June 2016 Br J Cardiol 2016;23:57–60 doi:10.5837/bjc.2016.019
Peysh A Patel, Murad Khan, Chia Yau, Simerjit Thapar, Sarah Taylor, Paul A Sainsbury
Introduction Angina results from myocardial ischaemia as a consequence of mismatch between supply and demand.1 Most cases are secondary to atherosclerotic disease of coronary arteries.2 Conventional therapy to manage such patients has relied on pharmacotherapy and revascularisation strategies. Pharmacological options routinely include aspirin, statin, rate-limiting therapy, such as beta blocker or calcium-channel antagonist, and vasodilators, such as isosorbide mononitrate and nicorandil. Revascularisation may be through percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).3 Chronic, refractory angina constitutes
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