This effect is dose clear granulocytes possess an electron-transport sys- dependent and occurs at clinically relevant concentra- tem that accepts electrons from NADPH in the cytosol tions [2].
The reactive oxygen species gener- in vitro [3]. The primary objective of this study was to ated are instrumental in killing pathogenic microor- determine whether these in vitro inhibitory effects ganisms [1]. Accord- cholamine concentration [5], whereas subsequent ing to random allocation, patients received either i. Laryngoscopy response to these manoeuvres [6].
Therefore, the potential exists the dedicated sampling cannula a prior to induction for lidocaine to decrease any inhibitory effect of laryn- of anaesthesia and fentanyl administration, b after goscopy and intubation on NRB. In vitro, lidocaine has induction of anaesthesia and immediately prior to a direct inhibitory effect on NRB [8].
In order to measure ROS production, 5 mL of blood was mixed with heparin 10 IU mL 1 in a Methods sterile plain tube, stored at room temperature and After institutional ethical approval, and having analysed within 2 h.
Three samples studied. Prior to coli bacteria. DNA staining was performed with mann's solution mL commenced. After preoxygen- values FL-1 E. One indicating the amount of rhodamine per cell. Swanton et al. Table 1.
Results Twenty patients were studied nine in group L and 11 Fig. Neutrophil respiratory burst activity. Sample times: in group S. Discussion In group S, respiratory burst activity remained depressed at 1 min Anaesthesiology [3]. This is a heterogeneous group with respect to political and cultural issues and also the develop- Methods ment of medicine. Only The ESA designed a questionnaire with ten ques- descriptive statistics were used average, standard tions.
The questionnaire was based on the previous deviation, range. The numbers shown correspond survey from and questions related to migra- only to the countries from which data were actually tion and shortage were added. The questionnaire received. All relative workforce figures are given as was sent to the president of the National Anaes- per of population.
Group averages for rela- thesia Society in each of the included European tive workforce figures e. We asked for the most recent data and to logists per population were calculated by indicate for which year the data were provided for. In case we had to follow-up on answers that tion in the more populated countries.
Also, group were unclear, interviewees were contacted again by averages were calculated only for the actual subgroup E-mail, fax or phone call. For all those countries of countries that use the respective type of workforce. These countries were not included to calculate the group average for the Country grouping number of anaesthesia nurses. This was done to study migration patterns and to Survey questions determine differences in the anaesthesia team Interviewees were asked the following questions composition.
In Group 2, there were anaes- or not. If for a board-certified anaesthesiologist. Groups 1 and 2 are taken together i. In Group the countries of origin or destination, inde- 3, there were 10 anaesthesiologists, the average pendent of citizenship of anaesthesiologists or number being 6.
The largest percentage of the female as a percentage of current workforce. In Europe, the workforce model of anaesthesia nurses or nurse anaesthetists is different to the US where the Type of practice: public vs. In some which the aspects of anaesthesia care are delegated Northern European countries Denmark, Norway, to the anaesthesia nurse differ within and between Finland, Ireland, UK , only a very small fraction of countries [5].
In Group 1, no gists in their country. If these Iceland and Portugal. Egger Halbeis et al Table 1. Number of anaesthesiologists, trainees, and anaesthesia nurses in Group 1. Anaesthesia workforce in Europe 5 Table 2. Number of anaesthesiologists, trainees and anaesthesia nurses in Group 2. In Group 3 median Czech Republic and Malta only. For Group 3, only the public anaesthesia practice dominates. Distribution of anaesthetic procedures In Group 1 Fig. Data relating to private anaesthesia Fig.
In work in private practice Fig. Anaesthesia Group 3 Fig. In both Groups 2 and 3, non-OR commitments by anaesthesiologists tend to be larger than those in Group 1. Egger Halbeis et al Table 3. Number of anaesthesiologists, trainees and anaesthesia nurses in Group 3.
Anaesthesia workforce in Europe 7 Figure 1. Distribution of anaesthetic procedures in Group 1. Figure 2. Distribution of anaesthetic procedures in Group 2.
Figure 3. Distribution of anaesthetic procedures in Group 3. Egger Halbeis et al Figure 4. Areas of professional activity in Group 1 public practice. Figure 5. Areas of professional activity in Group 1 private practice. Figure 6. Areas of professional activity in Group 2 public practice. In Group 3, the average percentage of physician trainees were recorded Tables 2—4.
