D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Estimation of cardiac risk prior to noncardiac surgery

PURPOSE OF PREOPERATIVE EVALUATION

-Evaluate patient’s current medical status -Provide clinical risk profile -Provide recommendations for management in the perioperative period -Not to give “cardiac clearance” -Alter or cancel the planned procedure -Recommend revascularization if outcome would be altered -Currently high-quality evidence suggests that coronary revascularization

before major noncardiac surgery is of limited or no benefit in stable patients; however, this cannot be generalized to patients with left main or severe triple vessel disease because of the absence of data in these groups.

-Importantly, the risk of thrombosis after PCI is high and the hypercoagulable perioperative state increases the probability of this occurring.

= Indiscriminate and extensive preoperative cardiac testing is an ineffective way of using health care funds and can lead to more unwarranted and risky procedures. In addition to the inappropriate expenditure of resources, unnecessary testing could cause harm to the patient by delaying surgery. 

--Three elements must be assessed to determine the risk of cardiac events:

Patient specific clinical variablesExercise capacitySurgery-specific risk

--The American College of Cardiology National Database Library defines recent MI as greater than seven days but ≤30 days..

Minor predictors:Minor risk factors are recognized markers for cardiovascular disease that have not been definitively proven to independently increase perioperative risk and were not included in the recommendations for treatment by the ACC/AHA perioperative guidelines:

-Advanced age (greater than 70 years of age)-Abnormal ECG (left ventricular hypertrophy, left bundle branch block, ST-T wave abnormalities)-Rhythm other than sinus (such as atrial fibrillation)-Uncontrolled systolic hypertension(The presence of more than one of these may lead to a higher suspicion of coronary artery disease.)

Surgical factors that influence cardiac risk:-Related to the urgency, invasiveness, type, and duration of the procedure, as well as the change in body core temperature, blood loss, and fluid shifts. -Every operation elicits a stress response initiated by tissue injury mediated by neuro-endocrine factors, and may induce sympathovagal imbalance. -Fluid shifts in the peri-operative period add to the surgical stress increases myocardial oxygen demand. -Surgery also causes alterations in the balance betweenprothrombotic and fibrinolytic factors, potentially resulting in increased coronary thrombogenicity.

=In general, endoscopic and endovascular techniques speed recovery, decrease hospital stay, and reduce the rate of complications.However, randomized clinical trials comparing laparoscopic with open techniques exclude older, sicker, and ’urgent’ patients, and results from an expert-based randomized trial (laparoscopic vs.open cholecystectomy) have shown no significant differences in conversion rate, pain, complications, length of hospital stay, or re-admissions.-Increased intra-abdominal pressure, pneumoperitoneum and Trendelenburg position increased mean arterial pressure, central venous pressure, mean pulmonary artery, pulmonary capillary wedge pressure, and systemic vascular resistance impairing cardiac function cardiac risk in patients with heart failureis not reduced in patients undergoing laparoscopy, and both should be evaluated in the sameway.

=Although it is a less-extensive intervention, infrainguinal revascularization entails a cardiac risk similar to—or even higher than—that of aortic procedures. This can be explained by the higher incidence of diabetes, renal dysfunction, IHD, andadvanced age in this patient group.

=Endovascular AAA repair (EVAR) has been associated with lower operative mortality and morbidity than open repair but this advantage reduces with time, due to more frequent graft-relatedcomplications and re-interventions in patients who underwent EVAR, resulting in similar long-term AAA-related mortality and total mortality.

=A meta-analysis of studies, comparing open surgical with percutaneous transluminal methods for the treatment of femoropopliteal arterial disease, showed that bypass surgery is associated with higher 30-day morbidity and lower technical failurethan endovascular treatment, with no differences in 30-day mortality;however, there were higher amputation-free and overall survival rates in the bypass group at 4 years. Therefore, multiple factors must be taken into consideration when deciding which type of procedure serves the patient best. -An endovascular-first approach may be advisable in patients with significant comorbidity, whereas a bypass procedure may be offered as a first-line interventional treatment for fit patients with a longer life expectancy

=Carotid artery stenting has appeared as an attractive, less-invasivealternative to CEA; however, although CAS reduces the rate of periprocedural myocardial infarction and cranial nerve palsy, thecombined 30-day rate of stroke or death is higher than CEA,particularly in symptomatic and older patients.-The benefit of carotid revascularization is particularly high inpatients with recent (<3 months) transient ischaemic attack(TIA) or stroke and a >60% carotid artery bifurcation stenosis.-In neurologically asymptomatic patients, carotid revascularizationbenefit is questionable, compared with modern medicaltherapy, except in patients with a >80% carotid stenosis and anestimated life expectancy of >5 years

History

--Known cardiac disease.--The assessment of functional ability provides valuable prognostic information, since patients with good functional status have a lower risk of complications. Functional status can be expressed in metabolic equivalents (1 MET is defined as 3.5 mL O2 uptake/kg per min, which is the resting oxygen uptake in a sitting position). Perioperative cardiac and long-term risk is increased in patients unable to meet a 4-MET demand during most normal daily activities:*Can take care of self, such as eat, dress or use the toilet (1 MET)*Can walk up a flight of steps or a hill (4 METs)*Can do heavy work around the house such as scrubbing floors or lifting or moving heavy furniture (between 4 and 10 METs)*Can participate in strenuous sports such as swimming, singles tennis, football, basketball, and skiing (>10 METs)-- However, the presence of PAD may be an important limitation to assessment of functional capacity since such patients often cannot exercise because of claudication.

Notably, when functional capacity is high, the prognosis is excellent, even in the presence of stable IHD or risk factors; otherwise, when functional capacity is poor or unknown, the presence and number of risk factors in relation to the risk of surgery will determine pre-operative risk stratification and peri-operative management.

Physical examination

--Blood pressure measurements in both arms--Analysis of carotid artery and jugular venous pulsations for the quality of the pulse contour and the presence of bruits--Auscultation of the lungs--Precordial palpation and auscultation--Abdominal palpation--Examination of the extremities for edema and vascular integrity. --Important findings include evidence of HF or a murmur suspicious for aortic stenosis (AS), since poorly controlled HF and significant AS increase perioperative risk.--The presence of Q waves or significant ST segment elevation or depression have been associated with an increased incidence of perioperative cardiac complications.

