Angioscopic Evaluation of Coronary-Artery Thrombi in Acute Coronary Syndromes

Mizuno, Kyoichi; Satomura, Kimio; Miyamoto, Akira; Arakawa, Ko; Shibuya, Toshio; Arai, Tsunenori; Kurita, Akira; Nakamura, Haruo; Ambrose, John A.

doi:10.1056/nejm199201303260502

Cited by 560 publications

(184 citation statements)

References 30 publications

Supporting

Mentioning

172

Contrasting

Unclassified

Order By: Relevance

“…If proximal thrombus apposition occurs in only 25% of cases as suggested by autopsy findings, 63 one would have to assume that the "head" of the occluding thrombus was directly visualized by angioscopy in three quarters of the patients. 66 The red color of all thrombi in the acute myocardial infarction group was consistent with the histological finding of a coagulation or mixed thrombus, rich in erythrocytes, at the site of plaque rupture in most cases of fatal transmural myocardial infarction. 63 Response to Pharmacological Interventions Failure of fibrinolytic therapy to achieve angiographically apparent improvement of the culprit lesion in patients with unstable angina pectoris was first reported by us 24 and definitively proven in the TIMI IIIA trial.…”

Section: Coronary Angioscopic Findingssupporting

confidence: 77%

See 1 more Smart Citation

Thrombi in Acute Coronary Syndromes

2000

Circulation

View full text Add to dashboard Cite

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...

show abstract

Section: Coronary Angioscopic Findingssupporting

confidence: 77%

“…In vivo evidence regarding the composition of occlusive thrombi has been provided by transcutaneous transluminal coronary angioscopy. 66 Of 16 patients with acute myocardial infarction undergoing coronary angioscopy, 15 had thrombi, all reddish. Thrombi were also found in 14 patients with unstable angina pectoris.…”

Section: Coronary Angioscopic Findingsmentioning

confidence: 99%

Thrombi in Acute Coronary Syndromes

2000

Circulation

View full text Add to dashboard Cite

show abstract

“…24,25 Enhanced platelet activation and thrombin generation after clot lysis that could exacerbate thrombus formation and precipitate MI could explain the paradoxical findings. 20,26 Unlike fibrinolytic agents, GP IIb/IIIa antagonists act on the process of thrombus formation by preventing platelet aggregation and thrombus growth and allowing effective endogenous thrombolysis to dissolve the clot.…”

Section: Discussionmentioning

confidence: 99%

“…On the basis of a high frequency of intracoronary thrombus detected angiographically in patients with UA or NQWMI 5,6,20 and of platelet-rich thrombus detected by angioscopy, as opposed to red fibrin-rich thrombus in patients with acute MI, 4 it was hypothesized that profound inhibition of platelet aggregation with tirofiban would reduce the intracoronary thrombus burden and improve coronary flow past the culprit lesion. The primary angiographic end point was the proportion of patients with each grade of TIMI thrombus (grades 0 to 5).…”

Section: Study Hypothesis and Primary And Secondary Angiographic End mentioning

confidence: 99%

See 1 more Smart Citation

Intracoronary Thrombus and Platelet Glycoprotein IIb/IIIa Receptor Blockade With Tirofiban in Unstable Angina or Non–Q-Wave Myocardial Infarction

et al. 1999

View full text Add to dashboard Cite

for the PRISM-PLUS InvestigatorsBackground-The present study describes the effects of tirofiban, a nonpeptide platelet glycoprotein (GP) IIb/IIIa receptor blocker, on the characteristics of culprit lesions in patients with unstable angina (UA) or non-Q-wave myocardial infarction (NQWMI). Methods and Results-Of 1915 patients enrolled in PRISM-PLUS, 1491 had a readable film obtained a median of 65 hours after randomization. A core laboratory examined the culprit lesions for intracoronary thrombus burden (primary end point) and for TIMI flow grade distribution and severity of the obstruction and of underlying coronary artery disease (secondary end points). The combination of tirofiban plus heparin compared with heparin alone significantly reduced the intracoronary thrombus burden of the culprit lesions (ORϭ0.77, Pϭ0.022), improved the perfusion grade (ORϭ0.65, Pϭ0.002), and decreased the severity of the obstruction (Pϭ0.037), but it did not influence the severity of the underlying plaque. Persistence of a thrombus in 45% of patients was associated with a 2.4-fold increase in the odds of death at 30 days (Pϭ0.005) and a 2-fold increase in the odds of myocardial infarction (Pϭ0.002). Conclusions-The addition of tirofiban to heparin reduced the thrombus burden of the culprit lesion and improved distal perfusion in patients with UA or NQWMI, which supports the clinical benefit observed with the combination treatment.

show abstract

Unstable Angina

Ambrose

Dangas²

2000

Arch Intern Med

Self Cite

View full text Add to dashboard Cite

During the past 15 years, we have learned an enormous amount about the pathogenesis and treatment of unstable angina. In most cases of unstable rest angina, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. However, any process that acutely changes the supply-demand ratio (decreased supply or increased demand in the presence of a decrease in supply) can precipitate the clinical presentation of unstable angina. Standard acute antithrombotic drug therapy is effective in decreasing progression to infarction. Newer agents (low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibitors) are more effective, and their use is evolving. Percutaneous intervention and bypass surgery can reduce symptoms and multiple hospitalizations, in most cases without a decrease in the long-term mortality rate. Because the cost of hospitalization is extremely high and the clinical presentation and outcome are heterogeneous, better triage methods are required.

show abstract

Angioscopic Evaluation of Coronary-Artery Thrombi in Acute Coronary Syndromes

Cited by 560 publications

References 30 publications

Thrombi in Acute Coronary Syndromes

Thrombi in Acute Coronary Syndromes

Intracoronary Thrombus and Platelet Glycoprotein IIb/IIIa Receptor Blockade With Tirofiban in Unstable Angina or Non–Q-Wave Myocardial Infarction

Unstable Angina

Contact Info

Product

Resources

About