CVPath and its research team, led by Renu Virmani, MD, have extensive research experience in the field of atherosclerosis, especially coronary and carotid arteries. We have recently shown that red cell membranes contribute to the enlargement of the necrotic core as well as deposition of free cholesterol. The mechanism of plaque hemorrhage in atherosclerotic disease is poorly understood and we are now beginning to learn more about plaque angiogenesis and its role in plaque hemorrhage. We would like to determine if the thin cap fibroatheroma (vulnerable plaque) is the precursor lesion to plaque rupture and hope to accomplish this through the establishment of an animal model of vulnerable plaque.
A further focus of our research in atherosclerosis is the mechanisms that lead to formation of plaque erosion. We have shown that such lesions occur frequently in young women, but the reasons are not yet understood. We have proposed that vasospasm may be the underlying mechanism and are engaged in active research to determine whether this is so.
We are also gathering information from the collection of stented human arteries, including drug- eluting stents (DES), seeking greater understanding of how these devices work and what types of histologic changes are induced by such interventions.
We have established a rabbit model of plaque hemorrhage. Our goal is to understand how and under what circumstances the plaque ruptures. Our model of atherosclerosis can also be used to study vessel wall stent interaction and healing. In normal stented rabbit arteries, we have shown that immunosuppressant and cytotoxic drugs can reduce neointimal formation. The impact of DES on vessel wall morphology is important and we have described some of the beneficial and untoward effects of DES. It is also important to study the impact of polymers on the induction of inflammatory reaction and how drugs could modify the inflammation and whether this desirable effect can be sustained.
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• Atherosclerotic Vascular Disease
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Plaque Rupture - Coronary artery (Gross, left; Movat stain, right)
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• Restenosis Stents/PIT (Fibro Intimal Thickening)
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In-Stent Restenosis (from a patient with stable angina)
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• Pharmocotherapy
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Rabbit iliac artery model at 28 days
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• Toxic Vascular Reactions
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