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 bargains experiences of up to date advances within the pathophysiological, diagnostic and healing continuum of ACS. It includes information on third-generation thrombolytic brokers, together with reteplase, and classes from the GUSTO trials.
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For example, active transforming growth factor beta or platelet-derived growth factor can stimulate de novo biosynthesis of interstitial forms of collagen by cultured human vascular smooth muscle cells. On the other hand, a cytokine known to be present in atherosclerotic plaques, interferon-g, can inhibit collagen production by human smooth muscle cells in culture. Of the cells associated with atheroma, only T lymphocytes can synthesize interferon-g. As alluded to above, interferon-g can induce the expression of the activation marker HLA-DR on human smooth muscle cells.
Title : Acute Coronary Syndromes author : Topol, Eric J. publisher : CRC Press isbn10 | asin : 0824701402 print isbn13 : 9780824701406 ebook isbn13 : 9780585158556 language : English subject Coronary heart disease, Myocardial Infarction--diagnosis, Myocardial Infarction--therapy, Fibrinolytic Agents--therapeutic use. 1/23 subject : Coronary heart disease, Myocardial Infarction--diagnosis, Myocardial Infarction--therapy, Fibrinolytic Agents--therapeutic use. Page i Acute Coronary Syndromes Edited by Eric J.
Thus, inflammation, mediated by cytokines, can lead to smooth muscle death, another mechanism that may impair the integrity of the plaque's fibrous cap. Page 13 Conclusions and Clinical/Therapeutic Implications We have considered various mechanisms that may lead to the acute coronary syndromes. In particular, we have focused on factors external to the plaque which may trigger disruption and hence thrombosis. Moreover, we have examined some of the recent work that has increased our understanding of the mechanisms that determine the susceptibility of a given atherosclerotic plaque to disruption.
Acute coronary syndromes by Eric J. Topol