Gabriel P. Krestin, MD, PhD

The deadline for implementation of the EU Physical Agents (Electromagnetic Field) Directive was originally set as April 2008. As this deadline approached, information about the legislation's likely impact on the daily use of MRI was distributed widely. Most radiologists in Europe were aware of the problems they were likely to face, in both routine clinical work and MR research. So when the European Commission announced in late October 2007 that the execution of the EMF Directive would be put on hold, the radiological community breathed a huge sigh of relief.

Many radiologists now have the impression that the threat has passed, that the fight against the European Commission has been won. Unfortunately, this is not the case. What we have obtained is merely a postponement until 30 April 2012, to allow time for a substantive amendment to be adopted.

So what is going to happen over the next three and a half years? We already have information showing how MR workers could exceed the proposed occupational exposure limits for EMF by performing certain activities. This is provided in a study by Prof. Stuart Crozier of the University of Queens-land, commissioned by the U.K. Health and Safety Executive,

 and in experimental data gathered from four MRI facilities at the request of the EC.2 No further work is needed in this area.

What we don't have is information on the effects of these magnetic fields on radiologists, anesthetists, nurses, medical physicists, and technicians. After all, the Directive is designed to protect workers. Professionals agree that exposure to EMF can induce some short-term physiological effects, such as peripheral nerve stimulation and a metallic taste in the mouth. It is thought that these effects are not harmful to health, but this is very difficult to prove.

As it stands, the directive does not consider the long-term or cumulative effects of exposure to EMF. The amended version may do so. This is another area that requires more research. The only information we have on long-lasting effects from EMF exposure is from animal studies. More data are needed on this topic.

The modified EMF Directive is expected to be available toward the end of 2009. It will include amended recommendations on exposure limits from the International Commission on Non-Ionizing Radiation Protection (ICNIRP). It will also take into account the results of a socioeconomic impact assessment, which has yet to be commissioned. After a period of public consultation, it is expected that the revised legislation will be adopted by April 2011 and implemented by all EU member states within the next 12 months.

This time frame is extremely tight. There will not be enough time to gather any substantial scientific data about the side effects of EMF exposure. The limits suggested by the ICNIRP in the original directive were cautious. We have no idea what the revised advice will be. This time the commisson may include limits on static fields, which were left out of the earlier version. We have no guarantee that the amended EMF Directive will cause fewer problems for the MRI community.

The Alliance for MRI is still lobbying hard. Ideally, we would like a derogation for MRI from this directive, though achieving this concession is going to be challenging. We believe that such a derogation is necessary to ensure the future unimpeded use of MRI, particularly for interventional procedures and cutting-edge research. 

The safety of MRI workers is already regulated by the EU Medical Devices Directive (amend. Direct 93/42/EEC) and the established MR safety standard IEC/EN 60601-2-33 (as amended to include users/workers), so they would not be unprotected.I do not want to play down what we have achieved already. This is the first time in the history of the European Commission that a directive has been withdrawn or postponed at such a late stage. Two EU countries-Slovakia and Italy-had even incorporated it into national law.

It is important, however, for the European radiological community to appreciate that the problem has not been solved. Work is still ongoing, and there may be more battles ahead. 

PROF. KRESTIN is head of radiology at the Erasmus Medical Center, University of Rotterdam, the Netherlands, and a member of the Alliance for MRI.

1. Assessment of electromagnetic fields around magnetic resonance imaging (MRI) equipment. U.K. Health and Safety Executive, 2007 (

).
2. An investigation into occupational exposure to electromagnetic fields for personnel working with and around medical magnetic resonance imaging equipment. EC Employment, Social ffairs nd Equal Opportunities DG, April 2008 (

www.myesr.org/html/img/pool/VT2007017FinalReportv04.pdf

Articles

The deadline for implementation of the EU Physical Agents (Electromagnetic Field) Directive was originally set as April 2008. As this deadline approached, information about the legislation's likely impact on the daily use of MRI was distributed widely.