-Each of the six risk factors was assigned one point. Patients with none, one, or two risk factor(s) were assigned to RCRI classes I, II, and III, respectively, and patients with three or more risk factors were considered class IV. -The risk associated with each class was 0.4%, 1%, 7%, and 11% for patients in classes I, II, III, and IV, respectively.

-However, developed years ago and many changes have since occurred in the treatment of IHD and in the anaesthetic, operative and peri-operative management of non-cardiac surgical patients.Gupta preoperative risk-However, some peri-operative cardiac complications such as pulmonary oedema and complete heart block, were not considered. By contrast, the Lee index allows estimation of the risk of peri-operative pulmonary oedema and of complete heart block, in addition to death and myocardial Infarction

=Risk models do not dictate management decisions but should beregarded as one piece of the puzzle to be evaluated, in concertwith the more traditional information

American Society of Anesthesiologists (ASA)

Biomarkers

Based on the existing data, assessment of serum biomarkers for patients undergoing non-cardiacsurgery cannot be proposed for routine use, but may be considered in high-risk patients (METs ≤4 or with a revised cardiac risk index value >1 for vascular surgery and >2 for non-vascular surgery).

Non-invasive testing

-Pre-operative LV systolic dysfunction, moderate-to-severe mitral regurgitation, and increased aortic valve gradients are associated with major cardiac events.-The limited predictive value of LV function assessment for peri-operative outcome may be related to the failure to detect severe underlyingIHD.

Exercise testing

--Exercise ECG testing is usually the preferred stress test since exercise tolerance is an important predictor of outcome that appears to be more important than the ECG response. --Exercise ECG testing is usually performed with perfusion imaging or echocardiography since imaging can better identify high-risk features that would warrant referral for angiography (eg, reversible large anterior wall defect, multiple reversible defects, ischemia occurring at a low heart rate, extensive stress-induced wall motion abnormalities, transient ischemic dilatation).

--In addition, concurrent imaging is essential if the resting ECG has abnormalities that can interfere with the detection of ischemia during exercise stress. These include preexcitation (Wolff-Parkinson-White) syndrome, a paced ventricular rhythm, more than 1 mm of ST depression at rest, complete left bundle branch block, and patients taking digoxin or with ECG criteria for left ventricular hypertrophy, even if they have less than 1 mm of baseline ST depression. --Pharmacologic stress testing is preferred in patients with abdominal aortic aneurysms ≥6.0 cm in diameter or aneurysms that are symptomatic. It is appropriate to control hypertension prior to stress testing in patients with aneurysms.

--Dipyridamole-thallium imaging is usually preferred in patients with known cardiac arrhythmias, since dobutamine can induce atrial or ventricular arrhythmias.--Dobutamine echocardiography is preferred in patients with bronchospastic lung disease and in those with severe carotid stenosis, because dipyridamole can induce bronchospasm and a decrease in blood pressure. It is also preferred when information about left ventricular function or valvular heart disease is desired. Dobutamine appears to be safe in patients with abdominal aortic aneurysms. {patients with ≥5 segments involved had more cardiac events than those with limited stress-induced ischemia }--DSE has some limitations: it should not, for example, be used in patients with severe arrhythmias, significant hypertension, large thrombus-laden aortic aneurysms, or hypotension.--DSE has a high negative predictive value and a negative test is associated with a very low incidence of cardiac events in patients undergoing surgery; however, the positive predictive value is relatively low (between 25% and 45%)

-The onset of a myocardial ischaemic response at low exercise workloads is associated with a significantly increased risk of peri-operative and long-term cardiac events. In contrast, the onset of myocardial ischaemiaat high workloads is associated with only a minor risk increase, but higher than a totally normal test.-Reversible ischaemia in <20% of the LV myocardium did not alter the likelihood of peri-operative cardiac events, compared with those without ischaemia*.

EXERCISE STRESS TESTING

Mean sensitivity for Dx of CAD 68%

Mean specificity77%

Sensitivity for 3-vessel dis.86%

Negative predictive value93%

**Patients with ACTIVE cardiac conditions (eg, unstable coronary syndromes, decompensated heart failure, significant arrhythmias, or severe valvular stenosis) not undergoing emergency surgery should first be managed according to ACC/AHA guidelines:

**Patients without active cardiac symptoms undergoing low risk surgery OR those with good functional capacity (MET level ≥4) require no preoperative testing aside from an ECG.

**Patients with poor or unknown functional capacity, or potential cardiac symptoms who are scheduled to undergo intermediate risk or vascular surgery are managed according to the number of clinical risk factors.

IHD

**The main indications for noninvasive testing in asymptomatic patients are estimated high risk (≥3 revised cardiac index criteria) or intermediate risk (1 to 2 revised cardiac index criteria) plus poor or indeterminate functional status, a history consistent with coronary disease, or high-risk surgery **2007 ACC/AHA guidelines (not changed in the 2009 focused update) and the 2009 ESC/ESA guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery, which recommend coronary revascularization for symptomatic patients with: (1) high-risk unstable angina or non-ST-elevation MI(2) acute ST-elevation MI(3) angina and left main or three-vessel disease(4) angina and two-vessel disease if this includes proximal LAD stenosis as well as LV dysfunction or ischemia on stress testing**Angiography is only warranted in a small number of asymptomatic patients undergoing noncardiac surgery (2 to 11 percent in series following the ACC/AHA and ESC/ESA algorithms).

Revascularization

-Control of myocardial ischaemia before surgery is recommended whenever non-cardiac surgery can be safely delayed. There is, however, no indication for routinely searching for the presence of myocardial (silent) ischaemia before non-cardiac surgery.-Coronary pathology underlying fatal peri-operative myocardialinfarctions revealed that two-thirds of the patients had significantleft-main or three-vessel disease Most of the patients did notexhibit plaque fissuring and only one-third had an intracoronarythrombussubstantial proportion of fatal peri-operative 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.

-CASS:protective effect of previous coronary revascularization was more pronounced in patients with triple-vessel CAD and/or depressed LV function, as well as in those undergoing highrisk surgery, and lasted for at least six years; however, the study was performed at a time when medical therapy did not meet currentstandards.-Covering 3949 patients enrolled in 10 studies between the years 1996 and 2006 (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 significantdifference between coronary revascularization andmedicalmanagement groups, in terms of post-operative mortality and myocardial infarction There were no long-term outcome benefits associated with prophylactic coronary revascularization

Recent PCI

--2007 ACC/AHA guideline (not changed in the 2009 focused update) suggested the following approach in patients who require PCI and need subsequent surgery:

*If the bleeding risk of surgery is low, stenting may be performed and dual antiplatelet therapy continued.*If the bleeding risk of surgery is not low, balloon angioplasty is suggested for surgery needed in 14 to 29 days {Delay surgery for at least one week to permit healing of vessel injury at the balloon treatment site }, bare metal stenting for surgery needed in 30 to 365 days (ESC 2014 minimumof 4weeks and ideally for up to 3 months ), and drug-eluting stenting for surgery needed after 365 days(ESC 2014 routine extension of DAPT beyond 6 months is no longer recommended in new generations)*Balloon angioplasty — <14 days: delay surgery; >14 days: proceed with aspirinBare metal stent: <30 to 45 days: delay surgery; >30 to 45 days: proceed with aspirinDrug eluting stent: <365 days: delay surgery; >365 days: proceed with aspirin

ESC/ESA 2014

In summary, it is recommended that DAPT be administered for at least 1 month after BMS implantation in stable CAD, for 6 months after new-generation DES implantation, and for up to 1 year in patients after ACS, irrespective of revascularization strategy. Importantly, a minimum of 1 (BMS) to 3 (new-generation DES) months of DAPT might be acceptable, independently of the acuteness of coronary disease, in cases when surgery cannot be delayed for a longer period

PCI+urgent surgery

--Platelet P2Y12 receptor blocker should be discontinued for as brief a period as possible while aspirin therapy continues uninterrupted. --The concept of bridging a gap in platelet P2Y12 receptor blocker therapy using an intravenous glycoprotein IIb/IIIa inhibitor such as tirofiban is under investigation .--Some experts are willing to recommend shorter discontinuation periods, perhaps up to three days before either cardiac or noncardiac surgery, and for procedures less likely to be associated with major bleeding. On the other hand, consideration may be given to discontinuing platelet P2Y12 receptor blocker at least seven days before intracranial surgery, given the potentially disastrous consequences of intracranial bleeding.--Platelet P2Y12 receptor blocker therapy should be restarted with a loading dose of 300 mg as soon as possible after surgery, perhaps even later in the day, if postoperative bleeding has stopped. Some experts recommend a higher loading dose of 600 mg to decrease time to effectiveness in the higher risk postoperative setting.--Aspirin should be continued during this period if possible and not be discontinued without confirming absolute necessity.

-Use of heparin or short-acting GP2b/3a inhibitors is not routinely recommended in patients being withdrawn from clopidogrel because of lack of evidence and concern for rebound platelet hyperactivity, especially in absence of ASA, with or without clopidogrel treatment.-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, the use of low-molecular-weight heparin (LMWH) for bridging in these patients should be avoided.-For patients receiving anti-platelet therapy, who have excessive or life-threatening peri-operative bleeding, transfusion of platelets is recommended.- ESC 2014 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-In addition, it is suggested that surgery be performed in centers with 24 hour interventional cardiology coverage . Thrombolysis is not very effective because stent thrombosis is mainly a platelet-mediated event.

ASA

--The use of low-dose aspirin in patients undergoingnon-cardiac surgery should be based on an individual decision, which depends on the peri-operative bleeding risk, weighed against the risk of thrombotic complications.--For patients undergoing spinal surgery or certain neurosurgical or ophthalmological operations,it is recommended that aspirin be discontinued for at least seven days.

Acute MI, high-riskACS, or high-riskcardiac anatomy

Bleeding risk of surgery

LowStent and continueddual-antiplatelettherapy

Not low

Timing of surgery

14 to 29 days 30 to 365 days > 365 days

Balloonangioplasty

Bare-metalstent

Drug-elutingstent

Valvular heart disease

--Echocardiography should be performed in order toassess its severity and consequences esp in cardiac murmur. --In the presence of severe VHD, clinical and echocardiographic evaluation be performed and, if necessary, treated before non-cardiac surgery.--The key issues:to assess the severity of VHD, the symptoms and their relationship to VHD, and the estimated risks of valvular intervention and of cardiac complications according to the type of non-cardiac surgery

Significant valvular heart disease: AS

--Percutaneous balloon valvotomy critically ill awaiting surgery , pregnant symptomatic{risky}--ACC/AHA guidelines concluded that most asymptomatic patients with severe AS can undergo urgent noncardiac surgery at relatively low risk with careful intraoperative and postoperative management, including monitoring of anesthesia and careful attention to fluid balance Balloon valvotomy was not recommended; aortic valve replacement should be considered if preoperative correction of AS is warranted----Control heart rate (particularly in MS), to avoid fluid overload as well as volume depletion and hypotension (particularly in AS)--European 2012

Mitral stenosis

--Non-cardiac surgery can be performed with relatively low levels of risk in patients with non-significant mitral stenosis (valve area> 1.5 cm2) and in asymptomatic patients with significant mitral stenosis (valve area <1.5 cm2) and systolic pulmonary artery pressure <50 mm Hg.--Control heart rate (particularly in MS), to avoid fluid overload

AR, MR

--Symptomatic patients—and those who are asymptomatic with severely impaired LVEF (<30%)—are at high risk of cardiovascular complications, and non-cardiac surgery should be performed only if necessary

--Secondary mitral regurgitation should undergoperi-operative evaluation and management according to the recommendations for LV systolic dysfunction or IHD

