Observations on the Morbid Anatomy of Coronary Artery Disease

Branwood, A. W.; Montgomery, G. L.

doi:10.1177/003693305600101201

Cited by 111 publications

(24 citation statements)

References 8 publications

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“…It is also closely linked to hypercholesterolaemia and has a dominant inflammatory phenotype. Classical histological features include a lipid rich pool, thin fibrous cap, paucity of vascular smooth muscle cells, and an intense inflammatory cell infiltrate 1 4–6…”

Section: Coronary Atherosclerosis and Thrombosismentioning

confidence: 99%

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Triggering of acute myocardial infarction: beyond the vulnerable plaque

Newby

2010

Heart

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Section: Coronary Atherosclerosis and Thrombosismentioning

confidence: 99%

“…Over 50 years ago, pathologists hotly debated the question of whether myocardial infarction was caused by coronary thrombosis 1. This reflected the observation that, in patients who had died from acute myocardial infarction (AMI), postmortem examinations often failed to demonstrate the presence of intracoronary thrombosis.…”

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confidence: 99%

Triggering of acute myocardial infarction: beyond the vulnerable plaque

Newby

2010

Heart

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“…"3 In recent years the primary role of coronary thrombus in precipitating AMI has been questioned. [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] To evaluate the significance of coronary thrombus in AMI, we examined in detail the coronary arteries containing thrombi in 54 necropsy patients with transmural AMI. Several previously undescribed observations on coronary thrombi resulted, which clarify the significance of coronary thrombi in AMI.…”

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confidence: 99%

Significance of coronary arterial thrombus in transmural acute myocardial infarction. A study of 54 necropsy patients.

Brosius

Roberts

1981

Circulation

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In 54 necropsy patients with transmural acute myocardial infarction (AMI) and coronary arterial thrombi, histologic sections of coronary arteries that contained the thrombi were examined by video-planimetry to determine if the amount of luminal narrowing caused by thrombi was comparable to that produced by underlying atherosclerotic plaques, and to determine the amount of luminal narrowing by plaques immediately proximal and distal to the thrombi. The 54 coronary arteries in the 54 patients were narrowed 33-98% (mean 81%) by atherosclerotic plaque alone in cross-sectional area at the site of the thrombus (occlusive in 47 and nonocclusive in seven), from 26-98% (mean 75%) within the 2-cm segment proximal to the thrombus, and from 43-98% (mean 79%) within the 2-cm segment distal to the thrombus. Of the 54 arteries, 52 (96%) were narrowed 76-98% in cross-sectional area by atherosclerotic plaque alone at or immediately proximal or distal to the thrombus and 26 (48%) were narrowed 91-98% by plaque alone. The thrombi were 0.1--6.0 mm2 (mean 1.4 mm2) in cross-sectional area and the underlying atherosclerotic plaques were 3.0-21.0 mm2 (mean 8.7 mm2). Thus, among necropsy patients with transmural AMI, coronary thrombi occur at sites already severely narrowed by atherosclerotic plaques.

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“…Although it has been claimed 19 ' 125 that coronary vasospasm has an important role in the pathogenesis of coronary occlusive disease, the prevailing opinion holds to an even stronger association between myocardial infarction -especially transmural myocardial infarction -and thrombotic coronary occlusion. Antemortem recanalization or spontaneous lysis of occlusive thrombi, as well as postmortem thrombolysis or clot retraction, might have generated the conflicting results of necropsy studies, 18 ' 19 6-2°3 which reported an incidence of coronary thrombosis associated with myocardial infarction ranging from 20% 196 to 90%. 200 More recent arteriographic findings 2 demonstrated total coronary occlusion in over 85% of cases during the first 4 to 6 hours after the onset of symptoms in transmural myocardial infarction.…”

Section: Thrombolytic Therapymentioning

confidence: 99%