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Safety of outpatient dental anaesthesia for children
adopted. Perhaps the question to ask now is whether the nursing of ventilated patients in the supine position is safe and necessary. Nigel R Webster Academic Unit of Anaesthesia and Intensive Care, University of Aberdeen, Institute of Medical Sciences, Aberdeen AB25 2ZD, UK 1
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Vincent JL, Bihari DJ, Suter PM et al. The prevalence of nosocomial infection in intensive care units in Europe: results of the European Prevalence of Infection in Intensive Care (EPIC) study. JAMA 1995; 274: 639–44. Kollef MH, Silver P, Murphy DM, Trovillion E. The effect of late-onset ventilator-associated pneumonia in determining patient mortality. Chest 1995; 108: 1655–62. Kollef MH. Ventilator-associated pneumonia: a multivariate analysis. JAMA 1993; 270: 1965–70. Torres A, Anzar R, Gatell JM, et al. Incidence, risk, and prognosis factors of nosocomial pneumonia in mechanically ventilated patients. Am Rev Respir Dis 1990; 142: 523–28. Centers for Disease Control and Prevention. Guidelines for prevention of nosocomial pneumonia. Morb MortalWkly Rep1997; 46: 1–79. Stoutenbeek CP, van Saene HK. Nonantibiotic measures in the prevention of ventilator-associated pneumonia. Semin Resp Infect 1997; 12: 294–99. Torres A,Serra-Batlles J, Ros E, et al. Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation: the effect of body position. Ann Intern Med 1992; 116: 540–43. Pingleton SK. Enteral nutrition as a risk factor for nosocomial pneumonia. Eur J Clin Microbiol Infect Dis 1989; 8: 51–55. Jacobs S, Chang RW, Lee B, Bartlett FW. Continuous enteral feeding: a major cause of pneumonia among ventilated intensive care patients. JPEN J Parenter Enteral Nutr 1990; 14: 353–56. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis in critically ill patients: resolving discordant meta-analyses. JAMA 1996; 275: 308–14. Stevenson GW, Hall SC, Rudnick S, Seleny FL, Stevenson HC. The effect of anesthetic agents on the human immune response. Anesthesiology 1990; 72: 542–52.
Safety of outpatient dental anaesthesia for children See page 1864 Every year in the UK, about one in 250 000 people undergoing dental anaesthesia die in the dentist’s chair.1 Most of those who die are young adults or children, and the deaths are attributed to respiratory difficulties or sudden cardiovascular collapse. Over the past decade in the USA, the annual incidence of death during anaesthesia for dental procedures was about one in 670 000 to 1 000 000. Although anaesthetic deaths may have occurred in healthy young people in the USA since 1994, in that year there were no deaths with the 69 795 general anaesthetics given in the state of Massachusetts. Only 12 of 317 673 patients receiving anaesthesia in dental offices in Massachusetts in 1994 were transferred to hospital.2 Arrhythmias requiring treatment were reported only in older adults. Is there a difference between the mortality rate during anaesthesia for dental procedures in the USA and the UK? Perhaps reporting is incomplete in the USA. Whether or not there is a difference, most clinicians would agree that even one preventable death is too many, and that further information is needed about the safety of outpatient dental anaesthesia. In today’s Lancet, Michael Blayney and colleagues report the results of a randomised trial of two anaesthetic agents given via nasal masks to children undergoing dental extraction. The investigators found a higher frequency of ventricular arrhythmias in children who received halothane than in those who received sevoflurane, and conclude that sevoflurane is a safer anaesthetic than halothane for 1836
paediatric dentistry. Bigeminy and short episodes of ventricular tachycardia occurred only in children who received halothane. These cardiac events were independent of the transient episodes of hypoxaemia that were as common during sevoflurane as during halothane anaesthesia. This study and others3–6 clearly show that sevoflurane has fewer cardiac side-effects than halothane. However, in the USA halothane is commonly given to children for complete oral check-ups and treatment, and cardiac side-effects are rarely reported. When the patient is under halothane anaesthesia in hospital, ventilation is controlled through an endotracheal tube and anticholinergic medication is commonly part of the general anaesthetic