Mitral stenosis

Prosthetic valves

-According to the ACC guidelines, those patients with a bileaflet mechanical AVR with no risk factors (ie, AF, previous thromboembolism, LV dysfunction, hypercoagulable conditions, older generation thrombogenic valves, mechanical tricuspid valves, or more than one mechanical valve) should stop their warfarin 48 to 72 hrs before the procedure (so the INR falls to 1.5) and restarted within 24 hrs after the procedure.Heparin is usually unnecessary. -In those patients at high risk of thrombosis (defined as those with any mechanical MV replacement, or a mechanical AVR with any risk factor), therapeutic doses of IV UFH should be started when the INR falls below 2.0 (typically 48 hrs before surgery), stopped 4 to 6 hrs before the procedure, restarted as early after surgery as bleeding stability allows, and continued until the INR is again therapeutic with warfarin therapy.-Certain underlying conditions such as previous bacterial endocarditis are associated with a relatively high risk of IE (ie, previous endocarditis, mechanical valve replacement, congenital heart disease with shunt and transplant valvulopathy).

Vitamin K antagonists

- (INR) is ≤1.5, surgery can be performed safely-Patients with a high risk of thrombo-embolism—for example, patients with:† AF with a CHA2DS2-VASc score of ≥4] or† mechanical prosthetic heart valves, newly inserted biological prosthetic heart valves, or† mitral valvular repair (within the past 3 months) or† recent venous thrombo-embolism (within 3 months) or† thrombophilia needbridging therapy with unfractionated heparin (UFH) or therapeutic-dose LMWH--It is recommended that VKAtreatment be stopped 3–5 days before surgery (depending on the type of VKA),with daily INR measurements, until ≤1.5 is reached, and thatLMWHor UFH therapy be started one day after discontinuation of VKA—or later, as soon as the INR is <2.0.-UFH is resumed after surgery until the INR is within the therapeutic range-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.

NOACs

-The overall recommendation is to stop NOACs for 2–3 times their respective biological half-lives prior to surgery in surgical interventions with ‘normal’ bleeding risk, and 4–5 times the biological half-lives before surgery in surgical interventions with high bleeding risk.-Because of the fast ‘on’-effect of NOACs (in comparison with VKAs), resumption of treatment after surgery should be delayed for 1–2 (in some cases 3–5) days, until post-surgical bleeding tendency is diminished.

AC+Emergency surgery

VKA:-(2.5–5.0 mg) intravenous or oral vitamin K is recommended. -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 tolow-dose intravenous or oral vitamin K.Heparin:-1 mg of protamine sulphate will usually neutralise at least 100 international units of mucous heparin or 80 units of lung heparin. The dose of protamine sulphate should be reduced if more than 15 minutes have elapsed since intravenous injection.-For example, if 30-60 minutes have elapsed since heparin was injected intravenously, 0.5-0.75 mg protamine sulphate per 100 units of mucous heparin is recommended. If two hours or more have elapsed, 0.25-0.375 mg per 100 units of mucous heparin should be administered.-If the patient is receiving an intravenous infusion of heparin, the infusion should be stopped and 25-50 mg of protamine sulphate given by slow intravenous injection.-If heparin was administered subcutaneously, 1 mg protamine sulphate should be given per 100 units of mucous heparin – 25-50 mg by slow intravenous injection and the balance by intravenous infusion over 8-16 hours.

LMWH:-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. If immediate reversal is required, intravenous protamine sulphate can be used, but anti-Xa activity is never completely neutralized (maximum 50%).(Protamine sulphate should be administered by slow intravenous injection over a period of ten minutes. Not more than 50 mg of protamine sulphate should be given in any one dose.)

Decompensated heart failure

--A reduced LVEF of ≤35% was found to be a strong predictor of post-operative cardiac events--Echocardiography is not routinely indicated for assessing left ventricular systolic function in clinically stable patients.--Echocardiography is reasonable in patients with symptoms or signs of new or worsening HF, evaluation of inferior vena cava diameter for the determination of volume status and right atrial pressure. --Asking patients about the distance they can walk and number of stairs they can climb can help stratify risk.--The cause of new or newly decompensated heart failure HF identified by preoperative history and physical examination should be evaluated before major elective surgery.--Signs of HF at the time of surgery probably confer greater risk than a history of prior HF that is compensated at the time of the preoperative examination.-- In the absence of new or active myocardial ischemia, postoperative pulmonary edema does not affect long-term prognosis.

--The best assessment of a patient’s overall functional capacity is achieved by performing a cardiopulmonary exercise test (CPX/ CPET). Both the cardiac and pulmonary reserve and their interaction can then be evaluated. --An anaerobic threshold of <11 mL O2/kg/min has been used as a marker of increased risk……Still waiting accumulation of data

--Decompensated HF should be optimally treated before major elective surgery, euvolemic before elective surgery, with stable blood pressure and optimal end-organ perfusion.. Postponement of surgery may be appropriate until this is accomplished.--Routine initiation of perioperative beta blocker therapy is of unproven benefit and associated with potential harm. There is some evidence supporting benefit in patients at particularly high risk (eg, revised Goldman cardiac risk index ≥3); HF is one risk factor in this model. In such patients, beta blocker therapy should optimally be initiated weeks or more before surgery.--The routine use of perioperative invasive monitoring is not recommended. Such monitoring may be considered in unstable patients with HF requiring immediate surgery.--Patients found to have postoperative HF should be evaluated for new or unstable myocardial ischemia. If there is no evidence for new or active ischemia, pulmonary edema should be initially managed with diuretics.

