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Fondaparinux was inferior to UFH in the setting of primary PCI in patients with STEMI (OASIS-6 trial) [ 256 ].

Bleeding contributes to worse outcome and can be prevented by implementing the following measures:

formally assess and document bleeding risk in every patient;

avoid crossover between UFH and LMWH;

adjust antithrombotic therapy doses based on weight and renal function ( Table 37

Table 37
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Recommendations of antithrombotic drug use in chronic kidney disease

Table 37
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Recommendations of antithrombotic drug use in chronic kidney disease

use radial access in patients at high risk of bleeding;

stop anticoagulation after PCI unless a specific indication exists;

adopt selective downstream use of GPIIb-IIIa inhibitors, as required in the catheterization laboratory, in preference to unselective upstream use.

1 month after BMS implantation in stable angina [ 55 , 60 , 94 ];

6–12 months after DES implantation in all patients [ 60 , 94 ];

1 year in all patients after ACS, irrespective of revascularization strategy.

Data suggest that certain patient populations (e.g. high risk for thromboembolic events, patients after SES or PES implantation), may benefit from prolonged DAPT beyond 1 year. The downside of this strategy is the increased rate of severe bleeding complications over time. Recent data suggest that DAPT for 6 months might be sufficient because late and very late stent thrombosis correlate poorly with discontinuation of DAPT.

Indications for DAPT and treatment duration depend primarily on the clinical indication (stable CAD, NSTE-ACS, STEMI), irrespective of the mode of revascularization. Secondary prevention demands lifelong antiplatelet therapy with 75–325 mg ASA daily (Section 13).

Antiplatelet agents also promote long-term graft patency, especially SVG. In cases of aspirin intolerance, clopidogrel should be used. There are no RCTs comparing the efficacy of clopidogrel or clopidogrel plus aspirin vs. aspirin alone on long-term graft patency.

Triple therapy consisting of ASA, clopidogrel (or prasugrel), and a vitamin K antagonist should only be given if a compelling indication exists, i.e. paroxysmal, persistent, or permanent AF with CHADS 2 score ≥ 2, mechanical valves, recent or recurrent history of deep venous thrombosis, or pulmonary embolism. Triple therapy should only be prescribed for the shortest necessary duration with frequent INR measurement (target INR 2–2.5) [ 257 ]. In patients with a compelling indication for long-term anticoagulation, BMS implantation or stand-alone balloon angioplasty or CABG should be preferred over DES to restrict the duration of triple therapy to 1 month.

In the multicellular preparations of the myocardium isolated from the epicardial border zone of the 5-day infarcted heart, the following abnormalities have been described: a decrease in resting potential, total AP amplitude and V̇ max , a reduction in AP duration at both 50 and 90% repolarization and a loss in the plateau potentials ( Fig. 1 ) [5] . However, when the cells of the epicardial border zone are dispersed and studied as isolated myocytes in vitro [10] , the resting potential is no different than control suggesting that other factors control resting membrane potential in the multicellular preparation. One likely factor may be extracellular ion accumulation, since in single cells electrical activity is studied after it is removed from the syncytium and superfused in an environment where immediate extracellular ion accumulation and depletion are not significant.

While resting potentials of the 5-day myocytes are similar to control values, APs of these myocytes show changes in the repolarization during the terminal portion of phase 3. Net membrane currents are significantly different between cell groups but I K1 appears to differ only at hyperpolarized potentials ( Fig. 2 ).

Fig. 2
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Average ‘steady-state’ net membrane current density voltage-relations of normal (NZVM, =28, filled circles) and 5-day infarct (IZVM, =44, unfilled circles) ventricular myocytes in nisoldipine-containing Tyrode’s solution. Currents were measured at the end of a 440-ms pulse from a holding potential of −40 mV to various test potentials (). Average capacitance of cells was 123±6 pF (NZVM) and 179±7 pF (IZVM) (<0.05). Note that the isochronal – curve of NZVM had a pronounced n-shape, compared to that of IZVM. The average resting potential −87±3 mV and −83±3 mV for NZVM and IZVM, respectively. For all IZVM studied, the average – differed from NZVM at test voltages −110 to −95 mV and at −80 to −30 mV. Inset shows cesium (Cs, 20 mM)-sensitive currents in a subset of cells (NZVM, =12; IZVM, =24). Cs-sensitive currents were n-shaped in both groups, depicting the – of the underlying (zero intercepts, NZVM=−90±2 mV; IZVM=−93±1 mV, >0.05). There was a significant reduction in IZVM density in the −110 to −90 mV range. * indicates significance at <0.05.

