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Coronary flow disturbance is a recognised pathophysiological process in patients with aortic stenosis.1 2 Resting flow is tightly controlled by a complex set of homeostatic mechanisms.3 In patients with left ventricular hypertrophy (LVH) as a result of aortic stenosis, autoregulation increases resting coronary flow to preserve myocardial perfusion.3 However, as the capacity of the microvasculature to respond to hyperaemia is relatively constant, coronary flow reserve (CFR) is curtailed. Together with the extravascular effects of LVH (increased systolic compression, decreased diastolic perfusion time, capillary rarefaction), hyperaemic myocardial perfusion becomes impaired. While there is much interest in the assessment of epicardial coronary artery disease in patients with severe aortic stenosis, the scientific literature on microvascular function in these patients is limited. A more detailed understanding of microvascular pathophysiology in aortic stenosis may pave the way to optimising the diagnostic management of affected patients.
To this end, Paolisso et al investigated coronary physiology in a propensity-score matched cohort of patients with and without severe aortic stenosis.4 All patients had resting and hyperaemic flow assessment in the left anterior descending artery (LAD) during elective coronary angiography. Cardiac CT scanning was also performed. Patient selection ensured exclusion of factors which would impact coronary physiology, including previous acute coronary syndromes or coronary artery bypass grafting in the LAD territory, epicardial stenosis >50% in the LAD, left bundle branch block, left ventricular ejection fraction <50% or previous aortic valve replacement. A control cohort was identified from patients undergoing assessment for angina with no obstructive epicardial coronary disease, and matched for significant factors including age, sex, diabetes and fractional flow reserve (FFR).
Coronary physiology was assessed using a combined pressure/temperature diagnostic guidewire positioned in the LAD. Absolute coronary flow …
Footnotes
Contributors JC and DA wrote the first draft. CB provided guidance and then reviewed and revised the manuscript and submitted the final version.
Funding CB has received research support from the British Heart Foundation (PG/17/2532884, FS/17/26/32744 and RE/18/6134217) and funding from the Chief Scientist Office, UKRI (COVID-HEART, reference MC/PC/20014), EPSRC (EP/N014642/1; EP/S030875/1), Medical Research Council (MR/S005714/1) and Wellcome Trust. JC, DA and CB are employed by the University of Glasgow which holds research and consultancy agreements with Abbot Vascular, AstraZeneca, Boehringer Ingelheim, Coroventis, GSK, HeartFlow, Menarini, Neovasc, Novartis, Opsens, Siemens Healthcare and Valo Health. These companies had no involvement in this manuscript.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.