Abstract
When the new victims of an acute myocardial ischemic syndrome — be it unstable angina, non-Q-wave, or Q-wave myocardial infarction (MI) — are suddenly and most often unexpectedly confronted with questions as to their odds for survival, it may be at least partially comforting to be told (if sudden death does not intervene ad interim) that the long-term prognosis of similar cases has steadily improved over the past three decades [1]. Nevertheless, coronary artery disease (CAD) is still the leading cause of morbidity and mortality in the United States; about seven million people have it as a confirmed diagnosis, and many more are known or suspected to harbor it in its clinically-silent variety [2] (Fig. 1). It was almost 80 years ago, in 1912, when Herrick first proposed that the pathological climax of this disease — an acute MI (as we now call it) — is due to the thrombosis of coronary artery [3]. The complexities of this issue are so intricate however, that less than ten years ago controversies still abounded as to what the actual mechanisms leading to coronary occlusion really are.
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Ferlinz, J. (1991). Origins, Evolution, and Prognosis of Acute Myocardial Ischemic Syndromes: Focus on Non-Q-Wave Myocardial Infarction. In: Vincent, J.L. (eds) Update 1991. Update in Intensive Care and Emergency Medicine, vol 14. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84423-2_6
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