Inflammatory burden and oedema provide complementary information on subsequent pericardial tethering in tuberculous pericarditis: a longitudinal segment-level CMR study.
The relationship between pericardial inflammation and subsequent constriction in tuberculous (TB) pericarditis remains poorly understood. Late gadolinium enhancement (LGE) has shown conflicting prognostic associations, suggesting that inflammation alone may not adequately reflect disease stage or reversibility. We hypothesised that inflammatory burden and oedema provide complementary information regarding subsequent pericardial tethering, and that segments without oedema would be more likely to demonstrate tethering at follow-up than oedematous segments.
Participants with TB pericarditis underwent baseline and 6-month cardiovascular magnetic resonance (CMR) imaging. Baseline inflammatory burden was quantified using pericardial LGE at 6 SD and 10 SD thresholds. Baseline oedema and 6-month visceral-parietal pericardial tethering were assessed segmentally using T2-weighted short tau inversion recovery imaging and radiofrequency tissue tagging, respectively, within a validated 20-segment pericardial model. Generalised estimating equation modelling was used to evaluate associations between baseline inflammatory burden, oedema and follow-up tethering.
Tethering at 6-month follow-up was present in 131/633 oedematous segments (20.7%) compared with 138/267 non-oedematous segments (51.7%; p<0.001). Greater baseline inflammatory burden was independently associated with subsequent tethering, while baseline oedema remained independently protective. In the 6 SD model, baseline oedema was independently associated with lower odds of subsequent tethering (OR 0.29, 95% CI 0.20 to 0.43; p<0.001), while greater baseline inflammatory burden was independently associated with higher odds of subsequent tethering (OR 1.32 per SD increase, 95% CI 1.12 to 1.55; p=0.0011). Similar findings were observed using 10 SD thresholds.
Pericardial inflammatory burden and oedema provide independent and complementary information regarding subsequent tethering in active TB pericarditis. Oedema may reflect a more acute, potentially reversible inflammatory phenotype, whereas intense inflammatory signal without oedema appears associated with a more fibrosis-prone state. These findings support multiparametric CMR for disease staging and provide longitudinal imaging evidence consistent with differing pathways of pericardial remodelling.
Participants with TB pericarditis underwent baseline and 6-month cardiovascular magnetic resonance (CMR) imaging. Baseline inflammatory burden was quantified using pericardial LGE at 6 SD and 10 SD thresholds. Baseline oedema and 6-month visceral-parietal pericardial tethering were assessed segmentally using T2-weighted short tau inversion recovery imaging and radiofrequency tissue tagging, respectively, within a validated 20-segment pericardial model. Generalised estimating equation modelling was used to evaluate associations between baseline inflammatory burden, oedema and follow-up tethering.
Tethering at 6-month follow-up was present in 131/633 oedematous segments (20.7%) compared with 138/267 non-oedematous segments (51.7%; p<0.001). Greater baseline inflammatory burden was independently associated with subsequent tethering, while baseline oedema remained independently protective. In the 6 SD model, baseline oedema was independently associated with lower odds of subsequent tethering (OR 0.29, 95% CI 0.20 to 0.43; p<0.001), while greater baseline inflammatory burden was independently associated with higher odds of subsequent tethering (OR 1.32 per SD increase, 95% CI 1.12 to 1.55; p=0.0011). Similar findings were observed using 10 SD thresholds.
Pericardial inflammatory burden and oedema provide independent and complementary information regarding subsequent tethering in active TB pericarditis. Oedema may reflect a more acute, potentially reversible inflammatory phenotype, whereas intense inflammatory signal without oedema appears associated with a more fibrosis-prone state. These findings support multiparametric CMR for disease staging and provide longitudinal imaging evidence consistent with differing pathways of pericardial remodelling.