Postępy w Kardiologii Interwencyjnej

Abstract

4/2025 vol. 21
Original paper

Coronary features in septic patients with elevated cardiac troponin

  1. Division of Cardiology, Department of Medicine, University Hospital of Verona, Italy
  2. Center for Intensive Internal Medicine, University Medical Center, Ljubljana, Slovenia
Adv Interv Cardiol 2025; 21, 4 (82): 521–525
Online publish date: 2025/10/28
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Introduction

Cardiac troponin, which is frequently elevated in septic patients, represents a diagnostic challenge in everyday clinical practice.

Aim

To investigate coronary features in septic patients with elevated cardiac troponin I (cTnI) and mechanisms of myocardial infarction.

Material and methods

A single-center retrospective observational study was conducted in consecutive cTnI-positive septic patients undergoing coronary angiography during index hospitalization.

Results

From January 2012 to December 2022, 74 patients with peak cTnI 16647 ng/l (normal < 40 ng/l), peak C-reactive protein 234 mg/l (normal < 5 mg/l), peak procalcitonin 14 µg/l (normal < 0.20 µg/l), arterial lactate 5.1 mmol/l (normal < 2.0 mmol/l), and positive hemocultures in 39% were enrolled. Obstructive coronary disease (> 70% diameter stenosis) was documented in 65%, with multivessel involvement in 51%. Chronic total occlusion (CTO) was present in 35%, and > 50% unprotected left main (ULM) stenosis in 22%. Definite or possible acute culprit lesions were documented in 9.5% and 6.8%, respectively. The median SYNTAX (Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery) score was 16 (25th and 75th IQR 0–34). Peak cTnI was significantly elevated in patients with a definite acute culprit lesion (67,659 ng/l) compared to a possible (18,422 ng/l; p = 0.030) or no acute culprit lesion (13,410 ng/l; p = 0.021). Only a weak, non-linear correlation between SYNTAX score and peak cTnI was documented (r2 = 0.088; p = 0.006).

Conclusions

Two-thirds of septic patients with elevated cTnI have obstructive coronary disease, with multivessel involvement in around 50%, significant ULM stenosis in 20%, and CTO in 40%. An acute culprit lesion, which is present in up to 10%, is associated with significantly elevated cTnI compared to patients with stable coronary disease.

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