EU restrictions may still pose threat to MRI

Acute coronary syndromes include ST-elevation myocardial infarction (STEMI) and unstable coronary artery disease. The latter includes non-ST-elevation myocardial infarction (NSTEMI) and unstable angina. 

Persistent ST-segment elevation generally reflects transmural ischemia by total coronary occlusion and characterizes evolving myocardial infarction (STEMI). This occurs in a relatively small population of patients with acute coronary syndrome. In these settings, the therapeutic objective is either primary angioplasty or fibrinolytic treatment to achieve rapid and complete recanalization.

Patients with NSTEMI or unstable angina present with chest pain associated with ST-depression, T-wave inversion, flat T waves, or nonspecific ECG changes; a normal ECG at presentation can also be the case. NSTEMI is distinguished from unstable angina by an elevation in serum biochemical markers of myocardial necrosis (troponin T or I). However, the elevation of troponin levels may also be caused by either transient occlusion or microembolization secondary to spontaneous thrombolysis (small infarcts), and hence in the absence of an epicardial coronary artery occlusion amenable to percutaneous revascularization.

Patients with unstable acute coronary syndrome are at risk for myocardial infarction, MI recurrence, or death. Diagnosis and risk stratification are pursued together: During the process of establishing the acute coronary syndrome diagnosis, risk is repeatedly assessed and used as guidance for choosing the best therapeutic strategy. According to the European Guidelines,2 risk stratification of patients with unstable angina/NSTEMI involves integrating relevant information from their histories; e.g., chest pain pattern, physical examination, ECG, and biochemical cardiac markers. 

Several clinical decision rules are available for risk stratification: the thrombosis in myocardial infarction (TIMI) score,

 the global registry of acute coronary events (GRACE) score, the fast revascularization in instability in coronary disease (FRISC) score,

 and the platelet glycoprotein IIb/IIIa in unstable angina receptor suppression using Integrilin (PURSUIT) score.

 According to these algorithms, patients can be assigned to low-, intermediate-, or high-risk categories. The presence of thrombus and extent of underlying coronary artery disease (CAD), in particular troponin elevation and signs and symptoms of ongoing myocardial ischemia, can modify a patient's risk category.

Optimal early management of patients with non-ST-elevation acute coronary syndrome is still being debated. Several large randomized trials

 compared a routine invasive strategy (i.e., early angiography possibly followed by revascularization) with a more conservative strategy (i.e., angiography and revascularization only if medical therapy failed or residual ischemia was documented).

 The early invasive strategy was found to be superior to the conservative strategy in reducing major cardiovascular events as well as severe angina and rehospitalization. In particular, RITA-3 (randomized intervention trial of unstable angina)

 was the first study reporting improved survival after early invasive intervention. 

 of 1200 patients with non-ST-elevation acute coronary syndrome demonstrated that if patients were optimally treated before, during, and after revascularization, early cardiac catheterization was not better than a more selective invasive strategy in terms of mortality and recurrence of acute myocardial infarction. These investigators reported that the restricted use of conventional angiography only in patients experiencing refractory angina or clinically significant ischemia on predischarge exercise tests saved 47% of catheterization procedures without any detrimental effect on long-term follow-up.

 A large number of these procedures were merely diagnostic and not followed by revascularization. Results were confirmed at four-year follow-up,

suggesting that only very high risk patients should undergo early invasive management. Medical therapy might be tailored to the patient's risk profile.

 compared multislice CT coronary angiography and conventional angiography for the detection of >50% coronary obstructions in 104 patients with NSTEMI. At a patient level, both sensitivity and negative predictive value of MSCT were 100%, with no difference between low-risk and high-risk patients. 

Dorgelo et al16 showed that MSCT could effectively be substituted for diagnostic conventional angiography in approximately one-third of patients with unstable CAD. It could be argued that a major limitation of MSCT is its inability to provide information on the hemodynamic significance of moderate (50% to 70%) lesions, which might lead to unnecessary catheterizations. However, these data showed that MSCT can rule out the diagnosis of acute coronary syndrome and has the potential to reduce hospital admissions.

