TITLE:
Systemic Inflammation and Subclinical Myocardial Injury: A Systematic Review of High-Sensitivity C-Reactive Protein and High-Sensitivity Troponin in Asymptomatic Adults
AUTHORS:
Vasisht Karri, Janvi N. Patel, Russell L. Kennedy
KEYWORDS:
Hs-CRP, High-Sensitivity Troponin, Inflammation, Subclinical Myocardial Injury, Heart Failure, Prevention, Colchicine, Canakinumab
JOURNAL NAME:
Open Access Library Journal,
Vol.13 No.5,
May
27,
2026
ABSTRACT: Background: High-sensitivity cardiac troponin (hs-cTn) detects low-level cardiomyocyte injury and predicts incident heart failure (HF), coronary events, and mortality in individuals without overt cardiovascular disease (CVD). High-sensitivity C-reactive protein (hs-CRP) captures systemic inflammatory burden and is associated with cardiometabolic risk and future atherosclerotic events. Whether systemic inflammation is consistently linked to subclinical myocardial injury across populations and how this relationship should inform preventive cardiology has not been synthesized in a single, clinically oriented systematic review. Objective: To systematically review epidemiologic, clinical, and translational evidence connecting systemic inflammation (hs-CRP and related pathways) with subclinical myocardial injury (hs-cTn) in asymptomatic adults, and to summarize preventive implications including risk stratification and anti-inflammatory interventions. Methods: A PRISMA-aligned systematic review was conducted using structured searches of PubMed and major publisher platforms (through February 2026). Eligible studies included 1) community-based cohorts or stable outpatient populations measuring hs-CRP and hs-cTn and reporting cross-sectional or longitudinal associations; 2) mechanistic and translational studies clarifying inflammatory pathways relevant to myocardial injury and remodeling; and 3) randomized trials evaluating anti-inflammatory strategies with cardiovascular outcomes. Evidence was synthesized narratively with emphasis on clinical interpretability and biologic plausibility. Results: Across large community cohorts, higher hs-CRP was repeatedly associated with detectable/elevated hs-cTn independent of traditional risk factors and renal function, supporting a graded inflammation-injury relationship. Longitudinal evidence consistently linked hs-cTn to future HF and mortality, and inflammatory modulation trials (IL-1β inhibition, low-dose colchicine) reduced cardiovascular events, reinforcing causal relevance of inflammatory pathways in CVD progression. Conclusions: The literature supports a coherent model in which systemic inflammation contributes to early myocardial vulnerability and low-level injury, measurable by hs-cTn, with downstream risk for HF and adverse cardiovascular events. Combined biomarker strategies and targeted anti-inflammatory interventions represent promising prevention directions, requiring prospective validation for implementation.