plan. Spontaneous ventilation during halothane anaesthesia may result in hypercapnia and precipitate ventricular tachycardia.7.8 General anaesthetics, sedatives, and narcotics all depress respiratory drive and lead to hypercapnia and hypoxaemia. These potentially life-threatening physiological abnormalities are easily treated or prevented by controlled ventilation.However, routine practice in dentists’ offices in the UK and the USA is not to place endotracheal tubes or to control ventilation. When the choice is made not to use skilled personnel to deliver general anaesthesia with controlled ventilation, the safety of the patient depends on his or her physiological state, the monitoring procedures used, the preparedness of the practitioner giving the anaesthetics, and the choice of drugs and doses given. In Blayney and colleagues’ study, inhalational anaesthetics were administered through a Goldman nasal mask: carbon dioxide concentrations in expired air were not monitored, and no anticholinergics or analgesics were given. Breathholding during induction of and emergence from anaesthesia and partial airway obstruction were the causes of hypoxaemia, but repositioning of the oral pack was the only manoeuvre needed to improve oxygenation—clearly these were skilled practitioners of dental anaesthesia. But it is very probable that hypercapnia was present in their patients. Pulse oximetry and monitoring of carbon dioxide concentrations can provide objective evidence of adequate ventilation.9 Use of a stethoscope, particularly a precordial stethoscope continuously connected to the anaesthetist’s ear, provides the earliest sign of altered respiratory function. Practice guidelines for the administration of sedatives and anaesthetics outside of the operating room were widely discussed in the 1980s, and professionals developed protocols suitable for the environment in their practices.10,11 One requirement in the guidelines is that practitioners giving sedation must be competent in basic life-support skills, such as maintenance of ventilation with a mask. But practice guidelines and monitoring standards will not in themselves ensure safety of patients. Those guidelines must be followed. The practitioner must also exercise judgment, both in the choice of drugs and in the timing of interventions to improve respiratory function. When guidelines developed by professional associations are not followed, the occurrence of serious adverse events may provoke tightening of legal restrictions on practice—at least in the USA. *Barbara W Brandom, Andrew Herlich *Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA 15213-2583; and Temple University, Philadelphia, PA ,U S A 1 2
Cartwright D. Death in the dental chair. Anaesthesia 1999; 54: 105–07. D’Eramo EM. Mortality and morbidity with outpatient anesthesia: the
THE LANCET • Vol 354 • November 27, 1999
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7 8
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Massachusetts experience. J Maxillofac Surg 1999; 57: 531–36. Wodey E, Pladys P, Copin C, et al. Comparative hemodynamic depression of sevoflurane ver sus halothane in infa n t s :a n echocardiographic study. Anesthesiology 1997; 87: 795–800. Lerman J, Davis PJ, Welborn LG, et al. Induction,recovery, and saety characteristics of sevoflurane in children undergoing ambulatory surgery. Anesthesiology 1996; 84: 1332–40. Skeehan T, Schuler HG, Riley JL. Comparison of the alteration of cardiac function by sevoflurane,isoflurane, and halothane in the isolated working rat heart. J Cardiothorac Vasc Anesth 1995; 9: 706–12. Crawford MW, Lerman J, Saldivia V, Carmiachel FJ. Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation. Anesth Analg 1992; 75: 1000–06. Sigurdsson GH, Lindahl S, Cardiac arrhythmias in intubated children during adenoidectomy. Acta Anaesthesiol Scand 1983; 27: 484–89. Thomas VJ, Thomas WJ,Thurlow AC, Cardiac arrhythmia during outpatient dental anaesthesia: the advantages of a controlled ventilation technique. Br J Anaesth 1976; 48: 919–22. Friesen RH, Alswang M. End-tidal PCO2 monitoring via nasal cannulae in pediatric patients:accuracy and sources of error. J Clin Monit 1996; 12: 155–59. American Academy of Pediatrics Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics 1992; 89: 1110–15. Weaver JM, Incorporating new ADA sedation-anesthesia practice guidelines into state dental board regulations. Anesth Prog 1999; 45: 131–33.
