LAUSR

Inflammation is the new frontier in the treatment of coronary artery disease. Following the seminal works by Libby et al. [1], recent trials such as CANTOS [2] and COLCOT [3] have shown the benefit of targeting inflammation to reduce cardiovascular events. However, not all were positive suggesting different types of inflammation may be in play [4]. In this issue of Acta, Dolu et al. present an observational study in which they correlate thrombus burden observed in STEMI with CRP and a simple inflammatory parameter, the systemic immune-inflammation index (SII) defined by the product of platelet and neutrophil counts divided by the lymphocyte count. This correlation implies that thrombus burden and therefore the mechanism of myocardial infarction is not only related to plaque characteristics but also to the general systemic inflammatory milieu. In other words, different mechanisms of acute coronary syndrome may be associated with different types and variable degrees of inflammation. Notwithstanding, myocardial infarctions with larger thrombi may also activate a different inflammation or a greater release of catecholamines. Thus, these findings might also be a consequence of the severity of the myocardial infarction rather than related to its cause. The clinical utility of the SII is reduced in the setting of primary PCI where results of haematology tests are usually obtained after coronary angiography and PCI, where thrombus burden is apparent and when the consequences of this thrombotic load are appreciated. Therefore, these findings probably pertain more to understanding how to prevent acute coronary syndromes than actually treating them. Nonetheless, this new data represent yet another stepping-stone on our way to understanding acute coronary syndromes.