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ARTICLES
Year : 2007  |  Volume : 51  |  Issue : 4  |  Page : 287 Table of Contents     

Perioperative myocardial ischaemia and infarction - a review


1 MD, Professor, Department Of Anaesthesia & Intensive Care, Government Medical College and Hospital, Sector 32, Chandigarh, India
2 P.G.Student, Department Of Anaesthesia & Intensive Care, Government Medical College and Hospital, Sector 32, Chandigarh, India
3 MD, Professor & Head, Department Of Anaesthesia & Intensive Care, Government Medical College and Hospital, Sector 32, Chandigarh, India

Date of Web Publication20-Mar-2010

Correspondence Address:
Satinder Gombar
#1111,Sector 32 B, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


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Keywords: Cardiac; Ischaemia; Infarction; Preoperative; Anaesthesia; Complications


How to cite this article:
Gombar S, Khanna AK, Gombar KK. Perioperative myocardial ischaemia and infarction - a review. Indian J Anaesth 2007;51:287

How to cite this URL:
Gombar S, Khanna AK, Gombar KK. Perioperative myocardial ischaemia and infarction - a review. Indian J Anaesth [serial online] 2007 [cited 2019 May 20];51:287. Available from: http://www.ijaweb.org/text.asp?2007/51/4/287/61158


   Introduction Top


Preoperative myocardial ischaemia and infarction (PMI) is a major cause of short and long term morbidity and mortality in the surgical population. It is estimated that more than one half of postoperative deaths are caused by cardiac events, most of which are ischaemic in origin. Over 50,000 patients each year sustain a perioperative MI at an average additional cost to the health infrastructure of $12,000 per patient. [1] Thus prevention of a PMI is important to improve overall postoperative outcome. However, the exact nature of perioperative myocardial injury remains elusive and an area of continued debate and controversy. [2] The following review will address these issues and the nature of perioperative ischaemia in both the cardiac and non-cardiac surgery scenarios along with its management, including both preventive and therapeutic aspects of the problem.


   Preoperative myocardial ischaemia and infarction (PMI): Defining the problem Top


Myocardial ischaemia is a dual state composed of in­ adequate myocardial oxygenation and accumulation of anaerobic metabolites and occurs when myocardial oxygen demand exceeds the supply. Myocardial infarction is defined as the death of myocardial myocytes due to prolonged ischaemia. [3] Though perioperative MI was thought to be re­lated to the presence of a perioperative ischaemia, it was not until the landmark article by Slogoff and Keats in 1985 that the association between the two was clearly established. [4]


   Incidence of PMI Top


In patients with, or at risk of coronary artery dis­ease (CAD), the reported incidence of perioperative myo­cardial ischaemia is 20 - 63%.Various studies have shown that postoperative myocardial ischaemia was consistently found to occur considerably more often than preoperative and intraoperative ischaemia (ratio approximately 3:1 and 5:1 respectively). Reported incidence of postoperative cardiac events (the combined incidence of non-fatal myo­cardial infarction, unstable angina, congestive heart fail­ure, cardiac death) is 5.5-53% and that of postoperative myocardial infarction between 1.4 and 38%. Postopera­tive myocardial infarction increased the odds for long­ term cardiac events 20-fold. [5],[6],[7] Unfortunately, there is no reliable data available on the incidence of perioperative ischaemia & infarction in our country.


   Pathophysiology Top


A. Myocardial ischaemia

Myocardial ischaemia is characterized by an imbal­ance between myocardial oxygen supply and demand. The two most common conditions that predispose to myocardial ischaemia are CAD and left ventricular hypertrophy(LVH). Reduced oxygen supply or low-flow ischaemia (coronary vasoconstriction, intracoronary platelet aggregation orthrom­bus formation) is largely responsible for myocardial infarc­tion and unstable angina. Increased myocardial oxygen de­mand or high-flow ischaemia is mostly responsible for ischaemic episodes in chronic stable angina (tachycardia, exercise or emotional stress) in the presence of fixed coro­nary artery stenosis. Often, myocardial ischaemia is a cul­mination of multiple factors and results from both a reduc­tion in supply and an increase in oxygen demand. [8]

Endothelial function is also impaired in CAD, and is an important cause of myocardial ischaemia. Increases in coronary blood flow secondary to an increase in myocar­dial oxygen demand and sympathetic nervous system ac­tivation (e.g. during exercise, mental stress or increase in heart rate) induce vasodilatation in normal coronary ar­teries but lead on to paradoxical vasoconstriction in the atherosclerotic vessels [9],[10] .Such limitation of coronary flow and the inability of vessels to dilate near the site of an atherosclerotic plaque may result in regional myocardial supply- or low-flow ischaemia. In the face of an unfavorable oxygen supply demand ratio, the manifestations of myocardial dysfunction progressively set in and subse­quently compromise tissue perfusion and cellular aerobic metabolism.

The clinical manifestations of myocardial ischaemia range from asymptomatic or "silent" episodes to angina, arrhythmia, conduction blocks, wall motion abnormalities, pulmonary congestion, infarction, and sudden cardiac death. Systolic (contractile) and diastolic (ventricular fill­ing) dysfunction occur first; followed by electrocardio­graphic changes, and finally by chest pain. All these events often occur in a short time course of less than 1 minute [Figure 1]. [11] An 80% reduction in coronary blood flow causes akinesis, whereas a 95% decrease causes dyskinesis. If the ischaemia becomes severe, the increase in left ven­tricular end-diastolic pressure may lead to pulmonary oedema. After a brief period of severe ischaemia, con­tractile function can return gradually (stunning).Alterna­tively, severe chronic ischaemia can result in diminished contractile performance, such as chronic regional wall motion abnormalities (hibernation). In stunning normal blood flow and energy metabolism are accompanied by reduced contractility, designated as 'flow-contractility mismatch'. Hibernation is characterized by reduced con­tractility accompanied by reduced oxygen consumption as a consequence of reduced blood flow. Partially dam­aged cardiomyocytes can be rescued to full function af­ter stunning as well as hibernation, provided normal blood flow is restored after the latter within the critical time period before irreversible cell damage has occurred. De­spite their distinct definition, stunning and hibernation may merely represent intermediary states in a continuum ex­tending from unimpaired functional myocytes to necro­sis. [12]

It is worth mentioning here that perioperatively, the single most common abnormality that is often associated with ischaemia is tachycardia, which by causing both an increase in demand and reduction in supply can in sus­ceptible patients jeopardize the myocardium and bring about ischaemic changes. [4] Preoperative tachycardia can result from many causes, including light plane of anesthesia, endotracheal intubation and extubation, hypov­olemia, fever, anaemia, congestive heart failure(CHF), and postoperative pain. Similarly hypertension can cause in­creased demand and hypotension can lead to decreased supply in the perioperative period.