Fig. 2
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Average ‘steady-state’ net membrane current density voltage-relations of normal (NZVM, =28, filled circles) and 5-day infarct (IZVM, =44, unfilled circles) ventricular myocytes in nisoldipine-containing Tyrode’s solution. Currents were measured at the end of a 440-ms pulse from a holding potential of −40 mV to various test potentials (). Average capacitance of cells was 123±6 pF (NZVM) and 179±7 pF (IZVM) (<0.05). Note that the isochronal – curve of NZVM had a pronounced n-shape, compared to that of IZVM. The average resting potential −87±3 mV and −83±3 mV for NZVM and IZVM, respectively. For all IZVM studied, the average – differed from NZVM at test voltages −110 to −95 mV and at −80 to −30 mV. Inset shows cesium (Cs, 20 mM)-sensitive currents in a subset of cells (NZVM, =12; IZVM, =24). Cs-sensitive currents were n-shaped in both groups, depicting the – of the underlying (zero intercepts, NZVM=−90±2 mV; IZVM=−93±1 mV, >0.05). There was a significant reduction in IZVM density in the −110 to −90 mV range. * indicates significance at <0.05.

Investigations of changes in the electrical function in the healing or healed infarct (weeks to months) include studies of cells overlying the infarct scar, known as the central ‘infarct zone’ cells, and those of the surrounding thin rim of cells called the lateral adjacent ‘border zone’ cells. In the feline healed infarct model, 50% of the hearts have ectopic activity [11,12] . The site of origin of these arrhythmias is not known but may be from cells within the healed border zone.

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Abstract

Objective

Higher risks of adverse outcomes have been reported for patients admitted acutely during off-hours. However, in relation to hip fracture, the evidence is inconsistent. We examined whether time of admission influenced compliance with performance measures, surgical delay and 30-day mortality in patients with hip fracture.

Design

Cohort study.

Setting

Data from The Danish Multidisciplinary Hip Fracture Registry linked with data from Danish National Registries.

Participants

Danish patients undergoing hip fracture surgery, aged >65 years, admitted 1 March 2010 to 30 November 2013 ( N = 25 305).

Exposure

Off-hours: weekday evenings and nights, and weekends.

Main Outcome Measures

Meeting specific performance measures, surgical delay and mortality.

Results

No differences were found in patient characteristics or in meeting performance measures (RRs from 0.99 [95% CI: 0.98–1.01] to 1.01 [95% CI: 0.99–1.02]. When comparing admission on weekdays (evenings and nights vs. days), off-hours admission was associated with a lower risk of surgical delay (adjusted OR 0.75 [95% CI: 0.66–0.85]) while no differences in 30-day mortality was found (adjusted OR 0.91 [95% CI: 0.80–1.04]. When comparing admission during weekends with admission during weekdays, off-hours admission was associated with a higher risk of surgical delay (adjusted OR 1.19 [95% CI: 1.05–1.37]) and a higher 30-day mortality risk (adjusted OR 1.13 [95% CI: 1.04–1.23]. The risk of surgical delay appeared not to explain the excess 30-day mortality.

Conclusions

Patients admitted off-hours and on-hours received similar quality of care. The risk of surgical delay and 30 days mortality was higher among patients admitted during weekends; explanations need to be clarified.

