Acute Coronary Syndromes

Abstract

Well into the 21st century, we still triage acute myocardial infarction based on the presence or absence of ST segment elevation, a century-old technology. Meanwhile, we have learned a great deal regarding the pathophysiology and mechanisms of acute coronary syndromes (ACS) at clinical, pathological, cellular, and molecular levels. Contemporary imaging studies have shed new light into the mechanisms of ACS. This review discusses these advances and their implications for clinical management of the ACS for the future. Plaque rupture has dominated our thinking about ACS pathophysiology for decades. Yet, current evidence suggests that a sole focus on plaque rupture vastly oversimplifies this complex collection of diseases, and obscures other mechanisms that may mandate different management strategies. We propose to segment coronary artery thrombosis due to plaque rupture into cases with or without signs of concomitant inflammation. This distinction may have substantial therapeutic implications as direct anti-inflammatory interventions for atherosclerosis emerge. Coronary artery thrombosis due to plaque erosion may be on the rise in an era of intense lipid lowering. Identification of patients with of ACS due to erosion may permit a less invasive approach to management than the current standard of care. We also now recognize ACS that occur without apparent epicardial coronary artery thrombus or stenosis. Such events may arise from spasm, microvascular disease, or other pathways. Emerging management strategies may likewise apply selectively to this category of ACS. We advocate this more mechanistic approach to the categorization of ACS to provide a framework for future tailoring, triage, and therapy for patients in a more personalized and precise manner.

Thrombotic Regulation From the Endothelial Cell Perspectives

“…Arterial thrombosis is commonly initiated by vascular endothelial erosions and ruptures of an atherosclerotic plaque 3,4 while venous thrombosis mainly stems from blood stasis. 5 Despite these differences, platelet adhesion/activation, and fibrin deposition as the result of coagulation constitute the fundamental processes of thrombus formation.…”

High-Sensitivity C-Reactive Protein and Acute Kidney Injury in Patients with Acute Myocardial Infarction: A Prospective Observational Study

“…Growing attention has been focused on C-reactive protein (CRP), a simply detectable inflammation biomarker, as a possible predictor of AKI and it has been recently recognized that CRP actively contributes in the pathogenesis and progression of AKI, by exacerbating local inflammation, impairing the proliferation of damaged tubular epithelial cells, and promoting the fibrosis of injured renal tissue [11][12][13][14][15]. Moreover, physicians have now become accustomed to use high-sensitivity CRP (hs-CRP), when considering vascular disease risk stratification, as opposed to the use of standard CRP assays that monitor infections and other inflammatory conditions [16][17][18]. In particular, to assess the cardiovascular risk, CRP should be measured by highly sensitive methods that are capable of reliably measuring concentrations within the healthy reference interval [16][17][18].Emerging evidence showed that serum level of CRP acts as a risk factor and, at the same time, as a potential causal factor for both AKI development and severity, which is also seen in AMI patients [15].…”

“…Moreover, physicians have now become accustomed to use high-sensitivity CRP (hs-CRP), when considering vascular disease risk stratification, as opposed to the use of standard CRP assays that monitor infections and other inflammatory conditions [16][17][18]. In particular, to assess the cardiovascular risk, CRP should be measured by highly sensitive methods that are capable of reliably measuring concentrations within the healthy reference interval [16][17][18].Emerging evidence showed that serum level of CRP acts as a risk factor and, at the same time, as a potential causal factor for both AKI development and severity, which is also seen in AMI patients [15]. In coronary artery disease patients, Gao et al [19], who were the first to perform a retrospective analysis on 4522 patients undergoing elective percutaneous coronary intervention (PCI) with drug-eluting stents, found that elevated pre-procedural CRP was associated with a progressively increased risk of contrast-induced AKI.…”

“…Moreover, physicians have now become accustomed to use high-sensitivity CRP (hs-CRP), when considering vascular disease risk stratification, as opposed to the use of standard CRP assays that monitor infections and other inflammatory conditions [16][17][18]. In particular, to assess the cardiovascular risk, CRP should be measured by highly sensitive methods that are capable of reliably measuring concentrations within the healthy reference interval [16][17][18].…”

Computational Fluid Dynamics as an Engineering Tool for the Reconstruction of Hemodynamics after Carotid Artery Stenosis Operation: A Case Study

“…On the other hand, some plaques are unstable and may “fracture” leading to rapid thrombus formation and severe ischemia of the upstream region [9]. In these cases, physicians may attempt to restore the patency by surgical or endovascular approach.…”