B. Myocardial infarction

Majority of perioperative infarctions occur in pa­tients with significant preexisting CAD, however hyper­tensive patients with LVH are also susceptible. The tran­sition from stable coronary artery disease to an acute coro­nary syndrome and infarction is characterized by coro­nary plaque disruption and subsequent thrombosis, which constitute the major pathogenic components of unstable or vulnerable plaques. [12]

A vulnerable plaque is an inflamed fibroatheroma with a lipid-rich core containing cholesterol crystals and necrotic debris, a thin fibrous cap with an infiltration of macrophages and lymphocytes, and low smooth muscle content. Inflammatory mediators closely regulate the bal­ance between the synthetic and degradative processes controlling the strength of the cap, specifically the syn­thesis of collagen. [8],[13]

When intraluminal thrombi attach to a ruptured atheromatous plaque, total occlusion of an epicardial coro­nary artery may occur, resulting in interruption of nutrient blood flow to the myocardium and death of myocardial myocytes. The situation may be worsened by distal em­bolization of microthrombi and by coronary vasoconstriction induced by local, mediator release-induced or sys­temic sympathetic activation. If coronary blood flow is interrupted for longer than 30 min, myocardial infarction may result. Loss of functional myocardium results in im­paired left ventricular function, which may impair quality of life and usually leads to premature death. [14] The pres­ence of myocardial ischaemia, nonfatal MI, or both within the first 7 postoperative days increases the risk of ad­verse cardiovascular events by 2- to 20-fold in the first 2 years after a noncardiac operation.

To put it in simple words , it is a complex and unpre­dictable interaction between the structural (central lipid core, thin cap) and functional (plaque thrombogenicity, intraplaque inflammatory cell infiltrate) intrinsic plaque factors as well as the exogenous factors (e.g. mechanical stress, vasomotor tone, infection, blood viscosity and co­agulability) which leads to the final outcome of myocar­dial ischaemic damage.

Most ischaemic episodes tend to start at the end of surgery and during emergence from anesthesia. This period is characterized by increases in heart rate (HR), arterial blood pressure (BP), sympathetic tone, and procoagulant activity. Increased sympathetic tone may lead to increases in coronary vasomotor tone and vascu­lar stress which in turn may trigger coronary vasospasm, plaque disruption and coronary thrombosis. Increases in HR & BP may lead to subendocardial ischaemia by in­creasing myocardial oxygen demand in the presence of limited coronary vasodilator reserve. Simultaneously, sur­gery induced procoagulant and anti-fibrinolytic activity may trigger coronary artery thrombosis during low flow conditions even in the absence of acute plaque disruption.


   Mechanisms and triggers of perioperative myocar­dial injury Top


Surgery, with its associated trauma, anesthesia and analgesia, intubation and extubation, pain, hypothermia, bleeding and anaemia, and fasting, is analogous to an ex­treme stress test. [Figure 2] illustrates how these factors ini­tiate inflammatory, hypercoagulable, stress and hypoxic state, which is associated with perioperative elevations in troponin levels, arterial thrombosis and mortality. [14]

Increasing grades of surgical trauma and general anaesthesia can initiate inflammatory and hypercoagulable states. The inflammatory state involves increases in tu­mour necrosis factor-alpha, interleukin (IL)-1, IL-6 and C-reactive protein; these factors may have a direct role in initiating plaque fissuring and acute coronary thrombosis. The hypercoagulable state involves increases in plasminogen activator inhibitor-1, factor VIII and platelet re­activity, as well as decreases in antithrombin III; all of these factors can lead to acute coronary thrombosis. The stress state involves increased levels of catecholamines (epinephrine and norepinephrine) and cortisol. Preoperative catecholamine and cortisol levels increase with general anesthesia, anaesthetic reversal, extubation, increasing pain scores, increasing grades of surgical trauma, anaemia, fasting and hypothermia. Increased stress hor­mone levels result in increases in blood pressure, heart rate, coronary artery sheer stress, relative insulin defi­ciency and free fatty acid levels all increase oxygen de­mand. Coronary artery shear stress may trigger plaque fissuring and acute coronary thrombosis. Factors that can initiate a hypoxic state include anaemia, hypothermia (through shivering), and anesthesia and analgesia (through suppression of breathing). Preoperative hypoxia can re­sult in myocardial ischaemia in the setting of a haemodynamically significant coronary artery stenosis. [14]


   Making a diagnosis Top


A. Definition and diagnosis of perioperative myo­cardial ischaemia:

Though there is no accepted gold standard for the diagnosis of myocardial ischaemia, the diagnosis can usu­ally be based on clinical, haemodynamic (pulmonary ar­tery capillary wedge and/or left atrial pressure wave), elec­trocardiographic (ECG), functional (echocardiogram), metabolic (coronary lactate production), biochemical (re­lease of creatine kinase-MB isoenzyme and/or troponin) or regional perfusion (scintigram) parameters. [8] All these techniques in the setting of ischaemia or infarction detec­tion have considerable limitations, varying sensitivity and specificity and poor inter technique correlation [Table 1] [15] .

Chest pain: The onset of new cardiac pain can be extremely important when one is diagnosing myocardial ischaemia preoperatively, during surgery under local or regional anesthesia and in the recovery room. Typically cardiac pain is a sense of chest constriction and may be referred to arm, neck, jaw, teeth or even post scapular area. However diabetics may have silent ischaemia be­cause pain pathways are impaired by diabetic neuropa­thy. In fact, it is reported that 70 % of myocardial ischaemic episodes in fully awake humans are asymptomatic.

