[Show abstract][Hide abstract] ABSTRACT: Thrombophilia may cause severe complications in cardiac surgical patients. We analyzed our experience with symptomatic factor V Leiden patients.
Over an eight-year period, 14 symptomatic patients previously diagnosed with activated protein C resistance,caused by factor V Leiden, underwent a cardiac surgical procedure. We retrospectively reviewed the clinical data, operative and postoperative courses, and the intermediate-term results of these patients.
Procedures performed were coronary artery bypass grafting (CABG, 10 patients), aortic valve replacement+ CABG, pulmonary thromboendarterectomy, left ventricular thrombus removal, and aortic valve reconstruction(one patient each). Eleven patients survived; three patients died perioperatively, one from sepsis (25 days after surgery), one from recurrent stroke (28 days after surgery), and one from multiorgan failure following perioperative stroke (31 days after surgery). In one patient, all bypass grafts occluded intraoperatively.Three patients underwent cardiac surgery under continuous anticoagulation with phenprocoumon. In these three patients, no perioperative thromboembolic events occurred. At a mean follow-up of 32 months,three patients had suffered from cerebral stroke, two from graft occlusion, of which one was recurrent. Two more patients had died (one after cerebral stroke and one from cerebral metastases of a renal cell carcinoma).
In 14 patients with symptomatic factor V Leiden who underwent cardiac surgery, we observed a considerable number of fatal and nonfatal thromboembolic events in the perioperative period and during a 32 months' follow-up. As conducted in three patients, continued anticoagulation with coumarin was safe and prevented perioperative thromboembolic events.
Journal of Cardiac Surgery 12/2008; 24(4):379-82. · 1.35 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Principally, there are two reasons why the pharmacological response to antiplatelet drugs should be measured: on the one hand, an insufficient inhibition of platelet function may result in atherothrombotic complications; on the other hand, an excessive inhibition of platelet function may lead to bleeding complications. The clinical importance to measure the effects of antiplatelet drugs is demonstrated by increasingly growing evidence for an association of resistance to antiplatelet drugs with thromboembolic events. It is often claimed that there is no generally accepted definition of "resistance" and, instead, there is an ongoing semantic discussion about the correct term to be used to describe this phenomenon. From the pharmacological point of view, there is only one acceptable definition of "resistance" to antiplatelet drugs: the term "resistance" should be used when a drug is unable to hit its pharmacological target. Thus, laboratory methods used to evaluate the effects of antiplatelet drugs should be designed to measure the direct pharmacodynamic effect of a drug, rather than the consequences for global platelet function. Based on physiological/pathophysiological, pharmacological, and practical considerations, the authors propose the following assays to be used to measure the effects of oral antiplatelet drugs: for the detection of aspirin actions, thromboxane or arachidonic acid-induced responses (light aggregometry, whole-blood aggregometry) should be measured; for the detection of clopidogrel actions, VASP (vasodilator-stimulated phosphoprotein) phosphorylation (flow cytometry) or ADP-(adenosine diphosphate-)induced responses (light aggregometry, whole-blood aggregometry, possibly also flow cytometry) should be measured.
[Show abstract][Hide abstract] ABSTRACT: Based on the concept that the so-called resistance to anti-platelet drugs is meant to describe a phenomenon where the drug does not hit its direct pharmacodynamic target, assays, used to evaluated the effects of anti-platelet drugs, should as closely as possible measure the direct pharmacodynamic effect of a particular drug. Thus, for the detection of aspirin effects, thromboxane concentrations or arachidonic acid-induced responses (light aggregometry, whole-blood aggregometry) should be measured. For the detection of clopidogrel actions, VASP phosphorylation (flow cytometry) or ADP-induced responses (light aggregometry, whole blood aggregometry) should be analysed.
[Show abstract][Hide abstract] ABSTRACT: Thrombophilic diathesis may cause severe problems in cardiac surgical patients. Among these, protein S deficiency is a coagulation disorder associated with recurrent thromboembolic events. We analyzed our experience with 7 patients with protein S deficiency who underwent cardiac surgery.
We retrospectively reviewed the clinical data, operative and postoperative courses, and the long-term results of 7 patients who were diagnosed to have protein S deficiency. Six of them were operated on using cardiopulmonary bypass, one was operated on with an off-pump procedure.
Procedures performed were emergent pulmonary embolectomy (patient 1), aortic valve replacement and coronary artery bypass grafting (CABG, patient 2), re-CABG (patients 3 and 7), and CABG (patients 4, 5, and 6). In patients 1, 2, 3, and 7, the diagnosis was made perioperatively. Patients 4, 5, and 6 were treated with a modified regimen of warfarin or protamine. All of the latter 3 patients had an uneventful perioperative course without thromboembolic complication. At follow-up, all but 1 of the 7 patients were on continuous warfarin, and were well and without any further thromboembolic events.
In patients with a past medical history of thromboembolic events or with a perioperative thromboembolic complication, elaborate laboratory investigation should lead to a definite diagnosis. For instance, patients with protein S deficiency undergoing cardiac surgery belong to a high-risk subgroup. Although rare, this and other coagulation disorders can be a critical issue in cardiac surgery. In such patients, we suggest perioperative warfarin therapy with a target international normalized ratio of 2.0 and incomplete protamine antagonism to minimize the risk of a perioperative thromboembolic event.
The Annals of thoracic surgery 01/2007; 82(6):2187-91. · 3.45 Impact Factor