Although only a minority of patients classified as low risk actually suffer from myocardial ischemia,

 it has been reported that up to 8% of patients who actually have acute coronary syndrome are inappropriately discharged home.

 These patients have increased morbidity and mortality. Because the consequences of missing the diagnosis are so severe, it has been standard practice to evaluate all patients with suspected acute coronary syndrome (including low-risk patients) with serial ECG and cardiac enzymes, followed by a rest and/or stress-imaging study. Such an approach is time-consuming and costly. 

Goldstein et al20 randomized 197 low-risk chest pain patients to either ECG-gated MSCT coronary angiography or standard diagnostic evaluation. In the MSCT group, 67% of patients had minimal CAD and were discharged immediately; 8% had at least one stenosis >70% and were referred for catheterization. The MSCT scan alone could immediately identify or exclude coronary disease as the cause of chest pain in 75% of patients. The remaining patients had intermediate lesions on MSCT or nondiagnostic scans, thus underwent stress testing. Stress testing was negative in 20% of patients, who were discharged directly from the emergency department during the index visit; importantly, none of these patients suffered from major acute cardiac events over the six-month follow-up period. In patients who required further testing, the MSCT strategy ultimately arrived at a correct diagnosis in 95% of cases.

 prospectively studied 58 patients with chest pain of uncertain origin. These authors reported 100% sensitivity, 92% specificity, and 100% negative predictive value for MSCT compared with standard diagnostic tests (i.e., new biomarker elevation, abnormal myocardial perfusion scintigraphy, and/or invasive angiography) in the diagnosis of acute coronary syndrome. At 15-month follow-up, sensitivity of MSCT for predicting major cardiovascular events was 92%, specificity 76%, and negative predictive value 97%.21 

The potential to visualize the coronary artery wall and several characteristics of atherosclerotic plaques noninvasively, rather than with such invasive techniques as intravascular ultrasound (IVUS), has raised interest in plaque imaging to define patient risk.

Noninvasive identification of the vulnerable plaque (i.e., the plaque that will rupture and cause an acute event) is probably an elusive goal with current imaging technology. Nevertheless, MSCT can detect obstructive/nonobstructive lesions, evaluate location/distribution of CAD, and estimate left ventricular function. MSCT might allow a patient to be reclassified from the low-risk category to a higher risk category when three-vessel disease, involvement of the left main stem, or impaired LV function is seen. 

 that mixed plaques were independent predictors of acute events in patients with CAD. Mixed plaques may contain a necrotic component (necrotic core) and be associated with higher risk of rupture than densely calcified plaques. The detection and differentiation of noncalcified plaque components from calcified plaque components is feasible with MSCT; the distinction between necrotic areas and fibrous areas, conversely, is more challenging. Nevertheless, some studies have explored the ability of MSCT coronary angiography to differentiate large necrotic cores from fibrous lesions by measuring the CT attenuation values within the plaques.

 Although these studies report significant variation of attenuation values within plaques of the same type, plaques with a necrotic core demonstrated by IVUS consistently showed lower CT attenuation values than fibrous plaques (Figure 1).

Bugiardini et al26 evaluated a large cohort of non-ST-elevation acute coronary syndrome patients drawn from several international multicenter trials.

 This study showed that most of the patients classified as low risk had nonobstructive CAD or normal coronary arteries. Importantly, the presence of nonobstructive CAD detected by conventional angiography was associated with a higher risk of events (one-year follow-up) than that associated with normal coronary angiograms. 

 performed MSCT in 103 chest pain patients presenting at the emergency department with no ischemic ECG changes and negative initial biomarkers. This study found that the absence of coronary artery plaque or obstructions at MSCT had a high negative predictive value for the subsequent diagnosis of acute coronary syndrome. Moreover, the presence of any plaque or coronary obstruction provided information incremental to conventional risk factors in predicting the risk of acute coronary syndrome.

 reported on the prognostic value of MSCT coronary angiography in symptomatic patients with known or suspected CAD and a high prevalence of conventional risk factors. At 16 months, a 100% event-free survival was noted in patients with normal MSCT coronary angiography. Patients with coronary atherosclerosis identified on MSCT had a worse prognosis. Although the risk of events was the highest in patients with obstructive CAD, the risk associated with nonobstructive CAD (Figure 2) was higher than that associated with a normal MSCT study. 