Electrocardiography (ECG): Preoperative myo­cardial ischaemia has predominantly been detected and defined by ECG. The reported incidence of perioperative myocardial ischaemia greatly depends on choice and num­ber of precordial leads, on the definition of ischaemic ST­segment change (extent and duration of ST-segment change), and on the mode of data acquisition (continuous vs intermittent). [16]

The standard ECG consists of 12 leads, however, during anesthesia, monitoring is usually limited to five or seven leads. Blackburn et al demonstrated that 89% of significant ST depression was found in precordial lead V 5 . They also demonstrated that 100% of ST segment changes can be detected by recording leads V 3 -V 6 and leads II and a VF. [17] In routine practice, leads II and V 5 are continuously monitored, giving views of inferior and lat­eral myocardium. The ECG must be calibrated to give a pen deflection of 10mm for 1mV potential. This is impor­tant because excessive gain can give false ST depression and inadequate gain can mask such depression. Proper diagnosis of ischaemia from ECG depends on the diag­nostic mode which brackets a frequency bandwidth of 0.05-100 Hz. It is equally important to have a working knowledge of critical ST segment analysis. Horizontal or down sloping ST segment depression of 1mm or more in­dicates significant subendocardial ischaemia while ST segment elevation greater than 1mm indicates severe transmural ischaemia. Patients with left ventricular hy­pertrophy, left bundle branch block (LBBB), digitalis ef­fect, ventricular pacing and those not in sinus rhythm are not suitable for ECG-derived diagnosis of myocardial is­chaemia. In addition, perioperative changes in acid-base balance and electrolytes can affect the ECG in a way that interferes with ischaemia detection. [16]

Pulmonary artery pressure: The quantitative in­crease in pulmonary capillary wedge pressure and char­acteristic changes in its waveform have been suggested as an ischaemia monitor, but it is believed that the pulmo­nary artery catheter is an insensitive monitor of myocar­dial ischaemia and should not be inserted with this as a primary indication. In addition, the use of pulmonary ar­tery catheters in the perioperative period may actually contribute to increased morbidity. [11]

Transoesophageal echocardiography (TEE): TEE is a highly sensitive ischaemia monitor and demon­strates development of new regional wall motion abnor­malities, decreased systolic wall thickening, and ventricu­lar dilation as a result of ischaemic events. Usually, a transgastric cross-sectional view of the left ventricle is imaged because this view displays the myocardial perfu­sion territories of the three major coronary arteries. The use of TEE has become increasingly common in the op­erating room for cardiac surgery but is less frequently used in noncardiac surgery. In addition to cost, significant limitations exist to the routine use of TEE as an ischaemia monitor. Pre-intubation events are missed, and the image plane may miss events in other areas of the myocardium. It has been shown that if the anaesthesiologist has the training, experience and equipment to perform TEE, it can be valuable in the early detection of myocardial is­chaemia. [16] However, the incremental value of adding TEE to electrocardiographic monitoring in noncardiac surgery is unclear at this time.

Myocardial lactate: Although used mainly as a re­search tool, the coronary sinus catheter represents the ac­cepted standard for myocardial ischaemia monitors. How­ever, the coronary sinus catheter requires the use of fluo­roscopy, echocardiography, or both for proper placement. In addition, small areas of ischaemia may not be recog­nized because the lactate produced from these areas will be diluted by the blood from nonischaemic regions. [18]

The use of numerical indices of myocardial oxygen consumption (MVO 2 ) has been popular in general car­diologic practice. Unfortunately, their theoretical advan­tages have failed validation in anaesthetized patients. The rate-pressure product (RPP = systolic blood pressure × heart rate) has been shown to be a useful measure of MVO 2 in awake patients, but direct correlation of this index to MVO 2 measurement in anaesthetized patients has been unreliable. Other indices developed to overcome the deficiencies of the rate-pressure product have also failed validation in anaesthetized patients, probably be­cause it has been shown that most intraoperative ischaemia is related to decrease supply rather than increased de­mand. Most intraoperative ischaemic events occur with relatively normal haemodynamic parameters. Thus, the indices that are based on increased demand have little sensitivity for intraoperative ischaemia. Although heart rates above 110 beats/minute double the incidence of myocardial ischaemia, ischaemia frequently occurs even with heart rates between 60 and 80 beats/minute. [11]

In summary, there is no single best indicator of intraoperative myocardial ischaemia. Use of an array of monitoring modalities may facilitate the highest yield of ischaemic episodes.

B. Definition and diagnosis of perioperative myo­cardial infarction

According to the definition of the World Health Or­ganization (WHO), at least two of three criteria must be fulfilled to diagnose myocardial infarction: typical ischaemic chest pain; increased serum concentration of creatine kinase-MB isoenzyme; and typical electrocardio­graphic findings, including development of pathological Q-­waves. [19] This definition provides adequate specificity but lacks high sensitivity.

Clinical presentation: Patients receiving GA ob­viously will not complain of chest pain but may have hy­potension, arrhythmias, and signs of congestive heart fail­ure. Most postoperative myocardial infarctions occur early after surgery and are asymptomatic.

ECG: ECG may show changes of subendocardial or transmural ischaemia (ST elevation >1mm).The vast majority of perioperative myocardial infarctions are of the non-Q-wave type and preceded by episodes of ST-seg­ment depression and T wave inversion. [2] Long-duration (single duration >20-30 min or cumulative duration >1-2 h) ST-segment change, rather than merely the presence of postoperative ST-segment depression, seems to be as­sociated with adverse cardiac outcome. [4],[18]

The development of assays for the cardiac troponins T and I, which are highly specific and sensitive for myocar­dial injury, formed the basis of a revised definition of myo­cardial infarction proposed by the European Society of Car­diology and the American College of Cardiology. [19] The fol­lowing two criteria satisfy the diagnosis of an acute, evolv­ing or recent myocardial infarction: (i) a typical increase and gradual decrease in troponin concentrations or more rapid increase and decrease in creatine kinase-MB con­centration in combination with at least one of the following: (a) typical ischaemic symptoms, (b) development of patho­logical Q-waves in the ECG, (c) ECG changes indicative of myocardial ischaemia(ST-segment elevation or depression), and (d) coronary artery intervention; and (ii) pathological findings of an acute myocardial infarction.

Biochemical markers: Increased concentration of CPK-MB is not useful intraoperatively because the leak­age of these enzymes into the circulation can occur 8-24 hours after an MI. Because of the inherent limitations of CPK-MB concentration and lack of specificity, MI may be best detected with cardiac TnT concentrations. TnT binds to tropomyosin, troponin C binds to Ca ++ ,and tropo­nin I (TnI) binds to actin and inhibits actin-myosin inter­actions. While CPK-MB concentrations may rise only 10-20 times of normal during infarction and return to nor­mal within 72 hrs, TnT and TnI levels may rise more than 20 times above the reference range within 3 hrs after onset of chest pain and may persist for up to 10-14 days [Figure 3].This may assist in late diagnosis of infarction. [16]

Evidence is accumulating that other biochemical markers may further enhance sensitivity or improve risk stratification in patients with ACS including myoglobin (earliest rise after MI), C-reactive protein( a marker of inflammation that is increasingly appreciated as the pri­mary acute physiological process leading to plaque rup­ture and thrombosis) and B-type natriuretic peptide ( sen­sitive but non-specific response to left ventricular pres­sure or volume overload caused by severe ischaemia or heart failure) [20],[21]

TEE : The sudden appearance of severe wall mo­tion abnormalities in patients being monitored by TEE may also indicate MI, though it may be difficult to distinguish evolving infarction, stunned myocardium and hibernating myocardium using TEE. [16]

The question remains whether a reported incidence of perioperative myocardial injury based on the traditional definition underestimates the true incidence of clinically relevant myocardial injury or whether a reported incidence based on serum concentrations of troponins overestimates it. When using exclusively biochemical markers, specific­ity may be sacrificed for sensitivity. Given accumulating evidence that even low levels of troponin elevation in oth­erwise asymptomatic patients are associated with higher long term (6months -1 year) morbidity and mortality, it appears that they are accurate in detecting perioperative myocardial injury. At present there is a paucity of formal guidelines on this topic which clearly specify the ideal diagnostic criteria for perioperative infarction. [18]

Despite widespread use of the TEE and the PA catheter, the ECG is still the best validated tool for detec­tion of ischaemic episodes postoperatively.

The ACC/AHA Guidelines [Table 2] on perioperative evaluation provide specific recommenda­tions for perioperative surveillance and evaluation of such patients that is applicable in most settings. [22] We need more intensive investigations to determine whether this warrants a change in the current patterns of perioperative care.


   Preoperative risk assessment Top


Non cardiac surgery

The fundamental purpose of ascertaining the pres­ence of coronary artery disease, myocardial ischaemia, or both preoperatively is (1) to determine which patients are at risk and whether any further preoperative treatment is necessary, (2) to design an intraoperative management plan to reduce the incidence and consequences of ischaemia in patients at risk, and (3) in these at risk patients attempt to reduce the risk of adverse outcome by implementing ag­gressive preventive and treatment modalities. Interventions based on this assessment may include preoperative medi­cal optimization, coronary revascularization or both. His­tory and physical examination can identify variables asso­ciated with postoperative ischaemia: LVH, hypertension, diabetes mellitus, definite coronary artery disease, smoking and use of digoxin or any other medications. The incidence of postoperative ischaemia increases from 22% in patients with none of these variables to 77% in patients with four variables present. [11]

The Goldman Cardiac Risk Index (1977) [23] first identi­fied the importance of surgery-specific risks, which was validated in large prospective series of general surgery patients. Subsequently, Detsky et al in large prospective studies in the 1980s confirmed and refined the original Goldman index by adding categories of angina and prior history of congestive heart failure. [24] An alternate clini­cal risk prediction tool, the Revised Cardiac Risk Index (RCRI) [25] may equally predict risk. It involves the pres­ence or absence of six clinical risk factors. Zero, one, two, or three (or more) risk factors are categorized into Class I, II, III, or IV respectively. The corresponding postoperative cardiac complication rates range from less than 1% to over 10%.

American Heart Association/American College of Cardiology (AHA/ACC) published a guideline for perioperative cardiovascular evaluation for noncardiac surgery in 1996.This guideline has been recently updated in 2002 and offers the most comprehensive approach to preoperative cardiac evaluation for noncardiac surger­ies. [22] It focuses clinicians' attention on three major areas:

  • clinical risk predictors,
  • surgery-specific risks, and
  • functional capacity
The guideline stratifies clinical risk predictors into minor, intermediate, or major based on estimated risk of postop­erative cardiac events. Minor risk factors are not known to be associated with postoperative cardiac events, while the presence of major risk predictors warrants prompt and aggressive investigation and treatment. [Table 3]. [22]

The duration of the procedure, site of operation, and amount of tissue handling combine to confer different risks associated with various types of surgeries. The AHA/ ACC guideline included a more detailed estimate of sur­gery-specific risks based on postoperative cardiac events for each type of surgery based on the Coronary Artery Surgery Study (CASS) registry. [26] Surgeries were then categorized into low, intermediate, and high-risk surgical groups.[Table 4] A patient with minor clinical predictors has an overall low risk except for high risk or urgent/ emergent surgeries. Conversely, a patient with major clini­cal predictors who is in stable condition has an accept­able overall risk if the proposed procedure is a low risk procedure. The final major component of this evaluation is an assessment of current functional capacity. This as­sessment is based on metabolic equivalents (METs)

(1 MET= O2 consumption at rest- 3.5ml.kg -1 .min -1 )

Functional capacity of less than 4 METs of activity confers a 4% risk of postoperative cardiac events, whereas the risk is as low as 0.7% in patients with greater than 4 METS of capacity. Examples of exercise equal to 4 METs being, climbing a flight of stairs/walking up a hill/ walking on level ground at 4mph/running a short distance

Careful consideration of all three aspects, including clinical characteristics, functional capacity, and surgery­ specific risk in accordance with the published AHA/ACC guideline, form the basis for informed decision making regarding further diagnostic testing and/or risk reduction interventions. [26]


   Cardiac surgery Top


In patients undergoing CABG, myocardial ischaemia that occurs during the intraoperative period has the stron­gest correlation with perioperative MI. Looking at the cardiac patient in the cardiac surgical setting, it is impor­tant to realize that the lesion causing ischaemic changes in the pre operative period is usually remedied in the post­operative period thus outcomes are favourable as com­pared to the non cardiac surgery patient who has to go through the post operative vulnerable period with an ischaemic myocardium.

Various studies in the cardiac surgery population have identified certain factors namely, NYHA functional class, urgency of surgery, valvular lesions secondary to ischaemia, mean PAP>30mmHg, ejection fraction <40% and a low cardiac index as being predictors of poor out­ comes after cardiac surgery. [27],[28]


   Preoperative evaluation Top


While clinical assessment of risk is necessary for every patient, in populations deemed to be at high risk we need a more definitive assessment in the form of preop­erative non-invasive testing. Although a battery of such tests are now available, recent guidelines by the AHA/ ACC clearly state the class I indications for pre operative evaluation in the cardiac patient and limit testing only to the population groups deemed to be at the highest risk (e.g, patients undergoing vascular operations). A number of non invasive tests have been used and studied.

