By Eric J. Topol
From vintage ST-segment elevation myocardial infarction (MI) and non-Q (non ST-segment elevation) MI to risky angina, this paintings addresses acute coronary syndromes (ACS). It deals stories of up to date advances within the pathophysiological, diagnostic and healing continuum of ACS. It comprises information on third-generation thrombolytic brokers, together with reteplase, and classes from the GUSTO trials.
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Additional resources for Acute coronary syndromes
Quantitative and qualitative variations in plasminogen activator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis, correlate with acute coronary events, particularly acute myocardial infarction in relatively young individuals (15,16). Diminished fibrinolytic potential could stabilize clots and, like hyperfibrinogenemia, render it more likely that a plaque disruption would provoke an evident acute thrombotic event rather than remaining clinically silent. An additional plasma factor correlated with coronary risk may influence fibrinolysis.
Yet other members of the matrix metalloproteinase family such as stromelysin can break down elastin, the core proteins of proteoglycans, and activate the precursor forms of other members of the matrix metalloproteinase family, a step required for them to act enzymatically. Under ordinary circumstances, cells within human arteries contain negligible amounts of the active forms of these specialized matrix-degrading enzymes (30). However, various cell types in vulnerable regions of human atherosclerotic plaques can express interstitial collagenase, gelatinases, and stromelysin (30,31).
Inhibitors of these enzymes do exist, and there is interest in exploring their utility as therapeutic agents in the context of the acute coronary syndromes. Certainly, experimental data suggest that metalloproteinase inhibition can delay intimal thickening postinjury in rats (43). However, appropriate animal models for testing the effects of such agents in preventing plaque rupture do not yet exist. Another therapeutic strategy might target the cytokines that mediate many of the aspects of plaque biology that can lead to vulnerability.
Acute coronary syndromes by Eric J. Topol