Abstract

Transient coronary insufficiency (TCI) is a combination of two syndromes -ischemic and reperfusion [4, 8, 9] . The writers showed previously that development of both syndromes is based on pathogenetic mechanisms some of which are common to both whereas others are characteristic of each separately [4, 5, 7-9]. In our view, in the course of development of both the ischemic and the reperfusion syndromes of TCI, factors changing the state of the clotting and anticlotting systems of the blood are initiated and (or) activated. An important argument in support of this view is given by experimental and clinical data on significant deviations of the parameters of hemostasis in animals with myocardial ischemia (MI) and also in patients with different forms of coronary insufficiency -angina pectoris, preinfarction, and myocardial infarction [2, 9, i0, 14]. However, the results of these investigations demonstrate deviations in the hemostasis system mainly in MI and they do not allow their changes to be judged at different stages of postischemic resumption of the coronary blood flow. At the same time, we know that the initial period of reperfusion (RP) often is not accompanied by resumption of microcirculation in various parts of the previously ischemized zone of the heart. This phenomenon has been called the postischemic "no reflow phenomenon." One possible cause of this phenomenon could be intravascular thrombosis or aggregation of blood cells.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call