The standard 12-lead electrocardiogram is an in­sensitive test of the risk for myocardial ischaemia. It is normal in up to 50% of patients with CAD, and some patients have conduction defects that render the electro­cardiogram uninterpretable for ischaemia. When further workup is required cardiac stress testing is used. The purpose of a stress test is to determine

  • The status of ventricular function,
  • The amount of myocardium at risk for ischaemia, and
  • The need for further interventions, e.g., medication, angioplasty, or coronary artery bypass grafting, be­fore the proposed surgical procedure.
Stress testing can be subdivided into exercise and pharmacologic testing. Each test method stresses the com­ponents of myocardial oxygen consumption (contractility, heart rate, and afterload) to varying degrees. [29]

Exercise stress testing assesses a patient's func­tional capacity. The ability to achieve a target heart rate of >100/min or 85% of the maximum predicted HR pre­dicts a low complication rate. ST segment depression greater than 0.1 mV on a preoperative exercise stress test is an independent predictor of perioperative cardiac complications.

When exercise testing is contraindicated (LBBB, significant arrhythmias, CHF) or if patient is unable to exercise because of claudication , pharmacologic and other testing is substituted which include ischaemia moni­toring by ambulatory ECG (AECG),ejection fraction esti­mation by radionuclide ventriculography (RNV), dipy­ridamole thallium scintigraphy (DTS),and dobutamine stress echocardiography. The dipyridamole-thallium stress test reduces after load and thereby alters supply; whereas dobutamine stress echocardiography test increases de­mand. Mantha et al believe that DSE may show the great­est promise in predicting cardiac events. [29]

AHA/ACC guidelines also try and answer a ques­tion that so often comes up in the mind of every perioperative physician "Should patients with signifi­cant coronary artery disease undergo 'prophylactic' coronary artery bypass grafting or percutaneous coronary intervention before non-cardiac surgery?" Patients with a severe pattern of coronary disease, such as a critical left main stem stenosis or severe proximal three vessel coronary disease have a poor prognosis and, irrespective of planned surgery, should be urgently considered for coronary revascularization. This intervention significantly improves prognosis especially where an ex­ercise test is strongly positive or left ventricular function is impaired. Preoperative percutaneous coronary inter­vention with angioplasty and stenting, on the other hand, exposes destabilized plaque and coronary stent to the prothrombotic post-operative milieu with potentially cata­strophic consequences and thus its role as a prophylactic intervention to tide over a high risk non cardiac surgery is questionable if not worth condemning. [22]

The underlying theme of these guidelines is that any intervention in the form of prophylactic revascularization procedures should be reserved for those who warrant such therapy independent of their surgical procedure. [22] Otherwise medical optimization is needed.


   Preoperative interventions for prevention of perioperative MI Top


Two principal strategies used in an attempt to re­duce the incidence of PMIs and other cardiac events are

  1. Preoperative coronary revascularization- PCI or CABG
  2. Pharmacological interventions
The decision for or against preoperative coronary revascularization- PCI or CABG, should be based entirely on universally accepted medical indications for coronary revascularization. The philosophy of performing preop­erative coronary revascularization merely 'to get the patient through surgery' is contrary to all available evidence. If the decision for preoperative coronary revascularization is made, then timing with respect to the subsequent surgery appears crucial. [18]


   Coronary artery stenting - challenges and contro­versies Top


The advent of coronary artery stenting adds further complexity to perioperative management. Since placement of coronary stents denudes the arterial endothelial sur­face, the risk of intrastent thrombosis is high for the first several weeks after the procedure. The use of aspirin and clopidogrel decreases this risk, but if surgery must occur in the first several weeks after stent placement, the risk of intrastent thrombosis is high, and may occur even when aspirin and clopidogrel are continued. This is likely due both to the activation of the sympathetic nervous sys­tem and to the hypercoagulable state which occurs perioperatively. Current guidelines advocate continuing combination anti platelet therapy for a minimum of 2-3 weeks and ideally for 3 months post stent placement to allow for complete re-endothelialization of the stent. [26] The advent of drug-eluting stents may further complicate perioperative care. These stents prolong the re­-endothelialization of coronary arteries, thus increasing the period of thrombotic risk for surgical patients with new stents. Initial guidelines recommended 3 months of com­bination antiplatelet therapy for patients with the sirolimus­eluting stent and 6 months for those with the paclitaxel­eluting stent which have now been extended for upto one year uniformly and continuation of aspirin upto the day of the planned surgical procedure has also been made man­datory, unless the risks of bleeding are significantly more than those of perioperative stent thrombosis [30] . If angioplasty must occur before the surgical procedure, some authors recommend either plain angioplasty with­out a stent, or use of a bare metal stent followed by 2 weeks of aspirin and clopidogrel before proceeding to noncardiac surgery, since the highest risk of stent throm­bosis appears to occur in the first two weeks. [18] Close preoperative consultation between the interventionalist and anaesthetist is required to minimize the risk of perioperative cardiac morbidity and mortality.


   Pharmacological interventions Top


Several classes of drugs have been proposed in or­der to reduce the risk of ischaemic complications of ana­esthesia and surgery. However, based on current clinical data, only aspirin, beta-blockers, alpha 2 -adrenoceptor ago­nists, and statins may have the potential to affect perioperative cardiovascular outcome.

1.β-blockers

These drugs, at present, occupy centre stage both for cardiac prophylaxis and treatment following an ACS. Several studies have shown a reduction in the incidence of cardiac complications of anaesthesia and surgery in patients deliberately given beta-blockers prophylactically. Cardio protective effects of β-blockers are attributed to numerous cardiovascular and other effects (anti-arrhyth­mic, anti-inflammatory, altered gene expression, protec­tion against apoptosis etc). [31] Randomized trials in at risk patients having non-cardiac surgery [32] and high-risk patients having vascular surgery [33] have supported the use of perioperative beta-blockade. According to the recent up-date by the AHA/ACC unless there is a clear contrain­dication, perioperative beta-blocker therapy should be given to all patients who are to have vascular surgery and to most patients with cardiovascular disease who are to un­dergo major non-cardiac surgery and also those group of patients who test positive for inducible ischaemia in a myocardial stress test. Withdrawal of chronic beta-blocker therapy may have serious adverse effects. [34],[35] It is impor­tant that beta-blocker therapy is maintained perioperatively in at risk patients and a rebound 'withdrawal syndrome' must be avoided. Beta-blockers may be given intrave­nously during or after surgery in patients unable to take oral drugs.

