ESOC 2025 | A meta-analysis investigating inflammatory mechanisms in stroke pathogenesis with atherosclerosis

So we know for quite a long time now that inflammatory mechanisms are implicated in stroke pathogenesis and we have been investigating this area in Dublin for quite a long time now. One of the issues that has been slow to resolve is whether or not inflammatory mechanisms are implicated in patients with atherosclerosis, or if they are also implicated in non-atherosclerotic mechanisms. This is a particularly important topic at present due to the recent results of the CONVINCE trial that was published at the European Stroke Conference in 2024. In that trial, colchicine did not demonstrate benefit over usual care for the reduction of major adverse cardiovascular events. CONVINCE enrolled patients both with atherosclerotic stroke and non-atherosclerotic stroke and it has been suggested that the reason for the neutral trial results may have been due to the inclusion of non-atherosclerotic patients. One of the easiest ways to measure systemic inflammation in our patients with stroke is to measure circulating high sensitivity C-reactive protein or interleukin-6 in blood samples of our stroke patients. We have previously shown that these markers are independently associated with major adverse cardiovascular events, including recurrent stroke after ischemic stroke or TIA. And this has been reported after performing a systematic review and meta-analysis. We approached a number of authors of previously published research that had investigated this question. These authors took part in the Blood Inflammatory Markers and Stroke Collaboration, or BISC, which was established in 2020. And using data from this data set, we had data from over 10,000 participants and quite a high number of recurrent vascular events in the region of 1400 major adverse cardiovascular events during follow-up. And using this data we asked whether or not a history of systemic atherosclerotic events modified the association between inflammatory markers and recurrence and so we compared patients with and without atherosclerosis which was defined as a stroke due to large artery atherosclerosis, or a previous history of coronary artery disease, irrespective of stroke subtype, or a previous history of peripheral arterial disease. And what we showed was that, irrespective of atherosclerotic status, there were independent associations between inflammatory markers and recurrent major adverse cardiovascular events and this is important data because it suggests that inflammatory mechanisms are implicated in post-stroke recurrence in patients with and without atherosclerosis and they also lend support to the future enrolment of patients irrespective of atherosclerosis status in future randomized control trials of anti-inflammatory therapies. And finally they also add further weighting to the concept that we should preferentially include patients with objective evidence of residual inflammatory risk, i.e. elevated CRP or interleukin-6, preferentially in future trials of anti-inflammatory therapy. And the rationale for this approach would be that these patients are most likely to benefit from these therapies in the future, and excluding patients without objective evidence of inflammation may improve the tailoring of the right treatment for the right patient.

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