Association between myocardial fibrosis, as assessed with cardiac magnetic resonance T1 mapping, and persistent dyspnea after pulmonary embolism.

BACKGROUND

Persistent dyspnea is a common symptom after pulmonary embolism (PE). However, the pathophysiology of persistent dyspnea is not fully clarified. This study aimed to explore possible associations between diffuse myocardial fibrosis, as assessed by cardiac magnetic resonance (CMR) T1 mapping, and persistent dyspnea in patients with a history of PE.

METHODS

CMR with T1 mapping and extracellular volume fraction (ECV) calculations were performed after PE in 51 patients with persistent dyspnea and in 50 non-dyspneic patients. Patients with known pulmonary disease, heart disease and CTEPH were excluded.

RESULTS

Native T1 was higher in the interventricular septum in dyspneic patients compared to non-dyspneic patients; difference 13 ms (95% CI: 2-23 ms). ECV was also significantly higher in patients with dyspnea; difference 0.9 percent points (95% CI: 0.04-1.8 pp). There was no difference in native T1 or ECV in the left ventricular lateral wall. Native T1 in the interventricular septum had an adjusted Odds Ratio of 1.18 per 10 ms increase (95% CI: 0.99-1.42) in predicting dyspnea, and an adjusted Odds Ratio of 1.47 per 10 ms increase (95% CI: 1.10-1.96) in predicting Incremental Shuttle Walk Test (ISWT) score < 1020 m.

CONCLUSION

Septal native T1 and ECV values were higher in patients with dyspnea after PE compared with those who were fully recovered suggesting a possible pathological role of myocardial fibrosis in the development of dyspnea after PE. Further studies are needed to validate our findings and to explore their pathophysiological role and clinical significance.

Informations de copyright

© 2021 The Author(s).

Déclaration de conflit d'intérêts

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: [W. Ghanima reports personal fees for lectures and participation in advisory board from Novartis, Amgen, Grifols, SOBI, UCB, ARGENX, Sanofi, Principia biophrma, Pfizer, BMS and Bayer and grants from Bayer and, PfizerBMS, all outside the submitted work. Dr. FA Klok reports research support from Bayer, Bristol-Myers Squibb, Boehringer-Ingelheim, MSD, Daiichi-Sankyo, Actelion, the Dutch thrombosis association, The Netherlands Organization for Health Research and Development and the Dutch Heart foundation. J. Gleditsch, Ø. Jervan, M. Tavoly, O. Geier, R. Holst and E. Hopp report no relationships that could be construed as a conflict of interest. The project received an unrestricted grant from the Norwegian patient organizations “Fredrikstad Tuberkuloseforenings Stiftelse” and “Landsforeningen for hjerte- og lungesyke”.].