2.Antiplatelet therapy (APA)-aspirin, clopidogrel and glycoprotein IIb/IIIa inhibitors

Aspirin forms an integral part of the acute therapy not only after an ACS but also in patients not known to have a pre existing CAD. It eliminates the diurnal varia­tion in plaque rupture. Apart from reducing platelet ag­gregation, its anti-inflammatory effect may be additive to its antithrombotic effect in patients with plaque instabil­ity. [18] Perioperative antiplatelet therapy presents both ben­efits and risks. For elective surgery the practice of with­drawing all forms of APA has been challenged because of fear of an unopposed and even increased risk of ischaemic events. Most experts recommend surgery while continuing APA for most vascular procedures and in set­tings where bleeding risk is likely to be low. [36] French So­ciety of anaesthesiology and intensive care (SFAR) rec­ommends that "aspirin can be discontinued in the perioperative period only when, compared with benefits, the specific haemorrhagic risks inherent to the interven­tion is definitely greater than the cardiovascular risk as­sociated with discontinuation". [37] For those patients who are on combination of two APA, the anaesthesiologist needs to discuss the risk benefit ratio with the surgical team and preferably put the patient on monotherapy at least 5 days preoperatively.

3.Alpha 2 -adrenoceptor agonists

Alpha-2 adrenoceptor agonists improve cardiovas­cular morbidity and mortality following cardiac and non­cardiac surgery. [38] These drugs attenuate perioperative haemodynamic instability, inhibit central sympathetic discharge, reduce peripheral norepinephrine release, and dilate post-stenotic coronary vessels. [39]

4. Statins

Hydroxymethylglutaryl coenzyme A (HMGCoA) reductase inhibitors or statin therapy is associated with major benefits in patients with vascular disease. 'Pleio­tropic' effects of statins independent of their lipid lower­ing action have been proposed as the mechanism of their beneficial effects. [18] These benefits are now recognized to occur not only in patients with coronary artery disease, but also in patients with peripheral vascular disease, cere­brovascular disease, and those with multiple risk fac­tors. [40],[41] These benefits may, in part, relate to the stabili­zation of the atherosclerotic plaque surface and cap, making plaque rupture less likely and enhancing plaque remodel­ling. All patients with vascular disease should be estab­lished on a statin, given the powerful evidence provided by the Heart Protection Study, statin therapy may be even more critical in the perioperative period. [40] In a recent meta analysis Biccard et al concluded that statin therapy is not only preventive but also is of proven benefit in the early stabilization of patients following the occurrence of an ACS in the perioperative period. [42]

5. Nitroglycerine

While nitroglycerine is used successfully in the treat­ment of myocardial ischaemia, there is no evidence that its prophylactic administration before anaesthesia and surgery decreases the risk of perioperative cardiac complications. [39]

6. Miscellaneous

Though effective in the management of ischaemic heart disease, Ca 2+ channel blockers have never been shown to offer any protection against perioperative car­diac complications of anaesthesia and surgery. [39],[43]

ACE inhibitors have a proven benefit in patients with a recent ACS and also in patients with vascular disease and normal left ventricular function. [44] These benefits ex­tend to patients with diabetes mellitus where there is the added advantage of a reduction in progression to microalbuminuria. Patients with vascular disease or dia­betes mellitus should be maintained on angiotensin con­verting enzyme inhibitor therapy perioperatively.ACE in­hibitors have anti-ischaemic actions with a 20% relative reduction for myocardial infarction. [44],[45]

The balance of benefits and risks of ACE inhibition in the perioperative period is uncertain. Inhibition of both the sympathetic nervous system with a beta-blocker and the renin-angiotensin system with an ACE inhibitor removes the major protective reflexes for intravascular volume regu­lation and homeostasis. Such combination therapy may re­sult in a greater risk of hypotension and may necessitate more detailed and invasive haemodynamic monitoring and more frequent intervention. In the presence of ACE inhibi­tion, acute renal failure can be precipitated by hypotension, hypovolaemia, radiocontrast, or NSAID administration. [46]

Antithrombin therapy (Heparin) has been used effec­tively in the management of unstable angina or acute PMI, both as a single agent or as a part of combination therapy with aspirin and thrombolytics. These patients are high risk candidates for perioperative embolic events and are often on subcutaneous low molecular weight heparin (LMWH) to reduce the risk of deep vein thrombosis and pulmonary em­bolism. Low dose heparin has been shown to reduce hyper­coagul ability after elective abdominal aortic surgery. [47]

Adenosine modulators facilitate the release of the coronary vasodilator adenosine by the ischaemic myocar­dium, thereby improving collateral blood flow toward the compromised area. Promising results have been obtained, [48] with the only agent tested in clinical trials, acadesine.

Nicorandil is both a nitrate and a K ATP channel opener. It is effective in the management of ischaemic heart dis­ease and its associated dysrhythmias. It may prove useful in the perioperative prevention of cardiac complications. In clinical practice, nicorandil, a K ATP channel opener and nitrate, is widely used in the treatment of angina. It ap­pears to protect by opening K ATP channels and to interact with ischaemic preconditioning and appears to offer addi­tional protection when administered with isoflurane, in terms of functional recovery of the stunned myocardium. [49]

Preoperative medication: High risk patients ben­efit from optimal preoperative anti-ischaemia and antihy­pertensive therapy which should be continued in perioperative period. Pharmacological and psychological attempts should be made to allay anxiety, the goals being to produce maximum sedation without undesirable circu­latory and ventilatory depression.


   Intraoperative management Top


The basic challenge during the perioperative period is to prevent myocardial ischaemia, this goal is logically achieved by maintaining the balance between myocardial oxygen delivery and demand. [Table 5] summarizes the various intraoperative events that can adversely influence this balance, and hence should be avoided.


   Choice of anaesthetic technique Top


Induction of anaesthesia in patient with IHD should be smooth and attempts should be made to minimize pressor response to laryngoscopy and intubation. Various drugs like lidocaine, nitroprusside, esmolol, fentanyl, nitroglycerine etc. have been used for this purpose.

