Single-centre experience with the Thoratec® paracorporeal ventricular assist device for patients with primary cardiac failure

SummaryBackgroundTemporary mechanical circulatory support may be indicated in some patients with cardiac failure refractory to conventional therapy, as a bridge to myocardial recovery or transplantation.AimsTo evaluate outcomes in cardiogenic shock patients managed by the primary use of a paracorporeal ventricular assist device (p-VAD).MethodsWe did a retrospective analysis of demographics, clinical characteristics and survival of patients assisted with a Thoratec® p-VAD.Resultsp-VADs were used in 84 patients with cardiogenic shock secondary to acute myocardial infarction (35%), idiopathic (31%) or ischaemic (12%) cardiomyopathy, myocarditis or other causes (23%). Before implantation, 23% had cardiac arrest, 38% were on a ventilator and 31% were on an intra-aortic balloon pump. Cardiac index was 1.6±0.5 L/min/m2 and total bilirubin levels were 39±59μmol/L. During support, 29 patients (35%) died in the intensive care unit and seven (10%) died after leaving. Forty-seven patients (56%) were weaned or transplanted, with one still under support. Despite significantly more advanced preoperative end-organ dysfunction, survival rates were similar in patients with biventricular devices (74%) and those undergoing isolated left ventricular support (24%) (63% versus 45%, respectively; p=0.2). Actuarial survival estimates after transplantation were 78.7±6.3%, 73.4±6.9% and 62.6±8.3% at 1, 3 and 5 years, respectively.ConclusionsOur experience validates the use of p-VAD as a primary device to support patients with cardiogenic shock. In contrast to short-term devices, p-VADs provide immediate ventricular unloading and pulsatile perfusion in a single procedure. Biventricular support should be used liberally in patients with end-organ dysfunction

Defective collagen-induced platelet activation in two patients with malignant haemopathies is related to a defect in the GPVI-coupled signalling pathway.

The occurrence of a thrombocytopathy concomitantly to the development of a malignant haemopathy has been reported for some time, but little is known about the mechanism(s) involved in the platelet dysfunction. Platelet glycoprotein VI (GPVI) has now been identified as a principal platelet receptor for collagen. In this paper, we report the cases of two patients with a myelodysplasia and a B lymphopathy, respectively, who presented with thrombocytopathy in relation to a defective GPVI-mediated platelet reactivity to collagen. Thus, with regard to the different steps of adhesion, activation secretion or aggregation, patients' platelet responses to collagen and to the GPVI specific agonists, collagen related peptide (CRP) or convulxin were null or dramatically impaired. Platelet responses to other agonists ADP, TRAP, Arachidonic acid were normal or showed only a moderate decrease. GPVI content was repeatedly normal, and binding of specific ligands, such as convulxin, satisfactory. Nevertheless, specific activating monoclonal antibodies and convulxin failed to induce platelet secretion; collagen, CRP or convulxin were unable to provoke calcium mobilisation. Furthermore, using a perfusion chamber model, we showed that ex vivo collagen-induced thrombi formation was very impaired. Taken together, these data provide evidence, for the first time, of an acquired defect in GPVI-mediated platelet reactivity to collagen, which reflects data observed in constitutional GPVI deficiencies, in two patients with malignant haemopathies

257 Prevalence of aspirin resistance in stable coronary heart diseased patients and correlation with platelet turn-over

BackgroundAspirin resistance has been widely reported but the underlying mechanisms remain unclear. Previous studies have suggested a relationship between accelerated platelet turn-over and aspirin resistance in patients with coronary artery disease. The purpose of this study was to determine whether aspirin resistance could be linked to accelerated platetet turn-over.MethodsWe performed a prospective monocentric study including 50 consecutive patients with stable coronary artery disease treated by aspirin (75 to 250mg/day) without any other antiaggregant treatment. Aspirin resistance was characterized 24 hours after aspirin intake by light transmission aggregometry using 0.5mg/mL arachidonic acid. Aspirin resistance was defined as >20% residual agregation. Platelet turn-over was estimated at the same time by measurement of mean platelet volume, % of reticulated platelets, serum P-selectin, platelet P-selectin and serum thrombopoietin.ResultsAmong 50 patients (70 ± 11 y.o. mean ± 1,5, 76% male, 52% type 2 diabetes mellitus, 16% active smokers), 18 (36%) were identified as aspirin resistants. Table 1 shows the mean value of markers currently linked to platelet turn-over depending on the presence of aspirin resistance. Serum thrombopoietin was significantly increased in patients with aspirin resistance compared to patients with no aspirin resistance. No statistical difference was demonstrated for mean platelet volume, reticulated platelets, platelet P-selectin and serum P-selectin. Serum thrombopoietin values were not correlated with other platelet turn-over parameters. There was no significant correlation between serum thrombopoietin and inflammatory markers.ConclusionSerum thrombopoietin is associated with aspirin resistance, but no other parameters currently linked to platelet turn-over. Further studies are needed to determine whether serum thrombopoietin can predict aspirin resistance in a larger cohort.Aspirin sensitiveAspirin resistantpPlatelet volume (fl)8.78 ± 0.268.82 ± 0.300.92Reticulated platelet (%)8.4 ± 0.528.6 ± 0.760.82Serup P selectin (ng/ml)42.6 ± 4.2942.9 ± 4.750.97Platelet P selectin (%)11.1 ± 1.09.5 ± 1.50.35Serum thrombopoietin (pg/ml)130.6 ± 11.3319.9 ± 97.80.0