-Consider the possibility of giving the medications via nasogastric tube or bioequivalent intravenous dose.-Regarding patients with LV-assist devices, who arescheduled for non-cardiac surgery, they should be evaluated pre-operatively by the centre responsible for implantation and follow-up--HF-PEF:Adequate peri-operative monitoring, attention tovolume status, control of afterload, and adequate diuretic treatment

Arrhythmias

--Ventricular arrhythmias, including ventricular premature beats (VPBs) and ventricular tachycardia (VT) are particularly common in high-risk patients. --Monomorphic VT may result from myocardial scarring, and polymorphic VT is a common result of acute myocardial ischaemia.--Pre-operative detection of these arrhythmias should therefore lead to evaluation including methods such as echocardiography, coronary angiography (with revascularization) and, in selected cases, invasive electrophysiological study, as appropriate. --Treatment steps for VPBs include identifying and correcting the reversible causes (e.g. hypoxia, hypokalemia and hypomagnesaemia).There is no evidence that VPBs or non-sustained VTs alone are associated with aworse prognosis or that suppressive therapy is beneficial.--Sustained monomorphic VT with haemodynamic compromise must be treated promptly with electric cardioversion. Intravenous amiodarone can be used for initial treatment of patients with stable sustained monomorphic VT, to prevent recurrences

--Beta-blockers are useful in patients with recurrent sustained polymorphic VT, especially if ischaemia is suspected or cannot be excluded. --Amiodarone is reasonable for patients with recurrent sustained polymorphic VT in the absence of long QT syndrome. --Torsades de pointes (TdP) : -Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended. -Management with magnesium sulphate should be considered for patients with TdP and long QT syndrome. -Beta-blockade, combined with temporary pacing, is suggested in patients with TdP and sinus bradycardia. -Isoproterenol is recommended in patients with recurrent, pause-dependent TdP, who do not have congenital long QT syndrome.--If the diagnosis is unclear, wide-QRS tachycardia should be presumed to be VT until proven otherwise. --Calcium channel blockers, such as verapamil and diltiazem, should not be used in patients to terminate wide-QRS-complex tachycardia of unknown origin

SVT, AF

--While initiating specific drug therapy, possible aggravating factors such as respiratory failure or electrolyte imbalance should also be corrected--No medication is recommended to suppress supraventricular premature beats--Vagal manoeuvres may terminate SVT in some cases; they usually respond well to treatment with adenosine. --In cases with incessant or commonly recurring SVT, beta-blockers, calcium channel blockers, or amiodarone treatment can be used.--In rare cases (and taking into account the urgency and nature of planned surgery), pre-operative catheter ablation of the arrhythmia substrate may be considered, e.g. for patients with Wolff-Parkinson- White syndrome and pre-excited AF.--The objective in managing peri-operative AF is usually ventricular rate control beta-blockers and calcium channel blockers (verapamil, diltiazem) are the drugs of choice--Amiodarone can be used as a first-line drug in patients with heart failure, since digoxin is frequently ineffective in high adrenergic states such as surgery. --Beta-blockers have been shown to accelerate the conversion of AF to sinus rhythmin the intensive care unit (ICU) after non-cardiac surgery. --Anticoagulation must be based on the individual clinical situation.

Peri-operative bradyarrhythmias

--Usually respond well to short term pharmacological therapy; temporary cardiac pacing is rarely required.--Pre-operative establishment of temporary or permanent cardiac pacing may be appropriate for patients with complete heart block or symptomatic asystolic episodes.--Asymptomatic bifascicular block, with or withoutfirst-degree atrioventricular block, is not an indication for temporary pacing; however, the availability of an external pacemaker is appropriate.

Peri-operative management of patients withpacemaker/implantable cardioverter defibrillator

--The use of unipolar electrocautery represents a significant risk, as the electrical stimulus from electrocautery may inhibit ’demand’ pacemakers, or may reprogram the pacemaker. --These problems can be avoided or minimized by*using bipolar electrocautery*correct positioning the ground plate for the electrical circuit. *Keeping the electrocautery device away from the pacemaker*giving only brief bursts*using the lowest possible amplitude. *The pacemaker should be set in an asynchronous or non-sensing mode inpatients who are pacemaker-dependent. This is most easily done inthe operating room by placing a magnet on the skin over the pacemaker.*Patients whose underlying rhythm is unreliable should have pacemaker interrogation after surgery, to ensure appropriate programming and sensing-pacing thresholds.--The defibrillator function of an ICD can be temporarily deactivated by placing a magnet on the skin over the ICD. While the device is deactivated, an external defibrillator should be immediately available

Congenital heart disease

--When the defect is simple, the circulation physiologically normal and the patient well compensated, the risk may be quite low--However, complicated patients with congenital heart disease should only undergo non-cardiac surgery after thorough evaluation by a multidisciplinary team in a specialized centre. --Prophylaxis for endocarditis should be initiated according to the ESC Guidelines on congenitalheart disease and infective endocarditis

Beta blockers

--Possible mechanisms for such a benefit include a reduction in myocardial oxygen demand, as postoperative stress and high catecholamine levels can lead to adverse cardiac events, an increase in myocardial oxygen delivery due to prolongation of coronary diastolic filling time, prevention of fatal ventricular arrhythmias, and protection against plaque rupture in the setting of increased sympathetic activity.--Given the results of POISE and the subsequent meta-analysis, the evidence does not support the initiation of prophylactic perioperative beta blocker therapy in most patients undergoing noncardiac surgery (RCRI ≤2). While beta blockers appear to decrease the risk of perioperative MI, the observed increases in the rate of stroke (hypotension), and possibly in the rate total mortality, more than nullified this benefit in POISE. A majority of the myocardial infarctions will be asymptomatic, but a few will result in serious complications in the perioperative period. In contrast, most of the strokes will be seriously disabling or incapacitating.--POISE does not exclude benefit in high-risk patients (RCRI ≥3), but such patients comprised only 2 percent.Similarly, POISE does not exclude benefit of beta blockers in patients with evidence of significant ischemia by stress tests who do not undergo preoperative coronary revascularization, in patients undergoing high-risk vascular surgery nor in those receiving lower doses of perioperative beta blockers.--It is suggested to start beta blockers at least one and preferably four weeks before surgery may lessen the chance that they will cause or contribute to hypotension in the perioperative period, taper carefully postoperative.

