Why the study?
Differentiating myocarditis, cardiac sarcoidosis, and non-confirmed cardiomyopathy within the diverse spectrum of inflammatory myocardial disease remains diagnostically and prognostically challenging.
Cohort (n=218)
Although myocarditis, cardiac sarcoidosis, and non-confirmed cardiomyopathy present with distinct clinical phenotypes and transcriptomic signatures, adjusted long-term clinical outcomes (mortality, mechanical circulatory support, or transplant) do not significantly differ between groups.
Answers are grounded in this paper and cite their sources.
No outcome differences despite distinct phenotypes; leaves open whether transcriptomics identify modifiable risks in inflammatory cardiomyopathy.
Background Inflammatory myocardial disease encompasses diverse clinical phenotypes, from subtle symptoms to fulminant heart failure. Differentiating myocarditis, cardiac sarcoidosis (CS), and non-confirmed cardiomyopathy (NC) remains diagnostically and prognostically challenging. We compared clinical presentation, outcomes, and myocardial transcriptomic profiles across these groups. Methods In this prospective cohort study, 218 adults undergoing evaluation for cardiomyopathy were classified as myocarditis ( n = 81), CS ( n = 84), or NC ( n = 53). The primary composite outcome was all-cause mortality, mechanical circulatory support, or heart transplantation. RNA sequencing of endomyocardial biopsies was performed in 53 patients with differential expression analysis adjusted for age, RNA integrity number, and systolic blood pressure. Results Patients with myocarditis were younger than those with CS or NC (34.7 ± 15.8 vs 57.4 ± 8.7 vs 57.6 ± 14.0 years); 70–75% were male. Myocarditis was characterized by chest pain and elevated inflammatory biomarkers, whereas CS was associated with arrhythmias and right ventricular dysfunction. Although unadjusted Kaplan–Meier analysis suggested differences in event-free survival, adjusted Cox regression showed no significant between-group differences (myocarditis vs NC: HR 0.99, 95% CI 0.22–4.43, p = 0.985; CS vs NC: HR 1.67, 95% CI 0.63–4.43, p = 0.307). Transcriptomic profiling revealed a more pronounced inflammatory gene expression profile in myocarditis, whereas CS showed limited differential expression and substantial overlap with NC. Conclusions Inflammatory myocardial disease shows distinct clinical presentations, while adjusted analyses did not demonstrate significant differences in long-term outcomes. Myocarditis showed a stronger inflammatory transcriptional signature, whereas CS exhibited limited transcriptomic differences. These findings support further investigation of RNA-based profiling as a complementary tool.
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Björkenstam et al. (2026) conducted a cohort in Inflammatory myocardial disease / cardiomyopathy (myocarditis, cardiac sarcoidosis, or non-confirmed cardiomyopathy) (n=218). Myocarditis or cardiac sarcoidosis phenotype vs. Non-confirmed cardiomyopathy (NC) was evaluated on Composite of all-cause mortality, mechanical circulatory support, or heart transplantation (HR 0.99 (myocarditis vs NC); HR 1.67 (CS vs NC), 95% CI 0.22-4.43 (myocarditis vs NC); 0.63-4.43 (CS vs NC), p=0.985 (myocarditis vs NC); 0.307 (CS vs NC)).
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