Why the study?
Persistent dyspnea is common after pulmonary embolism, but its pathophysiology is not fully clarified.
Is diffuse myocardial fibrosis, as assessed by CMR T1 mapping, associated with persistent dyspnea in patients with a history of pulmonary embolism?
Is diffuse myocardial fibrosis, as assessed by CMR T1 mapping, associated with persistent dyspnea in patients with a history of pulmonary embolism?
Septal native T1 and ECV values are elevated in patients with persistent dyspnea after pulmonary embolism, suggesting a potential role of myocardial fibrosis in post-PE dyspnea.
Answers are grounded in this paper and cite their sources.
Myocardial fibrosis may contribute to post-PE dyspnea; leaves open causal role and clinical relevance pending prospective studies.
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.
No takes yet. Share an insight, caveat, or question.
Gleditsch et al. (2021) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: