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Coronary atherosclerosis and interventions: pathological sequences and restenosis
C Yutani1, M Imakita, H Ishibashi-Ueda
1Department of Pathology, National Cardiovascular Center, Suita, Osaka, Japan. cyutani@hsp.ncvc.go.jp
Insights
Atherosclerosis, a leading cause of heart disease, involves plaque rupture influenced by composition, not just size. Restenosis after stenting involves vascular remodeling and intimal hyperplasia.
Area of Science:
- Cardiovascular Pathology
- Interventional Cardiology
Background:
- Ischemic heart disease, primarily caused by atherosclerosis, is a major cause of death globally.
- Atherosclerosis involves complex lesion development, with Stary's classification offering detailed morphological and biochemical insights.
- Acute coronary syndrome is often linked to the rupture of vulnerable atherosclerotic plaques.
Purpose of the Study:
- To clarify the mechanisms of atherosclerotic plaque disruption.
- To elucidate the relationship between plaque disruption and coronary risk factors in elderly Japanese patients with acute coronary syndrome.
- To describe the pathological mechanisms of restenosis following percutaneous transluminal coronary angioplasty (PTCA) and/or stent placement.
Main Methods:
- Utilized advanced imaging techniques like angioscopy and intravascular ultrasound.
- Analyzed autopsy studies of restenosis post-PTCA.
- Investigated the effect of tissue factor pathway inhibitor on interventional restenosis.
Main Results:
- Plaque composition, particularly high content of soft extracellular lipids and macrophages, increases vulnerability to rupture.
- Adventitial scarring and remodeling are identified as major contributors to restenosis after PTCA.
- Late in-stent restenosis remains a limitation, influenced by stent design and patient factors.
Conclusions:
- Understanding plaque composition is crucial for managing acute coronary syndrome.
- Adventitial remodeling and intimal hyperplasia are key pathological mechanisms of restenosis.
- Further research into interventions like tissue factor pathway inhibitors may help prevent restenosis.
Abstract:
The primary cause of cardiac morbidity and mortality in developed countries is ischemic (coronary) heart disease. The incidence of this disease is virtually all due to atherosclerosis, and ischemic heart disease is also the most prevalent disease in the industrialized world, causing over 40% of all deaths in the United States and Western Europe. In Japan, the incidence of ischemic heart disease due to coronary atherosclerosis is gradually increasing as well. Compared with the classical nomenclature of atherosclerosis; that is, fatty streak, fibrous plaque and complicated lesions, the term Stary's classification has been universally accepted because it reflects the more recently acquired knowledge about the morphological and biochemical details of the processes in coronary atherosclerosis, which have been obtained by new strategies such as angioscopy, intravascular ultrasound and molecular biological methods. The term Stary's classification has been applied for the coronary atherosclerosis of patients with acute coronary syndrome at the National Cardiovascular Center, for the analysis of predisposing atherosclerosis of these patients. The recent findings regarding acute coronary syndrome resulting from a rupture of coronary atherosclerotic plaques indicate that this syndrome is probably the most important mechanism underlying the sudden onset. It has been found that the risk of plaque rupture may depend more on plaque composition than on plaque size. Plaques rich in soft extracellular lipids and macrophages are possibly more vulnerable to plaque rupture. Two of the goals of the present review are to clarify how plaque disruption occurs and to elucidate the relationship between plaque disruption and coronary risk factors in elderly Japanese patients with acute coronary syndrome. Coronary stents have been shown to be efficacious in the treatment of acute and threatened closure complicating percutaneous transluminal coronary angioplasty (PTCA) and have produced encouraging initial results in the prevention of restenosis. In the autopsy study of restenosis after PTCA, it was observed that dense caps of collagen fibers in the adventitia in the vicinity of the disrupted internal elastic laminae were present in all of the remodeling lesions. It is suggested that remodeling, which resulted in adventitial scarring, is one of the major causative factors of restenosis after PTCA. The long-term success of stenting, however, remains limited by the occurrence of late in-stent restenosis, with an incidence of 20-42% depending on the stent design and the patient population studied. Another aim of the present review is to describe the pathological mechanism of restenosis after PTCA and/or stent replacement and, consequently, the vascular remodeling that occurs around adventitial tissue after PTCA and intimal hyperplasia that is chronically irritated by a foreign body granulomatous reaction after stenting. Finally, the results of the investigation of the effect of a tissue factor pathway inhibitor on the prevention of interventional restenosis is described.