Acute Myocardial Infarction Without Disrupted Yellow Plaque in Young Patients Below 50 Years Old

Ueda, Yasunori; Okada, Katsuki; Ogasawara, Nobuyuki; Oyabu, Jota; Hirayama, Atsushi

doi:10.1111/j.1540-8183.2007.00259.x

Cited by 9 publications

(13 citation statements)

References 11 publications

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“…Although the majority of culprit lesions of acute MI among aged patients had yellow plaque, young patients <40 years with acute MI had yellow plaque only in 44% of them and the rest had thrombus formation on white lesion [14]; therefore, the young patients with acute MI often have white erosive plaques as the culprit, which is different from the typical yellow erosive plaques detected in the culprit of aged patients. In a study that characterized the erosive culprit plaques of acute coronary syndrome defined by OCT as "intact fibrous-cap" plaque, the intact fibrous-cap culprit plaques had yellow color in 70% of them [15].…”

Section: Vulnerable Plaque and Vulnerable Patientmentioning

confidence: 81%

Transient increase in blood thrombogenicity may be a critical mechanism for the occurrence of acute myocardial infarction

Ueda

Kosugi

Abe

et al. 2021

Journal of Cardiology

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Section: Vulnerable Plaque and Vulnerable Patientmentioning

confidence: 81%

Transient increase in blood thrombogenicity may be a critical mechanism for the occurrence of acute myocardial infarction

Ueda

Kosugi

Abe

et al. 2021

Journal of Cardiology

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“…Therefore, in this case without disrupted yellow plaque or thrombus adhesion, the repeated occlusion of the culprit lesion and thus acute myocardial infarction was supposed to be caused by vasospasm. In young patients with acute myocardial infarction [3], the culprit lesion sometimes looks white but usually has thrombus adhesion (Fig. 6), which is compatible with the pathologically demonstrated culprit lesion of acute myocardial infarction with plaque erosion but without necrotic core.…”

Section: Discussionmentioning

confidence: 76%

“…6. The culprit of acute myocardial infarction in young patients (from Ueda et al [3]). According to our previous report, the culprit of acute myocardial infarction in young (<50 years old) patients had disrupted yellow plaque in 70% of cases (A) but did not have yellow plaque and looked white in 30% of cases (B), although both types of lesions had thrombus adhesion.…”

Section: Discussionmentioning

confidence: 98%

Vasospasm-induced acute myocardial infarction—Thrombus formation without thrombogenic lesion at the culprit

Kobayashi

Ueda

Matsuo

et al. 2013

Journal of Cardiology Cases

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a b s t r a c tAlthough plaque rupture is the major cause of acute myocardial infarction, vasospasm is also known as a potential cause of acute myocardial infarction. However, it is very rare and is sometimes difficult to diagnose correctly. A 30-year-old male patient with suspected unstable angina pectoris who received catheterization in 1999 had normal coronary artery but positive result in the provocation test of vasospasm. Although his angina had been suppressed by medications, he suffered ST-elevation acute myocardial infarction after the discontinuation of medication. The initial angiogram showed total occlusion of the proximal left anterior descending coronary artery. Thrombolysis and nitroglycerin achieved recanalization of the culprit lesion with only mild residual stenosis. Angioscopy revealed normal white luminal wall without any thrombogenic lesion. Therefore, the cause of coronary occlusion was diagnosed as vasospasm. However, since the repeated vasospastic occlusion of the culprit lesion regardless of repeated intra-coronary injection of nitroglycerin was observed, a stent was implanted and vasospasm was successfully prevented. It is not easy to judge from the angiogram that the cause of coronary occlusion in the patients with acute myocardial infarction is vasospasm. It is important to think routinely about the possibility of vasospasm as a cause of acute myocardial infarction.

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“…One clinical characteristic of these patients was a high prevalence of smoking, which is similar to that in the present study. 20 Smoking is a well-known coronary risk factor that promotes atherosclerosis. Smoking might have played a role in endothelial damage and consequent thrombosis in the present study.…”

Section: Discussionmentioning

confidence: 99%

Fluffy Luminal Surface of the Non-Stenotic Culprit Coronary Artery in Patients With Acute Coronary Syndrome - An Angioscopic Study -

Uchida

Sakurai

et al. 2010

Circ J

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Background: Approximately 15% of acute coronary syndrome (ACS) cases have no significant coronary stenosis. Mechanisms underlying the attacks are, however, unknown. Methods and Results:The clinical study had 254 patients with ACS; 38 patients (31 females and 7 males; aged 51.0±8.0 years) had no significant coronary stenosis on angiography. They underwent a dye-staining angioscopy of the suspected culprit coronary artery using Evans blue, which selectively stains fibrin and damaged endothelial cells. A fluffy coronary luminal surface was observed in the suspected culprit artery in all 38 patients. The fluffy luminal surface was stained blue with Evans blue. In animal experiments involving 5 beagles, 10% hydrogen peroxide solution was injected into the iliac arteries to damage endothelial cells, which was then followed by blood reperfusion, and then the artery was examined by intravascular microscopy and histology. In the beagles, the arterial segment, where the thrombus had been formed, exhibited a fluffy luminal surface after a washout of the thrombus, and the surface was stained blue. Histologically, the fluffy surfaces were composed of damaged endothelial cells attached by multiple fibrin threads and platelets. Conclusions:It was considered that the coronary segment exhibiting a fluffy luminal surface was the culprit lesion and that the fluffy surface was caused by residual thrombi after dispersion of an occlusive thrombus, which had formed on the damaged endothelial cells. (Circ J 2010; 74: 2379 - 2385

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Acute Myocardial Infarction Without Disrupted Yellow Plaque in Young Patients Below 50 Years Old

Abstract: Patients with acute MI < 50 years, especially <40 years, had lower prevalence of DYP&T but higher prevalence of smoking, obesity, and hypercholesterolemia. Smoking may play an important role for thrombotic occlusion at lesions with relatively low thrombogenic potential.

Cited by 9 publications

References 11 publications

Transient increase in blood thrombogenicity may be a critical mechanism for the occurrence of acute myocardial infarction

Transient increase in blood thrombogenicity may be a critical mechanism for the occurrence of acute myocardial infarction

Vasospasm-induced acute myocardial infarction—Thrombus formation without thrombogenic lesion at the culprit

Fluffy Luminal Surface of the Non-Stenotic Culprit Coronary Artery in Patients With Acute Coronary Syndrome - An Angioscopic Study -

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