No abstract

We develop and validate a high-order reconstruction (HOR) method for the phase-resolved reconstruction of a nonlinear wave field given a set of wave measurements. HOR optimizes the amplitude and phase of $L$ free wave components of the wave field, accounting for nonlinear wave interactions up to order $M$ in the evolution, to obtain a wave field that minimizes the reconstruction error between the reconstructed wave field and the given measurements. For a given reconstruction tolerance, $L$ and $M$ are provided in the HOR scheme itself. To demonstrate the validity and efficacy of HOR, we perform extensive tests of general two- and three-dimensional wave fields specified by theoretical Stokes waves, nonlinear simulations and physical wave fields in tank experiments which we conduct. The necessary $L$, for general broad-banded wave fields, is shown to be substantially less than the free and locked modes needed for the nonlinear evolution. We find that, even for relatively small wave steepness, the inclusion of high-order effects in HOR is important for prediction of wave kinematics not in the measurements. For all the cases we consider, HOR converges to the underlying wave field within a nonlinear spatial-temporal predictable zone ${\mathcal{P}}_{NL}$ which depends on the measurements and wave nonlinearity. For infinitesimal waves, ${\mathcal{P}}_{NL}$ matches the linear predictable zone ${\mathcal{P}}_{L}$, verifying the analytic solution presented in Qi et al. (Wave Motion, vol. 77, 2018, pp. 195–213). With increasing wave nonlinearity, we find that ${\mathcal{P}}_{NL}$ contains and is generally greater than ${\mathcal{P}}_{L}$. Thus ${\mathcal{P}}_{L}$ provides a (conservative) estimate of ${\mathcal{P}}_{NL}$ when the underlying wave field is not known.

Cardiogenic shock was a new predictor of new-onset AF in STEMI patients.

Background: Ticagrelor reduced the rate of myocardial infarction and death compared with clopidogrel in patients with acute coronary syndrome. However, little is understood about chronic treatment of ticagrelor on microvascular dysfunction. The objective of this study was to assess the impact of ticagrelor maintenance treatment on microvascular system and coronary flow in comparison with clopidogrel. Methods: This study was a nonblinded, open-label, parallel-group, prospective, randomized controlled trial that enrolled 120 patients with acute coronary syndrome requiring stent implantation. Patients were randomized into the ticagrelor (180 mg loading dose, 90 mg twice daily thereafter) or clopidogrel (300 to 600 mg loading dose, 75 mg daily thereafter) group. The primary end point was coronary microvascular dysfunction as measured by an index of microcirculatory resistance (IMR) at 6 months after treatment. Results: The baseline clinical characteristics and physiological parameters, such as fractional flow reserve, coronary flow reserve, and IMR, did not differ between the ticagrelor and clopidogrel groups. Six-month follow-up physiological data showed that the IMR value was significantly lower in the ticagrelor group than the clopidogrel group (15.57±5.65 versus 21.15±8.39, P <0.01), and coronary flow reserve was higher in the ticagrelor group than in the clopidogrel group (3.85±0.72 versus 3.37±0.76, P <0.01). However, there was no difference in fractional flow reserve (0.87±0.08 versus 0.87±0.09, P =0.94) between the 2 groups. The improvement in IMR after 6 months of treatment was higher in the ticagrelor group ( P <0.01). Analyses of 223 nonculprit vessels of registered patients based on physiological results showed no differences in baseline fractional flow reserve (0.93±0.13 versus 0.92±0.09, P =0.58), coronary flow reserve (3.62±1.27 versus 3.51±1.24, P =0.16), or IMR (21.37±12.37 versus 24.19±21.08, P =0.22) or in follow-up fractional flow reserve (0.91±0.09 versus 0.91±0.08, P =0.67), coronary flow reserve (3.91±1.22 versus 3.75±1.16, P =0.36), or IMR (19.43±10.32 versus 21.52±18.90, P =0.34) between the 2 groups. Conclusions: Compared with clopidogrel, 6 months of ticagrelor therapy significantly improved microvascular dysfunction in acute coronary syndrome patients with stent implantation. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02618733.