The pathological basis and microanatomy of occlusive thrombus formation in human coronary arteries

Abstract

Myocardial necrosis, usually called infarction, occurs in different patterns. A common form is necrosis of one segment of the left ventricle, i.e., anterior, septal, lateral or posterior. This regional infarction is consistently associated with an acute occlusive thrombosis of the artery supply that region. Diffuse necrosis involving the whole circumference, usually the subendocardial zone, of the ventricle is not consistently associated with thrombi. Occlusive thrombi identified in post-mortem coronary arterio-grams have been reconstructed in their entirety from serial sections at 150 micron intervals. Most occlusive thrombi were found to be associated with a dissection track into the intima at an atheromatous plaque. The break into the plaque usually extended over several millimeters, often in spirals, so that a mass of thrombus within the plaque compressed the original lumen. Previous accounts of plaque rupture or cracking greatly underestimated the magnitude of the dissection of blood into the intima.

Prevention of reoccluding platelet-rich thrombi in canine femoral arteries with a novel peptide antagonist of platelet glycoprotein IIb/IIIa receptors.

“…16 Several studies have shown that platelet activation is likely to play a key role in the recurrence of thrombosis after initially successful thrombolysis. [1][2][3][4][5][6][7][8][9][10][11][12][13][14]17 The platelet membrane GP JIb/lIla receptors are attractive targets for inhibition of platelet aggregation because they mediate binding of fibrinogen, an obligatory component of normal aggregation in Vivo.18 These receptors also mediate binding of von Willebrand factor and fibronectin, which may participate in platelet adhesion to the subendothelium and subsequent spreading.18 Association of several different adhesive proteins with the same receptor complex appears to result from recognition of a common amino acid sequence, Arg-Gly-Asp (RGD), in each. Thus, interaction of these proteins with GP llb/Illa receptors and subsequent platelet aggregation have been inhibited competitively by monoclonal antibodies to GP lIb/Illa receptors'9 and by naturally occurring and synthetic peptides containing the RGD sequence.…”

“…3 The composition of reoccluding thrombi may be similar to that observed after persistent arterial thrombosis, that is, there may be a plateletrich mass overlying the damaged vessel wall contiguous with a meshwork of fibrin and blood cells. 4,5 Because the proportions of fibrin and platelets in reoccluding thrombi may vary, it is important to determine the efficacy of agents with the potential to prevent reocclusion under experimental conditions that influence the relative amounts of fibrin See p 1920 and platelets in thrombi. Accordingly, we modified two preparations that were partially characterized previously, one in which injury to the arterial endothelium was induced by anodal current resulting in a platelet-rich thrombus6 and a second one developed in our laboratory in which an intraluminal coil of copper wire was used to produce a relatively fibrin-rich thrombus.…”

Increased platelet deposition on atherosclerotic coronary arteries.

“…Key words: atherosclerosis * thrombosis -platelet receptors * vessel wall proteins * perfusion system Myocardial infarction is in > 90% of cases caused by an occlusive thrombus in a coronary artery branch (1 ). The underlying substrate for thrombus formation is usually a ruptured atherosclerotic plaque (2)(3)(4)(5). This leads to exposure of deeper layers of the plaque to flowing blood.…”

An Overview of Antiplatelet and Antithrombotic Drugs

“…Rupture, cracking, or ulceration of atherosclerotic plaques is a common autopsy finding in patients with coronary atheroscle rotic disease [Constantinides, 1966;Horie et al, 1978;Davies and Thomas, 1981;Falk, 1983]. In more than half of the ruptured ath erosclerotic plaques the predominant feature is hemorrhage only from the lumen through the break (dissecting hemorrhage); this type of rupture tends to occur in plaques causing ste nosis of 50-85% of the coronary lumen [Falk, 1983] and usually the hemorrhage does not cause any further compromise of the coronary lumen.…”