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- Perioperative care
- myocardial infarction
- coronary thrombosis
- risk reduction
- platelet aggregation inhibitors
- risk stratification
- acute coronary syndrome
- antiplatelet treatment
- oral anticoagulants
Undergoing surgery imposes certain risks on the patient, such as impaired wound heeling, bleeding complications, perforations, nerve damage, and infection. These are all well known points of attention when planning a surgical procedure. Apart from these apparent risks directly related to the target area of the surgical procedure, there are other surgery related factors contributing to the outcome, that tend to be overlooked by the treating physicians. Of all contributors to poor postoperative outcome, cardiac complications are the most important, including myocardial infarction, congestive heart failure, stroke, and arrhythmias. An estimated 10–40% of postoperative mortality is attributed to myocardial infarction. With over 230 million surgical procedures being performed worldwide each year, the perioperative period is also a “golden hour” to initiate secondary prevention. Identification of risk factors for perioperative cardiac adverse events and risk stratification of surgery patients are the pillars for reducing cardiovascular complication rates.
The overall theme for perioperative care is to find the balance between risk reduction strategies, with a potential delay of the index surgical procedures, and its impact on the operation—for example, how to handle the controversy between haemorrhagic control and prevention of thrombosis related complications, such as myocardial infarction and stroke. Patients receiving antiplatelet therapy represent a surgical challenge, in terms of bleeding risk, while withdrawal can increase the risk of coronary thrombosis.
In this paper we aim to provide a comprehensive overview of the optimal medical management around the time of surgery, shedding light on all key issues.
Pathophysiology of surgical risks
Surgery causes physiological changes, affecting many organs apart from the primary target of the procedure. These changes can increase myocardial oxygen demand and reduce supply because of thrombosis, both leading to (fatal) myocardial ischaemia. The most important contributors to these pathophysiological pathways will be outlined briefly.
Stress and the oxygen mismatch
In the perioperative period, surgical stress induces a catecholamine surge, prompted by incisional tissue injury and mediated by neuroendocrine factors. The surgical stress causes an increase in heart rate and myocardial contractility, leading to an increased myocardial oxygen demand. Subsequently, an oxygen supply–demand mismatch can occur in patients with coronary artery disease. Another pathway of stress causing perioperative ischaemia is plaque rupture. The stress-induced increased mechanical activity of the heart can lead to shear stress on coronary plaques, increasing plaque instability with subsequent rupture or emboli. Plaque rupture and emboli decrease the oxygen supply, thus causing an increase in the oxygen mismatch, and the risk for myocardial infarction.
Inflammation and the oxygen mismatch
Apart from focal damage, surgery induces a generalised inflammatory response, with an increase of circulating C reactive protein, interleukin 6 (IL6), and tumour necrosis factor α. This response is further increased by the use of general anaesthesia. The progression of atherosclerosis can be propelled by increased IL6 and other inflammatory cytokines, leading to the genesis of more lesions and growth of existing atherosclerotic plaques. Increased levels of inflammation have also been linked to coronary plaque vulnerability and rupture.1 In short, the surgical inflammatory response can lead to a narrowing of the coronary lumina, and possible plaque rupture—both decreasing the oxygen supply to the myocardium.
Laparoscopy and thrombosis
Laparoscopic procedures cause minimal incisional tissue damage, but have another pathway leading to an increased cardiac risk. The increase in intra-abdominal pressure—due to the pneumoperitoneum created during surgery—reduces the venous return and therefore decreases cardiac output, increasing systemic vascular resistance. The decreased flow velocity that follows increases the risk of thrombus formation and growth. Taking this into account, patients undergoing minimally invasive surgery should be regarded as equivalent to those undergoing open surgery, in terms of cardiac risk stratification.
Hypercoagulability and thrombosis
Another consequence of surgery is a change in the balance of prothrombotic versus fibrinolytic factors (figure 1). Platelet activation and aggregation, with elevation of coagulation factors (eg, fibrinogen) on the one side, and a decrease in fibrinolysis on the other, can result in a state of hypercoagulability, increasing the risk of coronary artery thrombosis. This process predisposes to myocardial ischaemia and heart failure during and after the surgical procedure.
