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

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.

A Combination of Drug-Eluting Stents and Bioresorbable Vascular Scaffolds in the Treatment of Multivessel Coronary Artery Disease.

Optimal management of multivessel coronary artery disease can be complex. We report a 67-year-old male patient who was admitted to the Padua University Hospital, Padua, Italy, in 2014 with a non-ST-elevation myocardial infarction. Coronary angiography showed diffuse multiple sub-occlusive lesions of the proximal and distal left coronary vessels involving a long segment of the vessel. On intravascular ultrasonography (IVUS), the left main artery was moderately diseased with critically stenotic and calcified branch ostia. A successful percutaneous coronary intervention using the T-stenting and small protrusion technique with two drug-eluting stents (DES) was performed on the left main artery and its main branches. Two bioresorbable vascular scaffolds were also deployed in overlap at the mid to distal segments of the left anterior descending artery and overlapping a previous DES at the proximal segment. The full expansion and apposition of the struts and scaffolds to the vessel wall without residual stenosis was confirmed by IVUS.

Development and Validation of a Distal Embolization Risk Score During Primary Angioplasty in ST-Elevation Myocardial Infarction.

This study aims to develop and validate a new angiographic risk score to predict the risk of distal embolization (DE) during primary percutaneous coronary intervention (p-PCI) for ST-elevation myocardial infarction. Study included data from 1,200 patients who underwent p-PCI. The cohort was randomly split into a derivation cohort (n = 814) and a validation cohort (n = 386). Logistic regression was used to examine the relation between risk factors and the occurrence of DE. To each covariate in the model was assigned an integer score based on the regression coefficients. Variables included in the risk score, according to multivariable analysis, were occlusion pattern of infarct-related artery, Thrombolysis In Myocardial Infarction Thrombus Score 2 to 4, reference vessel diameter ≥3.5 mm, and lesion length >20 mm. To each variable was assigned a 0- to +2-point score according to the strength of the statistical association. Rates of DE in low-, intermediate-, and high-risk groups were 5.6%, 15.8%, and 40% in the derivation cohort (p for trend <0.0001; C-statistic 0.70) and 7.5%, 12.1%, and 37.9% in the validation cohort (p for trend <0.0001; C-statistic 0.62), respectively. In conclusion, the individual risk of DE in patients who underwent p-PCI can be predicted using a simple 4-variables model based on angiographic features.

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.

Thrombus burden and myocardial damage during primary percutaneous coronary intervention.

Large thrombus burden (LTB) lesions in the context of primary percutaneous coronary intervention (p-PCI) have been related to unsuccessful angiographic reperfusion and unfavorable clinical outcomes. However, the hazard of LTB treatment on myocardial damage has not been evaluated. We investigated the impact of LTB on myocardial damage using contrast-enhanced cardiac magnetic resonance (CE-CMR) in the setting of p-PCI. In 327 patients, who underwent p-PCI without thrombus aspiration within 12 hours from symptom onset, we prospectively assessed the impact of LTB on infarct size and microvascular damage using CE-CMR. LTB was defined by the presence of Thrombolysis In Myocardial Infarction thrombus score ≥3 in patent infarct-related artery (IRA); or by "cut-off" occlusion pattern and/or large reference vessel diameter (≥3.5 mm) in occluded IRA. One hundred ninety-seven patients (60.2%) showed LTB and 130 (39.8%) did not. Distal embolization occurred in 18.8% patients with versus 6.9% without LTB (p = 0.003). At CE-CMR, patients with LTB had larger infarct size index (27.5 ± 11.1 vs 22.1 ± 17.5, p = 0.009) and more often transmural necrosis (70.5% vs 55.4%, p = 0.008) compared with patients without LTB. Excluding patients with distal embolization, patients with LTB still had larger necrosis. At multivariate analysis, occluded (IRA) at baseline, anterior infarction, and presence of LTB predicted transmural necrosis. In conclusion, LTB in the setting of p-PCI is related to larger myocardial damage as detected by CE-CMR, regardless of angiographic detectable distal embolization.