Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569257
Title: The contribution of inflammatory mechanisms to microvascular injury in coronary angioplasty
Author: Patel, Billal
Awarding Body: University of Liverpool
Current Institution: University of Liverpool
Date of Award: 2012
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Abstract:
Coronary angioplasty is established as the most common form of revascularisation in IHD, yet despite major advances, failure of microvascular revascularisation is associated with poor prognosis. Inflammation is important in the natural progression of atherosclerosis from early stages through to progression to plaque rupture and acute myocardial infarction. In addition inflammatory mechanisms have a role in mediating adverse clinical outcomes during coronary reperfusion and revascularisation, although the underlying mechanisms remain unknown. The objective of this research was to assess the microvascular response to percutaneous coronary intervention (PCI) in patients with stable angina, and this study aimed to assess the relationship between changes in microvascular function in response to PCI with markers of systemic inflammation and endothelial activation. Also we aimed to detect localised myocardial inflammation in response to PCI in those patients who have microvascular injury following PCI. We measured fractional flow reserve (FFR), coronary flow reserve (CFR) and index of microcirculatory resistance (IMR) in both the vessel undergoing PCI and an adjacent vessel, before and after PCI. We assessed the inflammatory response to PCI and the relationship between markers of systemic inflammation and microvascular function. A subgroup of 9 patients underwent radiolabelling of leukocytes and myocardial SPECT scans before and after PCI to detect areas of localised inflammation. A total of 39 patients were included in the study. Patients demonstrated a heterogenous response on IMR following PCI. There was an increase of microvascular resistance in the vessel undergoing PCI in a third of subjects. There was a reduction of IMR in the reference vessel in response to PCI in the target vessel (23.7[15.8-31.4] vs. 17.9[12.4-24.1] n=34 p<0.01) Basal inflammation was not predictive of microvascular dysfunction but the inflammatory response as measured by CRP and ET -1 was associated with microvascular dysfunction (R=0.42 p
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.569257  DOI: Not available
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