Preoperative risk assessment
An adequate risk assessment can serve multiple purposes. The predicted risk guides the preoperative workup, such as initiation of risk reduction strategies, and helps the selection of the best surgical and anaesthesiological techniques. Preoperatively, both the risk of the surgical procedure as well as the cardiac risk of the individual patient should be taken into account.
A distinction is made between surgical procedures with high, intermediate, and low cardiovascular risk. Based on estimates from Boersma et al, high risk surgery has an estimated 30 day postoperative cardiac event rate of >5%, intermediate risk surgery a 1–5% event rate, and low risk surgery <1%.2
The risk of cardiac complications should be assessed for each individual patient. Useful risk factors were identified by Lee et al in prospectively gathered data of 2893 patients, undergoing a variety of surgical procedures.3 Lee's risk index includes ischaemic heart disease (eg, angina pectoris or myocardial infarction), heart failure, stroke, diabetes, renal dysfunction, and surgical risk. With equal contributions from each risk factor, the incidence of cardiac complications increases with each added risk factor. In their paper, Lee et al found that in patients with 0, 1, 2, and ≥3 risk factors, the incidence of cardiac complications was 0.4%, 0.9%, 7%, and 11%, respectively. The predicted perioperative cardiac risk guides the initiation or continuation of medical treatments.
Antiplatelet management and thrombosis
Advances in interventional cardiology, radiology, and endovascular surgery have resulted in an increasing number of patients receiving antiplatelet therapy. Antiplatelet therapy is recommended for patients with, among others, atrial fibrillation, coronary artery disease, acute coronary syndrome (ACS), cerebrovascular disease, and chronic peripheral arterial disease, as well as patients who have been treated with bare metal stents (BMS), drug eluting stents (DES), endovascular prostheses or via carotid endarterectomy.4 According to existing guidelines, duration of antiplatelet therapy can vary from 6 weeks (eg, after BMS placement) to a lifelong continuation for some indications.5 Guidelines even recommend dual antiplatelet therapy (ie, aspirin and clopidogrel) for patients with non-ST segment elevation ACS. High risk patients with recurrent ischaemia, ST segment depression, troponin release, and diabetes may also receive a glycoprotein (Gp) IIb/IIIa receptor inhibitor, on top of aspirin and clopidogrel, as triple therapy.
Surgeons must beware of the balance between bleeding risk, when performing surgery under antiplatelet therapy, and the risk for thrombotic complications when discontinuing the antiplatelet agents. Perioperative withdrawal from single antiplatelet therapy precedes 10% of cardiovascular events, according to a meta-analysis by Burger et al.6 Collet et al found that in patients treated with antiplatelets after having received a DES or BMS, interruption of antiplatelet therapy led to death in up 25–50% of cases.7 Furthermore, surgery related inflammatory response and hypercoagulability may be especially hazardous in these thrombogenic patients. Therefore, it is essential to have an understanding of how to manage a patient receiving antiplatelet therapy, when considering a surgical procedure.
The most widely prescribed antiplatelet agent is acetylsalicylic acid, or aspirin. Aspirin is an anti-thrombotic agent that acetylates part of cyclo-oxygenase 1 (COX 1). This inhibits the release of thromboxane A2, which acts as a stimulator of platelet activation. Since platelets are unable to generate new COX 1, the affected platelets are impaired for the duration of their life.
Surgeons tend to instruct patients to stop taking aspirin no less than a week before surgery, because of concern about bleeding complications. For example, a 1.5-fold increase in the risk of bleeding complications was reported in a meta-analysis by Burger et al, without an increase in the severity of haemorrhagic complications. However, in patients at risk for or with ischaemic heart disease, perioperative aspirin withdrawal was associated with a threefold higher risk for major adverse cardiac events.8 There are no specific guidelines on the treatment of major bleeding episodes in surgical patients currently receiving aspirin treatment, but discontinuation of aspirin and platelet transfusions is a possible option in the case of an emergency.
