Ahmed Hussien Hussien Al Mamary

On-treatment platelet reactivity in peripheral and coronary blood in patients undergoing primary PCI for ST-segment elevation myocardial infarction (STEMI)

Abstract Dual antiplatelet therapy is recommended in patients undergoing primary percutaneous coronary intervention (p-PCI) for ST-segment elevation myocardial infarction (STEMI). Pre-analytical variables may influence platelet function analysis results. Our aim was to evaluate the on-treatment platelet reactivity in peripheral artery vs coronary blood in patients with STEMI. We enrolled one hundred and nine patients who consecutively underwent p-PCI at Cardiology Unit of Padua University Hospital between June 2014 and June 2015. Before the procedure, all patients received intravenous aspirin 250 mg and either of the thienopyridines; clopidogrel 600 mg, prasugrel 60 mg or ticagrelor 180 mg. ASPI-test and ADP-test using multiple electrode aggregometry (MEA) were performed in samples collected from both a peripheral artery and the culprit coronary artery. ‘Low responders’ were patients with an ASPI-test or ADP-test value greater than or equal to a pre-established normal range. No significant differences were observed in ASPI-test values between peripheral (19 (median) [3–49 (10–90 percentiles)] U) vs coronary (12 [1–40] U, p = .06) blood and in ADP-test (40 [14–82] U vs 33 [7–79] U, p =.68) blood. In peripheral blood, fifteen (14%) patients were ‘low aspirin’ and forty-one (38%) ‘low thienopyridines’ responders. The prevalence of ‘low clopidogrel’ responders was higher (45%) than prasugrel (36%) and ticagrelor (33%). Similar results were observed in coronary blood. In patients undergoing p-PCI for STEMI, MEA platelet function observed in coronary arteries was consistent with peripheral artery blood’s independently of the antiplatelet drug used. The clinical significance of peripheral and coronary on-aspirin/thienopyridines platelet reactivity needs further clarification.

Neo-atherosclerosis in very late stent thrombosis of drug eluting stent.

BACKGROUND Recent studies have described neo-atherosclerosis, developing inside the stent, as cause of very late stent thrombosis. CASE REPORT A 59-year-old man, with family history of coronary artery disease, presented to our Department because of anterior ST-segment elevation myocardial infarction. Two years before he had underwent percutaneous coronary intervention with multiple drug-eluting stents (DES) implantation on proximal-mid left anterior descending artery (LAD), and mid-right coronary artery (RCA), respectively. The angiogram revealed stent thrombosis with total occlusion of proximal LAD. Multiple passages with manual thrombus-aspiration catheter were successfully performed with improvement in TIMI flow. Optical Coherence Tomography (OCT) imaging revealed fully expanded stents without areas of inappropriate apposition to vessel wall; and mild to moderate intimal hyperplasia throughout the stented segment, with full covered stent struts; areas of ulcerated and ruptured plaque within the proximal struts of stented segment was depicted with intraluminal protruding material. Thus, an additional bare metal stent (BMS) was deployed inside and overlapping the previous in order to seal this plaque. OCT post procedure revealed optimal stent expansion and apposition, without residual protruding material. At 9-month follow-up patient was alive and free from symptoms. Coronary angiogram revealed patency of implanted stents without significant restenosis. CONCLUSIONS Neo-atherosclerosis with thrombosis on top of ruptured necrotic plaque core may play a role in the pathophysiology of very late stent thrombosis in both BMS and DES. Our report highlights the role OCT to assess the mechanism of VLST.

Late stent fracture – A potential role of left ventricular dilatation

BACKGROUND Coronary stent fracture is an under-recognized event but one that has been reported frequently in the drug-eluting stent era. Most reported cases of stent fracture occurred within days to two years after implantation, and are related to stent thrombosis and restenosis. CASE REPORT Presentation of a 69-year-old male with a history of arterial hypertension and previous percutaneous coronary intervention (PCI), and with implantation of three overlapping drug-eluting stents (DES) on proximal-to-middle left anterior descending artery (LAD). At five-year outpatient evaluation, the patient was found to have a new left bundle branch block associated with mild elevation in Troponin-I value and severe left ventricular dysfunction. The patient recovered as non ST-segment elevation myocardial infarction (NSTEMI) and consequently a new coronary angiography showed total occlusion of proximal LAD with multiple stent fracture. Here we discuss the role of left ventricular dilatation as a contributing factor to late drug-eluting stent fracture. CONCLUSION Different anatomical coronary settings have been described as predisposing factors to stent fracture. Consequently, the remodeling of the left ventricle, together with the rise in diastolic pressure, may have affected the shear stress of LAD stents by increasing mechanical forces produced in the diastolic phase on the epicardial vessel. In addition, left ventricular enlargement could have increased the elongation forces on the stent frames by altering the curvature of the stent. All predisposing factors of stent fracture, including coronary and left ventricular issues, need to be considered before stent implantation to avoid stent fracture and clinical sequelae.

