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• W2022269966 abstract "In this issue of Anaesthesia, Breen and colleagues report that mortality after major vascular surgery was significantly worse in 34 patients who had undergone coronary artery bypass grafting (CABG) within the previous month, compared with those who had undergone CABG 1–2 or 2–3 months previously or had not undergone CABG within 3 months [1]. The incidences of renal and heart failure were significantly higher and there was a trend towards a higher incidence of non-fatal myocardial infarction (MI) after major vascular surgery within 1 month of CABG. Furthermore, peri-operative mortality was significantly higher compared with control patients specifically matched for established peri-operative cardiovascular risk factors and type of surgery (20.6% vs. 3.9%, respectively). These results appear to contradict the current consensus that, in selected patients, CABG protects against cardiovascular events following subsequent major or high-risk surgery for 4–6 years, as long as symptoms have not recurred [2-4]. In the largest single series, the incidence of postoperative deaths in patients undergoing high-risk non-cardiac surgery was lower in those who had had prior CABG compared with medical therapy alone (1.7% vs. 3.3%) [5]. A combined incidence of 1.6% for death or peri-operative MI was reported in patients undergoing a variety of surgical procedures at a mean interval of 29 months after CABG or percutaneous transluminal coronary angioplasty (PTCA) [6]. CABG should only be performed if indicated because of the severity of coronary artery disease and not with the sole aim of improving outcome after planned subsequent non-cardiac surgery [2, 7]. However, most published data refer to patients in whom the interval between CABG and subsequent surgery was several months or years, many of the early studies predate modern cardiological practice including thrombolytic therapy and percutaneous coronary interventions (PCIs) and there are no randomised prospective studies of either the reduction in risk provided by prior CABG or the timing of CABG or PCIs on mortality after subsequent major surgery. Such studies would be difficult to perform and persisting controversies include: What is the optimal timing of subsequent planned surgery after CABG? What is the role of PCIs? Is there a role for combined coronary revascularisation and non-cardiac surgery, particularly if planned surgery is urgent? What is the optimum management for patients not amenable to coronary revascularisation? The study of Breen and colleagues has some limitations, including its retrospective design, the lack of data concerning peri-operative beta-blockade or angina in the control group, and the relatively small size of the subgroups. The dataset partially precedes recent guidelines on the indications for CABG [8] and on the management and investigations for patients with cardiovascular disease undergoing non-cardiac surgery [2, 3]. Aspects of peri-operative management (e.g. the use of beta blockade, statins and aspirin) and the indications for CABG have also changed during the study period. Nonetheless, Breen's 30-day mortality was low (1.5% overall, and 3.9% in the control group who had a high prevalence of known risk factors), comparing favourably with other large series [5, 9] so the high incidence of peri-operative mortality (20.6%) and complications in patients within 1 month after CABG (but no deaths in the 1–3 month groups) is conspicuous. Causes of death varied but were mostly cardiovascular (one embolic CVA, one sepsis and renal failure, three MIs and two sudden cardiac arrest; KW Park, personal communication). The incidence of postoperative renal failure was also unusually high, although chronic renal insufficiency was present in 29% and diabetes in 41%. Peri-operative death and complication rates are appreciably higher than previous reports where the CABG to non-cardiac surgery interval was much longer [5, 6, 9, 10]. The few reports of elective non-cardiac surgery within a short period (< 3 months) of CABG are all retrospective, most concern major vascular surgery and report low mortality rates [11-13], although reporting bias is likely. So how should we interpret Breen's data, which clearly suggest that performing non-cardiac surgery early after CABG carries significant risks? The indications for CABG are not clear but it seems likely that the non-cardiac surgery was deemed urgent. Since CABG can cause major changes in inflammatory, coagulation and fibrinolytic pathways with widespread cardiovascular, respiratory, renal and neurological effects, it is intuitive that sufficient time be allowed before subsequent non-cardiac surgery to permit adequate recovery. The American College of Cardiology (ACC) guidelines are not proscriptive but a minimum interval of 6 weeks between procedures is often assumed and an interval of 3 months has been recommended [14]. We should remember that, even without other surgery, overall mortality is greater in the first year after CABG compared with medical therapy [4]. In the absence of definitive data, decisions regarding the order and timing of CABG and non-cardiac surgery depend on the indications, risks and urgency of both [15]. PTCA and other PCIs are increasingly being used as alternatives to CABG in suitable patients. Initial complication rates from PTCA are lower, and overall short- and long-term outcomes are similar to CABG, although more subsequent interventions may be required. Early retrospective studies suggested good outcomes from non-cardiac surgery within weeks or months after PTCA [6, 16-18]. Conversely, Posner and colleagues reported that 