Before planning surgery, the procedural bleeding risk and the individual risk of ischaemic events should be carefully weighed. In most cases, including minor and endoscopic surgery, continuing aspirin perioperatively is safe and advisable. Except for prostatectomy and intracranial surgery, low dose aspirin is not associated with an increased severity of bleeding nor perioperative mortality because of bleeding complications. If a planned surgical procedure is expected to experience very difficult haemostatic control, withdrawal from aspirin treatment 7 days before surgery can be considered. Not much guidance is available on preoperative aspirin withdrawal, or on restarting aspirin postoperatively. Future publication of the ASPIRIN trial (Antiplatelet Strategies in the Perioperative Period in Patients at Risk of Ischaemic Events) may provide definitive guidelines for patients taking aspirin in the perioperative period.4
Thienopyridines, of which clopidogrel is the most prescribed agent, have a different site of action on platelets, and therefore can be prescribed as double therapy beside aspirin, or as solitary prevention therapy in patients with high thromboembolic risk (eg, after coronary DES placement). Guidelines have recommended the implementation of clopidogrel following percutaneous coronary interventions (PCIs) and (non) ST-segment elevation myocardial infarction (STEMI).5 These indications illustrate the strong necessity for antiplatelet therapy, at the risk of (stent) thrombosis and cardiac ischaemia. Meta-analysis has shown that patients who prematurely discontinue clopidogrel treatment after coronary stent insertion are 10 times more likely to die or be readmitted during the following year.6 In comparison with aspirin, this new generation antiplatelet agent is more powerful, and has been called ‘a surgeon's headache’, due to its capacity to cause bleeding.
If a patient receiving clopidogrel treatment is planned for an operation, surgeons tend to discontinue the clopidogrel. However, consulting a cardiologist before discontinuation is warranted, considering the high thrombotic risk following clopidogrel withdrawal. In a report by Wilson et al, early (<6 weeks after coronary stenting) surgery with premature clopidogrel withdrawal was associated with an incidence of death, myocardial infarction or stent thrombosis of 4.8%, compared to no acute events in patients who underwent surgery >6 weeks after coronary stent placement.9
Collet and Montalescot designed an algorithm for patients receiving dual antiplatelet therapy after DES insertion, undergoing surgery.7 In this approach, bleeding risk and stent thrombosis risk should be assessed by the surgeon, an anaesthetist, and a cardiologist. If the risk for both bleeding and stent thrombosis is large, surgery should be postponed until the clopidogrel treatment is stopped—an approach supported by a review by Thachil et al.10 If delay is inadmissible, clopidogrel should be discontinued 5 days before surgery and aspirin should be continued. If the bleeding risk is small and there is a major risk of stent thrombosis, surgery should be performed under dual antiplatelet therapy.
If surgery is performed in a patient currently receiving clopidogrel therapy and a severe bleeding episode occurs, the drug should then be discontinued in agreement with a cardiologist. To reverse the effect of clopidogrel in severe bleeding cases, platelet transfusions can be considered, as well as administration of antifibrinolytic agents or recombinant factor VIIa, although these courses of action remain the subject of further investigation.
Prasugrel is a potent novel thienopyridine antiplatelet agent and has been shown in preclinical and clinical studies to achieve faster onset, higher levels of platelet inhibition, and less response variability than clopidogrel. This antiplatelet profile reflects more efficient generation of the active metabolite of prasugrel. As a consequence, the TRITON-TIMI 38 trial found that prasugrel was superior to clopidogrel, as measured by the composite end point of cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke in patients with ACS undergoing PCI, but was associated with a minor increase in the risk of bleeding. Future studies may address the additional perioperative bleeding risk of prasugrel, and the thrombotic risk of perioperative withdrawal, in (non) cardiac surgery.
Gp IIb/IIIa inhibitors
The third major class of antiplatelet agents are inhibitors of the Gp IIb/IIIa receptor, which plays a key role in the linking of activated platelets and the formation of platelet thrombi. These agents (ie, abciximab, cilostazol) have been tested in patients admitted with an ACS, patients undergoing thrombolytic therapy for acute myocardial infarction, and patients undergoing PCI or coronary artery bypass grafting (CABG).4 Triple therapy has been reported to improve cardiac outcome and survival in patients with acute STEMI undergoing PCI.11 Further studies and guidelines on the usefulness of Gp IIb/IIIa inhibitors in patients undergoing non-cardiac surgery have yet to be published.
Antiplatelet therapy and surgery
Alterations in antiplatelet therapy can best be deliberated between surgeon, anaesthetist, and cardiologist to ensure an optimal balance between the chance of bleeding and the risk of ischaemia.
Aspirin should be continued in surgery patients, unless there is a severe bleeding risk.
Clopidogrel should be discontinued before surgery.
However, if clinically admissible, delaying surgery until clopidogrel can be terminated safely is warranted.