The study by Bugiardini shows that low-risk patients might be a heterogeneous group and risk stratification should be improved in these patients.

All three studies support the concept that detecting the presence of CAD may be used for improving risk definition within the low-risk patient category.

More hard data are needed to define the clinical and prognostic value of specific MSCT findings in patients with acute coronary syndrome. Large trials will have to prove the clinical meaning of mixed/noncalcified plaques, plaque location, and plaque distribution. In spite of tremendous technical developments, the resolution of MSCT is still far from what is needed to visualize individual structures of the atheroma such as the fibrous cap, which is regarded as the pathological marker of vulnerable plaques. The reproducibility and inter-reader agreement in MSCT coronary plaque imaging will also have to be tested in the real world.

Nevertheless, the available data consistently support the excellent negative predictive value of a normal MSCT in patients with suspected acute coronary syndrome. Using these data may consistently reduce the number of unnecessary hospital admissions. The finding that not only obstructive lesions but also nonobstructive CAD and mixed plaques are associated with a worse prognosis,

 is in keeping with the notion that many patients are entirely asymptomatic up to their first acute event and that plaque composition, in addition to stenosis severity, contributes to the occurrence of events.

Although the routine use of MSCT in patients with suspected acute coronary syndrome is not supported yet by practice guidelines, the concepts discussed here lay the foundation for use of MSCT in these patients. MSCT might find a role in the diagnostic algorithm of low-risk patients with non-ST-elevation acute coronary syndromes to rule out obstructive CAD.

DR. PUGLIESE is a radiologist, and PROF. KRESTIN is the radiology chair, both at Erasmus MC University Medical Centre Rotterdam, the Netherlands.

References
1. Bertrand ME, Simoons ML, Fox KA, et al. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 2002;23(23):1809-1840.
2. Bassand JP, Hamm CW, Ardissino D, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology. Eur Heart J 2007;28(13):1598-1660.
3. Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA 2000;284(7):835-842.
4. Eagle KA, Lim MJ, Dabbous OH, et al. A validated prediction model for all forms of acute coronary syndrome: estimating the risk of 6-month postdischarge death in an international registry. JAMA 2004;291(22):2727-2733.
5. Lagerqvist B, Diderholm E, Lindahl B, et al. FRISC score for selection of patients for an early invasive treatment stra¬¬tegy in unstable coronary artery disease. Heart 2005;91(8):1047-1052.
6. Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation 2000;101(22):2557-2567.
7. Invasive compared with non-invasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in Coronary artery disease Investigators. Lancet 1999;354(9180):708-715.
8. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. NEJM 2001;344(25):1879-1887.
9. Fox KA, Poole-Wilson PA, Henderson RA, et al. Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of unstable Angina. Lancet 2002;360(9335):743-751.
10. Mehta SR, Cannon CP, Fox KA, et al. Routine vs selective invasive strategies in patients with acute coronary syndromes: a collaborative meta-analysis of randomized trials. JAMA 2005;293(23):2908-2917.
11. de Winter RJ, Windhausen F, Cornel JH, et al. Early invasive versus selectively invasive management for acute coronary syndromes. NEJM 2005;353(11):1095-1104.
12. Hirsch A, Windhausen F, Tijssen JG, et al. Long-term outcome after an early invasive versus selective invasive treatment strategy in patients with non-ST-elevation acute coronary syndrome and elevated cardiac troponin T (the ICTUS trial): a follow-up study. Lancet 2007;369(9564):827-835.
13. Calvin JE, Klein LW, VandenBerg EJ, et al. Validated risk stratification model accurately predicts low risk in patients with unstable angina. J Am Coll Cardiol 2000;36(6):1803-1808.
14. Cohen M, Demers C, Gurfinkel EP, et al. A comparison of low-molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events Study Group. NEJM 1997;337(7):447-452.
15. Meijboom WB, Mollet NR, van Mieghem CA, et al. 64-slice computed tomography coronary angiography in patients with non-ST elevation acute coronary syndrome. Heart 2007 (doi: 10.1136/hrt.2006.112771. Available online at 