ACCF/AHA

— The 2009 ACCF/AHA focused update (of the 2007 ACC/AHA guideline update on perioperative beta blocker therapy for noncardiac surgery) on perioperative beta blockade made the following recommendations:

-A strong recommendation to continue in patients previously on these agents.-A weak recommendation in patients undergoing vascular or intermediate-risk surgery who have coronary artery disease (CAD) OR more than one clinical risk factor-A very weak recommendation in patients undergoing vascular surgery who have a single clinical risk factor in the absence of CAD or in those who have no clinical risk factors-For those patients in whom a beta blocker should is started, the process should begin days to weeks before elective surgery and the dose should be carefully titrated. A heart rate of 60 to 80 beats per minute (in the absence of hypotension) in the perioperative period was thought reasonable.

ESC/ESA

— The 2009 ESC/ESA guidelines for pre-operative risk assessment and perioperative cardiac management in non-cardiac surgery made the following recommendations regarding perioperative beta blocker use:

Beta blockers should be given in all patients undergoing high-risk surgery, have ischemic heart disease (recommended), or have myocardial ischemia on pre-operative testing, and considered in patients undergoing intermediate-risk surgery or those undergoing low-risk surgery AND with risk factors. Continuation of beta blocker therapy was also considered useful in patients previously treatedTreatment should be initiated between 30 and 7 days before surgeryThe preferred initial drugs and doses were bisoprolol 2.5 mg or metoprolol succinate 50 mg daily. Adjustment before surgery should achieve a resting heart rate between 60 to 70 beats/min with a systolic blood pressure greater than 100 mmHg.

--Postoperative tachycardia should firstly lead to treatment of the underlying cause—for example, hypovolaemia, pain, blood loss, or infection—rather than simply increasing the beta-blocker dose.

ESC/ESA 2014

Statins

-- Patients with coronary disease or a coronary equivalent (diabetes mellitus, symptomatic carotid artery disease, peripheral artery disease, abdominal aortic aneurysm, chronic kidney disease, or multiple risk factors that confer a 10-year risk of CHD greater than 20 percent) should receive therapy with a statin unless it is not tolerated.--For patients on statin therapy undergoing urgent or emergent major vascular surgery continuing such therapy.--For patients not on statin therapy undergoing urgent or emergent major vascular surgery initiating therapy before surgery, if possible.--Over the long-term statin therapy be titrated to recommended goals.--Statins with a long half-life (e.g. atorvastatin) or extended release formulations (e.g. lovastatin) may be favoured to bridge the period immediately after surgery when oral intake is not feasible.

Intravenous nitroglycerin

--Intravenous nitroglycerin can reverse intraoperative myocardial ischemia. However, a small randomized trial questioned the effectiveness of prophylactic nitroglycerin in reducing perioperative ischemia . Furthermore, the decrease in preload induced by nitroglycerin may outweigh its benefits.

--The use of nitroglycerin must also be considered in conjunction with the type of anesthetics to be used, since some agents can mimic the venodilating and arterial dilating effects of nitroglycerin. **Transdermal nitroglycerin should not be given intraoperatively due to uneven absorption

CCB

--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.--The use of short-acting dihydropyridines—in particular, nifedipine capsules—should be avoided.

Alpha2 receptor agonists

--alpha2 receptor agonists should not be administeredto patients undergoing non-cardiac surgery.(clonidine increased the risk of clinically importanthypotension and non-fatal cardiac arrest*)

Diuretics

--Diuretic treatment—if necessary to control heart failure—should be continued to the day of surgery and resumed orally when possible. In the peri-operative period, volume status in patients with heart failure should be monitored carefullyand optimized by loop diuretics or fluids.--Any electrolyte disturbance—especially hypokalaemiaand hypomagnesaemia—should be corrected in due time beforesurgery. Acute pre-operative repletion in asymptomatic patientsmay be associated with more risks than benefits; thus, minor asymptomatic electrolyte disturbances should not delay acute surgery.

SUMMARY AND RECOMMENDATIONS

The process of estimating and reducing the risk of perioperative cardiac events (eg, cardiac death and nonfatal MI), includes the following four components:

--Defining the urgency of surgery. For instance, risk assessment may not alter the management of patients who need emergency surgery. --Initial risk assessment:*Does the patient have a high-risk condition that is considered a major predictor of risk in the ACC/AHA guidelines?* What is the surgery-specific risk of the planned operation?*What is the patient-specific risk?--Refinement of initial risk assessment with noninvasive testing in selected patients.--Efforts to reduce risk in high-risk patients (eg, beta blockers, revascularization).

General features

**These approaches all have the following general features that apply only to patients in different risk categories undergoing nonemergent surgery:

--Patients at low risk generally require no further evaluation before surgery.--Patients at high risk (eg, those with signs or symptoms of severe or unstable coronary disease) often undergo coronary arteriography to see if any correctable lesions are present.--Patients at intermediate risk : noninvasive testing can be used to identify the risk category of an individual patient. Noninvasive testing has a negative predictive value of almost 100 percent for perioperative death or nonfatal MI but a positive predictive value of less than 20 percent (eg, 98 and 18 percent, respectively in a review of five studies of dipyridamole-thallium imaging)

Peri-operative monitoringECG

--Continuous ECG monitoring is recommended for all patients undergoing anaesthesia--The duration of ST-segment changes correlates positively with the incidence of peri-operative myocardial infarction; therefore, when ST-segment changes occur, the clinician should assume that myocardial ischaemia is present if the patient has a history of pre-existing cardiac disease (Both ST-segment changes and regional wall motion abnormalities can be present in the absence of acute ischaemia.)--Although V5 has for many years been regarded as the best choice for the detection of intra-operative ischaemia, one study found that V4 was more sensitive and appropriate than V5 for detecting prolonged post-operative ischaemia and infarction--combining leads V4 and V5 increased the sensitivity to 90%.When theleads II, V4 andV5were used simultaneously, the sensitivity was greaterthan 95%.--12-lead ECG monitoring is recommended especially in high-risk patients, although correct positioning of 12 leads is not feasible in high abdominal and thoracic surgery

Transoesophageal echocardiography

--TOE is recommended if acute and severe haemodynamic instability or life-threatening abnormalities develop during or after surgery

--There appears to be no benefit and possible harm from perioperative use of pulmonary artery catheters (PAC). It has been concluded that no subgroups have been defined for which PAC provides more benefit than harm (PE). --In terms of postoperative monitoring, it has been suggested that a single postoperative ECG and troponin concentration should be measured in patients with established coronary heart disease or peripheral artery disease and in those at higher risk (eg, diabetes, cerebrovascular disease). Measurements should be repeated if cardiac symptoms occur or in the setting of hemodynamic instability.--High risk (high-risk surgery with one or more additional risk factors of the revised cardiac risk score) obtaining troponin at 6 to 12 hours and days 1, 2, and 3 after surgery. --Data are limited on the management of asymptomatic ischemia in an attempt to prevent cardiac complications. At the least, more careful monitoring is warranted.