If severe bleeding occurs in a surgical patient receiving clopidogrel treatment, discontinue clopidogrel in agreement with a cardiologist.
To counter the antiplatelet effect of clopidogrel, consider platelet transfusions.
More evidence is needed for guidelines on triple antiplatelet therapy around the time of non-cardiac surgery.
Anticoagulant management and thrombosis
In patients treated with oral vitamin K antagonists (VKA), more commonly known as coumarins (eg, warfarin, acenocoumarol, phenprocoumon), there is an increased risk of bleeding complications when performing non-cardiac surgery. In surgical procedures with an increased bleeding risk, anticoagulation should be discontinued. However, since these patients benefit from anticoagulant therapy, temporary cessation of these drugs can lead to thromboembolic events. There is a need for bridging therapy, consisting of low molecular weight heparin (LMWH) or unfractionated heparin (UFH). Thromboembolic risk is especially considered high in patients with atrial fibrillation, mechanical prosthetic heart valves, biological prosthetic heart valves or mitral valvular repair within the last 3 months, or recent venous thromboembolism (<3 months) plus thrombophilia, among other conditions.12 For bridging therapy, current guidelines prescribe discontinuation of VKA no less than 5 days before surgery, due to the long lasting biological availability of these agents. There are differences between agents in pharmacogenetics. For example, phenprocoumon has a longer lasting effect, and a more steady international normalised ratio (INR) throughout treatment, than acenocoumarol. Therefore, guidelines on anticoagulant withdrawal and INR control are generally helpful, but INR control in the individual patient is nevertheless warranted.
One day before surgery the INR should have decreased to <2.0, so that it can be expected to reach a level <1.5 on the day of surgery. Generally, if the INR is <1.5, any type of surgery can be performed safely.10 Otherwise, an oral dose of 1–2 mg of vitamin K1 can be administered 24 h before surgery, or considerations should be given to postponing the procedure.
The recommended daily dose of bridging LMWH is 70 anti-Xa U/kg, and should be administered subcutaneously. In high risk patients two daily doses should be administered. A timeline for discontinuation of VKA, bridging therapy and postoperative restarting of heparin and VKA is provided in the box below. As anticoagulation is restarted, extra attention should be paid to possible bleeding complications.
Anticoagulants and bridging therapy
Low bleeding risk
Continue anticoagulant therapy with INR in therapeutic range.
Low thromboembolic risk, high bleeding risk
Discontinue anticoagulants 5 days before surgery.
Start LMWH prophylaxis once daily or UFH intravenously 1 day after acenocoumarol interruption, and 2 days after warfarin interruption. Administer the last dose of LMWH at least 12 h before the procedure or give UFH intravenously up to 4 h before surgery.
Resume LMWH or UFH at preprocedure dose 1–2 days (at least 12 h) after the procedure according to haemostatic sufficiency. Resume VKA 1–2 days after surgery 150% of pre-procedure dose for 2 consecutive days according to haemostatic adequacy.
LMWH or UFH is continued until the INR returns to therapeutic levels.
High thromboembolic risk, high bleeding risk
Discontinue anticoagulants 5 days before procedure.
Start therapeutic LMWH twice daily or UFH intravenously 1 day after acenocoumarol interruption, and 2 days after warfarin interruption. Administer the last dose of LMWH at least 12 h before the procedure or give UFH intravenously up to 4 h before surgery.
Resume LMWH or UFH at preprocedure dose 1–2 days (at least 12 h) after the procedure according to haemostatic adequacy. Resume VKA 1–2 days after surgery 150% of pre-procedure dose for 2 consecutive days according to haemostatic sufficiency.
LMWH or UFH is continued until the INR has returned to therapeutic levels.
Medical management and oxygen mismatch
Risk reduction in the surgery patient population can be achieved by coronary revascularisation and medication. The focus for intervention is on plaque stabilisation and prevention of the oxygen supply/demand mismatch. Some perioperative medications (ie, β-blockers, statins) have been widely studied, and a good guideline on their treatment regimens has been published by Schouten et al.13 An update on the latest recommendations and developments on these agents are discussed briefly below.
