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Original research
Improvement in left ventricular mechanics following medical treatment of constrictive pericarditis
  1. Kimi Sato1,
  2. Ayman Ayache2,
  3. Arnav Kumar2,
  4. Paul C Cremer2,
  5. Brian Griffin2,
  6. Zoran B Popovic2,
  7. Christine Jellis2,
  8. Deborah H Kwon2,
  9. Michael Bolen3,
  10. Jay Ramchand2,
  11. Michael Chetrit2,
  12. Muhammad M Furqan2,
  13. Douglas Johnston2,
  14. Allan L Klein2
  1. 1Department of Cardiology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan
  2. 2Heart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland, Ohio, USA
  3. 3Imaging Institute, Cleveland Clinic, Cleveland, Ohio, USA
  1. Correspondence to Dr Allan L Klein, Department of Cardiovascular Medicine, Heart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland, OH 44195, USA; kleina{at}ccf.org

Abstract

Objective Patients with constrictive pericarditis (CP) with active inflammation may show resolution with anti-inflammatory therapy. We aimed to investigate the impact of anti-inflammatory medications on constrictive pathophysiology using echocardiography in patients with CP.

Methods We identified 35 patients with CP who were treated with anti-inflammatory medications (colchicine, prednisone, non-steroidal anti-inflammatory drugs) after diagnosis of CP (mean age 58±13; 80% male). Clinical resolution of CP (transient CP) was defined as improvement in New York Heart Association class during follow-up. We assessed constrictive pathophysiology using regional myocardial mechanics by the ratio of peak early diastolic tissue velocity (e’) at the lateral and septal mitral annulus by tissue Doppler imaging (lateral/septal e’) or the ratio of the left ventricular lateral and septal wall longitudinal strain (LSlateral/LSseptal) by two-dimensional speckle-tracking echocardiography. Longitudinal data were analysed using a mixed effects model.

Results During a median follow-up of 323 days, 20 patients had transient CP, whereas 15 patients had persistent CP. Transient CP had higher baseline erythrocyte sedimentation rates (ESR) (p=0.003) compared with persistent CP. There were no significant differences in LSlateral/LSseptal and lateral/septal e’. During follow-up, only transient CP showed improvement in lateral/septal e’ (p<0.001) and LSlateral/LSseptal (p=0.003), and recovery of inflammatory markers was similar between the two groups. In the logistic model, higher baseline ESR and greater improvement in lateral/septal e’ and LSlateral/LSseptal were associated with clinical resolution of CP using anti-inflammatory therapy.

Conclusions Improvement of constrictive physiology detected by lateral/septal e’ and LSlateral/LSseptal was associated with resolution of clinical symptoms after anti-inflammatory treatment. Serial monitoring of these markers could be used to identify transient CP.

  • echocardiography
  • pericardial constriction
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Footnotes

  • Contributors KS: conception of the study, data collection, data analysis, writing the manuscript. AA: conception of the study, data collection, writing of the manuscript. AK: data collection, critical review of the manuscript. PCC, BG, CJ, DHK, MB, JR, MC, MMF, DJ: critical review of the manuscript. ZBP: data analysis, critical review of the manuscript. ALK: critical review of the manuscript, responsible for the overall content as guarantor.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests ALK: research grant and scientific advisory board for Kiniksa; scientific advisory board for Sobi and Pfizer. PCC: scientific advisory board for Kiniksa.

  • Patient consent for publication Not required.

  • Ethics approval The study protocol was approved by the Cleveland Clinic Institutional Review Board.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available upon reasonable request to the corresponding author.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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