Why Does LDL-C Decrease With An MI?

I got this question from one of our cardiologists:

QUESTION: I was asked why LDL is fictitiously low for the 1st several months after acute coronary syndrome. I have to admit I do not know the mechanism…..

MY RESPONSE: I do not know the mechanism either, but the reduction in LDL can be great, up to a 50% or so LDL-cholesterol reduction. TGs go up. LDL is a “negative acute phase reactant”, it goes down with illness rather than up, so something with the infarct suppresses the level. The same thing happens with any illness or surgery. I saw it often before we had good drugs for familial hypercholesterolemia because my patients would have unexpectedly low levels and I would say, “Let me guess, you had the flu last week”. I was usually correct, and they feign being impressed. Beyond that, I am clueless as to the mechanism. The classic paper on the cholesterol /LDL reduction is by Rob Rosenson in 1993 and the citation and abstract are below. Look at the size of the LDL reductions! I am not sure the changes with an acute MI are as great in the present era because many people get prompt angioplasty so have less tissue injury. My guess is they also get less change in their LDL…I do not know of data to support that opinion, however.

Reference & Abstract to the Acute MI response: Rosenson RS. Myocardial injury: the acute phase response and lipoprotein metabolism.J Am Coll Cardiol. 1993 Sep;22(3):933–40.

Abstract — Myocardial infarction and other types of tissue injury generate changes in plasma proteins known as the acute phase response. Variations in lipid and lipoprotein levels after acute myocardial infarction are manifest within 24 to 48 h after the onset of chest pain. Maximal postinfarction reductions in total cholesterol occur at days 4 to 5 with levels 47% below baseline; low and high density lipoprotein cholesterol fractions decrease to their nadir on day 7 to concentrations that are 48% and 32% below baseline, respectively. Triglyceride levels increase after acute myocardial infarction to a maximal level that is 58% above baseline on day 7. These alterations in lipid and lipoprotein levels generally stabilize by 2 months after the acute event. Screening for dyslipidemias in survivors of myocardial infarction requires clinical decision-making based on accurate and reliable measurements. The clinician must be familiar with characteristic changes in acute phase lipids and lipoproteins to ensure that patients receive appropriate, potentially life-saving therapy.

Paul D. Thompson, MD

Chief of Cardiology — Emeritus, Hartford Hospital

Professor of Medicine, University of Connecticut

Telephone: 860–972–1793

Blog — https://medium.com/@pauldthompsonmd

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