Is simple clinical assessment adequate for cardiac risk stratification before elective non-cardiac surgery? With surgical outcomes being the subject of increasing medical and non-medical scrutiny, there is pressure to identify patients at high risk of perioperative cardiac events, most importantly fatal and non-fatal myocardial infarction. Thomas Lee and colleagues1 have shown that a simple clinical assessment is the only risk-stratifying measure required for most patients being considered for major non-cardiac surgery. Their revised Cardiac Risk Index, based on the type of surgery and risk factors related to the individual (panel) is derived from multipleregression analysis of a large cohort of patients (2893 in the derivation set, 1422 in the validation set) and represents a helpful simplification and improvement of their original scoring system developed in the 1970s. Patients with fewer than two risk factors, who made up 75% of the population, had a risk of a major cardiac event of less than 1%. Patients with two or more factors had a 6% risk. Lee and colleagues’ approach contrasts with the prevailing trend in many centres, where clinicians rely on an objective non-invasive risk-stratifying investigation, with significant resource implications, rather than trust their clinical judgment, aided by routine investigations. Patients undergoing minor surgery do not require elaborate cardiac investigation preoperatively, since the identification of obstructive coronary disease will not alter how they are managed. An analysis of the CASS (Coronary Artery Surgery Study) Registry showed that patients who underwent operations with a less than 4% rate of perioperative death or non-fatal myocardial infarction (eg, urological, orthopaedic, breast) were at the same low risk (about 2%) whether or not they had coronary disease, and whether or not they had undergone surgical revascularisation.2 Patients undergoing more major surgery (eg, abdominal or thoracic) but who are at intrinsically low clinical risk (revised index less than 2) will also not benefit from further investigation, since no noninvasive test will have a positive predictive accuracy sufficient to stratify further a group already known to be at
THE LANCET • Vol 354 • November 27, 1999
Revised Cardiac Risk Index Risk factor
Criteria
High-risk surgery Ischaemic heart disease Congestive heart failure Cerebrovascular disease Insulin-treated diabetes Creatinine >177 mol/L
AAA repair, thoracic, abdominal MI, Q, angina, nitrates, EST+ History, examination, CXR Stroke, TIA
Number of factors
Proportion of population
Major cardiac complications*
0 1 2 ⭓3
36% 39% 18% 7%
0·4% 1·1% 4·6% 9·7%
*Myocardial infarction, pulmonary oedema, ventricular fibrillation or primary cardiac arrest, complete heart block. Abbreviations: AAA=abdominal aortic aneurysm; MI=history of myocardial infarction; Q=Q-waves; EST+=history of positive exercise electrocardiogram; CXR=chest radiograph; TIA=transient ischaemic attack.
less than 1% risk. Patients with angina need specialist cardiac assessments with non-invasive tests and, when indicated, coronary angiography, whether or not non-cardiac surgery is planned. According to the revised index, the risk of a perioperative cardiac event for patients with angina undergoing major surgery (abdominal or thoracic) is greater than 5%. However, the CASS data suggest that, after successful coronary bypass surgery, the risk of a cardiac event after subsequent non-cardiac surgery for patients with multivessel coronary disease falls from 6% to 2·5%.2 Thus, if elective non-cardiac surgery is planned for patients with angina, the investigations and any treatment should be completed before the date of the operation. The most difficult group of patients to assess and manage are those without symptoms of coronary disease who are nevertheless at high risk (5% or more) of a perioperative cardiac event on clinical grounds (revised index 2 or more). Many patients being considered for noncardiac vascular surgery are in this category, since 40% of those without any cardiac symptoms have obstructive coronary disease on angiography, which leads to a perioperative cardiac event rate for all vascular operations of about 8%.3,4 It is these symptom-free but high-risk patients for whom further risk stratification with noninvasive stress-based imaging investigations is most useful. Both dipyridamole thallium perfusion scintigraphy and dobutamine stress echocardiography are widely used and well validated in the preoperative setting.4,5 The choice of test depends primarily on local expertise, and