QFR was correlated highly with iFR as well as FFR. Like FFR and iFR, QFR might be reliable for assessing the physiological severity of coronary stenosis in the angiographic intermediate lesions.
Age-related loss of skeletal muscle mass and function is associated with some predisposing factors that increase the risk of vascular damage. This study aimed to examine whether muscle mass reduction, low muscle strength, and their combination were related to arterial stiffness in community-dwelling elderly population. Study participants consisted of 1046 elderly individuals (aged 72 ± 5 years) without cardiovascular disease, chronic kidney disease, or liver disease. Bioelectrical impedance analysis was performed to estimate appendicular skeletal muscle mass (ASM). A value for ASM was normalized for height (ASM index, kg/m 2). Handgrip strength (HGS) was measured using a Smedley grip dynamometer. Brachial-ankle pulse wave velocity (baPWV) was evaluated as an index of arterial stiffness using a simple automatic oscillometric technique. When participants were stratified based on baPWV cutoff values (< 1800 cm/s, 1800 to 1999 cm/s, ≥ 2000 cm/s), ASM index and HGS progressively decreased with an increase in baPWV levels (P for trend < 0.001). In multiple regression analysis, baPWV was significantly associated with ASM index (β = −0.270, P < 0.001) and HGS (β = −0.102, P < 0.001) independent of potential confounding factors. The baPWV of the subgroup with low ASM index and low HGS was significantly higher than that of those with only low ASM index or low HGS (P < 0.001). These results suggest that loss of skeletal muscle mass and function is associated with increased arterial stiffness in the elderly population, and the combination of muscle mass reduction and low muscle strength may lead to greater arterial stiffness than each of the individual conditions.
related coronary arteries. Angiographically severe stenoses in prior-MI-related coronary arteries are not necessary to induce myocardial ischemia because the amount of viable myocardium is reduced. 9-11 Previous studies have demonstrated that FFR can accurately assess the degree of ischemia even in prior-MI-related coronary arteries, 11,12 but QFR may not consider the amount of viable myocardium because this index is estimated from the anatomic information of the epicardial coronary artery. Therefore, we investigated the diagnostic accuracy of QFR in prior-MI-related coronary arteries as compared with FFR. Methods Study PopulationThe present study was a retrospective, single-center study of patients who underwent CAG and FFR. We analyzed a consecutive series of 75 prior-MI-related coronary arteries (examined in 75 patients between July 2012 and December 2016) and a consecutive series of 75 non-prior-MI-related F ractional flow reserve (FFR) is a useful index of the functional significance of a coronary stenosis. 1 It is obtained during routine coronary angiography (CAG) by using a pressure wire. 2 FFR is independent of heart rate, systemic blood pressure and cardiac output and takes into account myocardial territory and viability and collateral perfusion. 2-5 However, FFR has some disadvantages, such as risks of pressure wire injury, side effects of hyperemic agents and additional costs.Quantitative flow ratio (QFR) is a novel approach to assessing the functional severity of a coronary stenosis. It is calculated from 3D quantitative CAG (3D-QCA) using an advanced algorithm that enables fast computation of the pressure drop caused by coronary stenosis.
Aims The ability of optical coherence tomography (OCT) to detect plaques at high risk of developing acute coronary syndrome (ACS) remains unclear. The aim of this study was to evaluate the association between non-culprit plaques characterized as both lipid-rich plaque (LRP) and thin-cap fibroatheroma (TCFA) by OCT and the risk of subsequent ACS events at the lesion level. Methods and results In 1378 patients who underwent OCT, 3533 non-culprit plaques were analysed for the presence of LRP (maximum lipid arc > 180°) and TCFA (minimum fibrous cap thickness < 65 μm). The median follow-up period was 6 years [interquartile range (IQR): 5–9 years]. Seventy-two ACS arose from non-culprit plaques imaged by baseline OCT. ACS was more often associated with lipidic plaques that were characterized as both LRP and TCFA vs. lipidic plaques that did not have these characteristics [33% vs. 2%, hazard ratio 19.14 (95% confidence interval: 11.74–31.20), P < 0.001]. The sensitivity and specificity of the presence of both LRP and TCFA for predicting ACS was 38% and 97%, respectively. A larger maximum lipid arc [1.01° (IQR: 1.01–1.01°)], thinner minimum fibrous cap thickness [0.99 μm (IQR: 0.98–0.99 μm)], and smaller minimum lumen area [0.78 mm2 (IQR: 0.67–0.90 mm2), P < 0.001] were independently associated with ACS. Conclusion Non-culprit plaques characterized by OCT as both LRP and TCFA were associated with an increased risk of subsequent ACS at the lesion level. Therefore, OCT might be able to detect vulnerable plaques.
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