http://heart.bmj.com/cgi/content/abstract/hrt.2006.112771v1

).
16. Dorgelo J, Willems TP, Geluk CA, et al. Multidetector computed tomography-guided treatment strategy in patients with non-ST elevation acute coronary syndromes: a pilot study. Eur Radiol 2005;15(4):708-713.
17. Reilly BM, Evans AT, Schaider JJ, et al. Impact of a clinical decision rule on hospital triage of patients with suspected acute cardiac ischemia in the emergency department. JAMA 2002;288(3):342-350.
18. McCarthy BD, Beshansky JR, D'Agostino RB, Selker HP. Missed diagnoses of acute myocardial infarction in the emergency department: results from a multicenter study. Ann Emerg Med 1993;22(3):579-582.
19. Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses of acute cardiac ischemia in the emergency department. NEJM 2000;342(16):1163-1170.
20. Goldstein JA, Gallagher MJ, O'Neill WW, et al. A randomized controlled trial of multi-slice coronary computed tomography for evaluation of acute chest pain. J Am Coll Cardiol 2007;49(8):863-871.
21. Rubinshtein R, Halon DA, Gaspar T, et al. Usefulness of 64-slice cardiac computed tomographic angiography for diagnosing acute coronary syndromes and predicting clinical outcome in emergency department patients with chest pain of uncertain origin. Circulation 2007;115(13):1762-1768.
22. Pundziute G, Schuijf JD, Jukema JW, et al. Prognostic value of multislice computed tomography coronary angiography in patients with known or suspected coronary artery disease. J Am Coll Cardiol 2007;49(1):62-70.
23. Schroeder S, Kopp AF, Baumbach A, et al. Noninvasive detection and evaluation of atherosclerotic coronary plaques with multislice computed tomography. J Am Coll Cardiol 2001;37(5):1430-1435.
24. Schroeder S, Kuettner A, Leitritz M, et al. Reliability of differentiating human coronary plaque morphology using contrast-enhanced multislice spiral computed tomography: a comparison with histology. JCAT 2004;28(4):449-454.
25. Leber AW, Knez A, Becker A, et al. Accuracy of multidetector spiral computed tomography in identifying and differentiating the composition of coronary atherosclerotic plaques: a comparative study with intracoronary ultrasound. J Am Coll Cardiol 2004;43(7):1241-1247.
26. Bugiardini R, Manfrini O, De Ferrari GM. Unanswered questions for management of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. Arch Intern Med 2006;166(13):1391-1395.
27. Antman EM, McCabe CH, Gurfinkel EP, et al. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction. Results of the thrombolysis in myocardial infarction (TIMI) 11B trial. Circulation 1999;100(15):1593-1601.
28. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. NEJM 2004;350(15):1495-1504.
29. Cannon CP, McCabe CH, Wilcox RG, et al. Oral glycoprotein IIb/IIIa inhibition with orbofiban in patients with unstable coronary syndromes (OPUS-TIMI 16) trial. Circulation 2000;102(2):149-156.
30. Lindahl B, Venge P, Wallentin L. Relation between troponin T and the risk of subsequent cardiac events in unstable coronary artery disease. The FRISC study group. Circulation 1996;93(9):1651-1657.
31. Morrow DA, Cannon CP, Rifai N, et al. Ability of minor elevations of troponins I and T to predict benefit from an early invasive strategy in patients with unstable angina and non-ST elevation myocardial infarction: results from a randomized trial. JAMA 2001;286(19):2405-2412.
32. Schwartz GG, Olsson AG, Ezekowitz MD, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA 2001;285(13):1711-1718.
33. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. NEJM 2001;345(7):494-502.
34. Hoffmann U, Nagurney JT, Moselewski F, et al. Coronary multidetector computed tomography in the assessment of patients with acute chest pain. Circulation 2006;114(21):2251-2260.