In the UK report no use of anaesthesia nurses5. Areas of professional activity in Group 3 public practice. Table 4. Trainees and duration of European anaesthesia physician training programmes. Armenia 1. Uzbekistan 0. Egger Halbeis et al Table 5. Monthly salary for Board-certified anaesthesiologist in Europe h per month. In Group 2 Fig. In patients with intermittent claudication, beta-blockers have not been shown to worsen symptoms and are therefore not contra-indicated.
In the absence of contra-indications, beta-blocker dose should be slowly up-titrated, starting at a low dose of a beta1-selective agent, to achieve a resting heart rate between 60 and 70 beats per minute bpm.
Beta1-selective blockers without intrinsic sympathomimetic activity are favoured and evidence exists that atenolol and bisoprolol are superior to metoprolol, 97 , — possibly due to the CYP2D6-dependent metabolism of metoprolol. Trials using metoprolol did not show a clear benefit. Initiation of treatment and the optimal choice of beta-blocker dose are closely linked. Bradycardia and hypotension should be avoided. It is important to prevent overtreatment with fixed, high, initial doses, and doses should be decreased if this occurs.
Beta-blocker dose should be slowly up-titrated and tailored to appropriate heart rate and blood pressure targets, requiring that treatment be initiated ideally more than 1 day when possible at least 1 week and up to 30 days before surgery, starting with a low dose. High doses should be avoided, particularly immediately before surgery.
A retrospective study suggests that intra-operative mean arterial pressure should remain above 55 mm Hg. When beta-blockers are indicated, the optimal duration of perioperative beta-blockade cannot be derived from randomized trials. The occurrence of delayed cardiac events indicates a need to continue beta-blocker therapy for several months. For patients testing positive for pre-operative stress, long-term beta-blocker therapy should be used. A high priority needs to be given to new, randomized, clinical trials to better identify which patients derive benefit from beta-blocker therapy in the perioperative setting, and to determine the optimal method of beta-blockade.
Patients with non-coronary atherosclerosis carotid, peripheral, aortic, renal should receive statin therapy for secondary prevention, irrespective of non-cardiac surgery. Statins also induce coronary plaque stabilization through pleiotropic effects, which may prevent plaque rupture and subsequent myocardial infarction in the perioperative period.
Multiple observational studies have suggested that perioperative statin use has a beneficial effect on the day rate of death or myocardial infarction, and on long-term mortality and cardiovascular event rates. In patients in whom statins were introduced before intervention, two meta-analyses showed a significant reduction in the risk of post-operative myocardial infarction following invasive procedures, , however, these meta-analyses included more clinical trials relating to cardiac surgery or percutaneous procedures than to non-cardiac surgery.
All-cause post-operative mortality was not reduced in most series, except in one observational study that used propensity score adjustment to account for differences in patient characteristics according to the treatment. Observational series suggest that perioperative statin therapy is also associated with a lower risk of acute renal failure and with lower mortality in patients experiencing post-operative complications or multiple organ dysfunction syndrome.
Statin withdrawal more than four days after aortic surgery is associated with a three-fold higher risk of post-operative myocardial ischaemia. A concern relating to the use of perioperative statin therapy has been the risk of statin-induced myopathy and rhabdomyolysis. Perioperatively, factors increasing the risk of statin-induced myopathy are numerous, e. Early introduction of statins allows for better detection of potential side-effects. According to current guidelines, most patients with peripheral artery disease PAD should receive statins.
If they have to undergo open vascular surgery or endovascular intervention, statins should be continued afterwards. In patients not previously treated, statins should ideally be initiated at least 2 weeks before intervention for maximal plaque-stabilizing effects and continued for at least 1 month after surgery.
In patients undergoing non-vascular surgery, there is no evidence to support pre-operative statin treatment if there is no other indication. Nitroglycerine is well known for reversing myocardial ischaemia.
The effect of perioperative intravenous nitroglycerine on perioperative ischaemia is a matter of debate and no effect has been demonstrated on the incidence of myocardial infarction or cardiac death. Also perioperative use of nitroglycerine may pose a significant haemodynamic risk to patients, since decreased pre-load may lead to tachycardia and hypotension. Additionally, perioperative use of ACEIs or ARBs carries a risk of severe hypotension under anaesthesia, in particular following induction and concomitant beta-blocker use.