TCT-256 Distal Embolization and Myocardial Damage during Primary-Percutaneous Coronary Intervention: The Relevance of Thrombus Burden

performed a study to assess long-term survival in OHCA patients managed with CA on admission and PCI if indicated and to compare survival between patients with and without acute myocardial infarction (AMI). Methods: Retrospective single-centre study including patients 18 y.o. resuscitated from an OHCA without an obvious non-cardiac cause. AMI was diagnosed angiographically as lesions suggestive of ruptured plaques with fresh thrombus and critical stenosis easily crossed by an angioplasty wire. Survival was recorded at discharge and 5-years survival probability was estimated by Kaplan-Meier survival curves. Data are expressed as numbers (percentages) and median (interquartile range-IQR). Results: 300 comatose patients aged 56 (48-67) were included from 2002 to 2011. 130 patients (43%) had ventricular fibrillation, 116 (39%) asystole, 54 (18%) had other/unknown initial rhythm. All patients had CA on admission and 93 (31%) had an AMI. PCI was attempted in 85 (91%) of AMI patients, successful in 79. Therapeutic hypothermia was performed in 256 (84%) patients. Survival at discharge was 32.3% (97/300). After discharge, 5-year probability of survival was 81.7 5.4%. Probability of survival from admission to 5 years was 26.2% 2.8%. AMI patients had better survival at discharge, 40.8% (38/93) versus 28.5% (59/207) in non-AMI, p1⁄40.047. Probability of survival from discharge to 5 years in AMI patients was 92.2% 5.4% versus 73.4 8.6% in non-AMI, hazard ratio (HR)1⁄42.7, confidence interval (CI)1⁄4(0.8-8.9), p1⁄40.1. Survival probability from admission to 5 years was better for AMI patients, 37.4% 5.2% versus, 20.7% 3.0% in non-AMI, HR1⁄41.5, CI1⁄4(1.122.0), p1⁄40.0067. Conclusions: We observed a very favourable post-discharge prognosis in OHCA patients undergoing on-admission CA with PCI if indicated. Patients suffering OHCA due to AMI had better survival to discharge and at 5 years follow-up than patients suffering OHCA due to other causes.

TCT-258 Elaboration of a New Risk Score for Predicting Distal Embolization during Primary Angioplasty in ST-Elevation Myocardial Infarction

P O S T E R S cardiac arrest (OHCA) patients, but data on the long-term survival are scarce. We performed a study to assess long-term survival in OHCA patients managed with CA on admission and PCI if indicated and to compare survival between patients with and without acute myocardial infarction (AMI). Methods: Retrospective single-centre study including patients 18 y.o. resuscitated from an OHCA without an obvious non-cardiac cause. AMI was diagnosed angiographically as lesions suggestive of ruptured plaques with fresh thrombus and critical stenosis easily crossed by an angioplasty wire. Survival was recorded at discharge and 5-years survival probability was estimated by Kaplan-Meier survival curves. Data are expressed as numbers (percentages) and median (interquartile range-IQR). Results: 300 comatose patients aged 56 (48-67) were included from 2002 to 2011. 130 patients (43%) had ventricular fibrillation, 116 (39%) asystole, 54 (18%) had other/unknown initial rhythm. All patients had CA on admission and 93 (31%) had an AMI. PCI was attempted in 85 (91%) of AMI patients, successful in 79. Therapeutic hypothermia was performed in 256 (84%) patients. Survival at discharge was 32.3% (97/300). After discharge, 5-year probability of survival was 81.7 5.4%. Probability of survival from admission to 5 years was 26.2% 2.8%. AMI patients had better survival at discharge, 40.8% (38/93) versus 28.5% (59/207) in non-AMI, p1⁄40.047. Probability of survival from discharge to 5 years in AMI patients was 92.2% 5.4% versus 73.4 8.6% in non-AMI, hazard ratio (HR)1⁄42.7, confidence interval (CI)1⁄4(0.8-8.9), p1⁄40.1. Survival probability from admission to 5 years was better for AMI patients, 37.4% 5.2% versus, 20.7% 3.0% in non-AMI, HR1⁄41.5, CI1⁄4(1.122.0), p1⁄40.0067. Conclusions: We observed a very favourable post-discharge prognosis in OHCA patients undergoing on-admission CA with PCI if indicated. Patients suffering OHCA due to AMI had better survival to discharge and at 5 years follow-up than patients suffering OHCA due to other causes.