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The following search terms (or combination of terms) were considered: \u201cacute pericarditis,\u201d \u201crecurrent pericarditis,\u201d \u201cmyocarditis,\u201d \u201ccardiac sarcoidosis,\u201d \u201catherosclerosis,\u201d \u201cacute myocardial infarction,\u201d \u201cinflammation,\u201d \u201cNLRP3 inflammasome,\u201d \u201cInterleukin\u20101\u201d and \u201ctreatment.\u201d<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Recent evidence supports the role of inflammation across a wide spectrum of CVDs including myocarditis, pericarditis, inflammatory cardiomyopathies (i.e. cardiac sarcoidosis) as well as atherosclerotic CVD and heart failure. Interleukins (ILs) are the signalling mediators of the inflammatory response. The NACHT, leucine\u2010rich repeat and pyrin\u2010domain containing protein 3 (NLRP3) inflammasome play a key role in producing IL\u20101\u03b2, the prototypical pro\u2010inflammatory cytokine involved in CVDs. Other pro\u2010inflammatory cytokines (e.g. tumour necrosis factor) have been implicated in cardiac sarcoidosis. As a proof of this, IL\u20101 blockade has been proven efficacious in pericarditis and chronic coronary syndrome.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Tailored strategies aiming at quenching the inflammatory response have emerged as promising to treat CVDs. In this review article, we summarize recent evidence regarding the role of inflammation across a broad spectrum of CVDs. 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