disease and if so do you consider treatment to be primary or secondary?