Stent Thrombosis is the Primary Cause of ST-Segment Elevation Myocardial Infarction following Coronary Stent Implantation: A Five Year Follow-Up of the SORT OUT II Study

Abstract

BackgroundThe widespread use of coronary stents has exposed a growing population to the risk of stent thrombosis, but the importance in terms of risk of ST-segment elevation myocardial infarctions (STEMIs) remains unclear.MethodsWe studied five years follow-up data for 2,098 all-comer patients treated with coronary stents in the randomized SORT OUT II trial (mean age 63.6 yrs. 74.8% men). Patients who following stent implantation were readmitted with STEMI were included and each patient was categorized ranging from definite- to ruled-out stent thrombosis according to the Academic Research Consortium definitions. Multivariate logistic regression was performed on selected covariates to assess odds ratios (ORs) for definite stent thrombosis.Results85 patients (4.1%), mean age 62.7 years, 77.1% men, were admitted with a total of 96 STEMIs, of whom 60 (62.5%) had definite stent thrombosis. Notably, definite stent thrombosis was more frequent in female than male STEMI patients (81.8% vs. 56.8%, p = 0.09), and in very late STEMIs (p = 0.06). Female sex (OR 3.53 [1.01–12.59]) and clopidogrel (OR 4.43 [1.03–19.01]) was associated with increased for definite stent thrombosis, whereas age, time since stent implantation, use of statins, initial PCI urgency (STEMI [primary PCI], NSTEMI/unstable angina [subacute PCI] or stable angina [elective PCI]), and glucose-lowering agents did not seem to influence risk of stent thrombosis.ConclusionIn a contemporary cohort of coronary stented patients, stent thrombosis was evident in more than 60% of subsequent STEMIs.

Inflammatory Bowel Disease as a Risk Factor for Premature Coronary Artery Disease

“…This study found that IBD patients were at an increase risk of CV events during periods of active disease. The use of TNF alpha inhibitors was one of the markers used to define periods of active disease/flares [ 20 ].…”

“…It is likely that the systemic inflammatory state alone is not sufficient to generate CV disease events but rather that the chronic inflammation wrought by IBD plays a role in facilitating an already present underlying process such as the intimal lipid particle oxidation in hyperlipidemic patients which is known to be the necessary catalyst for endothelial adhesion molecule production. This then leads to inflammatory cell attachment to the endothelium and the genesis of CAD [ 20 ]. What is clear is that more randomized control trials assessing the interplay between these two processes are necessary, and whether active effective therapy to suppress inflammation in these patients could alter the natural progression of CV disease.…”

Vascular response and intrastent thrombus in the early phase after drug‐eluting versus bare‐metal stent implantation in patients with ST‐segment elevation myocardial infarction: An observational, single‐center study

“…The causes of thrombus formation and subsequent clinical events after coronary stent implantation are considered to be the accumulation of unfavorable factors in patient (eg, diabetes and hereditary drug withdrawal), procedural (eg, suboptimal stenting), device (eg, metal and polymer), lesion (eg, residual thrombus and lipid‐rich plaque), and pharmacological responses to antiplatelet drugs . Renewed technologies in G2‐DES such as biocompatible polymers, improved drug‐eluting kinetics, thinner struts, and a well‐designed platform with better conformability may contribute to the reduction of thrombus formation and clinical events compared with first‐generation DES and BMS .…”

“…The causes of thrombus formation and subsequent clinical events after coronary stent implantation are considered to be the accumulation of unfavorable factors in patient (eg, diabetes and hereditary drug withdrawal), procedural (eg, suboptimal stenting), device (eg, metal and polymer), lesion (eg, residual thrombus and lipid-rich plaque), and pharmacological responses to antiplatelet drugs. [24][25][26][27][28] Renewed technologies in G2-DES such as biocompatible polymers, improved drugeluting kinetics, thinner struts, and a well-designed platform with better conformability may contribute to the reduction of thrombus formation and clinical events compared with first-generation DES and BMS. [1][2][3][4] Although the exact mechanism of smaller thrombus burden in G2-DES compared with BMS in the present study still remains unclear, the presence of biocompatible polymer in G2-DES might play an important role as a protective factor for thrombus formation, among several differences between them.…”

When the Coronary Anomaly Saves Your Life: a Very Rare Ischemic Coronary Presentation - Our Cardiac Catheterization Laboratory Experience and New Way of Treatment

“…In fact, in a hard situation as STEMI, the risk of ISR is higher because the interventional cardiologists don't have the real vessel size due to inflammation vasoconstriction, spasm and thrombotic stratification and this is the reason for a higher rate of stent thrombosis too [12].…”