, , , , ,
Topic:
Issue Section:

Studies have reported that patients admitted to hospitals during off-hours with acute medical conditions may experience a higher risk of death and other adverse outcomes compared with those admitted during regular hospital hours [ 1–12 ]. The most commonly cited explanatory factors for the increased adverse effects following off-hours admission (off-hours-effect) include differences in patient characteristics, staffing levels/compositions, and the organization of care. To disentangle the roles of these factors and to provide clarification on the mechanisms driving off-hours-effects studies, with detailed data on unselected patients, are needed.

Hip fracture is among the most common causes for hospital admissions among the older population. The risk of dying within 1 month after a hip fracture is ∼10%; however, more than 10% of the patients that survive a hip fracture face disabilities that prevent return to living in their own homes [ 13 , 14 ]. Studies have provided inconsistent results on admission-time-related variations in patient outcomes following a hip fracture treatment [ 4 , 15–23 ]. To our knowledge, no study has examined the association between admission time and quality of care, as reflected in process performance measures.

The analysis of plaque composition based on radio-frequency backscatter, so-called ‘virtual histology’, characterizes plaques as fibrotic, fibrofatty with or without a necrotic core, or calcific. Although the PROSPECT trial [ 243 ] provided new insights regarding indications for stent implantation, the role of tissue characterization for everyday practice remains to be established.

Optical coherence tomography (OCT) is a light-based modality of intravascular imaging with higher spatial resolution than IVUS (15 vs. 100 μm). Its penetration is lower than IVUS but it provides detailed imaging of the endoluminal borders. At present, OCT is a valuable research tool.

Although non-invasive stress imaging should be the gold standard for evaluation of patients with known or suspected CAD, many patients come to the catheterization laboratory without prior functional testing. When a non-invasive imaging stress test is unavailable, FFR can be useful, especially in the presence of MVD. The concept that avoiding unnecessary stenting actually improves outcome was demonstrated in the DEFER [ 15 ] and FAME [ 28 ] trials. FFR is a valuable tool to determine whether or not an intermediate stenotic segment can cause downstream ischaemia in stable and unstable patients with MVD, in-stent restenosis, LM stenosis, and post-MI.

Treatment of CAD patients often requires the combination of anti-platelet and antithrombotic therapies to prevent thrombosis from activation of both platelets and the coagulation system. The choice, initiation, and duration of antithrombotic strategies for myocardial revascularization depend on the clinical setting (elective, acute, or urgent intervention). To maximize the effectiveness of therapy and reduce the hazard of bleeding, ischaemic and bleeding risks should be evaluated on an individual basis. A well-validated score for estimating bleeding risk is eagerly awaited.

DAPT includes acetylsalicylic acid (ASA) 150–300 mg per os or 250 (−500) mg bolus i.v. followed by 75–100 mg per os daily for all patients plus clopidogrel 300 (600)-mg loading dose followed by 75 mg daily for all patients [ 55 ].

Since the vast majority of PCI procedures eventually conclude with stent implantation, every patient scheduled for PCI should be considered for pre-treatment with clopidogrel, regardless of whether stent implantation is intended or not. To ensure full antiplatelet activity, clopidogrel should be initiated at least 6h prior to the procedure with a loading dose of 300mg, ideally administered the day before a planned PCI. If this is not possible, a loading dose of 600mg should be administered at least 2 h before PCI. Of note, this pre-loading strategy was not shown to improve outcome. A 600-mg clopidogrel loading dose may be preferable because of greater platelet inhibition than with the 300-mg standard dose, even if this is given > 6 h before PCI. When diagnostic angiography is negative or no intervention is performed, clopidogrel can be stopped. When a 300-mg loading dose has been given and ad hoc PCI is performed, another 300-mg dose can be given. The use of a higher maintenance dose (150 mg) has been proposed in patients with high thrombotic risk (e.g. in diabetics, patients after recurrent MI, after early and late stent thrombosis, for complex lesions, or in life-threatening situations should occlusion occur). GPIIb-IIIa inhibitors should be used only in ‘bail-out’ situations (thrombus, slow flow, vessel closure, very complex lesions) [ 55 ]. Recent trials did not demonstrate additional benefit of GPIIb-IIIa inhibitors after a clopidogrel loading dose of 600mg.

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