Increased Inflammatory Activity in Patients 3 Months after Myocardial Infarction with Nonobstructive Coronary Arteries

Author:

Hjort Marcus12,Eggers Kai M1,Lindhagen Lars2,Agewall Stefan3,Brolin Elin B4,Collste Olov5,Daniel Maria5,Ekenbäck Christina6,Frick Mats5,Henareh Loghman7,Hofman-Bang Claes6,Malmqvist Karin6,Spaak Jonas6,Sörensson Peder8,Y-Hassan Shams7,Tornvall Per5,Lindahl Bertil12

Affiliation:

1. Department of Medical Sciences, and

2. Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden

3. Institute of Clinical Sciences, Oslo University Hospital, University of Oslo, Oslo, Norway

4. Department of Clinical Science, Intervention and Technology

5. Department of Clinical Sciences and Education, Södersjukhuset

6. Department of Clinical Sciences, Division of Cardiovascular Medicine, Danderyd Hospital

7. Heart and Vascular Theme, Department of Medicine, Karolinska University Hospital, and

8. Department of Molecular Medicine and Surgery, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden

Abstract

Abstract BACKGROUND Around 5%–10% of patients with myocardial infarction (MI) present with nonobstructive coronary arteries (MINOCA). We aimed to assess pathophysiological mechanisms in MINOCA by extensively evaluating cardiovascular biomarkers in the stable phase after an event, comparing MINOCA patients with cardiovascular healthy controls and MI patients with obstructive coronary artery disease (MI-CAD). METHODS Ninety-one biomarkers were measured with a proximity extension assay 3 months after MI in 97 MINOCA patients, 97 age- and sex-matched MI-CAD patients, and 98 controls. Lasso analyses (penalized logistic regression models) and adjusted multiple linear regression models were used for statistical analyses. RESULTS In the Lasso analysis (MINOCA vs MI-CAD), 8 biomarkers provided discriminatory value: P-selectin glycoprotein ligand 1, C-X-C motif chemokine 1, TNF-related activation-induced cytokine, and pappalysin-1 (PAPPA) with increasing probabilities of MINOCA, and tissue-type plasminogen activator, B-type natriuretic peptide, myeloperoxidase, and interleukin-1 receptor antagonist protein with increasing probabilities of MI-CAD. Comparing MINOCA vs controls, 7 biomarkers provided discriminatory value: N-terminal pro-B-type natriuretic peptide, renin, NF-κ-B essential modulator, PAPPA, interleukin-6, and soluble urokinase plasminogen activator surface receptor with increasing probabilities of MINOCA, and agouti-related protein with increasing probabilities of controls. Adjusted multiple linear regression analyses showed that group affiliation was associated with the concentrations of 7 of the 8 biomarkers in the comparison MINOCA vs MI-CAD and 5 of the 7 biomarkers in MINOCA vs controls. CONCLUSIONS Three months after the MI, the biomarker concentrations indicated greater inflammatory activity in MINOCA patients than in both MI-CAD patients and healthy controls, and a varying degree of myocardial dysfunction among the 3 cohorts.

Publisher

Oxford University Press (OUP)

Subject

Biochemistry, medical,Clinical Biochemistry

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