What does this research mean for the field?

Titin mRNA expression in peripheral blood mononuclear cells is significantly elevated in acute myocarditis patients and correlates strongly with left ventricular dysfunction and myocardial injury. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.ESTABLISHES_NEW_DIRECTION.

What question did this study set out to answer?

To evaluate titin (TTN) gene expression in monocytes as a potential biomarker for left ventricular dysfunction in acute myocarditis.

February 28, 2026Open Access

Monocyte Titin Gene Expression as a Biomarker of Left Ventricular Dysfunction in Acute Myocarditis

Key Result

Titin mRNA expression in PBMCs was 2.8-fold higher in acute myocarditis patients, strongly correlating with strain impairment (r=0.576) and inversely with LVEF (r=-0.421).

Key Points

To evaluate titin (TTN) gene expression in monocytes as a potential biomarker for left ventricular dysfunction in acute myocarditis.
Enrolled 29 patients with acute myocarditis and 10 healthy controls
Collected peripheral blood and isolated RNA from PBMCs
Quantified TTN mRNA expression
TTN expression was 2.8-fold higher in patients than controls (p = 0.015)
Strong positive correlation with global longitudinal strain impairment (r = 0.576, p < 0.001)
Moderate correlation with peak hs-cTnI levels (r = 0.435, p = 0.021)
Moderate inverse correlation with baseline LVEF (r = -0.421, p = 0.025)

Structured PICO

Does TTN mRNA expression in peripheral blood mononuclear cells correlate with left ventricular dysfunction and myocardial injury in patients with acute myocarditis?

Population

29 patients with acute myocarditis and 10 healthy individuals (total n=39)

Intervention

Measurement of Titin (TTN) mRNA expression in peripheral blood mononuclear cells (PBMCs)

Comparator

Healthy controls

Outcome

TTN mRNA expression levels in PBMCs and correlation with left ventricular dysfunction (global longitudinal strain, LVEF) and myocardial injury (peak hs-cTnI)surrogate

TTN mRNA expression in peripheral blood mononuclear cells is elevated in acute myocarditis and correlates with the severity of left ventricular dysfunction, suggesting its potential as a novel biomarker.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Background: Titin (TTN), a giant structural and signaling protein of striated muscle, participates in intracellular signaling networks and cytoskeletal organization, potentially influencing cell activation, trafficking, and interactions with other tissues, including the heart. Methods: In this pilot study, 29 patients with acute myocarditis and 10 healthy individuals were prospectively enrolled. Peripheral blood was obtained on the first day of hospital admission, total RNA was isolated from peripheral blood mononuclear cells (PBMCs), and TTN mRNA expression was quantified. Results: TTN expression in PBMCs was significantly higher in patients with acute myocarditis compared with healthy controls (p = 0.015), corresponding to a 2.8-fold median increase. Moreover, TTN expression showed a strong positive correlation with global longitudinal strain impairment (Spearman’s r = 0.576, p < 0.001), a moderate positive correlation with peak hs-cTnI levels (r = 0.435, p = 0.021; and a moderate inverse correlation with baseline LVEF (r = −0.421, p = 0.025). Conclusions: These findings support a pathophysiological link between TTN-related pathways in peripheral immune cells and myocardial injury in acute myocarditis and raise the hypothesis that TTN expression in PBMCs may serve as a novel biomarker of disease severity and long-term ventricular remodeling. Further studies in larger cohorts are warranted to validate these results and to elucidate the mechanistic role of titin in immune–cardiac cross-talk.