PMID- 35005213
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220430
IS  - 2352-9067 (Print)
IS  - 2352-9067 (Electronic)
IS  - 2352-9067 (Linking)
VI  - 38
DP  - 2022 Feb
TI  - Association between myocardial fibrosis, as assessed with cardiac magnetic 
      resonance T1 mapping, and persistent dyspnea after pulmonary embolism.
PG  - 100935
LID - 10.1016/j.ijcha.2021.100935 [doi]
LID - 100935
AB  - 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.
CI  - (c) 2021 The Author(s).
FAU - Gleditsch, Jostein
AU  - Gleditsch J
AD  - Department of Radiology, Ostfold Hospital, Kalnes, Norway.
AD  - Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
FAU - Jervan, Oyvind
AU  - Jervan O
AD  - Department of Cardiology, Ostfold Hospital, Kalnes, Norway.
AD  - Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
FAU - Tavoly, Mazdak
AU  - Tavoly M
AD  - Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
FAU - Geier, Oliver
AU  - Geier O
AD  - Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, 
      Norway.
FAU - Holst, Rene
AU  - Holst R
AD  - Department of Research, Ostfold Hospital, Kalnes, Norway.
AD  - Oslo Centre for Biostatistics and Epidemiology, University of Oslo and Oslo 
      University Hospital, Oslo, Norway.
FAU - Klok, Frederikus A
AU  - Klok FA
AD  - Department of Medicine - Thrombosis and Hemostasis, Leiden University Medical 
      Center, Leiden, the Netherlands.
FAU - Ghanima, Waleed
AU  - Ghanima W
AD  - Internal medicine clinic, Ostfold Hospital, Kalnes, Norway.
AD  - Department of hematology, Oslo University Hospital and Institute of Clinical 
      Medicine, University of Oslo, Oslo, Norway.
FAU - Hopp, Einar
AU  - Hopp E
AD  - Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, 
      Norway.
LA  - eng
PT  - Journal Article
DEP - 20211228
PL  - Ireland
TA  - Int J Cardiol Heart Vasc
JT  - International journal of cardiology. Heart & vasculature
JID - 101649525
PMC - PMC8717259
OTO - NOTNLM
OT  - Cardiac Magnetic Resonance
OT  - Dyspnea
OT  - Myocardial fibrosis
OT  - Pulmonary Embolism
OT  - T1-mapping
COIS- 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, O. 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".].
EDAT- 2022/01/11 06:00
MHDA- 2022/01/11 06:01
PMCR- 2021/12/28
CRDT- 2022/01/10 09:29
PHST- 2021/10/28 00:00 [received]
PHST- 2021/11/25 00:00 [revised]
PHST- 2021/12/19 00:00 [accepted]
PHST- 2022/01/10 09:29 [entrez]
PHST- 2022/01/11 06:00 [pubmed]
PHST- 2022/01/11 06:01 [medline]
PHST- 2021/12/28 00:00 [pmc-release]
AID - S2352-9067(21)00223-2 [pii]
AID - 100935 [pii]
AID - 10.1016/j.ijcha.2021.100935 [doi]
PST - epublish
SO  - Int J Cardiol Heart Vasc. 2021 Dec 28;38:100935. doi: 
      10.1016/j.ijcha.2021.100935. eCollection 2022 Feb.