-Oxidative stress (a major cause of macrovasculardisease) is triggered by swings in blood glucose, more than by sustainedand persistent hyperglycaemia

-reduction in mortality in those whose blood glucose control was less strict[7.8–10 mmol/L (140–180 mg/dL)] than in those in whom it was tightly controlled [4.5–6 mmol/L (81–108 mg/dL)], as well asfewer incidents of severe hypoglycaemia.

Perioperative myocardial infarction

--The 2007 Joint Task Force of the European Society of Cardiology, American College of Cardiology Foundation, the American Heart Association, and the World Health Federation (ESC/ACCF/AHA/WHF) defined acute MI as a clinical event consequent to the death of cardiac myocytes (myocardial necrosis) that is caused by ischemia (but not other etiologies such as myocarditis or trauma).-Mechanism:(i) a mismatch in the supply–demand ratio of blood flow, due to a coronary artery stenosis that may become flow-limiting by peri-operative haemodynamic fluctuations(ii) stress-induced rupture of a vulnerable atherosclerotic plaque in combination with vascular inflammation and altered vasomotion--In the setting of noncardiac surgery, MI has occurred if there is a typical rise and/or gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis after surgery in conjunction with ischemic symptoms or new or presumably new pathologic Q waves or changes of ischemia on the ECG.--Troponin is the preferred biomarker as CK-MB is less sensitive and less specific in perioperative patients.--Both short- and long-term survival are decreased in patients who have sustained a perioperative MI.--While less sensitive and less validated than troponin testing, obtain a 12-lead electrocardiogram in the perioperative period for the following patients:All patients with symptoms of myocardial ischemia.All patients with risk factors for perioperative MI (baseline and daily for two, and possibly, three days).

Management

--Statin and beta-blocker therapies should be initiated unless contraindicated.--Antithrombotic therapy, including oral antiplatelet therapy and intravenous anticoagulant and antiplatelet therapy are used in many patients with spontaneous myocardial infarction, which is often due to a plaque-rupture event. However, in patients who have undergone surgery recently, the risk of bleeding with these agents may be significantly increased. In addition, many of these patients have suffered an MI due to abnormalities in supply-demand balance. It is unclear that these patients need the aggressive antithrombotic therapy and early intervention that patients with plaque rupture require. The decision to start one or more of them should be made only after careful consideration of the risks and benefits.--Monitoring in an intensive care unit for at least 24 hours is advised, particularly if the diagnosis is made within the first 24 hours of surgery.--An echocardiogram should be obtained in most patients.--Further risk stratification for the extent of coronary artery disease should be performed when the patient’s clinical condition allows.

Obesity

**A 2009 American Heart Association (AHA) scientific advisory on obesity noted an association with cardiac and pulmonary diseases, which may negatively affect the outcome of surgery:-Heart failure and myocardial steatosis. -Sleep apnea with or without pulmonary hypertension, deep vein thrombosis, and pulmonary embolism.**The estimation of risk is more difficult in obese patients due to the uncertain significance of certain components of the history (dyspnea) and physical examination (lower-extremity edema). The generally poor exercise capacity of the obese further complicates risk assessment.

Renal disease

--Impaired renal function is associated with a significantly increased risk of CVD and is an independent risk factor for adverse post-operative cardiovascular outcomes--(eGFR) should be calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula

Contrast-induced AKI (CI-AKI)

--Defined as a rise of serum creatinine of 44 mmol/L (0.5 mg/dL) or a 25% relative rise from baseline at 48 hours (or 5–10% at 12 hours) following contrast administration.--in up to 15% of patients with chronic renal dysfunction who are undergoing radiographic procedures--Although most cases of CI-AKI are self-limiting, with renal function returning to normal within 7 days of the procedure, these patients occasionally (in 0.5–12% of cases) develop overt renal failure, associated with increased morbidity and mortality.--The pathogenesis of CI-AKI is multifactorial, and is thought to include a decrease in glomerular filtration and renal hypoperfusion, together with renal medullary ischaemia, direct tubular toxicity via reactive oxygen species, and direct cellulartoxicity from the contrast agent.--A range of strategies has been proposed to prevent CI-AKI, including minimizing the volume of contrast medium administered, use of less-nephrotoxic contrast agents, provision of prophylactic renal-replacement therapy, patient hydration, and use of pharmacological agents to counteract the nephrotoxicity of contrast agents--The relationship between the volume of contrast agent administeredand the development of CI-AKI is well known, and exceeding the maximum contrast dose (contrast volume/eGFR) is strongly associated with the development of CI-AKI

--The use of low osmolar contrast media (LOCM) or iso-osmolar contrast media (IOCM) is recommended in patients with mild, moderate, or severe CKD--Although renal-replacement therapy has a favourable effect, in terms of reducing CI-AKI in patients with stage 4 or 5 CKD, haemodialysis has been found to be non-beneficial (and potentially harmful) for the prevention of CI-AKI in those with baseline CKD stage ≤3.--Normal saline or isotonic sodium bicarbonate (1.26%)may be used and peripherally administered, with the advantage that it requires only one hour of pre-treatment--N-acetyl cysteine may be considered for prophylaxis of CI-AKI, given its low cost and toxicity profile; however, the evidence for its benefit remains inconclusive--A number of small studies undertaking alkalinization of urine using a range of agents(bicarbonate, sodium/potassium citrate, acetazolamide) have shown a reduction in the incidence of contrast-induced nephropathy--Recent information suggesting the use of high-dose statins in preventing CI-AKI is promising--diuretics are therefore not recommended for the prevention or treatmentof AKI.(no evidence)