Hypotension is less frequent when ACEIs are discontinued the day before surgery. Although this remains debatable, ACEIs withdrawal should be considered 24 hours before surgery when they are prescribed for hypertension. They should be resumed after surgery as soon as blood volume and pressure are stable. In patients with LV systolic dysfunction, who are in a stable clinical condition, it seems reasonable to continue treatment with ACEIs under close monitoring during the perioperative period.
When LV dysfunction is discovered during pre-operative evaluation in untreated patients in a stable condition, surgery should if possible be postponed, to allow for diagnosis of the underlying cause and the introduction of ACEIs and beta-blockers. The effect of calcium channel blockers on the balance between myocardial oxygen supply and demand makes them theoretically suitable for risk-reduction strategies.
It is necessary to distinguish between dihydropyridines, which do not act directly on heart rate, and diltiazem or verapamil, which lower the heart rate. The relevance of randomized trials assessing the perioperative effect of calcium channel blockers is limited by their small size, lack of risk stratification, and the absence of systematic reporting of cardiac death and myocardial infarction. A meta-analysis pooled 11 randomized trials totalling patients.
All patients underwent non-cardiac surgery under calcium channel blocker treatment. Subgroup analyses favoured diltiazem. Another study in patients undergoing acute or elective aortic aneurysm surgery showed that dihydropyridine use was independently associated with an increased incidence of perioperative mortality.
Thus, although heart rate-reducing calcium channel blockers are not indicated in patients with heart failure and systolic dysfunction, the continuation or introduction of heart rate-reducing calcium channel blockers may be considered in patients who do not tolerate beta-blockers.
Additionally, calcium channel blockers should be continued during non-cardiac surgery in patients with vasospastic angina. Alpha 2 receptor agonists reduce post-ganglionic noradrenaline output and might therefore reduce the catecholamine surge during surgery. The European Mivazerol trial randomized patients with IHD who underwent intermediate- or high-risk non-cardiac surgery.
Mivazerol did not decrease the incidence of death or myocardial infarction in the whole population; however, there was a reduction of post-operative death or myocardial infarction observed in a sub-population of patients undergoing vascular surgery. Clonidine did not reduce the rate of death or non-fatal myocardial infarction in general, or in patients undergoing vascular surgery relative risk 1.
On the other hand, clonidine increased the risk of clinically important hypotension relative risk 1. Diuretics are frequently used in patients with hypertension or heart failure. In general, diuretics for hypertension should be continued to the day of surgery and resumed orally when possible.
If blood pressure reduction is required before oral therapy can be continued, other antihypertensive agents may be considered. In heart failure, dosage increase should be considered if symptoms or signs of fluid retention are present.
Dosage reduction should be considered in patients with hypovolaemia, hypotension, or electrolyte disturbances. In general, diuretic treatment—if necessary to control heart failure—should be continued to the day of surgery and resumed orally when possible. In the perioperative period, volume status in patients with heart failure should be monitored carefully and optimized by loop diuretics or fluids.
The possibility of electrolyte disturbance should be considered in any patient receiving diuretics. It is well known to significantly increase the risk of ventricular fibrillation and cardiac arrest in cardiac disease. In a study of patients with cardiac disease undergoing non-cardiac surgery, hypokalaemia was independently associated with perioperative mortality.
Special attention should be given to patients taking diuretics and patients prone to developing arrhythmias. Any electrolyte disturbance—especially hypokalaemia and hypomagnesaemia—should be corrected in due time before surgery. Acute pre-operative repletion in asymptomatic patients may be associated with more risks than benefits; thus, minor asymptomatic electrolyte disturbances should not delay acute surgery.
Perioperative evaluation of the impact of aspirin continuation or cessation on serious cardiovascular events or bleeding has disclosed controversial results with, on the one hand, a reduction of intra- and perioperative stroke—but without influence on myocardial infarction during non-cardiac surgery—and, on the other hand, no statistical significance for the combined endpoint of vascular events.
Additionally, concerns of promoting perioperative haemorrhagic complications have often led to the discontinuation of aspirin in the perioperative period.