the overall strategy of which it forms a part is of far greater importance than the exact investigation chosen. Symptom-free but high-risk patients, whether identified on clinical grounds alone or following non-invasive testing, are conventionally assessed with coronary angiography for revascularisation. This strategy provides reassurance for the clinician, although there is little hard evidence to support it. Coronary bypass surgery in symptom-free patients has never been shown to reduce the risk of subsequent non-cardiac surgery, whatever the pattern of coronary disease. Percutaneous intervention is unlikely to improve prognosis because it cannot protect against plaque rupture over most of the length of the coronary artery. Current approaches cannot identify specific 1837
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Vincent JL, Bihari DJ, Suter PM et al. The prevalence of nosocomial infection in intensive care units in Europe: results of the European Prevalence of Infection in Intensive Care (EPIC) study. JAMA 1995; 274: 639–44. Kollef MH, Silver P, Murphy DM, Trovillion E. The effect of late-onset ventilator-associated pneumonia in determining patient mortality. Chest 1995; 108: 1655–62. Kollef MH. Ventilator-associated pneumonia: a multivariate analysis. JAMA 1993; 270: 1965–70. Torres A, Anzar R, Gatell JM, et al. Incidence, risk, and prognosis factors of nosocomial pneumonia in mechanically ventilated patients. Am Rev Respir Dis 1990; 142: 523–28. Centers for Disease Control and Prevention. Guidelines for prevention of nosocomial pneumonia. Morb MortalWkly Rep1997; 46: 1–79. Stoutenbeek CP, van Saene HK. Nonantibiotic measures in the prevention of ventilator-associated pneumonia. Semin Resp Infect 1997; 12: 294–99. Torres A,Serra-Batlles J, Ros E, et al. Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation: the effect of body position. Ann Intern Med 1992; 116: 540–43. Pingleton SK. Enteral nutrition as a risk factor for nosocomial pneumonia. Eur J Clin Microbiol Infect Dis 1989; 8: 51–55. Jacobs S, Chang RW, Lee B, Bartlett FW. Continuous enteral feeding: a major cause of pneumonia among ventilated intensive care patients. JPEN J Parenter Enteral Nutr 1990; 14: 353–56. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis in critically ill patients: resolving discordant meta-analyses. JAMA 1996; 275: 308–14. Stevenson GW, Hall SC, Rudnick S, Seleny FL, Stevenson HC. The effect of anesthetic agents on the human immune response. Anesthesiology 1990; 72: 542–52.
Safety of outpatient dental anaesthesia for children See page 1864 Every year in the UK, about one in 250 000 people undergoing dental anaesthesia die in the dentist’s chair.1 Most of those who die are young adults or children, and the deaths are attributed to respiratory difficulties or sudden cardiovascular collapse. Over the past decade in the USA, the annual incidence of death during anaesthesia for dental procedures was about one in 670 000 to 1 000 000. Although anaesthetic deaths may have occurred in healthy young people in the USA since 1994, in that year there were no deaths with the 69 795 general anaesthetics given in the state of Massachusetts. Only 12 of 317 673 patients receiving anaesthesia in dental offices in Massachusetts in 1994 were transferred to hospital.2 Arrhythmias requiring treatment were reported only in older adults. Is there a difference between the mortality rate during anaesthesia for dental procedures in the USA and the UK? Perhaps reporting is incomplete in the USA. Whether or not there is a difference, most clinicians would agree that even one preventable death is too many, and that further information is needed about the safety of outpatient dental anaesthesia. In today’s Lancet, Michael Blayney and colleagues report the results of a randomised trial of two anaesthetic agents given via nasal masks to children undergoing dental extraction. The investigators found a higher frequency of ventricular arrhythmias in children who received halothane than in those who received sevoflurane, and conclude that sevoflurane is a safer anaesthetic than halothane for 1836
