Zur Morphologie verschließender Koronarthromben

Sinapius, D.

doi:10.1055/s-0028-1107394

Cited by 39 publications

(18 citation statements)

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“…Extrusion of atheromatous material into the lumen was usually associated with a red or a mixed thrombus, not with a platelet thrombus. 63 Regressive changes in occlusive thrombi were not visible microscopically for Ն3 days after the infarct, which is significantly later than the time frame evident in mural thrombi. Furthermore, these regressive changes tended to be spotty rather than involving the entire thrombus.…”

Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%

“…17 The findings suggest that 80% of occlusive coronary thrombi are constituted predominantly of fibrin, which is a favorable substrate for thrombolytic therapy. 63 …”

Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%

“…1,3,41,62 In the most thorough autopsy study to date involving 91 cases of fatal transmural acute myocardial infarction, the composition of occlusive coronary thrombi was assessed by transverse sectioning and related to the underlying plaque pathology. 63 In only 15% (14 of 91) did the transverse sections at the site of plaque injury, corresponding to the "head" of the thrombus, reveal a pure platelet thrombus containing little or no fibrin. In 85% (77 of 91), occlusion was caused by thrombi rich in fibrin and erythrocytes.…”

Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%

“…Therefore, no more than Ϸ20% of all occlusive thrombi consisted exclusively or predominantly of platelets. 63 Plaque rupture frequently resulted in extrusion of atheromatous debris into the vessel lumen. 19,63 In rare cases, a prolapsed atheroma caused subtotal occlusion.…”

Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%

“…63 Plaque rupture frequently resulted in extrusion of atheromatous debris into the vessel lumen. 19,63 In rare cases, a prolapsed atheroma caused subtotal occlusion. Extrusion of atheromatous material into the lumen was usually associated with a red or a mixed thrombus, not with a platelet thrombus.…”

Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%

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Thrombi in Acute Coronary Syndromes

2000

Circulation

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O ver the past 35 years, the view has evolved that the acute coronary syndromes, ie, unstable angina pectoris, myocardial infarction, and sudden death, are caused by plaque rupture and formation of a platelet thrombus. There is at least a transient total or subtotal coronary occlusion in all cases of acute myocardial infarction. Q-wave infarcts are thought to differ from non-Q-wave infarcts by more stable platelet thrombi causing more prolonged and/or severe ischemia, leading to more extensive infarction. The greater platelet stability in transmural infarction is attributed to more severe or extensive plaque rupture. 1-3 Unstable angina and non-Qwave infarction, in the present view, are due to less extensive, less stable platelet thrombi that cause less severe, less extensive ischemia and/or infarction.However, autopsy data and more recent clinical findings require significant refinement of this viewpoint on the basis of the following observations. The occlusive thrombi causing Q-wave myocardial infarction contain more fibrin than the thrombi found in the other acute coronary syndromes that are characterized by more platelets and less fibrin. The higher fibrin content of thrombi causing Q-wave infarction explains their greater stability. Furthermore, this higher fibrin content suggests that the coagulation cascade is activated to a greater degree during Q-wave infarction than during non-Q-wave infarction in which platelets play a more dominant role. This review analyzes our evolving concepts focusing on the growing divergence of the different mechanisms underlying the different acute coronary syndromes and their clinical and therapeutic implications. Morphological Basis for the Current Concept of Acute Coronary SyndromesBy the mid-1930s, acute myocardial infarction was shown to be caused by coronary thrombosis resulting from intimal fissuring, which is often associated with dissecting hemorrhage into the underlying plaque. 4 -7 In the late 1930s, however, intimal fissuring was questioned and subendothelial hemorrhages were ascribed to rupture of capillaries within the plaque. 8,9 The causative role of coronary thrombosis became controversial in 1956 when pathologists first reported a low prevalence of thrombi in fatal infarction. 10 -16 The pendulum began to swing back in the mid-1960s because of improved autopsy techniques. Coronary thrombi were found in Ͼ90% of fatal infarcts, most being occlusive.Plaque hemorrhages, which were usually traceable to an intimal tear within the thrombosed segment, were found in most cases. [17][18][19][20][21] These observations reaffirmed that intimal rupture was the essential mechanism causing both subendothelial hemorrhage and intraluminal thrombosis. 22 Having found that three quarters of occlusive coronary thrombi were composed of layers of different ages, Sinapius 17,21 concluded that these thrombi developed in a protracted, recurring course. The oldest portion of thrombus usually sealed the intimal fissure and was rich in platelets. The finding that mural thrombus forma...

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Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%

“…17 The findings suggest that 80% of occlusive coronary thrombi are constituted predominantly of fibrin, which is a favorable substrate for thrombolytic therapy. 63 …”

Section: Histology Of the Occlusive Thrombusmentioning

confidence: 99%