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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Associate Professor Ellen Ostenfeld, Lund University, Sweden
- Second opponent: Professor Thomas Frauenfelder, University of Zurich, Switzerland
- Third member and chair of the evaluation committee: Professor Are Martin Holm, University of Oslo
Chair of the Defence
Associate Professor Gunnar Sandbæk, University of Oslo
Principal Supervisor
Consultant Radiologist Einar Hopp, Oslo University Hospital
Summary
Until recently, it was assumed that most patients became symptom-free shortly after an episode of acute pulmonary embolism (PE). However, a new discovery revealed that up to 50% of patients have persistent symptoms including as shortness of breath, reduced physical performance and reduced quality of life. This condition, now recognized as post-PE syndrome, has pathophysiological mechanisms that remain poorly understood.
The degree of diffuse myocardial fibrosis can be quantified using a cardiac magnetic resonance (CMR) technique known as T1 mapping. Myocardial fibrosis has been observed in diverse conditions, including in chronic thromboembolic pulmonary hypertension. Nevertheless, its role and impact in patients with dyspnea after PE require further investigation.
Post PE-patients without malignancy or comorbidities associated with dyspnea were invited to participate in a study. All participants performed CMR as well as pulmonary scintigraphy, walking tests and questionnaires. Patients who experienced dyspnea after PE had slightly higher myocardial T1 values compared to those who were fully recovered. No differences were found in other CMR parameters. A subset of post-PE patients with dyspnea performed a second CMR following completion of an 8-week exercise-based rehabilitation program. After rehabilitation, there was an improvement in patient-reported dyspnea, and minor changes in two of the measured CMR parameters.
Nearly all patients with clinical findings suggestive of PE undergo computed tomography pulmonary angiography (CTPA). While it has been proposed that clot burden as assessed by CTPA may have a value as a prognostic tool in acute PE, existing clot burden scoring systems are complex and not widely used in clinical practice. To address this, the “Mean bilateral proximal extension of the clot” score (MBPEC) was developed. The prognostic value of the MBPEC score was retrospectively assessed in a cohort of PE-patients. We found no clear association between the MBPEC score and mortality. However, patients with peripheral PE had higher mortality rates compared to those with centrally located PE.
In conclusion, we cannot rule out that myocardial fibrosis contributes to the development of dyspnea after PE in some patients, but the differences were modest. However, we consider it likely that other mechanisms are more important. Additionally, we did not observe any clear changes in myocardial function after rehabilitation, indicating that the symptomatic improvements were probably not related to alterations in cardiac function. Finally, we found no clear association between the MBPEC score and mortality, but our results indicate that peripheral PE also have clinical implications.
Additional information
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