paediatric dentistry. Bigeminy and short episodes of ventricular tachycardia occurred only in children who received halothane. These cardiac events were independent of the transient episodes of hypoxaemia that were as common during sevoflurane as during halothane anaesthesia. This study and others3–6 clearly show that sevoflurane has fewer cardiac side-effects than halothane. However, in the USA halothane is commonly given to children for complete oral check-ups and treatment, and cardiac side-effects are rarely reported. When the patient is under halothane anaesthesia in hospital, ventilation is controlled through an endotracheal tube and anticholinergic medication is commonly part of the general anaesthetic plan. Spontaneous ventilation during halothane anaesthesia may result in hypercapnia and precipitate ventricular tachycardia.7.8 General anaesthetics, sedatives, and narcotics all depress respiratory drive and lead to hypercapnia and hypoxaemia. These potentially life-threatening physiological abnormalities are easily treated or prevented by controlled ventilation.However, routine practice in dentists’ offices in the UK and the USA is not to place endotracheal tubes or to control ventilation. When the choice is made not to use skilled personnel to deliver general anaesthesia with controlled ventilation, the safety of the patient depends on his or her physiological state, the monitoring procedures used, the preparedness of the practitioner giving the anaesthetics, and the choice of drugs and doses given. In Blayney and colleagues’ study, inhalational anaesthetics were administered through a Goldman nasal mask: carbon dioxide concentrations in expired air were not monitored, and no anticholinergics or analgesics were given. Breathholding during induction of and emergence from anaesthesia and partial airway obstruction were the causes of hypoxaemia, but repositioning of the oral pack was the only manoeuvre needed to improve oxygenation—clearly these were skilled practitioners of dental anaesthesia. But it is very probable that hypercapnia was present in their patients. Pulse oximetry and monitoring of carbon dioxide concentrations can provide objective evidence of adequate ventilation.9 Use of a stethoscope, particularly a precordial stethoscope continuously connected to the anaesthetist’s ear, provides the earliest sign of altered respiratory function. Practice guidelines for the administration of sedatives and anaesthetics outside of the operating room were widely discussed in the 1980s, and professionals developed protocols suitable for the environment in their practices.10,11 One requirement in the guidelines is that practitioners giving sedation must be competent in basic life-support skills, such as maintenance of ventilation with a mask. But practice guidelines and monitoring standards will not in themselves ensure safety of patients. Those guidelines must be followed. The practitioner must also exercise judgment, both in the choice of drugs and in the timing of interventions to improve respiratory function. When guidelines developed by professional associations are not followed, the occurrence of serious adverse events may provoke tightening of legal restrictions on practice—at least in the USA. *Barbara W Brandom, Andrew Herlich *Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA 15213-2583; and Temple University, Philadelphia, PA ,U S A 1 2
Cartwright D. Death in the dental chair. Anaesthesia 1999; 54: 105–07. D’Eramo EM. Mortality and morbidity with outpatient anesthesia: the
THE LANCET • Vol 354 • November 27, 1999
3
4
5
6
7 8
9
10
11
Massachusetts experience. J Maxillofac Surg 1999; 57: 531–36. Wodey E, Pladys P, Copin C, et al. Comparative hemodynamic depression of sevoflurane ver sus halothane in infa n t s :a n echocardiographic study. Anesthesiology 1997; 87: 795–800. Lerman J, Davis PJ, Welborn LG, et al. Induction,recovery, and saety characteristics of sevoflurane in children undergoing ambulatory surgery. Anesthesiology 1996; 84: 1332–40. Skeehan T, Schuler HG, Riley JL. Comparison of the alteration of cardiac function by sevoflurane,isoflurane, and halothane in the isolated working rat heart. J Cardiothorac Vasc Anesth 1995; 9: 706–12. Crawford MW, Lerman J, Saldivia V, Carmiachel FJ. Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation. Anesth Analg 1992; 75: 1000–06. Sigurdsson GH, Lindahl S, Cardiac arrhythmias in intubated children during adenoidectomy. Acta Anaesthesiol Scand 1983; 27: 484–89. Thomas VJ, Thomas WJ,Thurlow AC, Cardiac arrhythmia during outpatient dental anaesthesia: the advantages of a controlled ventilation technique. Br J Anaesth 1976; 48: 919–22. Friesen RH, Alswang M. End-tidal PCO2 monitoring via nasal cannulae in pediatric patients:accuracy and sources of error. J Clin Monit 1996; 12: 155–59. American Academy of Pediatrics Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics 1992; 89: 1110–15. Weaver JM, Incorporating new ADA sedation-anesthesia practice guidelines into state dental board regulations. Anesth Prog 1999; 45: 131–33.
