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Significant platelet reactivity with endothelial damage may occur during percutaneous coronary intervention such as balloon angioplasty and elective stenting in patients with stenotic or occluded arteries in coronary artery disease. Activated platelets express several surface epitopes to aggregate and form heterotypic interactions with leukocytes and endothelial cells, secrete biomarkers to enhance their prothrombotic properties and also generate increased level of microparticles (PMPs). These events may contribute to subacute stent thrombosis induced by the procedure-mediated trauma. Our aim was to study the level of PMPs and other platelet activation markers at an early time point after stenting with bare metal stent in patients on aspirin antiplatelet pre-treatment, and these results were compared to data obtained from subjects with diagnostic catheterization alone. We found that at 15 minutes after the completion of stenting, the levels of PMPs (557 +/- 83/microl versus 325 +/- 42/microl), the platelet P-selectin expression (2.7 +/- 0.3% versus 1.99 +/- 0.1%) and the ratio of platelet-monocyte heterotypic aggregates (48 +/- 4% versus 38 +/- 3%) were significantly (p < 0.05) elevated in patients compared to unstented subjects, but no difference was found in soluble P-selectin values. We suggest that the observed cellular changes are early and sensitive markers to detect the platelet-activating effect of stent implantation.

Drug-eluting stenting (DES) has become a reliable tool for coronary stenting; however, its direct effects on platelet and endothelium function differ from those of bare-metal stenting (BMS). This study involved a periprocedural analysis of various biomarkers of cellular activation after elective DES (Xience®, Abbott Vascular, Santa Clara, CA, USA) or BMS (Integrity®, Medtronic, Minneapolis, MI, USA). Forty-nine stable angina patients were recruited: 28 underwent BMS, and 21 received everolimus-eluting stents. Samples were collected (i) prior to stenting, (ii) at 24 hours after procedure, and (iii) after 1 month of dual antiplatelet therapy. Platelet activation was analyzed by surface P-selectin positivity in parallel with plasma levels of soluble P-selectin, CD40L and platelet-derived growth factor (PDGF). Endothelial cell (EC) activation was detected by measuring markers of early (von Willebrand factor) and delayed response (VCAM-1, ICAM-1, E-selectin). Patients were followed for 6 months for the occurrence of restenosis or stent thrombosis. Increased platelet activation was sustained regardless of stent type or antiplatelet medication. Concentrations of most EC markers were more elevated after BMS than after DES. No stent thrombosis was seen, but six BMS subjects displayed restenosis with significantly higher sCD40L (779 [397–899] vs. 381 [229–498] pg/mL; p = 0.032) and sICAM-1 (222 [181–272] vs. 162 [153–223] ng/mL; p = 0.046) levels than in those without complication, while DES patients exhibited significantly decreased PDGF (572 [428–626] vs. 244 [228–311] pg/mL; p = 0.004) after 1 month. Nonresponsiveness to antiplatelet drugs did not influence these changes. In conclusion, the degree of platelet and EC activation suggests that Xience® DES may be regarded a safer coronary intervention than Integrity® BMS, with a lower risk of in-stent restenosis.

Left ventricular wall rupture after myocardial infarction is a mechanical complication that may result in a pseudoaneurysm. Between January 1994 and October 1996, false or pseudoaneurysms were detected in 6 (0.0026%) of 2,600 consecutive patients (4 women, 2 men; mean age 59.4 years) undergoing cardiac catheterization at University Medical School, Debrecen, Hungary. All patients had a history of cardiovascular disease, with diagnosis of pseudoaneurysm confirmed by echocardiography. The average time from the occurrence of acute infarction to diagnosis was 37.0 days (range 3–80 days). All patients were in New York Heart Association functional class IV congestive heart failure; in four patients cardiogenic shock was present. Five patients underwent coronary angiography, which demonstrated multivessel disease and occlusion of the infarct–related artery (TIMI 0) without adequate collateral circulation (grade 0–1). Five patients had surgical repair of the false aneurysm, and, in three patients, concomitant coronary bypass grafting was performed. The 2‐year mortality rate for all patients was 50%. Early diagnosis of false aneurysm is facilitated by echocardiography, and coronary angiography is required before surgery. Early surgical correction with coronary revascularization is advised.

Stents represent a thrombogenic surface where one of the earliest events is the deposition of platelets. Activated platelets express neoepitopes that enable them to form homo- and heterotypic aggregates and activate the coagulation system. In this study, we investigated the effects of ad hoc clopidogrel treatment compared to a clopidogrel pretreated group on platelet P-selectin expression. We found that after stent implantation in the ad hoc treated group, P-selectin expression decreased after 1 h, while the initial decrease in platelet count normalized after 4 h. Aspirin non-responsiveness did not influence the results. These data point to the beneficial effect of clopidogrel treatment in reducing platelet reactivity during stenting.

Access (Microsoft Office)-based software was developed to register the results of different cardiological investigations (echocardiography, coronarography and SPECT) in 16 left ventricular segments in a polar map display in order to compare the anatomical and functional data. Ten patients with previous myocardial infarction were selected (mean age: 48 years, EF: 36.1/spl plusmn/7.2%). They had 14 totally or subtotally occluded coronary branches. The overlap between the occlusion-associated regions derived by angiography and the corresponding defects on MIBI SPECT, and also the echocardiographic segmental wall motion scores were evaluated. The distribution of the total of 160 segments with rest perfusion defects on MIBI SPECT and the wall motion abnormalities detected by echocardiogaphy gave positive and negative predictive values of coronary occlusion of 0.94 and 0.81 against SPECT and 0.82 and 0.76 against echocardiography, respectively. Further analysis revealed that the relative MIBI activities of the individual segments correlated significantly with the wall motion scores (r=-0.87). It is concluded that the direct comparison of tomographic imaging and echocardiography with the angiogram on the polar map display in order to measure the functional consequences of coronary artery disease may help to indicate an intervention on an individual coronary lesion.

With high pressure stent deployment and combined of the long subtotal occlusion, a 3.0/12 mm S670x (Medantiplatelet therapy the incidence of subacute stent thrombosis is currently 1–2%. Increased risk for stent thrombosis includes lower stent diameter, longer or more implanted stents and acute conditions with intracoronary thrombus formation. Failure of adequate stent expansion to the vessel wall also inclines to thrombus formation in the treated coronary segment [1,2]. The importance of the potential of distal embolisation during intervention on a coronary lesion is increasingly recognised as an advent result for the distal coronary perfusion. This risk is the most prominent during recanalisation of a totally and acutely occluded artery in the case of acute myocardial infarction, but other scenarios (chronically occluded artery, unstable coronary plaque with thrombus apposition or degenerated venous grafts) are also prone to distal embolisation [3,4]. After the coronary intervention, the possibility of distal embolisation in the case of a newly generated thrombus is clear, but according to our knowledge spontaneous distal macroembolisation had not been reported after coronary stent implantation. We report a patient with inferior acute myocardial infarction treated by rescue percutaneous coronary intervention with stent implantation whose symptoms recurred on the third day caused by the occlusion of a distal branch that had been intact before. Angiographic signs revealed thrombus formation inside the stent as the source of distal macroembolisation. Recanalisation of the distal occlusion with balloon dilatation and redilatation of the stent was performed successfully and the further course of the patient was uneventful. A 68-year-old male patient in acute inferior myocardial infarction treated by streptokinase was transferred for rescue PCI because of ongoing ischaemic signs. After predilatation