Literature DB >> 11044421

Considerable time from the onset of plaque rupture and/or thrombi until the onset of acute myocardial infarction in humans: coronary angiographic findings within 1 week before the onset of infarction.

S Ojio1, H Takatsu, T Tanaka, K Ueno, K Yokoya, T Matsubara, T Suzuki, S Watanabe, N Morita, M Kawasaki, T Nagano, I Nishio, K Sakai, K Nishigaki, G Takemura, T Noda, S Minatoguchi, H Fujiwara.   

Abstract

BACKGROUND: It has been thought that the thrombi and bleeding in plaques that occur after plaque rupture or endothelial damage from vessels with mild stenosis suddenly occlude the lumen and cause acute myocardial infarction (AMI). However, our hypothesis is that thrombi and bleeding may not suddenly occlude the lumen. METHODS AND
RESULTS: The study group consisted of 20 patients who had coronary angiograms performed within 1 week (3+/-3 days) before AMI and 20 control patients who had coronary angiograms performed 6 to 18 months (282+/-49 days) before AMI. The features of infarct-related coronary segments (IRCS) at 3 days before AMI were the presence of a significant stenosis of >50% (95% in incidence and 71+/-12% diameter stenosis) and Ambrose's type II eccentric lesions (plus multiple irregularities), an indicator of plaque rupture and/or thrombi (60% [70%]), and the features at 1 year before AMI were mild stenosis of <50% (95% incidence and 30+/-18% diameter stenosis) with rare Ambrose's type II eccentric lesions (plus multiple irregularities) (10% [10%]). The same relation was observed in each of the 4 subgroups with Q-wave infarction, non-Q-wave infarction, preceding effort angina within 1 month before AMI, and no preceding effort angina.
CONCLUSIONS: The appearance of marked progression and Ambrose's type II eccentric lesion on coronary angiograms 3 days before AMI suggests the presence of a considerable time from the onset of plaque rupture and/or thrombi until the onset of AMI. These features may be predictors of AMI. The concept provides new insight into the mechanism and prevention of human AMIs.

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Mesh:

Year:  2000        PMID: 11044421     DOI: 10.1161/01.cir.102.17.2063

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  25 in total

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Review 2.  Molecular imaging by MRI.

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Review 4.  Acute coronary events.

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Review 5.  Coronary magnetic resonance imaging: visualization of the vessel lumen and the vessel wall and molecular imaging of arteriothrombosis.

Authors:  Elmar Spuentrup; Rene M Botnar
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6.  High-grade culprit lesions are a common cause of ST-segment elevation myocardial infarction.

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Review 7.  Molecular imaging in atherosclerosis.

Authors:  Andor W J M Glaudemans; Riemer H J A Slart; Alessandro Bozzao; Elena Bonanno; Marcello Arca; Rudi A J O Dierckx; Alberto Signore
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8.  Distance from the coronary ostium to the culprit lesion in acute ST-elevation myocardial infarction and its implications regarding the potential prevention of proximal plaque rupture.

Authors:  C Michael Gibson; Ajay J Kirtane; Sabina A Murphy; Juhana Karha; Christopher P Cannon; Robert P Giugliano; Mathew T Roe; Robert A Harrington; E Magnus Ohman; Elliott M Antman
Journal:  J Thromb Thrombolysis       Date:  2003-06       Impact factor: 2.300

9.  MR imaging of thrombi using EP-2104R, a fibrin-specific contrast agent: initial results in patients.

Authors:  Elmar Spuentrup; Rene M Botnar; Andrea J Wiethoff; Tareq Ibrahim; Sebastian Kelle; Marcus Katoh; Murat Ozgun; Eike Nagel; Josef Vymazal; Phil B Graham; Rolf W Günther; David Maintz
Journal:  Eur Radiol       Date:  2008-04-19       Impact factor: 5.315

10.  Eccentric stenosis of the carotid artery associated with ipsilateral cerebrovascular events.

Authors:  T Ohara; K Toyoda; R Otsubo; K Nagatsuka; Y Kubota; M Yasaka; H Naritomi; K Minematsu
Journal:  AJNR Am J Neuroradiol       Date:  2008-03-13       Impact factor: 3.825

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