A large meta-analysis, including 41 studies in 49 patients, which compared peri-procedural withdrawal vs. Patients less than six weeks after placement of a bare metal coronary stent, or less than one year after placement of a drug-eluting coronary stent, were excluded from the trial and the number of stented patients outside these time intervals was too small to draw firm conclusions as to the risk—benefit ratio. Patients started taking aspirin at a dose of mg or placebo just before surgery and continued it daily at a dose of mg for 30 days in the initiation stratum and for 7 days in the continuation stratum, after which they resumed their regular aspirin regimen.
Aspirin did not reduce the rates of death or non-fatal myocardial infarction at 30 days 7. Major bleeding was more common in the aspirin group than in the placebo group 4. The primary and secondary outcome results were similar in the two aspirin strata. The trial results do not support routine use of aspirin in patients undergoing non-cardiac surgery, but it is uncertain whether patients with a low perioperative bleeding risk and a high risk of thrombo-embolic events could benefit from low-dose aspirin.
Aspirin should be discontinued if the bleeding risk outweighs the potential cardiovascular benefit. In conclusion, the use of low-dose aspirin in patients undergoing non-cardiac surgery should be based on an individual decision, which depends on the perioperative bleeding risk, weighed against the risk of thrombotic complications. Five to twenty-five percent of patients with coronary stents require non-cardiac surgery within 5 years following stent implantation.
The prognosis of stent thrombosis appears to be worse than for de novo coronary occlusion, and premature cessation of dual anti-platelet therapy DAPT in patients with recent coronary stent implantation is the most powerful predictor for stent thrombosis. The consequences of stent thrombosis will vary according to the site of stent deployment, e. The management of anti-platelet therapy, in patients who have undergone recent coronary stent treatment and are scheduled for non-cardiac surgery, should be discussed between the surgeon and the cardiologist, so that the balance between the risk of life-threatening surgical bleeding on anti-platelet therapy—best understood by the surgeon—and the risk of life-threatening stent thrombosis off DAPT—best understood by the cardiologist—can be considered.
To reduce risk of bleeding and transfusion, current Guidelines recommend delaying elective non-cardiac surgery until completion of the full course of DAPT and, whenever possible, performing surgery without discontinuation of aspirin. While non-cardiac surgery performed early after balloon angioplasty is not associated with an increased risk of cardiac events, stenting dramatically changes the scenario.
Importantly, whenever possible, aspirin should be continued throughout surgery. A higher risk of non-cardiac surgery early after DES placement has been reported, and a higher risk for major adverse cardiac events has also been shown during the first weeks after non-cardiac surgery in patients with implanted stents.
Observational data from new-generation zotarolimus-eluting and everolimus-eluting stents suggest that even shorter durations of DAPT may be sufficient, and a randomized study showed a similar outcome in patients treated with 3 and 12 months of DAPT after PCI. In patients undergoing myocardial revascularization for high-risk ACS, DAPT treatment is recommended for 1 year irrespective of stent type. Overall, in patients undergoing non-cardiac surgery after recent ACS or stent implantation, the benefits of early surgery for a specific pathology e.
Independently of the timeframe between DES implantation and surgery, single anti-platelet therapy preferably with aspirin should be continued. In patients needing surgery within a few days, current ESC Guidelines recommend withholding clopidogrel and ticagrelor for five days and prasugrel for seven days prior to surgery unless there is a high risk of thrombosis.
For patients with a very high risk of stent thrombosis, bridging therapy with intravenous, reversible glycoprotein inhibitors, such as eptifibatide or tirofiban, should be considered. Cangrelor, the new reversible intravenous P2Y 12 -inhibitor, has been shown to provide effective platelet inhibition but is not yet available. Dual anti-platelet therapy should be resumed as soon as possible after surgery and, if possible, within 48 hours.
For patients receiving anti-platelet therapy, who have excessive or life-threatening perioperative bleeding, transfusion of platelets is recommended. Anticoagulant therapy is associated with increased risk of bleeding during non-cardiac surgery. In some patients, this risk will be outweighed by the benefit of anticoagulants and drug therapy should be maintained or modified, whereas, in patients at low risk of thrombosis, anticoagulation therapy should be stopped to minimize bleeding complications.
Patients treated with oral anticoagulant therapy using vitamin K antagonists VKAs are subject to an increased risk of peri- and post-procedural bleeding. In patients with a high thrombo-embolic risk, therapeutic doses of LMWH twice daily are recommended, and prophylactic once-daily doses in low-risk patients. Further adjustment of dose is necessary in patients with moderate-to-high kidney function impairment.
