# Cardiovascular Disease and COVID-19: Is There a Place for Mid-Regional Pro-Adrenomedullin? Preliminary Data from a Clinical Cohort

**Authors:** Paulina Pietraszko, Marcin Żórawski, Emilia Bielecka-Richter, Małgorzata Gryciuk, Kacper Mil, Aleksandra Zbroch, Edyta Zbroch

PMC · DOI: 10.3390/ijms262010081 · 2025-10-16

## TL;DR

This study examined mid-regional pro-adrenomedullin (MR-proADM) levels in patients with and without cardiovascular disease and COVID-19 to determine its role in predicting heart complications.

## Contribution

The study provides preliminary evidence that MR-proADM does not offer additional prognostic value for cardiovascular complications in the context of COVID-19.

## Key findings

- MR-proADM levels did not differ significantly between patients with and without COVID-19 or cardiovascular disease.
- MR-proADM was not predictive of chronic heart failure or myocardial infarction.
- No significant correlations were found between MR-proADM and standard cardiac biomarkers like troponin or proBNP.

## Abstract

Mid-regional pro-adrenomedullin (MR-proADM) has emerged as a promising biomarker reflecting endothelial dysfunction and systemic inflammation. Its prognostic role in cardiovascular complications, particularly in the context of COVID-19 infection, remains under investigation. This study aimed to evaluate MR-proADM concentrations in patients with and without cardiovascular disease and COVID-19 and to assess its association with cardiac complications and biomarkers of myocardial injury. A total of 157 patients (mean age: 72.3 years; 66 men) hospitalized in a tertiary referral center were enrolled. The study population consisted of three groups: patients with cardiovascular disease and COVID-19 (n = 64), patients with cardiovascular disease but no COVID-19 (n = 74), and a control group without cardiovascular disease or COVID-19 (n = 17). Plasma MR-proADM levels were measured, and their relationship with cardiovascular complications (chronic heart failure and myocardial infarction) and standard cardiac biomarkers (troponin T, troponin I, and proBNP) was analyzed. The mean MR-proADM concentration in the overall cohort was 91.48 ± 71.96 pmol/L (median: 77.95; range: 5.81–429.20). Distributions of MR-proADM, troponin T (M = 143.12 ± 733.93 ng/L), troponin I (M = 143.37 ± 749.85 ng/L), and proBNP (M = 2080.29 ± 3632.03 pg/mL) deviated significantly from normality (Shapiro–Wilk, all p < 0.001). No significant differences in MR-proADM concentrations were observed between patients with COVID-19 vs. without (93.78 ± 56.94 vs. 92.08 ± 82.82 pmol/L, p = 0.842) and between active infection vs. past COVID-19 (93.78 ± 56.94 vs. 85.98 ± 50.39 pmol/L, p = 0.869). A trend toward higher MR-proADM concentrations was observed in patients with cardiovascular disease compared to those without, with mean levels of 93.56 ± 74.90 vs. 74.33 ± 37.43 pmol/L, respectively. The frequency of chronic heart failure (55.0% vs. 54.5%, p = 1.000) and myocardial infarction (11.3% vs. 20.8%, p = 0.128) did not differ between patients with low vs. high MR-proADM (cut-off: median). Logistic regression confirmed that MR-proADM did not significantly predict either chronic heart failure (Nagelkerke R2 = 0.002, p = 0.660) or myocardial infarction (Nagelkerke R2 = 0.006, p = 0.465). Correlation analysis showed no significant associations between MR-proADM and proBNP (ρ = 0.09, p = 0.323), troponin T (ρ = 0.22, p = 0.065), or troponin I (ρ = 0.16, p = 0.088). MR-proADM levels did not differ significantly between patients stratified by COVID-19 infection or cardiovascular disease and were not predictive of heart failure or myocardial infarction. Moreover, no correlations were found with standard cardiac biomarkers. These results suggest that, in this cohort, MR-proADM did not provide additional prognostic information for cardiovascular complications.

## Linked entities

- **Proteins:** TNNT3 (troponin T3, fast skeletal type), LOC105904758 (troponin I, fast skeletal muscle-like)
- **Diseases:** cardiovascular disease (MONDO:0004995), myocardial infarction (MONDO:0005068), COVID-19 (MONDO:0100096)

## Full-text entities

- **Diseases:** systemic (MESH:D015619), heart failure (MESH:D006333), COVID-19 (MESH:D000086382), myocardial infarction (MESH:D009203), infection (MESH:D007239), cardiac complications (MESH:D006331), Cardiovascular Disease (MESH:D002318), myocardial injury (MESH:D009202), endothelial dysfunction (MESH:D014652), inflammation (MESH:D007249)
- **Chemicals:** proADM (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12562633/full.md

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Source: https://tomesphere.com/paper/PMC12562633