Prevalence and severity spectrum of lymphocytic myocarditis in a dilated cardiomyopathy phenotype endomyocardial biopsy cohort, classified by the Seaport criteria

Background/Aim In patients with a dilated cardiomyopathy (DCM) phenotype, endomyocardial biopsy (EMB) can improve diagnostic certainty across the spectrum of lymphocytic myocarditis and inflammatory cardiomyopathy and may support targeted therapy. In practice, heterogeneous reporting language (e.g., “borderline/compatible”), sampling variability, and uncertainty about the clinical meaning of qualitative viral PCR can add variability to clinical decisions. In addition, narrative terms implying cardiomyocyte injury (e.g., myocytolysis/necrosis/degeneration/cardiomyocyte loss) may be inconsistently incorporated yet influence the interpretation of an “active process.” The Seaport criteria (SCVP/AECVP) aim to reduce heterogeneity via a CD3-based grading system (Grade 1–3) and the category of SITUS (Scattered Increased T lymphocytes of Undetermined Significance). We aimed to define the prevalence and severity spectrum of lymphocytic myocarditis by Seaport criteria in consecutive DCM phenotype cases undergoing EMB. Methods Consecutive DCM phenotype patients undergoing EMB (2015–2020) were retrospectively reviewed. Samples were re-graded in a reference laboratory according to Seaport criteria (no myocarditis, SITUS, Grade 1–3). Viral genome/PCR (present/absent) and immunomodulatory treatment planning/recommendations from clinical records were collected. The analysis was descriptive, focusing on parallelism between standardized tissue classification and real-world clinical planning. Mean follow-up was 12 months; baseline and follow-up LVEF were recorded. Results Twenty-two patients were included (mean age 38±14 years; 77% male [17/22]). Baseline LVEF was 26.5±6.8%. Among 19 patients with follow-up echocardiography, LVEF increased to 40.1±9.0% (mean Δ +12.5 percentage points). By Seaport grading, 41% (9/22) had no myocarditis, 9% (2/22) SITUS, and 50% (11/22) Grade 1–3 myocarditis (Grade 1: 32% [7/22], Grade 2: 14% [3/22], Grade 3: 5% [1/22]). Immunomodulatory planning/recommendations were documented in 73% (16/22): present in 100% (11/11) of Grade 1–3, but also in no myocarditis (44% [4/9]) and SITUS (50% [1/2]), suggesting decisions were not fully explained by standardized grading alone. Injury-oriented narrative terms appeared in 32% (7/22); only one was Grade 3, while others were distributed across Grade 1/SITUS/no myocarditis, suggesting “active process” wording may influence planning beyond standardized classification. Conclusion In a DCM phenotype EMB cohort, Seaport criteria meaningfully reclassify histopathological diagnosis and reveal discordance between standardized tissue grading and real-world immunomodulatory treatment planning. Future studies should test whether Seaport-based standardization improves appropriateness of immunomodulatory strategies and clinical outcomes.