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We began analyzing https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.117.029870, but it redirected us to https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.117.029870. The analysis below is for the second page.

Title[redir]:
Acute Coronary Syndromes | Circulation
Description:
Well into the 21st century, we still triage acute myocardial infarction on the basis of the presence or absence of ST-segment elevation, a century-old technology. Meanwhile, we have learned a great deal about the pathophysiology and mechanisms of acute coronary syndromes (ACS) at the clinical, pathological, cellular, and molecular levels. Contemporary imaging studies have shed new light on 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. However, 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 segmenting coronary artery thrombosis caused by 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 caused by plaque erosion may be on the rise in an era of intense lipid lowering. Identification of patients with of ACS resulting from 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.

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🏙️ Massive Traffic: 50M - 100M visitors per month

Based on our best estimate, this website will receive around 94,026,998 visitors per month in the current month.

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Keywords {🔍}

coronary, crossref, google, scholar, pubmed, plaque, doi, patients, acs, acute, rupture, erosion, inflammation, cells, heart, mechanisms, spasm, circulation, libby, artery, atherosclerosis, study, crea, myocardial, thrombosis, plaques, atherosclerotic, cardiovascular, cardiol, syndromes, cholesterol, endothelial, clinical, disease, local, therapeutic, systemic, fibrous, infarction, figure, arterial, superficial, thrombus, events, human, cap, tcell, receptor, syndrome, ischemia,

Topics {✒️}

aha/asa scientific statements hps/timi55-reveal collaborative group time-honored anti-inflammatory drug cd31-negative t-cell subset st-segment–myocardial infarction versus synthetic cd31-derived peptide st-segment–elevation myocardial infarction lipid-rich necrotic core high-sensitivity c-reactive protein harbor large collections american heart association american heart journal transforming growth factor-β rho-kinase inhibitor fasudil lowering low-density lipoprotein transforming growth factor-β1 plasma low-density lipoprotein modulate t-cell functions solid-state reactor st-segment–myocardial infarction monoclonal t-cell proliferation micro-optical coherence tomography high-density lipoprotein concentrations raises high-density lipoprotein raising high-density lipoprotein virtual screening-driven repositioning direct anti-inflammatory interventions releasing anti-inflammatory cytokines gov/ct2/show/nct02551094 specialized pro‐resolving mediators high-sensitivity [hscrp] assay myocardial infarction-prone strain healthy control subjects serum mir-142-5p serves supplements download pdf red ™ aha submit effective anti-thrombotic therapy upstream t-cell receptor mrc-ila heart study st-segment–elevation acs rho kinase inhibitor traditional risk factors human regulatory t-cells blood c-reactive protein intensive lipid-lowering treatment address triglyceride-rich lipoproteins circulating t-cell subsets acute coronary-artery lesions main content advertisement

Questions {❓}

Although this approach remains the appropriate evidence-based strategy today, aiming toward the future goal of more individualized therapy, can we apply a more pathophysiologically based categorization of the acute coronary syndromes (ACS)?
How does lipid lowering prevent coronary events?
Regulation of matrix metalloproteinase expression in human vascular smooth muscle cells by T lymphocytes: a role for CD40 signaling in plaque rupture?
Triglycerides on the rise: should we swap seats on the seesaw?

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