Ethnic variations in post ST elevation myocardial infarction inflammatory kinetics
Authors: Sadler M , Cannata A , Argunhan F , Mackie S , Mondi Anandhakrishna R , Quek L , Mcdonagh T , Bromage D 
Published: October 2024

Introduction

Sterile inflammation post myocardial infarction (MI) is essential to activation reparative mechanisms. However, excessive inflammation contributes to detrimental recovery and adverse outcomes(1). Several studies have reported an association between elevated leucocyte subpopulations and neutrophil-lymphocyte ratio (NLR) with poor prognosis after MI(2). In healthy volunteers, it is known that black individuals have a lower diurnal neutrophil, basophil, and monocyte count and the term ‘benign ethnic neutropenia’ has been used(3). However, the effect of ethnicity on leucocyte counts after MI is not known.

Purpose

We aimed to assess the interaction between ethnicity and leucocyte subpopulations and NLR. Understanding post-MI inflammation and its interaction with ethnicity is essential in providing personalised patient management and prognostication.

Methods

We conducted a single centre retrospective observational study of consecutive patients presenting with ST-segment elevation MI (STEMI) between 2016 and 2022. Patients were divided into white and other ethnic groups combined (‘ethnic minorities’) based on self-reported ethnicity. Leucocyte subpopulations, neutrophil and monocyte lymphocyte ratios (NLR and MLR, respectively) at baseline and for 4 days post admission were compared. Baseline variables were analysed with Shapiro-Wilk testing and presented as median (IQR). Area under the curve (AUC) was used to analyse magnitude of change in longitudinal analysis with smoothed conditional means (LOESS) to display trends in the data. Univariate and multivariate linear regression analyses were used to investigate for an association between ethnicity and baseline clinical variables.

Results

We included 1933 STEMI patients, of whom 1477 (76%) were white and 456 (24%) were from ethnic minority groups. Baseline neutrophils (7.73 [5.9-10] vs 9.04 [6.7-11.9] x109/L), monocytes (0.52 [0.38-0.69] vs 0.6 [0.44-0.82] x109/L), basophils (0.03 [0.02-0.04] vs 0.04 [0.02-0.06] x109/L), NLR (4.47 [2.93-7.19] vs 5.61 [3.64-8.89]) and MLR (0.3 [0.21-0.43] vs 0.36 [0.26-0.53]) were significantly lower (all p&lt;0.001) in ethnic minority vs white patients. There were no differences in peak troponin T or CRP. Longitudinal assessment of leucocyte subgroups and NLR showed that white patients had a significantly higher AUC and difference between minimum and maximum values (delta) for neutrophils, monocytes, basophils and NLR (Panel 1). After correction, we observed a negative association between being in the ethnic minority group and baseline NLR (p=0.005) and basophil count (p&lt;0.001).

Conclusions

Despite baseline differences in leucocyte subgroups and NLR according to ethnicity, there is a distinct interaction among patients with STEMI suggesting an ethnicity-specific inflammatory profile. Blunting of the magnitude and duration of leucocyte response is novel, and future work will focus on the implications for prognosis and tailored therapy.