Safety and Efficacy of FAP iCDC in Ischemic Cardiomyopathy

Ischemic heart disease (IHD) is becoming an increasingly serious global public health challenge due to its rising prevalence and the continuous increase in human life expectancy. Despite substantial advances in reperfusion therapy, pharmacological treatment, and risk factor management in recent decades, clinical prognosis remains poor. Many patients continue to experience adverse cardiac remodeling after the initial ischemic injury and eventually progress to heart failure. This persistent residual risk suggests that current therapeutic strategies do not fully address key pathogenic mechanisms underlying disease progression. Inflammation plays a central role in linking acute myocardial injury to chronic cardiac remodeling.

Dendritic cells (DCs), as professional antigen-presenting cells, function at the interface between innate and adaptive immunity and play a critical role in coordinating immune responses within the tissue microenvironment. Recent advances in the study of tolerogenic dendritic cells (tolerogenic DCs) have provided new insights into their potential application in cardiovascular diseases. Unlike conventional immunostimulatory DCs, tolerogenic DCs can induce antigen-specific immune tolerance through multiple mechanisms, including secretion of regulatory cytokines, expression of co-inhibitory ligands, suppression of effector T-cell responses, and induction of regulatory T cells. These properties make DCs a promising but underexplored platform for immune modulation.

This study evaluates a novel therapeutic strategy using fibroblast activation protein (FAP)-targeted autologous immunosuppressive chimeric antigen receptor dendritic cell (CAR-DC) therapy, also referred to as iCDC therapy, in patients with ischemic cardiomyopathy. This approach is designed to direct engineered dendritic cells to sites of cardiac injury and fibrosis, with the goal of modulating the balance between injurious and reparative immune responses. By targeting local immune regulation at the site of injury, this strategy may help attenuate adverse cardiac remodeling while potentially avoiding the systemic immunosuppression associated with conventional therapies.

• Change in Left Ventricular Ejection Fraction (LVEF) by Echocardiography [Срок оценки: Baseline, 3 months, 6 months]
• Change in left ventricular end-systolic volume (LVESV) as assessed by Echocardiography [Срок оценки: Baseline, 3 months, and 6 months]
• Change in left ventricular end-diastolic volume (LVEDV) by Echocardiography [Срок оценки: Baseline, 3 months, and 6 months]
• Change in global longitudinal strain (GLS) measured by Echocardiography [Срок оценки: Baseline, 3 months, 6 months]
• Change in wall motion score index (WMSI) measured by Echocardiography [Срок оценки: Baseline, 3 months, 6 months]
• Change in left ventricular ejection fraction (LVEF) by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline, 6 months]
• Change in left ventricular end-systolic volume (LVESV) by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline and 6 months]
• Change in left ventricular end-diastolic volume (LVEDV) by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline, 6 months]
• Change in stroke volume (SV) by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline and 6 months]
• Change in Myocardial Late Gadolinium Enhancement Volume by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline and 6 months]
• Change in Extracellular Volume Fraction in Remote Myocardium by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline and 6 months]
• Change in Myocardial Scar Transmurality by Cardiac Magnetic Resonance Imaging [Срок оценки: Baseline and 6 months]