CTA seeks niche triage role in unstable angina patients

Coronary CT angiography has been found to be a powerful tool to evaluate patients suspected of coronary artery disease who are at low to intermediate risk. The task now for many researchers is to further refine specific patient populations for whom coronary CTA can be beneficial. One such patient niche being explored is the group with unstable angina and/or non-ST-segment elevation myocardial infarction.

Persistent ST-segment elevation generally reflects transmural ischemia by total coronary occlusion and characterizes evolving myocardial infarction (STEMI). This occurs in a relatively small population of patients with acute coronary syndrome. In these settings, the therapeutic objective is either primary angioplasty or fibrinolytic treatment to achieve rapid and complete recanalization (Figure 1).1

Patients with non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina present with chest pain associated with ST-depression, T-wave inversion, flat T waves, or nonspecific ECG changes; a normal ECG at presentation can also be the case.

NSTEMI is distinguished from unstable angina by an elevation in serum biochemical markers of myocardial necrosis (troponin T or I). However, the elevation of troponin levels may also be caused by either transient occlusion or microembolization secondary to spontaneous thrombolysis (small infarcts), and hence in the absence of an epicardial coronary artery occlusion, it may be amenable to percutaneous revascularization.

Patients with unstable acute coronary syndrome are at risk for myocardial infarction, MI recurrence, or death. Diagnosis and risk stratification are pursued together: During the process of establishing the acute coronary syndrome diagnosis, risk is repeatedly assessed and used as guidance for choosing the best therapeutic strategy. According to the European Guidelines,2 risk stratification of patients with unstable angina/NSTEMI involves integrating relevant information from their histories; e.g., chest pain pattern, physical examination, ECG, and biochemical cardiac markers.

Several clinical decision rules are available for risk stratification.3-6 According to these algorithms, patients can be assigned to low-, intermediate-, or high-risk categories. The presence of thrombus and extent of underlying coronary artery disease (CAD), in particular troponin elevation and signs and symptoms of ongoing myocardial ischemia, can modify a patient's risk category.

Optimal early management of patients with non-ST-elevation acute coronary syndrome is still being debated. Several large randomized trials7-9 and a meta-analysis compared a routine invasive strategy (i.e., early angiography possibly followed by revascularization) with a more conservative strategy (i.e., angiography and revascularization only if medical therapy failed or residual ischemia was documented).10 The early invasive strategy was found to be superior to the conservative strategy in reducing major cardiovascular events as well as severe angina and rehospitalization. RITA-3 (randomized intervention trial of unstable angina)9 was the first study reporting improved survival after early invasive intervention.

Another study11 of 1200 patients with non-ST-elevation acute coronary syndrome demonstrated that if patients were optimally treated before, during, and after revascularization, early cardiac catheterization was not better than a more selective invasive strategy in terms of mortality and recurrence of acute myocardial infarction.

These investigators reported that the restricted use of conventional angiography only in patients experiencing refractory angina or clinically significant ischemia on predischarge exercise tests saved 47% of catheterization procedures without any detrimental effect on long-term follow-up.11 Indeed, a large number of these procedures were merely diagnostic and not followed by revascularization. Results were confirmed at four-year follow-up,12 suggesting that only very high risk patients should undergo early invasive management. Medical therapy might also be tailored to the patient's risk profile.3,6,13,14

Meijboom et al15 compared MSCT coronary angiography and conventional angiography for the detection of > 50% coronary obstructions in 104 patients with NSTEMI. At a patient level, both sensitivity and negative predictive value of MSCT were 100%, with no difference between low-risk and high-risk patients. Another study, by Dorgelo et al,16 showed that MSCT could effectively be substituted for diagnostic conventional angiography in approximately one-third of patients with unstable CAD.

