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. 1991;18(4):243–247.

Unstable Angina Pectoris and the Progression to Acute Myocardial Infarction

Role of Platelets and Platelet-Derived Mediators

James T Willerson 1,2,3,4, Sheng-Kun Yao 1,2,3,4, James J Ferguson 1,2,3,4, H Vernon Anderson 1,2,3,4, Paolo Golino 1,2,3,4, L Maximilian Buja 1,2,3,4
PMCID: PMC326348  PMID: 15227406

Abstract

The conversion from stable to unstable angina and the further progression to myocardial infarction are usually associated with atherosclerotic plaque fissuring or ulceration at sites of coronary artery stenosis and subsequent development of a thrombus. This thrombus formation is initiated by platelet adhesion and aggregation; these, in turn, are promoted by the local release and accumulation of thromboxane A2 and serotonin. This accumulation and the resulting platelet aggregation at sites of endothelial injury cause dynamic vasoconstriction. With time, the platelet-initiated thrombus expands to include white and red blood cells in a fibrin mesh. Thus, a fully occlusive coronary thrombus may develop and cause the progression from unstable angina to acute myocardial infarction, often Q-wave myocardial infarction. We believe that the connection between unstable angina and acute myocardial infarction is a continuum relative to the processes of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary stenosis lasts only a few minutes and is repetitive, unstable angina or non-Q wave myocardial infarction occurs. However, when complete coronary artery occlusion lasts for longer than 4 hours, a transmural or Q-wave myocardial infarction results.

Recently, in experimental animal models with mechanically induced coronary artery stenoses and endothelial injury, we have found that other mediators, including adenosine diphosphate and thrombin, also contribute to coronary artery thrombosis. Moreover, in humans with limiting angina, we have identified spontaneous coronary blood flow variations in a pattern similar to the variations caused by alternating platelet attachment and dislodgement in experimental canine modes. In this review, we add information to our previous observations in order to present the possible mechanisms of conversion from chronic to acute coronary heart disease syndromes. (Texas Heart Institute Journal 1991; 18:243-7)

Keywords: Adenosine diphosphate

Keywords: angina pectoris

Keywords: blood flow velocity

Keywords: coronary disease/coronary thrombosis

Keywords: endothelium, vascular

Keywords: heparin

Keywords: myocardial infarction

Keywords: platelet aggregation

Keywords: platelet activating factor

Keywords: serotonin

Keywords: thrombin

Keywords: thromboxane A2

Keywords: vasoconstriction

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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