The use of β-adrenoreceptor antagonists, or β-blockers, is primarily aimed at reducing the heart rate, counteracting the effect of the catecholamine surge, and reducing the oxygen supply–demand mismatch in order to prevent myocardial ischaemia occurring. A recent meta-analysis of 12 306 patients underlined the effect of β-blockade in high risk surgery patients on all cause mortality (63% decreased risk) and non-fatal myocardial infarction (44% decreased risk). In intermediate surgical risk patients, a 30% reduction of the risk of non-fatal myocardial infarction was found, at the expense of an increased risk of all cause mortality, non-fatal stroke, and hypotension.14 This was challenged by a recent randomised controlled trial in intermediate surgical risk patients, which showed improved perioperative outcome, without an increased rate of these complications.15
The introduction of esmolol, an ultra-short acting β-blocker, has provided a new tool to mitigate heart rate better but prevent hypotension. A recent meta-analysis including 1765 patients showed a decrease of myocardial ischaemia in non-cardiac surgery, without an increase in the rate of hypotension or bradycardia.16 In future guidelines, perhaps esmolol will take a prominent place in perioperative medical management.
Dosage and timing of β-blocker therapy have great influence on the treatment effect. According to guidelines, medical treatment should commence 30 days before surgery, with a low starting dose of 2.5 mg bisoprolol or 50 mg metoprolol succinate. Subsequently, the dose can be titrated to the preferred range of resting heart rate, which is around 60–70 beats/min.12 Peri- and postoperatively, intravenous β-blockade is warranted when oral administration is not possible.
Cardioprotective measures: β-blockers
β-blockers are recommended in patients with ischaemic heart disease or myocardial ischaemia on preoperative stress testing.
β-blockers are highly recommended in high risk surgery patients.
β-blockers are recommended in intermediate risk surgery patients.
β-blockers should be administered 30 days before surgery.
β-blockers should be titrated to a heart rate of 60–70 beats/min.
Short acting β-blockers can decrease hypotension and bradycardia rates.
In the process of cholesterol synthesis, the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA) plays a crucial role. HMG-CoA inhibitors, better known as statins, directly influence this process. Generally prescribed to patients for primary or secondary prevention of cardiac ischaemia, statins are renowned for their lipid lowering effect. Additionally, statins have so-called pleiotropic effects, adding to their cardioprotective value. These include decreasing lipid oxidation, inflammation, matrix metalloproteinase and cell death, and increasing tissue inhibitor of metallo-proteinase and collagen. It is these effects that may prevent plaque instability and subsequent rupture around the time of surgery.
Several reports on the effects of perioperative statins showed improved cardiac outcome, especially in high risk surgery patients. Meta-analysis of 18 studies including a total of 799 632 patients showed a 30–42% reduction of perioperative rates of death or ACS in patients taking statins.17 However, large prospective studies had not yet been performed. In the recently published DECREASE III trial by Schouten et al, a randomised controlled trial involving 497 vascular surgery patients, fluvastatin use (80 mg extended release) was associated with 10.8% myocardial ischaemia, compared to 19.0% in the placebo group.18
Lacking evidence in intermediate and low risk surgery, perioperative statin therapy is not recommended for these types of surgery. However, discontinuation of statins may be harmful, independent of surgery. Therefore, perioperative statin continuation is recommended regardless of the type of surgery. Lacking intravenous substitutes, the use of statins with a prolonged half-life (eg, atorvastatin or fluvastatin extended release) is preferable, to bridge the immediate postoperative period in which oral statin administration is impaired.12
Cardioprotective measures: statins
Perioperative continuation of current statin therapy is recommended.
Statins should be started 30 days before high risk surgery.
Statins with prolonged half-life are preferable.
Statins should be restarted as soon as possible, following postoperative withdrawal.
Angiotensin converting enzyme (ACE) inhibitors can be prescribed for patients with left ventricular (LV) systolic dysfunction (eg, postmyocardial infarction) as well as for hypertensive patients. ACE inhibitors have several effects on endothelial function and atherosclerosis, adding to the treatment effect in especially high risk patients. Regarding surgical patients, current studies do not support perioperative ACE inhibitor therapy as having added cardioprotective value.19 However, if a patient is receiving ACE inhibitor therapy preoperatively for LV dysfunction instead of hypertension, this should not be discontinued. If LV dysfunction is discovered preoperatively, it is preferable to start ACE inhibitor and β-blocker therapy, and therefore temporarily postpone surgery.20 Considering the type of surgery, starting perioperative ACE inhibitor therapy for LV systolic dysfunction in stable patients is more strongly advised in high risk surgery than intermediate risk surgery.12
Cardioprotective measures: ACE inhibitors
Withdrawal of ACE inhibitors for hypertension can be considered before non-cardiac surgery.