Choice of drugs for maintenance depends on left ventricular function as determined by preoperative evalu­ation. In patients with normal LV function, a combination of N 2 O-opioid with addition of volatile agent (isoflurane, desflurane, sevoflurane) is acceptable. In patients with severely impaired LV function, a high dose opioid (fenta­nyl 50-100 µg.kg -1 IV )may be utilized as sole anaesthetic. [50] Opioid-based anaesthetics have become popular because of the cardiovascular stability associated with their use. The use of high doses, however, is associated with the need for postoperative ventilation. Because weaning from the ventilator in an intensive care setting has been associ­ated with myocardial ischaemia, this feature is important in the overall risk-benefit equation.

Neuraxial anaesthetic techniques can result in sympathetic blockade, resulting in decreases in both preload and after load. The decision to use neuraxial ana­esthesia for the high-risk cardiac patient may be influ­enced by the dermatomal level of the surgical procedure. Infrainguinal procedures can be performed under spinal or epidural anaesthesia with minimal haemodynamic changes if neuraxial blockade is limited to those der­matomes. Abdominal procedures can also be performed using neuraxial techniques; however, high dermatomal levels of anaesthesia may be required and may be associ­ated with significant haemodynamic effects. High der­matomal levels can potentially result in hypotension and reflex tachycardia if preload becomes compromised or blockade of the cardioaccelerators occurs. Studies that have evaluated regional vs. general anaesthesia for high ­risk patients undergoing noncardiac surgery found no dif­ference in outcome in terms of cardiac morbidity. [22]

Monitored anaesthesia care by an anaesthesia caregiver includes the use of local anaesthesia supple­mented with intravenous sedation/analgesia and is believed by some to be associated with the greatest safety margin. Although this technique can eliminate some of the unde­sirable effects of general or neuraxial anaesthesia, it pro­vides poor blockade of the stress response unless the lo­cal anaesthetic provides profound anaesthesia of the af­fected area. If the local anaesthetic block is less than satisfactory or cannot be used at all, monitored anaesthe­sia care could result in an increased incidence of myocar­dial ischaemia and cardiac dysfunction compared with general or regional anaesthesia. To achieve the desired effect, excess sedation can occur. Therefore, there may be no significant difference in overall safety with moni­tored anaesthesia care, and general or regional anaesthe­sia may be preferable.


   Perioperative pain management Top


From the cardiac perspective, pain management may be a crucial aspect of perioperative care. Because the majority of cardiac events in noncardiac surgical patients occur postoperatively, the postoperative period may be the time during which ablation of stress, adverse haemodynamics, and hypercoagulable responses is most critical. Although no randomized, controlled study specifi­cally addressing analgesic regimens has demonstrated improvement in outcome, patient-controlled analgesia tech­niques are associated with greater patient satisfaction and lower pain scores. Epidural or spinal opiates are becom­ing more popular and have several theoretical advantages. The patients having epidural anaesthesia/analgesia have demonstrated lower opiate dosages, better ablation of the catecholamine response, and a less hypercoagulable state. Most importantly , an effective analgesic (i.e., one that blunts the stress response) regimen must be included in the perioperative plan. [51],[52]


   Maintenance of body temperature Top


Hypothermia is common during the perioperative period in the absence of active warming of patients. Sev­eral methods of maintaining normothermia are available in clinical practice, the most widely studied being forced­ air warming. Perioperative morbid cardiac events have been found to occur less frequently in the normothermic population than in the hypothermic group.


   Treatment of perioperative myocardial ischaemia Top


1. Prevention of myocardial ischaemia: Careful attention to prevention of tachycardia during anaesthesia is extremely important. Maintenance of adequate depth of anaesthesia along with judicious use of ultra short act­ing â blockers can be very useful in preventing tachycar­dia. Apart from this, one should take adequate measures to attenuate pressor responses to laryngoscopy and en­dotracheal intubation. If haemodynamic aberrations are associated with myocardial ischaemia, they may precede and be the cause of ischaemia ;or ischaemia may pre­cede and may cause haemodynamic aberrations. For ex­ample if an anaesthetized patient has normal ST segment and then develops tachycardia followed by ST depres­sion, one should assume tachycardia as the cause of is­chaemia, so efforts should be made to reduce the rate. However, if hypovolemic hypotension precedes the onset of ST depression, perhaps the hypotension and conse­quent decrease in myocardial oxygen supply is the cause, which should be managed accordingly. [16]

2. Treatment of myocardial ischaemia without accompanying haemodynamic alterations: In suscep­tible patients, myocardial ischaemia often occurs without attendant haemodynamic alterations. In these patients ni­troglycerine (sublingual or intranasal) can be useful. Ni­troglycerine decreases preload and wall tension, dilates epicardial coronary arteries, and increases subendocar­dial blood flow.

3. Treatment of myocardial ischaemia accompa­nied by tachycardia and hypertension: A combination of tachycardia and hypertension can precipitate myocar­dial ischaemia by disturbing the myocardial oxygen demand and supply balance. After ensuring adequate ventilation, oxygenation and anaesthetic depth, â blockers (esmolol or metoprolol) may be administered in a titrated manner pro­vided there is no evidence of CHF or bronchospasm.

4. Treatment of myocardial ischaemia accom­panied by tachycardia and hypotension: A combina­tion of tachycardia and hypotension (mostly due to hypo­volemia) can precipitate myocardial ischaemia because both can drastically reduce myocardial oxygen supply. Apart from volume replacement, it is important to restore coronary perfusion pressure and slow the rate.

5. Severe resistant myocardial ischaemia: Oc­casionally one may come across severe myocardial is­chaemia, which is resistant to all antianginal drugs. Here intraaortic balloon pump (IABP) can be useful; it acutely decreases myocardial oxygen requirements and may in­crease myocardial oxygen supply.


   Treatment of perioperative myocardial infarction Top


Cardiologists usually do treatment of an acute pre or postoperative MI; however, in the intraoperative set­ting the anaesthesiologist has a major role to play. Once the diagnosis of acute MI is made, it is important to moni­tor the patient carefully: pulse oximetry, automated noninvasive blood pressure and in selected cases a radial arterial line should be inserted to have a continuous moni­toring. 100% oxygen should be administered and volatile agent discontinued. As soon as PMI is diagnosed, aspirin 325 mg is administered orally (through ryle's tube if un­able to take orally) and is continued thereafter. Prompt and aggressive treatment of changes in HR and/or BP is indicated. Tachycardia is treated with IV β blockers like esmolol while nitroglycerine is the drug of choice in the presence of normal to modestly elevated systemic BP. Class I recommendations for intraoperative nitroglycer­ine include high-risk patients previously taking nitroglyc­erine, who have active signs of myocardial ischaemia with­ out hypotension. [22]

Morphine is a venodilator that reduces ventricular preload and oxygen requirements. It is the analgesic of choice for continuing pain unresponsive to nitrates, and it is also effective in patients with pulmonary vascular con­gestion complicating ACS.