In patients with mechanical prosthetic heart valves, the evidence in favour of intravenous UFH is more solid; thus in some centres these patients are hospitalized and treated with UFH until four hours before surgery, and treatment with UFH is resumed after surgery until the INR is within the therapeutic range. LMWH or UFH is resumed at the pre-procedural dose 1—2 days after surgery, depending on the patient's haemostatic status, but at least 12 hours after the procedure.
Furthermore, the type of surgical procedure should be taken into consideration, as the bleeding risk varies considerably and affects haemostatic control. Procedures with a high risk of serious bleeding complications are those where compression cannot be performed. In these cases, discontinuation of oral anticoagulants and bridging therapy with LMWH are warranted.
In patients undergoing surgery with a low risk of serious bleeding, such as cataract- or minor skin surgery, no change in oral anticoagulation therapy is needed; however, it is wise to keep INR levels in the lower therapeutic range. An exception to this rule is the patient with high thrombo-embolic risk, whose surgical intervention is delayed for several days. In general, reduced kidney function or moderate-to-high increased bleeding risk should lead to earlier cessation of NOACs.
In patients who are receiving VKAs and who require reversal of the anticoagulant effect for an urgent surgical procedure, low-dose 2. The effect of vitamin K on INR will first be apparent after 6—12 hours.
If more immediate reversal of the anticoagulant effect of VKAs is needed, treatment with fresh-frozen plasma or prothrombin complex concentrate PCC , is recommended, in addition to low-dose intravenous or oral vitamin K. In patients receiving UFH and requiring reversal of the anticoagulant effect for an urgent surgical procedure, cessation of therapy is sufficient, because coagulation is usually normal four hours after cessation. When UFH is given subcutaneously, the anticoagulant effect is more prolonged.
For immediate reversal, the antidote is protamine sulphate. The dose of protamine sulphate can be calculated by assessment of the amount of heparin received in the previous two hours. The dose of protamine sulphate for reversal of a heparin infusion is 1 U per 1 U of heparin sodium. In patients who are receiving LMWHs, the anticoagulant effect may be reversed within eight hours of the last dose because of the short half-life.
When severe bleeding complications occur under the influence of NOACs, symptomatic treatment should be initiated Figure 2 because of the lack of specific antidotes these are currently under development. Preliminary data have shown a potential benefit for the use of PCC or activated PCC when bleeding occurs under the direct factor Xa inhibitor rivaroxaban, and is also applicable to apixaban and dabigatran, whereas haemodialysis is an effective method for eliminating dabigatran from the circulation but does not help when a direct factor Xa inhibitor has been used Figure 2.
Management of bleeding in patients taking non-vitamin K antagonist direct oral anticoagulants. From Camm et al. The role of routine, prophylactic, invasive, coronary diagnostic evaluation and revascularization in reducing coronary risk for non-cardiac surgery remains ill-defined.
Indications for pre-operative coronary angiography and revascularization, in patients with known or suspected IHD who are scheduled for major non-cardiac surgery, are similar to those in the non-surgical setting. There is, however, no indication for routinely searching for the presence of myocardial silent ischaemia before non-cardiac surgery. Coronary pathology underlying fatal perioperative myocardial infarctions revealed that two-thirds of the patients had significant left-main or three-vessel disease.
These findings suggest that a substantial proportion of fatal perioperative myocardial infarctions may have resulted from low-flow, high-demand ischaemia, owing to the stress of the operation in the presence of fixed coronary artery stenoses and therefore amenable to revascularization. In patients who underwent coronary angiography before vascular surgery, a number of non-fatal perioperative myocardial infarctions occurred as a consequence of plaque rupture in arteries without high-grade stenosis.
These results are not surprising, considering the extreme and complex stress situations associated with surgery—such as trauma, inflammation, anaesthesia, intubation, pain, hypothermia, bleeding, anaemia, fasting, and hypercoagulability—which may induce multiple and complex pathophysiological responses. Furthermore, the study showed that patients who were clinically stable in the years after CABG had a reduced risk of cardiac complications in the event that they required non-cardiac surgery.
