Abdul R Sheikh1, Christopher J Zeitz2, Sharmalar Rajendran2, David P Di Fiore1, Rosanna Tavella3, John F Beltrame4. 1. Discipline of Medicine, University of Adelaide, Adelaide, South Australia 5005, Australia; Cardiology Department, The Queen Elizabeth & Royal Adelaide Hospitals, Central Adelaide Local Health Network, Adelaide, South Australia, Australia; Basil Hetzel Institute for Translational Health Research, 37 Woodville Road, Woodville South, South Australia 5011, Australia. 2. Discipline of Medicine, University of Adelaide, Adelaide, South Australia 5005, Australia; Cardiology Department, The Queen Elizabeth & Royal Adelaide Hospitals, Central Adelaide Local Health Network, Adelaide, South Australia, Australia; Cardiology Unit, Lyell McEwin Hospital, Northern Adelaide Local Health Network, Haydown Road, Elizabeth Vale, South Australia 5112, Australia. 3. Discipline of Medicine, University of Adelaide, Adelaide, South Australia 5005, Australia; Basil Hetzel Institute for Translational Health Research, 37 Woodville Road, Woodville South, South Australia 5011, Australia. 4. Discipline of Medicine, University of Adelaide, Adelaide, South Australia 5005, Australia; Cardiology Department, The Queen Elizabeth & Royal Adelaide Hospitals, Central Adelaide Local Health Network, Adelaide, South Australia, Australia; Basil Hetzel Institute for Translational Health Research, 37 Woodville Road, Woodville South, South Australia 5011, Australia. Electronic address: john.beltrame@adelaide.edu.au.
Abstract
BACKGROUND: Coronary haemodynamic testing frequently identifies abnormal pathophysiological parameters in patients with angina and non-obstructed coronaries on angiography (NoCAD) but the clinical utility of these measures has received limited attention. OBJECTIVE: This study aims to identify the clinical and coronary haemodynamic determinants of recurrent chest pain at one month in patients with NoCAD. METHODS: Patients with angina, NoCAD (<50% stenosis) and normal LV systolic function underwent invasive coronary haemodynamic testing involving: (1) angiographic TIMI frame and opacification rate, (2) microvascular functional measures including coronary flow reserve (CFR) and hyperaemic microvascular resistance (HMR), (3) coronary endothelial function assessment with low dose intracoronary acetylcholine (IC-ACh) infusions (0.18 μg/min & 1.8 μg/min over 2 min), and (4) Provocative spasm testing with high dose IC-ACh boluses (25, 50 and 100 μg). Clinical and health status were assessed at baseline and one month. RESULTS: In the 49 NoCAD patients (78% female, mean age of 54 ± 11) undergoing comprehensive coronary haemodynamic testing, 33 (67%) continued to experience chest pain at one month. Determinants of recurrent chest pain on univariate analysis included baseline chest pain status or a HMR > 1.9. Multivariate logistic regression analysis identified frequent angina at baseline (OR: 68.9 [4.1, 1165.0], p = 0.003), previous unstable angina admission (OR: 43.9 [3.5, 547.9], p = 0.003) and a HMR > 1.9 (OR: 15.6 [2.1, 114.0], p = 0.007) as independent predictors of recurrent chest pain. CONCLUSION: In this small pilot study, an abnormal HMR was the only coronary haemodynamic parameter that was a determinant of ongoing angina at short-term follow-up.
BACKGROUND: Coronary haemodynamic testing frequently identifies abnormal pathophysiological parameters in patients with angina and non-obstructed coronaries on angiography (NoCAD) but the clinical utility of these measures has received limited attention. OBJECTIVE: This study aims to identify the clinical and coronary haemodynamic determinants of recurrent chest pain at one month in patients with NoCAD. METHODS:Patients with angina, NoCAD (<50% stenosis) and normal LV systolic function underwent invasive coronary haemodynamic testing involving: (1) angiographic TIMI frame and opacification rate, (2) microvascular functional measures including coronary flow reserve (CFR) and hyperaemic microvascular resistance (HMR), (3) coronary endothelial function assessment with low dose intracoronary acetylcholine (IC-ACh) infusions (0.18 μg/min & 1.8 μg/min over 2 min), and (4) Provocative spasm testing with high dose IC-ACh boluses (25, 50 and 100 μg). Clinical and health status were assessed at baseline and one month. RESULTS: In the 49 NoCADpatients (78% female, mean age of 54 ± 11) undergoing comprehensive coronary haemodynamic testing, 33 (67%) continued to experience chest pain at one month. Determinants of recurrent chest pain on univariate analysis included baseline chest pain status or a HMR > 1.9. Multivariate logistic regression analysis identified frequent angina at baseline (OR: 68.9 [4.1, 1165.0], p = 0.003), previous unstable angina admission (OR: 43.9 [3.5, 547.9], p = 0.003) and a HMR > 1.9 (OR: 15.6 [2.1, 114.0], p = 0.007) as independent predictors of recurrent chest pain. CONCLUSION: In this small pilot study, an abnormal HMR was the only coronary haemodynamic parameter that was a determinant of ongoing angina at short-term follow-up.
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