The Sooner, the Better: Anti-inflammation in Acutemyocardial Infarction

Thomas F. Lüscher


Eur Heart J. 2020;41(42):4100-4102. 

In This Article

Rediscovering Inflammation

However, there was a remaining cardiovascular risk, and this led to the rediscovery of the true meaning of Virchow's seminal statement. First of all, it appeared from experimental studies that oxidized or otherwise modified cholesterol rather than native LDL-cholesterol (LDL-C)[5,6] was involved and that dysfunctional HDL-C lost its protective function.[7,8] The expression of adhesion molecules and, in turn, the presence of white blood cells such as monocytes, macrophages, and T cells in atherosclerotic plaques[9] and the occluding thrombus in acute coronary syndromes (ACS)[10] further corroborated the concept that inflammation might play a role. In 1994, the group of Attilio Maseris showed that acute phase proteins such as C-reactive protein (CRP) and serum amyloid A (SAA) predicted future cardiovascular events in patients with unstable angina.[11] This observation was soon extended by Charles Hennekens and Paul Ridker to healthy individuals.[12] In individuals at high cardiovascular risk with elevated CRP, but normal or midly elevated cholesterol, rosuvastatin lowered not only CRP, but also major cardiovascular events (MACE).[13] Indeed, a mild anti-inflammatory action of statins had previously been demonstrated in small experimental trials. Thus, Virchow's vision was indeed prophetic. However, how can this information be used clinically to the benefit of patients?