ACE inhibitor therapy in stable patients with LV systolic dysfunction should be continued during non-cardiac surgery.
Upon discovery of LV systolic dysfunction, ACE inhibitors should be started before high risk surgery.
Upon discovery of LV systolic dysfunction, starting ACE inhibitors can be considered before intermediate risk surgery.
Due to technical advancement and improved life expectancy, the surgical patient population is increasing in age and level of comorbidities. In an effort to decrease postoperative cardiac complications and death, optimal medical management is essential. Undergoing surgery has an accelerating effect on coronary atherosclerosis, increases inflammation, and induces a state of hypercoagulability in patients. Therefore, cardioprotective measures should be taken, especially in patients with a high risk of cardiac complications after surgery. Furthermore, increasing numbers of patients scheduled for surgery are treated with antiplatelet and/or anticoagulant therapy. These agents require strict management around the time of surgery, due to their ability to cause haemorrhage on the one hand and increased cardiac risks of withdrawal on the other.
As planning for surgery begins, cardioprotective measures are best initiated. Optimally, 30 days before surgery both β-blockade and statin therapy are recommended to start. Especially in high cardiac risk patients, these medications have proven to be beneficial in the perioperative period and in long term follow-up. Additionally, the use of antiplatelet therapy should be assessed. A cardiologist and an anaesthetist should be consulted if the planned procedure has such a high bleeding risk that withdrawal from antiplatelet therapy is considered by the surgeon. Antiplatelet—especially clopidogrel—withdrawal is often hazardous to the patient, and surgery should therefore be postponed until clopidogrel therapy has stopped, if possible.
Patients with current anticoagulant treatment should discontinue their therapy 5 days before most types of surgery. This will reduce the risk of bleeding during surgery, but it will increase the risk for thrombosis. In general, LMWH will be used as bridging therapy to reduce the perioperative thrombotic risk. LMWH therapy should commence 1 day after acenocoumarol or 2 days after warfarin, and be continued until 12 h before surgery. One or two days, and certainly no less than 12 h after surgery, LMWH bridging therapy can be continued. One or 2 days after surgery, anticoagulant therapy should be restarted at 150% of the preoperative daily dose for 2 days, and then continued at the preoperative daily dose. Heparin is discontinued when the INR reaches the therapeutic range.
This paper provides a comprehensive outline of the optimal perioperative medical management concerning cardiac risk in any surgical population, based on recent guidelines. We emphasise that knowledge of, and adherence to, current guidelines is essential for optimal care and safety of surgical patients.
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Review article providing insight into the association between inflammatory and morphological aspects of atherosclerotic lesions and vulnerability of the plaques.
Excellent review on different antiplatelet agents and their consequences in the perioperative period.
Practical review on management of surgical patients with current anticoagulant and antiplatelet therapy.
Retrospective analysis of 4203 STEMI patients who underwent PCI with drug eluting stents. This report shows a benefit for triple antiplatelet therapy (including cilostazol) in these patients, over dual therapy with aspirin and clopidogrel.
Most recent ESC guidelines for preoperative cardiac risk assessment and perioperative cardiac management in non-cardiac surgery. The ESC guidelines provide an overview of both evidence based and authority based information on the approach of a variety of patients in the perioperative period.
A comprehensive guideline on risk assessment and cardioprotective medication.
Randomised study in a two by two design with both bisoprolol and fluvastatin. This study shows the benefit of perioperative β-blockade but not of perioperative statin treatment in intermediate risk surgery patients.
Meta-analysis that assesses the possible benefit of esmolol as a new perioperative tool for cardiac risk reduction.
Large systematic review including 799 632 patients, to assess the value of statins as perioperative cardioprotective medication. This paper shows that especially high risk surgery patients may benefit, but little evidence is presented for routine administration of statins perioperatively.
Randomised controlled trial among 497 vascular surgery patients on the benefit of fluvastatin extended release as perioperative cardioprotective medication. This paper provides proof that, in high risk patients, statins have added value as perioperative cardioprotection.
Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. The authors have no competing interests.
Provenance and peer review Commissioned; not externally peer reviewed.
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