H�ufigkeit und Morphologie der Coronarthrombose und ihre Beziehungen zur antithrombotischen und fibrinolytischen Behandlung

Sinapius, D.

doi:10.1007/bf01485588

Cited by 32 publications

(8 citation statements)

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“…[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.…”

Section: Morphological Basis For the Current Concept Of Acute Coronarmentioning

confidence: 86%

“…Furthermore, these regressive changes tended to be spotty rather than involving the entire thrombus. 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: 98%

“…The finding that mural thrombus formation frequently coincided with the onset of preinfarction unstable angina pectoris provided the basis for the present pathogenetic concept of unstable angina pectoris, ie, plaque rupture and deposition of a mural platelet thrombus with an abrupt reduction in coronary artery lumen. 17,21,22 These mechanisms were not generally accepted throughout the 1970s. The skeptics suggested that plaque fissures were artifacts caused by sectioning arteries and that coronary thrombi resulted from a prolonged low-output state associated with large infarcts.…”

Section: Morphological Basis For the Current Concept Of Acute Coronarmentioning

confidence: 99%

“…Fibrinolytic agents cannot diffuse easily into compressed mural thrombi, which makes them poor targets for such drugs. 17 …”

Section: Histology Of Mural Thrombimentioning

confidence: 99%

“…1,17,41 However, controversy remains about the composition of the terminal thrombus that causes total occlusion of the vessel. The concept that total coronary occlusion always results from growth of mural platelet thrombi was first proposed in 1969 61 and gained wide acceptance, although it is unconfirmed by scientific data.…”

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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