Non-thromboembolic pulmonary hypertension in multiple myeloma, after thalidomide treatment: a pilot study

C Lafaras1, E Mandala, E Verrou

  • 1Department of Cardiology, Theagenion Cancer Hospital, Thessaloniki, Greece. iatros@the.forthnet.gr

Abstract

Insights

Pulmonary hypertension (PH) was detected in 4.87% of multiple myeloma patients treated with thalidomide. Pre-existing heart conditions, not age or gender, correlated with PH development, suggesting thalidomide may exacerbate existing cardiac issues.

Area of Science:

  • Cardiology
  • Hematology
  • Pulmonology

Background:

  • Multiple myeloma (MM) is associated with thrombotic events and endothelial damage.
  • Thalidomide treatment in MM patients carries a risk of thromboembolic pulmonary hypertension (PH).
  • Non-thromboembolic PH has also been observed in MM patients during thalidomide therapy.

Purpose of the Study:

  • To detect clinical and subclinical nonthromboembolic pulmonary hypertension (PH) in multiple myeloma (MM) patients undergoing thalidomide treatment.
  • Investigate the incidence and potential contributing factors of PH in this patient cohort.

Main Methods:

  • Eighty-two MM patients were evaluated using echocardiography at baseline, 1 month, and 6 months post-treatment.
  • Echocardiographic signs indicative of PH were specifically identified.
  • Diagnostic methods were employed to exclude thromboembolic causes of PH.

Main Results:

  • Four out of 82 patients (4.87%) were diagnosed with PH.
  • Thromboembolic PH was ruled out through comprehensive diagnostic evaluations.
  • A significant correlation was found between structural heart disease and the development of PH (r = 14.078; P = 0.008).
  • No significant correlation was observed between PH and patient age, gender, or International Staging System (ISS) score.

Conclusions:

  • Pre-existing endothelial dysfunction, often linked to structural cardiac disease, may predispose MM patients to PH.
  • Thalidomide might induce an imbalance between vasodilation and vasoconstriction, contributing to abnormal pulmonary vascular responses and perpetuating PH.
  • Structural cardiac disease is a key factor in the development of non-thromboembolic PH in MM patients treated with thalidomide.