ABO blood types: Influence on infarct size, procedural characteristics and prognosis

Abstract

Introduction

Patients with non-O blood groups have higher plasma von Willebrand factor (vWF) levels than those with type O. vWF mediates platelet adhesion, aggregation and thrombosis. These considerations likely explain the prior observations that non-O patients have higher rates of arterial and venous thromboembolic events. However, the effect of blood group status on size of MI, procedural findings and outcomes after PCI for MI have not been reported.

Methods

We analyzed 1198 patients who underwent percutaneous coronary intervention for acute myocardial infarction between 10/03 and 8/06, and who had ABO blood group status and clinical follow-up.

Results and conclusions

Patients with O blood type were slightly older (62 ± 13 vs. 60 ± 13years; p = 0.017) had a higher prevalence of hypercholesterolemia (67% vs. 58%; p = 0.002), and had a higher burden of atherosclerosis with more vascular disease (17% vs. 13%; p = 0.017) and higher prevalence of previous PCI (22% vs. 17%; p = 0.025). Non-O blood group patients had larger infarcts as measured by median peak troponin (33 vs. 24; p = 0.037), total CK (721 vs. 532; p = 0.012) and CK-MB (101 vs. 68; p = 0.010). At PCI, non-O patients had increased visible thrombus and reduced TIMI flow pre-procedure. However, there were no differences in procedural success, in-hospital blood transfusion or occurrence of MACE at 1year follow-up. Our data demonstrate that non-O compared to O blood groups patients have higher thrombus burden despite less extensive atherosclerosis. Nevertheless, outcomes at 1year were similar.

Introduction

The ABO blood group and the Rh (D) antigen status are major considerations in providing safe blood transfusion and tissue transplantation. Not limited to red cell membranes, ABO antigens are found on all tissues and are also expressed on several plasma proteins including von Willebrand factor (vWF), FVIII and α₂-macroglobulin [1]. On vWF, ABO blood group antigens are attached via N-linked oligosaccharides, with two at N1515 and N1574, near where ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 repeats-13) cleaves vWF [2]. The efficiency of proteolysis by ADAMTS13 at residues Tyr1605–Met1606 is influenced by these neighboring ABO antigens, occurring more readily with O- than with non-O blood groups [3]. This finding has been proposed as the major mechanism for the reproducible observation that vWF levels are higher in non-O vs. O- blood group patients [3]. Since vWF is the plasma carrier for FVIII, non-O patients also have higher FVIII levels [4].

Von Willebrand factor is a major mediator of platelet adhesion to areas of arterial injury [5], [6]. Platelets bind to domain A1 vWF through the GpIb α domain of the GPIb/V/X receptor and via GPIIb/IIIa interaction with C1 domain of vWF [7]. Several prospective studies have shown that higher vWF levels predict future coronary heart disease events [5]. Similarly, a variety of prospective as well as case–control studies have shown an association between non-O blood groups and CHD events [8], [9], [10], [11], [12], [13], [14], [15].

The effect of ABO status on extent of myocardial necrosis and clinical events after an MI has not previously been studied. Since patients who undergo percutaneous coronary interventions routinely have a “type and screen”, this information is widely available. We postulated that areas of damaged artery, especially with concomitant stent placement would be susceptible to increased events as a result of the higher vWF levels observed in non-O patients. Accordingly, we examined the effect of ABO blood group status on baseline characteristics, procedural findings and clinical events at 1year follow-up.