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.
Background Fine particulate matter (PM2.5) has been associated with an increased risk of chronic kidney disease (CKD) and cardiovascular disease (CVD). However, the relationships between specific PM2.5 components and the dynamic cardiorenal trajectory remain uncertain. Methods Employing multistate and accelerated failure time (AFT) modeling in a prospective cohort of 307,639 participants, we examined the associations of 2-year exposure to PM2.5 and its components (sulfate [SO42−], nitrate [NO3−], ammonium [NH4+], organic matter [OM], and black carbon [BC]) with dynamic and accelerated progression from different kidney function categories (1–4, according to estimated glomerular filtration rate [eGFR] and self-reported CKD) to CVD, and ultimately to cardiovascular death. Results Over 1,058,210 person-years of follow-up, we documented 23,948 CVD cases and 7763 cardiovascular death cases. We observed that PM2.5 and its components were significantly associated with the dynamic cardiorenal trajectory, with SO42−, NO3−, and NH4+ exhibiting larger hazard ratios (HRs). Per-interquartile range (IQR) increments in SO42−, NO3−, and NH4+ were positively correlated with the transition from kidney function category 2 to 3, and the HRs were 1.273 (95% confidence interval [CI]: 1.257–1.289), 1.304 (95% CI: 1.290–1.317), and 1.280 (95% CI: 1.267–1.294), respectively. The AFT model indicated that higher levels of PM2.5 and its constituents significantly accelerated the dynamic cardiorenal trajectory. The predictive transition times from kidney function category 2 to 3 for 2-year NO3− exposure were 1727.43 days at 4.2 μg/m3 and 868.56 days at 7.0 μg/m3. Conclusions Our findings revealed that PM2.5 components (2-year exposure) may be important risk factors for adverse cardiorenal outcomes.
