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Aim: To explore associations between root filled teeth, primary and secondary apical periodontitis, and levels of inflammatory markers in blood from patients with a first myocardial infarction and matched controls. Methodology: Between May 2010 and February 2014, 805 patients with a first myocardial infarction and 805 controls, matched for sex, age, and postal code area, were recruited to the multicentre case–control study PAROKRANK (periodontitis and its relation to coronary artery disease). All participants underwent a physical and oral examination, as well as blood sampling. Using panoramic radiography, root filled teeth, primary apical periodontitis, and secondary apical periodontitis were assessed by three independent observers. Blood samples were analysed with enzyme‐linked immunosorbent assay method for the following inflammatory markers: interleukin‐1β (IL‐1β), IL‐2, IL‐6, IL‐8, IL‐12p70, tumour necrosis factor‐α, and high‐sensitivity C‐reactive protein (hsCRP). Additionally, white blood cell count and plasma‐fibrinogen were analysed. Associations between endodontic variables and the levels of inflammatory markers were statistically analysed with Mann–Whitney U‐test and Spearman correlation, adjusted for confounding effects of baseline factors (sex, age, myocardial infarction, current smoking, diabetes, family history of cardiovascular disease, education, marital status, and periodontal disease). Results: Mean age of the cohort was 62 years, and 81% were males. Root fillings were present in 8.4% of the 39 978 examined teeth and were associated with higher levels of hsCRP, fibrinogen, and leukocyte count, but lower levels of IL‐2 and IL‐12p70. After adjusting for confounders, root filled teeth remained associated with higher levels of fibrinogen, but lower levels of IL‐1β, IL‐2, IL‐6, and IL‐12p70. Primary apical periodontitis was found in 1.2% of non‐root filled teeth and associated with higher levels of IL‐8 (correlation 0.06, p =.025). Secondary apical periodontitis was found in 29.6% of root filled teeth but did not relate to the levels of any of the inflammatory markers. Conclusions: This study supports the notion that inflammation at the periapex is more than a local process and that systemic influences cannot be disregarded. Whether the observed alterations in plasma levels of inflammatory markers have any dismal effects on systemic health is presently unknown but, considering the present results, in demand of further investigation. [ABSTRACT FROM AUTHOR]