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. 2021 Jan 13;10(2):275.
doi: 10.3390/jcm10020275.

Mitochondrial Biomarkers in Patients with ST-Elevation Myocardial Infarction and Their Potential Prognostic Implications: A Prospective Observational Study

Nicola Cosentino  1 , Jeness Campodonico  1 , Marco Moltrasio  1 , Claudia Lucci  1 , Valentina Milazzo  1 , Mara Rubino  1 , Monica De Metrio  1 , Ivana Marana  1 , Marco Grazi  1 , Alice Bonomi  1 , Fabrizio Veglia  1 , Gianfranco Lauri  1 , Antonio L Bartorelli  1   2 , Giancarlo Marenzi  1
Affiliations

Mitochondrial Biomarkers in Patients with ST-Elevation Myocardial Infarction and Their Potential Prognostic Implications: A Prospective Observational Study

Nicola Cosentino et al. J Clin Med. .

Abstract

Background: Mitochondrial biomarkers have been investigated in different critical settings, including ST-elevation myocardial infarction (STEMI). Whether they provide prognostic information in STEMI, complementary to troponins, has not been fully elucidated. We prospectively explored the in-hospital and long-term prognostic implications of cytochrome c and cell-free mitochondrial DNA (mtDNA) in STEMI patients undergoing primary percutaneous coronary intervention.

Methods: We measured cytochrome c and mtDNA at admission in 466 patients. Patients were grouped according to mitochondrial biomarkers detection: group 1 (-/-; no biomarker detected; n = 28); group 2 (-/+; only one biomarker detected; n = 283); group 3 (+/+; both biomarkers detected; n = 155). A composite of in-hospital mortality, cardiogenic shock, and acute pulmonary edema was the primary endpoint. Four-year all-cause mortality was the secondary endpoint.

Results: Progressively lower left ventricular ejection fractions (52 ± 8%, 49 ± 8%, 47 ± 9%; p = 0.006) and higher troponin I peaks (54 ± 44, 73 ± 66, 106 ± 81 ng/mL; p = 0.001) were found across the groups. An increase in primary (4%, 14%, 19%; p = 0.03) and secondary (10%, 15%, 23%; p = 0.02) endpoint rate was observed going from group 1 to group 3. The adjusted odds ratio increment of the primary endpoint from one group to the next was 1.65 (95% CI 1.04-2.61; p = 0.03), while the adjusted hazard ratio increment of the secondary endpoint was 1.55 (95% CI 1.12-2.52; p = 0.03). The addition of study group allocation to admission troponin I reclassified 12% and 22% of patients for the primary and secondary endpoint, respectively.

Conclusions: Detection of mitochondrial biomarkers is common in STEMI and seems to be associated with in-hospital and long-term outcome independently of troponin.

Keywords: ST-elevation myocardial infarction; cell-free mitochondrial DNA; cytochrome c; prognosis; troponin I.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study, in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results

Figures

Figure 1
Figure 1
Left ventricular ejection fraction (LVEF; upper panel) and high-sensitivity troponin I (hs-TnI; lower panel) peak values stratified according to cytochrome c and/or mtDNA detection at hospital admission (group 1 (−/−; none mitochondrial biomarker detected) vs. group 2 (−/+; only one of the two biomarkers detected) vs. group 3 (+/+; both biomarkers detected)). p value for trend was obtained by one-way analysis of covariance (ANCOVA).
Figure 2
Figure 2
Rate of the primary endpoint (in-hospital mortality, acute pulmonary edema, and cardiogenic shock). Group 1 (−/−; no mitochondrial biomarker detected) vs. group 2 (−/+; only one of the two biomarkers detected) vs. group 3 (+/+; both biomarkers detected)). p value for trend was obtained by Mantel–Haenszel chi-square.
Figure 3
Figure 3
Kaplan–Meier curve analysis for long-term all-cause mortality stratified according to cytochrome c and/or mtDNA detection at hospital admission (group 1 (−/−; no mitochondrial biomarker detected) vs. group 2 (−/+; only one of the two biomarkers detected) vs. group 3 (+/+; both biomarkers detected)). p value was obtained by log-rank test.
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