26% of 686 patients undergoing PTCA within 90 days of subsequent non-cardiac surgery had adverse cardiac outcomes and twice the incidence of peri-operative MI compared with matched controls with uncorrected coronary artery disease (CAD) [19]. Over the last decade, several varieties of intracoronary stents (ICS), laser ablation, brachytherapy and thrombo-atherectomy have been introduced as adjuncts to PTCA. These have a better angiographic outcome, less requirements for emergency CABG and a lower rate of coronary restenosis than PTCA alone [20]. Early ICS were associated with a high risk of stent thrombosis and MI within the first 2 weeks [21, 22] and although the incidences of these are now < 1% as a result of advances in stent technology and antiplatelet drug regimens, the patient remains at risk until re-endothelialisation at the ICS site has occurred. Although theoretically attractive, the role of PCIs before planned non-cardiac surgery is not established. Disastrous results were reported in 40 patients undergoing non-cardiac surgery within 2 weeks after ICS placement but no deaths or MIs if surgery was performed at 2–6 weeks [23]. Eight of 25 patients undergoing surgery within 11 days of ICS died, and seven suffered MI. In addition, major haemorrhage occurred in 11 patients, five of whom died. Another study found a 4% incidence of death or MI in patients undergoing non-cardiac surgery within 6 weeks after ICS placement but no events when surgery occurred after 7–9 weeks [24]. Several mechanisms may contribute to this excessive peri-operative mortality early after PTCA or ICS. PTCA and ICS themselves stimulate systemic inflammatory and auto-immune responses with activation of platelets, coagulation and fibrinolytic pathways. The angioplasty site or ICS device is at risk of acute thrombosis particularly in the first few hours or days until re-endothelialisation at the site, but endothelial dysfunction may persist for some months [25]. Intimal hyperplasia may develop over the first few months leading to late coronary restenosis [4]. The additional effects of early non-cardiac surgery on the inflammatory, coagulation and fibrinolytic cascades may predispose to both bleeding and thrombotic complications, especially if antiplatelet therapy is interrupted [23]. In the absence of prospective data, the optimal timing of surgery after PCIs is uncertain but elective surgery should be postponed for 4–6 weeks after ICS insertion to allow re-endothelialisation under cover of antiplatelet medication [2, 24]. A recent review has suggested a delay of 3 months unless surgery is more urgent [14]. In patients with CAD who require elective non-cardiac surgery, coronary revascularisation (if indicated) should usually be performed first, provided the non-cardiac surgery can be delayed safely. However, in some cases (e.g. surgery for cancer, impending aneurysm rupture, trauma or limb salvage) non-cardiac surgery is urgent and delay for cardiological investigations or interventions would be harmful. Options here include reduction in the magnitude or cancellation of non-cardiac surgery, performance of non-cardiac surgery with appropriate cardioprotective measures, or simultaneous CABG and non-cardiac surgery. Although published data from some specialised centres suggest low mortality rates (4.8% or less) from simultaneous CABG and non-cardiac surgery [26, 27], other series describe mortality that is significantly higher and may exceed that from procedures performed separately [28]. Newer developments in cardiac surgery (e.g. off-pump bypass) may increase the feasibility of the combined approach. For example, recent series have reported no mortality from combined off-pump CABG and abdominal aortic aneurysm (AAA) repair and less morbidity compared with conventional CABG and AAA repair [29, 30]. Some patients with CAD are ineligible for coronary revascularisation, the indications for which depend on individual symptoms, coronary anatomy, cardiac function, coexisting disease and the potential to produce long-term benefit [8]. These patients are at high risk from peri-operative cardiac morbidity or death after major non-cardiac surgery, depending on their cardiac disease and comorbidity. Other groups at risk are those with CAD who require urgent non-cardiac surgery and those with CAD not amenable to revascularisation (because the CAD is diffuse or conversely not sufficiently severe to warrant intervention). Guidelines for investigation of these patients are established, but management is less well defined. Nevertheless, these situations occur frequently in clinical practice. If feasible, reduction in the magnitude of non-cardiac surgery (for example endoluminal AAA repair, laparoscopic or minimally invasive abdominal surgery or peripheral arterial angioplasty rather than conventional surgery) should be considered. In certain cases, deferment or cancellation of surgery may be the best option. However, many of these patients would benefit from beta-blockade. Several prospective and retrospective studies have shown that peri-operative beta blockade reduces morbidity and mortality in patients with cardiovascular risk factors [31, 32], or documented inducible myocardial ischaemia undergoing major non-cardiac surgery [33-35], and it has been suggested that they are administered to almost all patients undergoing major surgery [36]. Studies showing benefit from peri-operative beta blockade have logically assumed that reduction of heart rate to below a critical threshold value associated with myocardial ischaemia is important [31-33, 37]. The ACC guidelines suggest a target heart rate of 50–60 beat.min−1 in those with proven inducible ischaemia only [2] but in lower risk patients this target may be unnecessary. Further analysis of all patients enrolled in the DECREASE study showed that relative risk reduction from peri-operative beta-blockade depends on the number of clinical risk factors (age > 70 years, a history of current or previous angina, MI, stroke or heart failure) and the presence or absence of inducible ischaemia. In patients with ≤ 2 clinical risk factors, the incidence of death or MI was lower in beta-blocked patients (0.9% vs. 3.0% in non-beta blocked patients). However, in patients with ≥ 3 risk factors and inducible ischaemia the incidence of adverse cardiac events was 10% despite beta-blockade [34], and others have confirmed that chronic beta-blockade does not protect higher risk patients from peri-operative cardiac morbidity [38, 39]. The reasons for this are unclear. Furthermore the optimum duration, dose and role of individual regimens for beta-blockade are not established. A second paper in this issue of Anaesthesia has confirmed wide variation in the practice of peri-operative beta-blockade between Australasian teaching hospitals [40]. Although beta-blockers are administered in most institutions, only 10% reported the use of specific protocols. Duration of therapy before and after surgery, and postoperative monitoring of beta-blockade vary considerably. Although conclusions must be limited by the response rate of 64%, this rapid availability and access to cardiologists and cardiological investigations is unusual by UK standards. The wide awareness of the literature but enormous variations in practice is very similar to that of Canadian and UK anaesthetists [41, 42] and may reflect the lack of conclusive evidence for beta-blockade in intermediate or low risk patients undergoing major surgery [43] as recognised by the ACC guidelines [2]. This question is now being addressed by ongoing multicentre studies, including the POISE study, which aims to recruit 10 000 patients worldwide. Definitive guidelines are impossible until such data are available and variations in practice are inevitable. Beta-blockers are often well tolerated in patients with traditional contraindications (e.g. diabetes, reactive airway disease or left ventricular dysfunction) if titrated carefully, although many high-risk surgical patients do not receive beta-blockers when indicated and they are frequently omitted inappropriately in the postoperative period [44]. Conversely, beta-blockade can cause hypotension in patients with hypovolaemia, sepsis or concomitant epidural anaesthesia and may not always be beneficial in these circumstances. We should remember that peri-operative myocardial infarction is not a single phenomenon [45]. The final common pathway is thought to be similar to non-peri-operative MI (i.e. rupture of an unstable coronary plaque causing thrombosis, coronary occlusion and myocardial necrosis) [46]. Postoperative sympathetic nervous activity and stress may contribute to this (via changes in arterial pressure, heart rate, coronary arterial tone, inflammatory mediators, endothelial function, platelet and fibrinolytic activity), but many postoperative MIs occur in the absence of plaque rupture and outside the territory served by the most severely stenosed coronary arteries [46, 47]; these infarcts may not have been amenable to pre-operative revascularisation. Although postoperative tachycardia and prolonged myocardial ischaemia cause infarction in some patients, other factors are involved [45]. Beta-blockers may have cardio-protective effects independent of heart rate reduction (by altering gene expression and receptor activity, protecting against apoptosis and antiarrhythmic effects) [48], but other strategies to prevent peri-operative myocardial infarction (antiplatelet, anti-inflammatory or lipid-lowering drugs) [49, 50] may also be important. For example, statin therapy is invaluable in primary and secondary prevention of MI in non-surgical patients and perhaps should be prescribed for all high-risk surgical patients; the additive effects of peri-operative beta-blocker and statin therapy are unknown but they could conceivably decrease the need for PCIs or CABG. In conclusion, despite intensive research over the last two decades with established guidelines for the investigation and management of patients with cardiac disease presenting for non-cardiac surgery, a number of questions remain. The comparative effects of PCIs, CABG or medical therapy on peri-operative complications are unknown. The benefits of CABG and PCIs accrue gradually; subsequent surgery should ideally be delayed for at least 6 weeks and longer if possible, but more urgent surgery requires clinical judgement as to the risks and benefits of several options including the timing of surgery and aspects of peri-operative management. The advantages of beta-blockade in some patients are clear, but the optimum regimen, duration and value in lower risk patients are uncertain. As several factors are important in the pathogenesis of peri-operative MI, universal beta-blockade may not be a panacea and other measures are likely to be useful. The wide variation in current practice reflects gaps in our knowledge and disparities in service provision. Further data will become available but in the meantime high-risk patients will continue to require surgery. However, widespread changes in practice outside recognised guidelines should wait whilst the quest for answers continues." @default.
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• W2022269966 title "Ideal peri-operative management of patients with cardiovascular disease: the quest continues" @default.
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