# Ischaemic heart disease is the factor associated with severe COVID-19 in the urban population of Uzbekistan: a single‑center retrospective study

## TL;DR

This study finds that ischaemic heart disease is a key factor in severe COVID-19 among Uzbeks, along with genetic and metabolic factors.

## Contribution

The study identifies ischaemic heart disease and ACE gene polymorphism as significant predictors of severe COVID-19 in the Uzbek population.

## Key findings

- Ischaemic heart disease (IHD) was the strongest predictor of severe COVID-19 in the Uzbek population.
- The ACE rs1799752 DD genotype, combined with clinical factors, helped distinguish severe cases.
- IL28B polymorphism had no significant effect on disease severity in this study.

## Abstract

The course of disease development during the coronavirus disease 2019 (COVID-19) pandemic has demonstrated a very wide spectrum, with the most vulnerable group of severe disease comprising > 10% of cases worldwide. Previously, several clinical and laboratory phenotypes have been suggested for the prediction of severe disease courses with different impacts in diverse populations.

Using a logistic regression model, we performed a study of 227 patients (37% with severe disease), all of whom were ethnically Uzbek, to identify predisease clinical phenotypes associated with disease severity, such as type 2 diabetes (T2D), obesity, hypertension and ischaemic heart disease (IHD), and ascertained the contribution of the angiotensin converting enzyme-encoding gene insertion/deletion (ACE I/D) rs1799752 and the interleukin-28 isoform B (IL28B) gene rs12979860 genetic markers.

We found that the greatest contribution to the severe disease group from IHD was observed before the start of infection, whereas the contributions of T2D and obesity were only nominally important for the model. Interestingly, the ACE rs1799752 DD genotype together with clinical phenotypes contributed to the discrimination of the severe disease group, but we detected no effect of the IL28B polymorphism. However, without the inclusion of clinical phenotypes in the model, we did not observe a significant ACE polymorphism association with COVID-19 severity (likelihood ratio test p = 0.1). We critically reviewed allelic frequencies for ACE rs1799752 in different populations and studies in an attempt to explain possible discrepancies in previously reported associations in diverse populations.

In a modest group of patients from the Uzbek population, we confirmed the importance of IHD, metabolic disorders and ACE genetics in the development of severe COVID-19 infection in this population.

Not applicable.

The online version contains supplementary material available at 10.1186/s12879-026-12798-6.