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Pathology of plaque haemorrhage and neovascularization of coronary artery
Takahide Kodama1, Nupoor Narula, Manuela Agozzino
1Centre for Inherited Cardiovascular Diseases, Foundation IRCCS Policlinico San Matteo, Pavia, Italy.
Insights
Intraplaque hemorrhage (IPH) drives atherosclerotic plaque progression and rupture, leading to acute coronary syndromes. Understanding IPH and plaque neovascularization is key to managing cardiovascular disease.
Area of Science:
- Cardiovascular Pathology
- Atherosclerosis Research
Background:
- Intraplaque hemorrhage (IPH) is implicated in atherosclerotic plaque progression and rupture.
- Acute coronary syndromes, a leading cause of mortality, are linked to these plaque events.
- IPH is a frequent finding in atherosclerotic plaques.
Purpose of the Study:
- To review the pathology and pathophysiology of IPH and plaque neovascularization.
- To discuss the clinical impact of IPH in atherosclerosis.
- To highlight unanswered questions regarding angioneogenesis in plaques.
Main Methods:
- Review of pathological and experimental studies on IPH.
- Utilizing anti-Glycophorin A antibodies for IPH detection.
- Focus on histopathological investigation of IPH and neovascularization.
Main Results:
- Studies confirm the significant role of IPH in plaque progression and complications.
- Plaque neovascularization is identified as the source of blood for IPH.
- Mechanisms of IPH impact on plaque instability are increasingly understood.
Conclusions:
- IPH and plaque neovascularization are critical factors in cardiovascular disease pathogenesis.
- Further research is needed to address the causes and treatment of plaque angioneogenesis.
- Histopathological examination is essential for studying IPH and its clinical implications.
Abstract:
Intraplaque haemorrhage (IPH) is thought to play crucial roles in plaque progression and plaque rupture, resulting in acute coronary syndromes, which are the leading causes of morbidity and mortality in the developed countries. IPH is a common finding in atherosclerotic plaques. In the past decade, the use of anti-Glycophorin A antibodies that specifically and uniquely label membranes of the red cells triggered a cascade of pathologic and experimental studies concordantly documenting not only the presence but also the major role of IPH in plaque progression and complications. Moreover, recent studies have shown that plaque neovascularization is essential to IPH as a source of blood content. Although the mechanisms by which IPH impacts plaque progression and plaque rupture gradually become clear, several questions such as causes of angioneogenesis, identification and treatment of plaques with angioneogenesis are still unanswered. Further studies are needed to resolve these issues; however, the investigation of IPH without a histopathological approach is unconceivable. This review will focus on the pathology of IPH and plaque neovascularization, pathophysiology and potential clinical impact.
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