It can be concluded that asymptomatic patients who underwent CABG within the previous six years are relatively protected from myocardial infarction complicating non-cardiac surgery and may undergo non-cardiac surgery without routine pre-operative stress testing.
As mentioned above, patients who have had a previous PCI may be at higher risk of cardiac events during or after subsequent non-cardiac surgery, particularly in cases of unplanned or urgent surgery following coronary stenting.
It is therefore preferable, whenever possible, to postpone elective surgery until 12 months after DES implantation. Giving clear recommendations on prophylactic revascularization in patients with asymptomatic or stable IHD is challenging, as most of the data are derived from retrospective studies and registries.
There was no difference in either mortality or perioperative myocardial infarction at 2. The results of the CARP study indicated that systematic prophylactic revascularization before vascular surgery does not improve clinical outcomes in stable patients.
A second prospective, randomized trial included patients, selected on the basis of a revised cardiac risk index, who were scheduled for major vascular surgery. While the rate of myocardial revascularization was higher in the systematic strategy group A recent randomized, prospective, controlled trial, focussing on a particular homogeneous subset of non-cardiac surgical interventions CEA , examined the value of pre-operative coronary angiography and stenting in patients without history of CAD or cardiac symptoms and with normal cardiac ultrasound and electrocardiography results.
The patients were randomized to pre-operative coronary angiography and—if needed—revascularization, or to no coronary angiography. The primary combined endpoint was the incidence of any post-operative myocardial ischaemic events combined with the incidence of complications of coronary angiography and stenting. In the non-angiography group, nine ischaemic events were observed 4. In this particular group of patients, the results suggest a short-term benefit of systematic coronary angiography.
Covering patients enrolled in 10 studies between the years and nine observational and the CARP randomized trial , a meta-analysis that addressed the value of pre-operative coronary revascularization before non-cardiac surgery revealed no significant difference between coronary revascularization and medical management groups, in terms of post-operative mortality and myocardial infarction OR 0.
Successful performance of a vascular procedure, without prophylactic revascularization, in a stable coronary patient, does not imply that the patient would not require subsequent revascularization.
Despite the lack of extensive scientific data, myocardial revascularization may be recommended in patients presenting with persistent signs of extensive ischaemia before elective non-cardiac surgery similar to non-surgical settings recommended by the ESC Guidelines. Occasionally, patients with stable IHD may require elective surgery, which may be postponed for several months and up to a year.
There are no solid data to guide a revascularization strategy in such a case. It seems reasonable to propose a cardiovascular work-up according to the ESC Guidelines on stable angina pectoris.
All patients considered for revascularization should receive optimal medical treatment. The timing of revascularization is critical and depends on the clinical presentation: stable vs. The type of revascularization, CABG vs. PCI, depends on the extent of CAD and technical feasibility and is discussed in detail in the ESC Guidelines on myocardial revascularization, 74 of which a new edition will be published in Percutaneous coronary intervention should be performed to improve symptoms in stable symptomatic patients with single or multi-vessel disease, in whom intervention is technically appropriate and procedural risk does not outweigh the potential benefit.
If PCI is performed before non-cardiac surgery, according to the previous edition of these Guidelines, BMS is advocated in order not to delay the surgery; however, if the data from recent trials evaluating newer DES devices are confirmed, this recommendation may no longer be valid and certain new-generation DES may be used in low-risk patients requiring early non-cardiac surgery. No trial has yet investigated the role of prophylactic revascularization in patients with NSTE-ACS requiring non-cardiac surgery; therefore, if the clinical condition requiring non-cardiac surgery is not life-threatening, priority should be given to the management of NSTE-ACS.
In the rare scenario of NSTE-ACS linked with the need for subsequent early non-cardiac surgery, at the time of PCI, preference should be given either to BMS, in order to avoid delaying surgery beyond 1 and preferably 3 months, or to new-generation DES if data from recent trials confirm non-inferiority.
The value of coronary revascularization for NSTE-ACS, in patients who later require non-cardiac surgery, has been addressed in a retrospective analysis covering 16 patients who, between and , had a myocardial infarction and underwent hip surgery, cholecystectomy, bowel resection, elective AAA repair, or lower extremity amputation in a period of up to three years following the myocardial infarction.
Drobnik, J. Knape, F. Petrini and L. Adriaensen, H. Blunnie, C. Carlsson, M. Dupont and T. Alahuhta, J.
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