Patients with rheumatic disease experiencing ST-elevation myocardial infarction have increased inflammatory- and neurohormonal response and higher 1-year mortality

Abstract

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): This work was supported by Righospitalets Forskningsfond (Grant number: 07IO). Lundbeck Foundation (R186-2015-2132). Background Patients with rheumatoid diseases have been reported to have increased risk of ST-elevation myocardial infarction (STEMI). However, little is known about mortality risk following STEMI in these patients. Furthermore, STEMI patients with increased neurohormonal- and inflammatory response have higher mortality compared to patients with low response. Purpose We sought to assess whether patients with a rheumatic disease (RD) have an increased inflammatory- and neurohormonal response to a STEMI and whether 1-year mortality was higher in these patients compared to patients without rheumatic disease. Methods In 1700 consecutive STEMI patients (comatose cardiac arrest- and cardiogenic shock patients were excluded) from two Danish tertiary heart centres were studied. Biomarkers reflecting neurohormonal activation (pro-atrial natriuretic peptide (proANP), copeptin, and mid-regional pro-adrenomedullin (MRproADM)) and inflammatory response (C-reactive protein (CRP) and ST2) were measured at in the catheterization laboratorium before the acute coronary angiogram was performed. Patients were stratified according to known RD or not. Results In total, 88 (5.2%) STEMI patients had a RD diagnosis. From these 28 (32%) had RA, 9 (10%) had psoriasis arthritis, and 23 (26%) had gout, while 28 (32%) had other RDs. Patients in the two groups were similar of age (no RD vs. RD, mean (SD): 63 (13) vs. 65 (14) years, p=0.22), mostly male (n (%) 1194 (74) vs 57 (66), p=0.08) with similar number of comorbidities, same LVEF (median (IQR) 50 (40-55) vs. 50 (40-55), p=0.58), and similar infarct size (maximum troponin T concentration 3050 (1150-6885) vs. 3030 (1500-7260) ng/L, p=0.79). In RD patients, admission concentration of MRproADM (median (IQR) 0.77 (0.63-0.98) vs. 0.71 (0.58-0.90) nmol/L, p=0.04), ST2 (43 (33-64) vs 39 (29-55) ng/ml, p=0.04), and CRP (6.8 (2.9-14) vs 3.3 (1.4-8.2) mg/L, p<0.0001) was higher compared to patients without RD. No difference in proANP and copeptin was detected. One-year all-cause mortality was higher in patients with RD (11% vs. 5.5%, p=0.02). When including patients with CS and patients comatose after cardiac arrest, the signal remained intact. Conclusion STEMI patients with RD have higher admission inflammatory response and neurohormonal activation compared to patients without. Furthermore, patients with RD have higher 1-year all-cause mortality.