"Real-world" outcomes of BVS showed acceptable rates of TLF at six months, although the rates of early and midterm scaffold thrombosis, mostly clustered within 30 days, were not negligible.

Background Inorganic nitrate (NO3−), abundant in certain vegetables, is converted to nitrite by bacteria in the oral cavity. Nitrite can be converted to nitric oxide (NO) in the setting of hypoxia. We tested the hypothesis that NO3− supplementation improves exercise capacity in HFpEF via specific adaptations to exercise. Methods Seventeen subjects participated in this randomized, double-blind, cross-over study comparing a single-dose of NO3-rich beetroot juice (NO3−:12.9 mmoles) versus an identical nitrate-depleted placebo. Subjects performed supine-cycle maximal-effort cardiopulmonary exercise tests, with measurements of cardiac output (CO) and skeletal muscle oxygenation. We also assessed skeletal muscle oxidative function. Study endpoints included exercise efficiency (total work/total oxygen consumed), peak VO2, total work performed, vasodilatory reserve, forearm mitochondrial oxidative function, and augmentation index (a marker of arterial wave reflections, measured via radial arterial tonometry). Results Supplementation increased plasma NO-metabolites (median 326 μM versus 10 μM; P=0.0003), peak VO2 (12.6±3.7 vs. 11.6±3.1 mL O2/min/kg; P=0.005), and total work performed (55.6±35.3 vs. 49.2±28.9 kJ; P=0.04). However, efficiency was unchanged. NO3− led to greater reductions in SVR (−42.4±16.6 vs. −31.8±20.3%; P=0.03) and increases in CO (121.2±59.9 vs. 88.7±53.3%; P=0.006) with exercise. NO3− reduced aortic augmentation index (132.2±16.7 vs. 141.4±21.9%, P=0.03) and tended to improve mitochondrial oxidative function. Conclusion NO3− increased exercise capacity in HFpEF by targeting peripheral abnormalities. Efficiency did not change due to parallel increases in total work and VO2. NO3− increased exercise vasodilatory and cardiac output reserves. NO3− also reduced arterial wave reflections, which are linked to left ventricular diastolic dysfunction and remodeling.

No abstract

No abstract

Consensus criteria for patient and lesion selection, BVS implantation and optimisation, use of intravascular imaging guidance, approach to multiple patient and lesion scenarios, and management of complications, were identified.

At one-year follow-up, the PSP-1 score was an independent predictor of DoCE. External validation and prospective studies are needed to determine the clinical usefulness of this score.

Quantification of pulmonary flow is clinically important in the evaluation of both congenital and acquired heart disease. Velocity-encoded cine magnetic resonance (MR) is a promising technique for measuring velocity and volume of blood flow. The authors report validation of the accuracy of velocity-encoded cine MR for measurement of oblique-angle flow in vitro, with use of a constant-flow phantom, and in vivo, with nine healthy volunteers in whom velocities were measured separately in the main, right, and left pulmonary arteries. Findings at MR were compared with findings at Doppler echocardiography. Velocity measurements in a flow phantom with cine MR correlated well with direct measurements at Doppler echocardiography. Velocity-encoded cine MR enabled accurate and reproducible measurement of absolute blood flow in healthy subjects. Oblique-gradient flow encoding (ie, flow-encoding direction coinciding with the true direction of flow) was the method of choice for velocity measurements in the right and left pulmonary arteries.

Abstract-Effective arterial elastance (E A ) was proposed as a lumped parameter that incorporates pulsatile and resistive afterload and is increasingly being used in clinical studies. Theoretical modeling studies suggest that E A is minimally affected by pulsatile load, but little human data are available. We assessed the relationship between E A and arterial load determined noninvasively from central pressure-flow analyses among middle-aged adults in the general population (n=2367) and a diverse clinical population of older adults (n=193). In a separate study, we investigated the sensitivity of E A to changes in pulsatile load induced by isometric exercise (n=73). The combination of systemic vascular resistance and heart rate predicted 95.6% and 97.8% of the variability in E A among middle-aged and older adults, respectively. E A demonstrated a quasi-perfect linear relationship with the ratio of systemic vascular resistance/heart period (middle-aged adults, R=0.972; older adults, R=0.99; P<0.0001). Aortic characteristic impedance, total arterial compliance, reflection magnitude, and timing accounted together for <1% of the variability in E A in either middle-aged or older adults. Despite pronounced changes in pulsatile load induced by isometric exercise, changes in E A were not independently associated with changes pulsatile load but were rather a nearly perfect linear function of the ratio of systemic vascular resistance/ heart period (R=0.99; P<0.0001). Our findings demonstrate that E A is simply a function of systemic vascular resistance and heart rate and is negligibly influenced by (and insensitive to) changes in pulsatile afterload in humans. Its current interpretation as a lumped parameter of pulsatile and resistive afterload should thus be reassessed.