Clinical and prognostic implications of C‐reactive protein levels in myocardial infarction with nonobstructive coronary arteries. Issue 7 (25th May 2021)

• Record Type: Journal Article
• Authors: Eggers, Kai M; Baron, Tomasz; Hjort, Marcus; Nordenskjöld, Anna M; Tornvall, Per; Lindahl, Bertil
• Is Part Of: Clinical cardiology. Volume 44:Issue 7(2021)
• Page Start: 1019
• Page End: 1027
• Publication Date: 2021-05-25
• Subjects: C‐reactive protein -- inflammation -- MINOCA -- myocardial infarction -- prognosis; Cardiology -- Periodicals; 616.12005
• DOI: 10.1002/clc.23651
• Languages: English
• ISSNs: 0160-9289

Abstract

Abstract: Background: Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a heterogeneous condition. Recent studies suggest that MINOCA patients may have a proinflammatory disposition. The role of inflammation in MINOCA may thus be distinct to myocardial infarction with significant coronary artery disease (MI‐CAD). Hypothesis: We hypothesized that inflammation reflected by C‐reactive protein (CRP) levels might carry unique clinical information in MINOCA. Methods: This retrospective registry‐based cohort study (SWEDEHEART) included 9916 patients with MINOCA and 97 970 MI‐CAD patients, used for comparisons. Multivariable‐adjusted regressions were applied to investigate the associations of CRP levels with clinical variables, all‐cause mortality and major cardiovascular events (MACE) during a median follow‐up of up to 5.3 years. Results: Median admission CRP levels in patients with MINOCA and MI‐CAD were 5.0 (interquartile range 2.0–9.0) mg/dl and 5.0 (interquartile range 2.1–10.0 mg/dl), respectively. CRP levels in MINOCA exhibited independent associations with various cardiovascular risk factors, comorbidities and estimates of myocardial damage. The association of CRP with peripheral artery disease tended to be stronger compared to MI‐CAD. The associations with female sex, renal dysfunction and myocardial damage were stronger in MI‐CAD. CRP independently predicted all‐cause mortality in MINOCA (hazard ratio 1.22 [95% confidence interval 1.17–1.26]), similar to MI‐CAD (p interaction = 0.904). CRP also predicted MACE (hazard ratio 1.08 [95% confidence interval 1.04–1.12]) but this association was weaker compared to MI‐CAD (p interaction<.001). Conclusions: We found no evidence indicating the presence of a specific inflammatory pattern in acute MINOCA compared to MI‐CAD. However, CRP levels were independently, albeit moderately associated with adverse outcome.