Platelet function in lung cancer patients undergoing lobectomy

Abstract

A growing interest concerns arterial thromboembolic disease in cancer patients. As platelets may be key players in this process, investigation of platelet aggregation in cancer patients is of importance. We aimed to investigate platelet aggregation in patients with lung cancer prior to surgery and during video-assisted thoracoscopic surgery (VATS) lobectomy compared with lobectomy performed through a thoracotomy. We included 93 patients (VATS + low molecular weight heparin (LMWH), n = 32; VATS no LMWH, n = 31; thoracotomy + LMWH, n = 30). Data obtained from 121 healthy individuals were used for comparison prior to surgery. Platelet aggregation was analysed by impedance aggregometry using adenosine diphosphate 6.5 μM (ADPtest) and collagen 3.2 μg/mL (COLtest) as agonists. Prior to surgery, platelet aggregation was significantly increased in both VATS-patients (ADPtest, p < .0001; COLtest, p = .0002) and patients undergoing thoracotomy (ADPtest, p < .0001; COLtest, p < .0001) compared with healthy individuals. Platelet aggregation did not differ between VATS-patients and thoracotomy patients prior to surgery (p-values >.11). At the first postoperative day, VATS-patients demonstrated significantly higher collagen-induced platelet aggregation than preoperatively (p = .001), but the increase in platelet aggregation did not differ significantly between VATS and thoracotomy patients (p-values ≥.24). At the second postoperative day, platelet aggregation was significantly reduced in thoracotomy patients compared with the preoperative level (ADPtest, p = .002; COLtest, p = .05). In conclusion, platelet aggregation was significantly increased in patients with primary lung cancer prior to surgery compared with healthy individuals. At the first postoperative day, platelet aggregation was significantly higher than the preoperative level in VATS-patients; however, this increase did not differ between patient groups.

Keywords:

• Platelet aggregation
• neoplasm
• surgery
• haemostasis
• lung cancer

Acknowledgements

The authors thank research nurse Vibeke Laursen for helping and coordinating the practical issues in regards of conducting this study and laboratory technician Mai Stenulm Veirup and Vivi Bo Mogensen for blood sampling and analyses. Hans Pilegaard, MD, and Professor Vibeke E. Hjortdal are thanked for making the study practical feasible.

Disclosure statement

None of the authors have any conflicts of interest regarding the present paper, but have the following general conflicts for interest: Thomas Decker Christensen has been on the speaker bureaus for AstraZeneca, Boehringer-Ingelheim, Pfizer, Roche Diagnostics, Takeda, and Bristol-Myers Squibb and has been in an Advisory Board for Bayer and Merck Sharp & Dohme (MSD). Anne-Mette Hvas has received speaker’s fees from CSL Behring, Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb, Astellas, and Leo Pharma and unrestricted research support from Octapharma, CSL Behring and Leo Pharma. Mads Nybo has received speaker’s fees from Astra Zeneca, Boehringer-Ingelheim, Pfizer, and Roche Diagnostics. Peter Licht has received speaker’s fees from Ethicon Endo-Surgery. Other authors – none declared.

Additional information

Funding

The study was financially supported by Arvid Nilssons fond, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsens Fond and Fru Agnes Niebuhr Andersons Cancerforskningsfonds pris. The work was done independent of the funders.