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of Newsday reported it is"the Giants' objective to negotiate with and sign Beckham to a contract."

"I'd be very surprised [if New York trades Beckham]," a source told Glauber and Rock.

Beckham will hold out and " not set foot on a field without a new contract extension," according to Ian Rapoport of NFL Network. The wideout's rookie deal expires after the 2018 season.

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of the New York Daily News reported Monday the team is "open to fielding offers for OBJ."

This comes after co-owner John Mara indicated the organization would be willing to let him go.

"I mean we're certainly not shopping him," Mara said Sunday at the owners meetings in Orlando, Florida, per. "But when you’re coming off a season where you're 3-13 and played as poorly as we played, I wouldn't say anyone's untouchable."

Some could look at his antics on the field and the recent video of Beckham as a reason to make a move. The Giants are seemingly far from contention, and Beckham is set to become a free agent. Per Spotrac , he is due $8.5 million in 2018 as part of his fifth-year option after he made just over $10 million in his first four years combined.

Trading him could land some quality assets and help kick-start a rebuild.

On the other hand, Beckham is clearly an impact player and worth building around if the two sides can come to an agreement. Although injuries limited him to just four games last season, he still has three Pro Bowl appearances in four years, totaling at least 90 catches, 1,300 yards and 10 touchdowns in each of his first three seasons.

Bivalirudin, a direct antithrombin, alone or in combination with GPIIb-IIIa inhibition, was compared with UFH/enoxaparin + GPIIb-IIIa inhibition. Bivalirudin monotherapy was superior to either regimen with respect to reduced bleeding, without increased ischaemic events [ 251 ].

DAPT consists of ASA 150–300 mg per os or 250 (−500) mg bolus i.v., followed by 75–100 mg daily, and prasugrel 60 mg loading dose, followed by 10 mg daily, or ticagrelor 180 mg loading dose, followed by 90mg twice daily, depending on drug availability [ 94 ]. Clopidogrel 600mg loading dose, followed by 75 mg daily, should be used primarily if the more effective ADP receptor blockers are contraindicated or unavailable.

Increasing the maintenance dose of clopidogrel for 1–2 weeks might be effective in STEMI patients, as shown in NSTE-ACS. Prasugrel is superior to clopidogrel (300mg loading dose, 75 mg maintenance dose) in reducing combined ischaemic endpoints and stent thrombosis in STEMI patients without increasing the risk of severe bleeding [ 252 ].

A predefined subgroup analysis has demonstrated that STEMI or NSTE-ACS patients referred for PCI significantly benefit from ticagrelor, vs. clopidogrel, with similar bleeding rates [ 253 ].

Most studies of GPIIb-IIIa inhibitors in STEMI have evaluated abciximab (0.25 mg/kg i.v. bolus followed by infusion of 0.125 μg/kg/min up to a maximum of 10 μg/min for 12 h). Findings are mixed regarding the effectiveness of facilitation (early administration) with GPIIb-IIIa inhibitors before catheterization. While the only available RCT [ 86 ] showed no benefit, registries, meta-analyses, and post hoc analyses of APEX-AMI [ 254 ] show positive results. The controversial literature data, the negative outcome of the only prospective RCT [ 86 ], and the beneficial effects of faster acting and more efficacious ADP receptor blockers in primary PCI do not support pre-hospital or pre-catheterization use of GPIIb-IIIa inhibitors.

Options for anticoagulation include UFH 60 IU/kg i.v. bolus with GPIIb-IIIa inhibitor or UFH 100 IU/kg i.v. bolus without GPIIb-IIIa inhibitor, or bivalirudin 0.75 mg/kg bolus followed by 1.75 mg/kg/h. Antithrombins can be stopped after PCI for STEMI with few exceptions (LV aneurysm and/or thrombus, AF, prolonged bed rest, deferred sheath removal).

A recent study suggested bivalirudin monotherapy as an alternative to UFH plus a GPIIb-IIIa inhibitor [ 255 ]. Significantly lower severe bleeding rates led to a beneficial net clinical outcome indicating that bivalirudin may be preferred in STEMI patients at high risk of bleeding. One-year outcome of the HORIZONS RCT confirmed the beneficial action of bivalirudin monotherapy vs. UFH and a GPIIb-IIIa inhibitor. Uncertainty remains in the early phase of primary PCI, when thrombotic complications seem to be higher with bivalirudin monotherapy. However, this had no effect on long-term clinical outcome, probably because acute in-hospital stent thrombosis can be promptly addressed, unlike late out-of-hospital stent thrombosis.

For the assessment of salvage in AMI, it is important to consider the timing of the scanning. During the first week after the AMI, LGE CMR tends to overestimate the size of FIS presumable due to contrast enhancement of oedematous but viable myocardial tissue. In contrast at 4 to 6 weeks after infarction, infarct volume may shrink due to replacement of necrotic muscle by scar. Therefore, it is critical to standardize the timing of the FIS measurement in the study design. The optimal time to evaluate myocardial salvage within one cardiac examination seems to be at 1 to 2 weeks post-infarction, since the size of FIS by LGE CMR remains almost constant after 1 week 58 and AAR remains stable for at least 7 days. 58

Since essentially all CMR methods for assessment of AAR relies on detection of myocardial oedema or gadolinium enhancement in regions with disruption of cell membranes, there is concern that an intervention itself may affect the formation of oedema and the size of the measured AAR. In the presence of an increase in salvage compared with standard treatment, postconditioning and administration of exenatide, a glucagon-like-peptide-1, at the time of reperfusion in patients with STEMI AAR was unaffected by treatment. 58 A few randomized single-centre trials have used myocardial salvage by CMR as an endpoint. 59–61 These trials are of proof-of-concept studies testing the potential efficacy of new therapeutic approaches and need confirmation in large-scale clinical outcome trials.

The greatest challenge in analysing CMR data for assessing myocardial salvage involves the segmentation of myocardial oedema on T2-weighted scans to depict AAR. Threshold techniques based on relative differences in signal intensity between oedematous and normal myocardium have mostly been used. However, segmentation based solely on threshold is inaccurate when there is more complex myocardial morphology such as in infarcts with microvascular obstruction or intramyocardial haemorrhage, which tends to create hypo-intense signal within the core of the infarcted area. 49 More recently acquisition of T1 maps 56 and T2 maps 62 to quantitate absolute values of T1 and T2 relaxation has been suggested. However, it remains to be shown whether such an approach will improve accuracy and avoid misinterpretation of the true size of AAR. A more simplified approach to segmentation of AAR involves delineation of the infarct-ESA on LGE images, presuming that the wave front of myocardial injury in AMI travels strictly along the endocardial borders. This may not be correct in patients with large salvage 56 where AAR and hence salvage are underestimated by ESA.

The immediate benefits of CMR compared with SPECT include the absence of radioactive tracers and a minor logistical challenge because CMR can potentially determine the AAR retrospectively from 24 h to several days after the infarction.

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