Is simple clinical assessment adequate for cardiac risk stratification before elective non-cardiac surgery? With surgical outcomes being the subject of increasing medical and non-medical scrutiny, there is pressure to identify patients at high risk of perioperative cardiac events, most importantly fatal and non-fatal myocardial infarction. Thomas Lee and colleagues1 have shown that a simple clinical assessment is the only risk-stratifying measure required for most patients being considered for major non-cardiac surgery. Their revised Cardiac Risk Index, based on the type of surgery and risk factors related to the individual (panel) is derived from multipleregression analysis of a large cohort of patients (2893 in the derivation set, 1422 in the validation set) and represents a helpful simplification and improvement of their original scoring system developed in the 1970s. Patients with fewer than two risk factors, who made up 75% of the population, had a risk of a major cardiac event of less than 1%. Patients with two or more factors had a 6% risk. Lee and colleagues’ approach contrasts with the prevailing trend in many centres, where clinicians rely on an objective non-invasive risk-stratifying investigation, with significant resource implications, rather than trust their clinical judgment, aided by routine investigations. Patients undergoing minor surgery do not require elaborate cardiac investigation preoperatively, since the identification of obstructive coronary disease will not alter how they are managed. An analysis of the CASS (Coronary Artery Surgery Study) Registry showed that patients who underwent operations with a less than 4% rate of perioperative death or non-fatal myocardial infarction (eg, urological, orthopaedic, breast) were at the same low risk (about 2%) whether or not they had coronary disease, and whether or not they had undergone surgical revascularisation.2 Patients undergoing more major surgery (eg, abdominal or thoracic) but who are at intrinsically low clinical risk (revised index less than 2) will also not benefit from further investigation, since no noninvasive test will have a positive predictive accuracy sufficient to stratify further a group already known to be at
THE LANCET • Vol 354 • November 27, 1999
Revised Cardiac Risk Index Risk factor
Criteria
High-risk surgery Ischaemic heart disease Congestive heart failure Cerebrovascular disease Insulin-treated diabetes Creatinine >177 mol/L
AAA repair, thoracic, abdominal MI, Q, angina, nitrates, EST+ History, examination, CXR Stroke, TIA
Number of factors
Proportion of population
Major cardiac complications*
0 1 2 ⭓3
36% 39% 18% 7%
0·4% 1·1% 4·6% 9·7%
*Myocardial infarction, pulmonary oedema, ventricular fibrillation or primary cardiac arrest, complete heart block. Abbreviations: AAA=abdominal aortic aneurysm; MI=history of myocardial infarction; Q=Q-waves; EST+=history of positive exercise electrocardiogram; CXR=chest radiograph; TIA=transient ischaemic attack.
less than 1% risk. Patients with angina need specialist cardiac assessments with non-invasive tests and, when indicated, coronary angiography, whether or not non-cardiac surgery is planned. According to the revised index, the risk of a perioperative cardiac event for patients with angina undergoing major surgery (abdominal or thoracic) is greater than 5%. However, the CASS data suggest that, after successful coronary bypass surgery, the risk of a cardiac event after subsequent non-cardiac surgery for patients with multivessel coronary disease falls from 6% to 2·5%.2 Thus, if elective non-cardiac surgery is planned for patients with angina, the investigations and any treatment should be completed before the date of the operation. The most difficult group of patients to assess and manage are those without symptoms of coronary disease who are nevertheless at high risk (5% or more) of a perioperative cardiac event on clinical grounds (revised index 2 or more). Many patients being considered for noncardiac vascular surgery are in this category, since 40% of those without any cardiac symptoms have obstructive coronary disease on angiography, which leads to a perioperative cardiac event rate for all vascular operations of about 8%.3,4 It is these symptom-free but high-risk patients for whom further risk stratification with noninvasive stress-based imaging investigations is most useful. Both dipyridamole thallium perfusion scintigraphy and dobutamine stress echocardiography are widely used and well validated in the preoperative setting.4,5 The choice of test depends primarily on local expertise, and the overall strategy of which it forms a part is of far greater importance than the exact investigation chosen. Symptom-free but high-risk patients, whether identified on clinical grounds alone or following non-invasive testing, are conventionally assessed with coronary angiography for revascularisation. This strategy provides reassurance for the clinician, although there is little hard evidence to support it. Coronary bypass surgery in symptom-free patients has never been shown to reduce the risk of subsequent non-cardiac surgery, whatever the pattern of coronary disease. Percutaneous intervention is unlikely to improve prognosis because it cannot protect against plaque rupture over most of the length of the coronary artery. Current approaches cannot identify specific 1837