Targeting inflammation to reduce recurrent stroke

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 Targeting inflammation to reduce recurrent stroke

Annaelle Zietzhttps://orcid.org/0000-0002-4362-24971,2, Sarah Gorey3,4,5, Peter J Kelly3,4,6, Mira Katan1,7, and John J McCabe3,4,5
Background: 

 

Approximately one in four stroke patients suffer from recurrent vascular events, underlying the necessity to improve secondary stroke prevention strategies. Immune mechanisms are causally associated with coronary atherosclerosis. However, stroke is a heterogeneous disease and the relative contribution of inflammation across stroke mechanisms is not well understood. The optimal design of future randomized control trials (RCTs) of anti-inflammatory therapies to prevent recurrence after stroke must be informed by a clear understanding of the prognostic role of inflammation according to stroke subtype and individual patient factors.
 

Aim:

 

 In this narrative review, we discuss (1) inflammatory pathways in the etiology of ischemic stroke subtypes; (2) the evidence on inflammatory markers and vascular recurrence after stroke; and (3) review RCT evidence of anti-inflammatory agents for vascular prevention.
 

Summary of review:

 Experimental work, genetic epidemiological data, and plaque-imaging studies all implicate inflammation in atherosclerotic stroke. However, emerging evidence also suggests that inflammatory mechanisms are also important in other stroke mechanisms. Advanced neuroimaging techniques support the role of neuroinflammation in blood–brain barrier dysfunction in cerebral small vessel disease (cSVD). Systemic inflammatory processes also promote atrial cardiopathy, incident and recurrent atrial fibrillation (AF). Although several inflammatory markers have been associated with recurrence after stroke, interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) are presently the most promising markers to identify patients at increased vascular risk. Several RCTs have shown that anti-inflammatory therapies reduce vascular risk, including stroke, in coronary artery disease (CAD). Some, but not all of these trials, selected patients on the basis of elevated hsCRP. Although unproven after stroke, targeting inflammation to reduce recurrence is a compelling strategy and several RCTs are ongoing.
 

Conclusion:

 

 Evidence points toward the importance of inflammation across multiple stroke etiologies and potential benefit of anti-inflammatory targets in secondary stroke prevention. Taking the heterogeneous stroke etiologies into account, the use of serum biomarkers could be useful to identify patients with residual inflammatory risk and perform biomarker-led patient selection for future RCTs.
Keywords
Stroke, stroke prevention, inflammation, inflammatory biomarkers, stroke etiology
1Department of Neurology and Stroke Center, University Hospital Basel and University of Basel, Basel, Switzerland
2Neurology and Neurorehabilitation, University Department of Geriatric Medicine Felix Platter, University of Basel, Basel, Switzerland
3Health Research Board (HRB) Stroke Clinical Trials Network Ireland (SCTNI), Dublin, Ireland
4School of Medicine, University College Dublin (UCD), Dublin, Ireland
5Department of Geriatric Medicine, Mater Misericordiae University Hospital, Dublin, Ireland
6Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland
7Department of Neurology, University Hospital and University of Zurich, Zurich, Switzerland
Corresponding author(s):
Mira Katan, Department of Neurology and Stroke Center, University Hospital Basel and University of Basel, 4031 Basel, Switzerland. Email: mira.katan@usb.ch