Hypotension should be rapidly treated in order to restore coronary perfusion pressure (CPP). Moderate hy­potension often responds to volume expansion with 300­-500ml of crystalloid. If severe hypotension (60-80mmHg systolic) persists despite volume expansion, vasoactive or inotropic drugs may be given to elevate CPP above criti­cal value.

In the presence of significant left ventricular dys­function, CVP monitoring may not be a good guide for fluid therapy so more invasive haemodynamic monitoring (pulmonary artery catheterization) is indicated in patients with refractory hypotension (unresponsive to volume ex­pansion), hypotension in the presence of CHF or haemodynamic deterioration severe enough to require vasopressors, vasodilators or an IABP. If PCWP is 12mmHgor less, volume expansion with crystalloid should continue. If PCWP is high, use of an inotropic agent like dopamine 3-5μg.kg -1 .min -1 or dobutamine 2.5-20 μg.kg­1 .min -1 is considered. If hypotension persists, consider epinephrine or milrinone. Milrinone is a class III cAMP phosphodiesterase inhibitor, 10 times more potent than amrinone, shorter half-life and less potential for thromb­ocytopenia. After a bolus of 25-50μg.kg -1 and infusion of 0.375 to 0.75μg.kg -1 .min -1 , cardiac output and blood pres­sure increase in a few minutes. In some patients who don't respond, use of percutaneous IABP is life saving. [16]


   Treatment of cardiac dysrrhythmias Top
[50]

Apart from attempts to increase the cardiac output, one should look for and correct metabolic acidosis (due to low cardiac output), electrolyte imbalance (esp hypokale­mia), ensure good oxygenation and treat arrhythmias. Si­nus bradycardia is common following acute MI especially inferior wall infarctions reflecting acute ischaemia of SA/ AV node. Treatment with atropine and a temporary pace­maker is needed when there is haemodynamic compro­mise. Some patients with severe bradycardia may require emergency cardiac pacing (transcutaneous or transvenous as appropriate).

Atrial fibrillation (AF) occurs in > 10 % of patients following acute MI and may result from an acute increase in left atrial pressure caused by LV dysfunction. When AF is haemodynamically significant, cardioversion should be promptly done however if AF is well tolerated, â-blocker therapy is indicated.

Ventricular tachycardia (VT) is common following acute MI. Sustained or haemodynamically significant VT is treated with electrical defibrillation while asymptom­atic VT is treated with lidocaine, procainamide, or amiodarone.

Ventricular fibrillation (VF) occurs in 3-5% of pa­tients with acute MI. Prophylactic lidocaine is no longer recommended because of an increased incidence of bradydysrhythmias and associated asystole. When VF occurs, rapid defibrillation with 120-200 Joules biphasic or 360 Joules monophasic current should be administered. Mortality is high when VF occurs in patients with hy­potension and/or CHF.

Thrombolytic or reperfusion therapy using thromboplastin activator (t-PA) or streptokinase is rec­ommended to minimize the damage caused by intraop­erative infarct. To be effective, they should be preferably given within 4 hrs (maximum up to 12 hrs).The major limitation is a predisposition for bleeding so it is contrain­dicated in patients with fresh surgical wounds however it may be useful in patients who have suffered PMI after procedures like cystoscopy or direct laryngoscopy.

In addition to thrombolytics, medical therapy with β blockers, antithrombotics and antiplatelet drugs can be started to ensure maximum myocardial salvage. Heparin should be started in patients in whom thrombolytic is not given. Heparin has been shown to reduce morbidity and mortality from thromboembolism and reinfarction. Early administration of (3 blockers may decrease the size of infarct, so all patients should receive intravenous β-blockers unless contraindications like CHF or large anterior wall MI with EF <40% exist. Such patients should receive ACE inhibitors.


   Intra-aortic balloon counterpulsation device Top


Placement of an intra-aortic balloon counterpulsa­tion device has been suggested as a means of reducing perioperative cardiac risk in noncardiac surgery. Although the rate of cardiac complications is low compared with other series of patients at similarly high risk, there are no randomized trials to assess its true effectiveness. There is currently insufficient evidence to determine the ben­efits vs. risks of prophylactic placement of an intra-aortic balloon counterpulsation device for high-risk noncardiac surgery.


   Conclusions Top


Perioperative myocardial infarction is a significant issue in patients undergoing not only high risk surgery but also those with clinical predictors that put them at a higher risk even with minor surgical interventions. Though the understanding of the pathophysiology and management of ischaemia in the perioperative period has increased tremendously over the last decade but lot of questions still remain unanswered. In view of the poor positive predic­tive value of non-invasive cardiac stress tests, the empha­sis is on a combination of selective non-invasive testing (to reliably identify those patients whotruly benefit from preoperative intervention such as preoperative coronary revascularization, initiation or optimization of cardio pro­tective medication, aggressive perioperative pharmacologi­cal therapy or cancellation of surgery).The perioperative period induces large, unpredictable and unphysiological changes in sympathetic tone, cardiovascular performance, coagulation and inflammatory response which in turn lead to alterations in plaque morphology and function. The im­portance of sympathetic activation in ischaemic syndromes leading to plaque rupture and secondary insults have tar­geted therapy towards stabilization of the so called vul­nerable plaque by pharmacological means (statins, aspi­rin, β-blockers)which may be as important in the preven­tion of PMI as an increase in myocardial oxygen supply (by coronary revascularization),or a reduction in myocar­dial oxygen demand (by β-blockers or α- 2 -agonists).

Having said that, there is still some way to go be­fore we can have formal strategies and guidelines for preventing, identifying and managing perioperative sub clinical myocardial injury and further research in this area is the need of the hour.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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  In this article
    Introduction
    Incidence of PMI
    Pathophysiology
    Mechanisms and t...
    Making a diagnosis
    Preoperative ris...
    Cardiac surgery
    Preoperative eva...
    Preoperative int...
    Coronary artery ...
    Pharmacological ...
    Intraoperative m...
    Choice of anaest...
    Perioperative pa...
    Maintenance of b...
    Treatment of per...
    Treatment of per...
    Intra-aortic bal...
    Conclusions
    Preoperative myo...
    Treatment of car...
    References
    Article Figures
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