Asian Cardiovasc Thorac Ann 2003;11:255-257
© 2003 Asia Publishing EXchange Ltd
Angioscopic Appearance and Histopathology of Coronary Artery Thrombi
Takayoshi Ohba, MD,
Noritake Hata, MD,
Yoshiharu Ohaki, MD1
Division of Intensive Care Unit
1 Division of Pathology, Chiba Hokusoh Hospital, Nippon Medical School, Chiba, Japan
For reprint information contact: Noritake Hata, MD Tel: 81 476 99 1111 Fax: 81 476 99 1911 email: hata-n{at}nms.ac.jp Division of Intensive Care Unit, Chiba Hokusoh Hospital, Nippon Medical School, 1715 Kamagari, Inbamura, Inbagun, Chiba 270-1694, Japan.
 |
ABSTRACT
|
|---|
A 70-year-old woman presented with acute coronary syndrome. Coronary angiography documented occlusion of the left circumflex coronary artery, and coronary angioscopy showed large red thrombi at the site of occlusion. These thrombi were aspirated using a RESCUE thrombectomy catheter, after which coronary flow was reestablished. Histological examination of the aspirated thrombi revealed platelets, irregularly intermingled erythrocytes, and a large number of leukocytes (mainly neutrophils); tissue resembling vascular endothelium also was present.
|
INTRODUCTION
|
|---|
Macrophages and T lymphocytes have been reported to be the dominant inflammatory cells in coronary thrombi, but few reports have noted neutrophils. However, study of the cellular composition of the thrombus may be inadequate because of disintegration of the thrombus during removal from the patient, while microscopic study of aspirated coronary thrombi is rare. We report a case of acute coronary syndrome that was treated by aspiration of the coronary thrombi and describe the histopathological evaluation of the thrombus.
|
CASE REPORT
|
|---|
A 70-year-old woman was admitted to the intensive care unit for evaluation and treatment of multiple episodes of intermittent chest pain lasting 30 minutes over the previous 2 days. Her past history was unremarkable. Electrocardiography on admission showed incomplete right bundle branch block and elevation of the ST segment in leads II, III, and aVF. Physical examination revealed no detectable cardiac murmurs or rales, and chest radiography indicated no cardiomegaly. Her total leukocyte count was 8,810 µL-1 with 84% neutrocytes. The serum concentration of creatine phosphokinase was 87 IU•L-1, C-reactive protein was 0.05 mg•dL-1, and glucose was 211 mg•dL-1. A diagnosis of acute coronary syndrome was made based on the characteristic history of frequent episodes of chest pain, persistent ST-segment elevation, and asynergy of the inferoposterior left ventricular walls on echocardiography.
Coronary angiography was performed immediately after admission to establish the diagnosis unequivocally prior to initiating thrombolytic therapy. It showed occlusion of the left circumflex coronary artery (American Heart Association segment 13); and coronary angioscopy, performed using a Vecmoba angioscopy catheter (Clinical Supply, Gifu, Japan), showed large red thrombi on a yellow plaque at the site of the lesion. To avoid distal embolism following direct coronary angioplasty, we elected to aspirate the thrombi using a RESCUE thrombectomy catheter (Boston Scientific, Maple Grove, MN, USA). After thrombectomy, no additional thrombus was seen at the lesion by either coronary angiography or angioscopy (Figure 1
). After thrombectomy, a 9-mm NIR stent (Boston Scientific, Boston, MA, USA) was implanted at the lesion.
We were able to aspirate a large red thrombus and obtained sufficient sample to examine microscopically (Figure 2). The specimens consisted of not only aggregations of platelets and erythrocytes but also leukocytes (mainly neutrophils). Many cells, especially neutrophils, showed leakage of nuclear material as a result of cell destruction. Endothelial tissue fragments also were identified along with some calcification. The thrombus was not organized. These findings indicate that it was a fresh thrombus.
View larger version (211K):
[in this window]
[in a new window]
|
Figure 2. (A) Aspirated intracoronary thrombi composed of aggregated platelets and erythrocytes, in addition to neutrophils. (B) Cells in the aggregation, especially neutrophils, showing leakage of nuclear material. Endothelial tissue fragments are also seen. (Hematoxylin–eosin stain, original magnification x5 for A and x10 for B.)
|
|
|
DISCUSSION
|
|---|
Inflammatory cells such as T lymphocytes and macrophages have been reported in coronary thrombi.1,2 However, few reports have noted neutrophils in fresh thrombi.2–4 Van der Wal and colleagues2 reported that plaque rupture was seen in 12 and superficial erosion in 8 of 20 patients with acute myocardial infarction. The ischemic coronary artery of these patients was found to contain predominantly macrophages and T lymphocytes at the site of rupture or erosion. More importantly, these sites were characterized by abundant expression of the HLA-DR antigen on leukocytes and the adjacent smooth muscle cells, suggesting an active inflammatory reaction. We confirmed this response by vascular endoscopy and thrombus aspiration in vivo. Naruko’s group5 found neutrophilic infiltration in addition to infiltration by macrophages and T lymphocytes. In our case, erythrocytes and thrombocytes were the dominant cells in the thrombus. These thrombi seem to be a mixture of red and white thrombi6 and might be rich in polymorphonuclear leukocytes. The appearance of polymorphonuclear leukocytes in the coronary artery was found to be associated with the endothelial expression of leukocyte adhesion molecules.7 Leukocytes may play an important role in the pathogenesis of acute coronary syndrome.8
Descriptions of the pathology of coronary artery disease have been based on specimens from postmortems, animal experiments, and directional coronary atherectomy. Most of the samples obtained by directional coronary atherectomy are fragmented and contain artifacts. We think that disintegration of the thrombus makes these specimens inadequate for study, whereas the coronary aspirate provides clinical material for study that has not been modified by mechanical force or enzymatic degradation. Moreover, treatment by aspiration is useful in patients with rich coronary thrombi.
|
REFERENCES
|
|---|
- Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N Engl J Med 1992;326:242–50.[Medline]
- Van der Wal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994;89:36–44.[Abstract/Free Full Text]
- Weiss SJ. Tissue destruction by neutrophils. N Engl J Med 1989;320:365–76.[Medline]
- Kloner RA, Giacomelli F, Alker KJ, Hale SL, Matthews R, Bellows S. Influx of neutrophils into the walls of large epicardial coronary arteries in response to ischemia/reperfusion. Circulation 1991;84:1758–72.[Abstract/Free Full Text]
- Naruko T, Ueda M, van der Wal AC, van der Loos CM, Itoh H, Nakao K, et al. C-type natriuretic peptide in human coronary atherosclerotic lesions. Circulation 1996;94:3103–8.[Abstract/Free Full Text]
- Mizuno K, Satomura K, Miyamoto A, Arakawa K, Shibuya T, Arai T, et al. Angioscopic evaluation of coronary-artery thrombi in acute coronary syndromes. N Engl J Med 1992;326:287–91.[Abstract]
- O’Brien KD, McDonald TO, Chait A, Allen MD, Alpers CE. Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content. Circulation 1996;93:672–82.[Abstract/Free Full Text]
- Suzuki T, Sakomura Y, Kebukawa K, Suzuki S, Horie T, Hosoda S. Histopathological characteristics of tissue specimens obtained during directional coronary atherectomy for acute coronary syndromes [Japanese]. Jpn J Interv Cardiol 1996;11:333–8.
TOP
ABSTRACT
Introduction
