Ischemic heart disease (IHD) is a major cause of death in the western world. Although the age-standardized mortality rates are decreasing, the burden of the disease remains high and novel therapeutic strategies are still needed to improve clinical outcome. In the past decades, inflammation has been recognized as an important factor throughout all stages of IHD. The increase in understanding the inflammatory mechanisms has uncovered an intriguing diversity of potentially targetable pathways. However, the exact role of inflammation still remains to be further elucidated. This thesis supports the hypothesis that inflammation plays an important role across all stages of IHD, varying from atherosclerosis to myocardial infarction, and eventually ischemic heart failure. Increased inflammation is associated with a decrease in cardiac function after myocardial infarction, but adequate anti-inflammatory therapies that may aid in reducing this decline remain to be developed or to be proven to be effective. It is therefore essential to further unravel the complex pathophysiological inflammatory mechanisms underlying IHD. New techniques such as single cell RNA sequencing, can help us to further study these complex mechanisms. Furthermore, accumulating evidence has suggested that the human gut microbiome may play an important role in the pathophysiology of IHD through the modulation of inflammation related to the event. Although the interplay of inflammation and the human gut microbiome in IHD is a relatively young field of research, a better understanding of these two may aid in the improvement of risk stratification, therapeutic treatment efficacy, and prognosis of IHD.
|Qualification||Doctor of Philosophy|
|Place of Publication||[Groningen]|
|Publication status||Published - 2021|