Quantitative and Qualitative Platelet Derangements in Cardiac Surgery and Extracorporeal Life Support.

Enrico Squiccimarro,Roberto Lorusso,Giuseppe Filiberto Serraino,Hugo ten Cate,Federica Jiritano,Domenico Paparella

doi:10.3390/jcm10040615

Abstract

Thrombocytopenia and impaired platelet function are known as intrinsic drawbacks of cardiac surgery and extracorporeal life supports (ECLS). A number of different factors influence platelet count and function including the inflammatory response to a cardiopulmonary bypass (CPB) or to ECLS, hemodilution, hypothermia, mechanical damage and preoperative treatment with platelet-inhibiting agents. Moreover, although underestimated, heparin-induced thrombocytopenia is still a hiccup in the perioperative management of cardiac surgical and, above all, ECLS patients. Moreover, recent investigations have highlighted how platelet disorders also affect patients undergoing biological prosthesis implantation. Though many hypotheses have been suggested, the mechanism underlying thrombocytopenia and platelet disorders is still to be cleared. This narrative review aims to offer clinicians a summary of their major causes in the cardiac surgery setting.

Highlights

Platelets are anucleated blood components with a pivotal role in hemostasis and other functions in the biology and pathophysiology of complex diseases [1]
Contemporary knowledge ascribes to platelets a key role in inflammation and innate immunity [2,3,4,5]
Quantitative and qualitative platelet derangements represent a shortcoming in cardiac surgery and extracorporeal life supports (ECLS)

Summary

Introduction

Platelets are anucleated blood components with a pivotal role in hemostasis and other functions in the biology and pathophysiology of complex diseases [1]. A platelet qualitative impairment such as a reduced surface GPIb expression was found to be associated with the overexpression of some miRNAs (i.e., mir-10b and mir-96) and with enhanced platelet Bax apoptotic signaling in cardiac surgery cohorts [38,39] Microcirculatory impairment is another factor associated with platelet dysfunction following heart procedures. A recent investigation showed how perivascular mast cells were activated through the release of the lipid mediator platelet activating factor (PAF) from gut microvascular endothelial-adherent platelets to explain the inflammatory mediated tissue damage and organ injury following a CPB [43] This mechanism might highlight platelets as a direct determinant of IRI related tissue damage

Platelets and Extracorporeal Membrane Oxygenation

Platelets and Aortic Biological Prosthesis

Heparin-Induced Thrombocytopenia

Points

Findings

Conclusions