Cardiac remodeling and ventricular pacing represent intertwined phenomena with profound implications for cardiovascular health and therapeutic interventions. This review explores the intricate relationship between cardiac remodeling and ventricular pacing, spanning from the molecular underpinnings to biomechanical alterations. Beginning with an examination of genetic predispositions and cellular signaling pathways, we delve into the mechanisms driving myocardial structural changes and electrical remodeling in response to pacing stimuli. Insights into the dynamic interplay between pacing strategies and adaptive or maladaptive remodeling processes are synthesized, shedding light on the clinical implications for patients with various cardiovascular pathologies. By bridging the gap between basic science discoveries and clinical translation, this review aims to provide a comprehensive understanding of cardiac remodeling in the context of ventricular pacing, paving the way for future advancements in cardiovascular care.

Pacing-induced cardiomyopathy (PiCM) significantly impacts patient morbidity and mortality, emphasizing the need for improved preventive and therapeutic strategies. This systematic review aimed to evaluate the effectiveness of resynchronization therapies compared to traditional right ventricular pacing (RVP). Emerging evidence supports the use of biventricular cardiac resynchronization therapy (BiV-CRT) and conduction system pacing (CSP) as effective alternatives to conventional RVP. Both strategies preserve ventricular synchrony, improve left ventricular (LV) function, and reduce adverse outcomes. Comparative studies suggest superior physiological and clinical benefits of CSP over BiV-CRT, including greater improvements in QRS duration, LV ejection fraction (LVEF), and functional status. In addition, pharmacological therapy-particularly combination ACEi/ARB with β-blockers-has shown potential in reducing the incidence of PiCM.

Residing in rural or remote areas is often linked to compromised access to health services, directly affecting the feasibility of follow-up on patients wit

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.

Purpose of Review : Pacing-induced cardiomyopathy (PiCM) significantly impacts patient morbidity and mortality, emphasizing the need for improved preventive and therapeutic strategies. This systematic review aimed to evaluate the effectiveness of resynchronization therapies compared to traditional right ventricular pacing (RVP). Recent Findings: Recent studies highlight advancements in therapeutic strategies for PiCM such as biventricular pacing (BiV-CRT) and Hiss-bundle pacing (HPCSP). These techniques improve left ventricular function and clinical outcomes while offering more physiological alternatives by preserving natural ventricular activation. Emerge evidence supports their efficacy in both preventing and managing PiCM. Summary : Both Both BiV-CRT and HPCSP significantly improved cardiac function, with increases in left ventricular ejection fraction (LVEF) and relief of clinical symptoms, as evidenced by improvements in NYHA functional class. Notably, superior benefits of HPCSP over BiV-CRT in QRS amplitude, LVEF, and clinical outcomes was highlighted in two studies. While resynchronization therapies have low complication rates, procedural challenges like venous access and lead placement persist. Additionally, these therapies demonstrate a promising preventive role, particularly in patients with high RVP burdens. Further research is essential to refine treatment strategies and optimize outcomes for PiCM patients.

Background/Objectives: Pacing-induced cardiomyopathy (PiCM) is a recognized complication of chronic right ventricular pacing (RVP), characterized by left ventricular (LV) dysfunction, adverse remodeling, and progression to heart failure. MicroRNAs (miRs) regulate gene expression and play an important role in ventricular remodeling. This study aimed to observe whether dynamic changes in miRs according to a novel peripheral blood mononuclear cell (PBMC)-based approach could serve as early predictive biomarkers of PiCM. Methods: A prospective, single-center cohort study was conducted in adult patients undergoing pacemaker implantation. Clinical characteristics, echocardiographic parameters and expression levels of miR-208b-3p and miR-9 were assessed immediately and 3 months post-pacemaker implantation. PiCM was defined as a ≥10% reduction in LVEF at one year, with no alternative cause. Statistical analyses included correlation testing, ROC curve analysis, and multivariate regression to identify factors associated with PiCM. Results: Among 126 patients, 11.1% developed PiCM. Compared with the non-PiCM group, those who developed PiCM exhibited more pronounced 3-month changes in miR-208b-3p (median Δ₃log miR: +1.3 vs. −0.4, p = 0.013) and miR-9 (median Δ₃log miR: −1.7 vs. +0.21, p = 0.011). In multivariate analyses, Δ₃LV-GLS, Δ₃logmiR-208b-3p, and Δ₃logmiR-9 were associated with a higher likelihood of PiCM. Among PiCM patients, Δ₃logmiR-208b-3p correlated inversely with Δ₃LV-GLS (r = −0.73, p = 0.016), while Δ₃logmiR-9 correlated positively (r = 0.88, p < 0.001). ROC analyses demonstrated good predictive ability for Δ₃LV-GLS (AUC = 0.924), Δ₃log miR-208b-3p (AUC = 0.783), and Δ₃log miR-9 (AUC = 0.835), with no significant differences between curves. Conclusions: Early LV-GLS deterioration and dynamic changes in expression of miR-208b-3p and miR-9 in PBMCs precede overt LV systolic dysfunction. These miRs may serve as early predictive biomarkers for PiCM.