Cerebrovascular disease

-Low incidence of peri-operative stroke (0.1%).-Mainly ischaemic and cardioembolic and AF is often the underlying leading condition withdrawal of anticoagulation and the hypercoagulable state related to surgery-Additional aetiologies include atheroembolism, originating from the aorta or the supra-aortic vessels, and local atherothrombosis in the presence of intracranial smallvessel disease. -Hypoperfusion—related to peri-operative arterial hypotension and/or severe stenosis of the cervicocranial vessels—is an unusual cause of peri-operative stroke-Rarely, peri-operative stroke may be due to air, fat, or paradoxical embolisms.-The occurrence of this adverse event was associated with a 700% increase in peri-operative mortality, corresponding to an absolute risk increase exceeding 20%. -Multivariate analysis identified age, history of myocardial infarction within 6 months prior to surgery, acute renal failure, history of stroke, history of TIA, dialysis, hypertension, chronic obstructive pulmonary disease (COPD), and current tobacco use as independent predictors of perioperative stroke, while high body mass index was found to be Protective

-Antiplatelet/anticoagulant treatments should be continued whenever possible throughout the peri-operative period. Alternatively, the period of drug withdrawal should be kept as short as possible while weighting thrombo-embolic and haemorrhagic risks-Adequate selection of the anaesthetic technique (regional vs. neuraxial vs. general anaesthesia), prevention and treatment of AF, euglycaemic control (avoiding both hyperglycaemia and hypoglycaemia), as well as meticulous peri-operative blood pressure control, may all contribute to reducing the risk of peri-operative stroke.

--Permanent changes in mental status may occur following non-cardiac surgery, including spatio-temporal disorientation, memory loss, hallucinations, anxiety or depression. The underlying mechanisms, often elusive, may include surgery-induced systemic inflammation and cerebral hypoperfusion.

Peripheral artery disease

--It is not recommended to routinely perform exercise or imaging test to detect cardiac ischaemia inPAD patients without clinical symptoms, unless the patient has more than two of the clinical risk factors--All patients with PAD should be treated with statins and platelet inhibitors according to guidelines. Blood pressure control and lifestyle measures should be attended to

-mean pulmonary arterialpressure >25 mm Hg at rest, as assessed by right heart catheterization

-even IV or inhalation if not oral

-pre-operative initiation of appropriate positive airway pressure therapy, and planning of peri-operative techniques(anaesthetic and surgical) and post-operative positive airway pressuremanagement

-increase association with CAD, PAD

Anaesthesia

--Preoperative risk assessment and pre-operative optimization of cardiac disease

should be performed as a team exercise

Pre-operatively and post-operatively,

patientswhocouldmost benefit fromBNPor high-

sensitivity troponinmeasurements are those with METs ≤4 or with a

revised cardiac riskindex value >1 for

vascular surgery and >2 for non-vascular surgery.

-take care of bleeding risk with antiplatelets, anticoagulants

Thank you

DECREASE-V pilot study

— A separate question is whether revascularization is of value in patients at somewhat higher risk than in CARP. This issue was addressed in 101 patients who had ≥3 risk factors and had extensive stress-induced ischemia on noninvasive testing in the DECREASE-V Pilot Study, which showed no benefit from preoperative coronary revascularization at 30 days, one year, or during a median follow-up of 2.8 years [16,17]. However, the study was underpowered and the revascularization group had more diabetes, angina, and prior strokes than the medical therapy group. Further study is needed in higher risk subgroups

CARP trial

— The Coronary Artery Revascularization Prophylaxis (CARP) trial was a randomized comparison of preoperative revascularization (with either PCI or CABG) and medical therapy in patients with stable coronary disease undergoing major vascular surgery [14]. Of 5859 patients scheduled for vascular operations, 1190 were considered to be at increased cardiac risk (based upon clinical factors and/or stress testing) and had no other exclusions to participation (urgent vascular surgery or severe coexisting illness). These patients underwent coronary angiography; an additional 680 patients were excluded because of left main coronary disease, severe left ventricular dysfunction (LVEF ≤20 percent), severe aortic stenosis, or coronary anatomy not suitable for revascularization.

The remaining 510 patients (representing only 9 percent of the original study candidates) were randomly assigned to preoperative revascularization or medical management. Forty-nine percent of patients had a revised cardiac risk index ≥2 and 13 percent had a score ≥3 (table 2). Two-thirds of the study subjects had either one- or two-vessel disease. Of those assigned to revascularization, 41 percent underwent CABG and 59 percent underwent PCI (based upon clinician preference). Subsequent vascular surgery was performed for either abdominal aortic aneurysm (33 percent) or lower extremity arterial disease (67 percent).

The trial was designed to have sufficient power to examine long-term mortality, but not to provide a definitive analysis of perioperative events. The following outcomes were observed:

Postoperative MI by cardiac enzymes occurred with comparable frequency in patients assigned to revascularization and those assigned to medical therapy (11.6 versus 14.3 percent).There were no differences between the revascularization and medical arms in left ventricular ejection fraction at three months (54 versus 55 percent).At a median of 2.7 years, the primary end point (all-cause mortality) was not significantly different in the revascularization and medical therapy groups (22 versus 23 percent, relative risk 0.98, 95% CI 0.70-1.37).The CARP trial was not designed to evaluate the best approach to screening or to decide who should undergo angiography. The study was also not large enough to provide a conclusive analysis of the potential benefit of revascularization in high-risk subgroups, such as those with a large stress-induced defect on radionuclide myocardial perfusion imaging or those with three vessel disease plus left ventricular dysfunction. However, a post-hoc, subset analysis did not show any significant lowering in the risk of death and nonfatal MI from preoperative revascularization in any risk groups, including the highest risk subsets [15].