Loss of high-molecular-weight von Willebrand multimers and platelet receptor shedding in mechanical circulatory support [descriptive label — exact article title VERIFICATION REQUIRED]

Certainty
Moderate
Chapters

29, 36, 39

Clinical implication

Most patients on support have acquired von Willebrand syndrome. But an unknown share of the platelet abnormality belongs to the disease that made the circuit necessary, not to the circuit — the same attribution correction the free-haemoglobin data force.

Comparator

Heart failure patients WITHOUT a device, and healthy donors — the design feature that makes this study useful

Design
Prospective cohort
Identifier

Lukito P, Wong A, Jing J, Arthur JF, Marasco SF, Murphy DA, Bergin PJ, Shaw JA, Collecutt M, Andrews RK, Gardiner EE, Davis AK. J Thromb Haemost 2016;14(11):2253-2260. DOI 10.1111/jth.13497

Intervention

Von Willebrand multimer analysis and platelet receptor measurement (soluble and surface glycoprotein VI, surface glycoprotein Ib-alpha)

Limitations

Single centre; 20 ECMO patients; cross-sectional

Link
Main result

Loss of high-molecular-weight multimers, consistent with acquired von Willebrand syndrome, in 14 of 20 ECMO patients and 18 of 19 device patients. Elevated soluble glycoprotein VI with significantly reduced surface glycoprotein Ib-alpha and glycoprotein VI versus healthy donors. Critically, platelet receptor levels were ALSO significantly reduced in the heart failure patients who had no device.

Population

21 continuous-flow ventricular assist device patients, 20 ECMO patients, 12 heart failure patients without a device, 7 with aortic stenosis, and healthy donors

Verified
Year
2016