It could be argued that a major limitation of MSCT is its inability to provide information on the hemodynamic significance of moderate (50% to 70%) lesions, which might lead to unnecessary catheterizations. However, these data showed that MSCT can rule out the diagnosis of acute coronary syndrome and has the potential to reduce hospital admissions.

Although only a minority of patients classified as low risk actually suffer from myocardial ischemia,17 it has been reported that up to 8% of patients who actually have acute coronary syndrome are inappropriately discharged home.18,19 These patients have increased morbidity and mortality. Because the consequences of missing the diagnosis are so severe, it has been standard practice to evaluate all patients with suspected acute coronary syndrome (including low-risk patients) with serial ECG and cardiac enzymes, followed by a rest and/or stress-imaging study. Such an approach is time-consuming and costly.

Goldstein et al20 randomized 197 low-risk chest pain patients to either ECG-gated MSCT coronary angiography or standard diagnostic evaluation. In the MSCT group, 67% of patients had minimal CAD and were discharged immediately; 8% had at least one stenosis > 70% and were referred for catheterization.

The MSCT scan alone could immediately identify or exclude coronary disease as the cause of chest pain in 75% of patients. The remaining patients had intermediate lesions on MSCT or nondiagnostic scans and thus underwent stress testing. Stress testing was negative in 20% of patients, who were discharged directly from the emergency department during the index visit; importantly, none of these patients suffered from major acute cardiac events over the six-month follow-up period. In patients who required further testing, the MSCT strategy ultimately arrived at a correct diagnosis in 95% of cases.

Rubinshtein et al21 prospectively studied 58 patients with chest pain of uncertain origin. These authors reported 100% sensitivity, 92% specificity, and 100% negative predictive value for MSCT compared with standard diagnostic tests (i.e., new biomarker elevation, abnormal myocardial perfusion scintigraphy, and/or invasive angiography) in the diagnosis of acute coronary syndrome. At 15-month follow-up, sensitivity of MSCT for predicting major cardiovascular events was 92%, specificity 76%, and negative predictive value 97%.21

The potential to visualize the coronary artery wall and several characteristics of atherosclerotic plaques noninvasively, rather than with such invasive techniques as intravascular ultrasound, has raised interest in plaque imaging to define patient risk.

Noninvasive identification of the vulnerable plaque; (i.e., plaque that will rupture and cause an acute event) is probably an elusive goal with current imaging technology. Nevertheless, MSCT can detect obstructive/nonobstructive lesions, evaluate location/distribution of CAD, and estimate left ventricular function. For instance, MSCT might allow a patient to be reclassified from the low-risk category to a higher risk category when three-vessel disease, involvement of the left main stem, or impaired LV function is seen.

It was recently shown22 that mixed plaques were independent predictors of acute events in patients with CAD. Mixed plaques may contain a necrotic component (necrotic core) and be associated with higher risk of rupture than densely calcified plaques. The detection and differentiation of noncalcified plaque components from calcified plaque components is feasible with MSCT; the distinction between necrotic areas and fibrous areas, conversely, is more challenging. Nevertheless, some studies have explored the ability of MSCT coronary angiography to differentiate large necrotic cores from fibrous lesions by measuring the CT attenuation values within the plaques.23-25 Although these studies report significant variation of attenuation values within plaques of the same type, plaques with a necrotic core demonstrated by IVUS consistently showed lower CT attenuation values than fibrous plaques (Figure 2).

Bugiardini et al26 evaluated a large cohort of non-ST-elevation acute coronary syndrome patients drawn from international multicenter trials.27-33 This study showed that most of the patients classified as low-risk had nonobstructive CAD or normal coronary arteries. The presence of nonobstructive CAD detected by conventional angiography was associated with a higher risk of events (one-year follow-up) than that associated with normal coronary angiograms.

Hoffmann et al34 performed MSCT in 103 chest pain patients presenting at the emergency department with no ischemic ECG changes and negative initial biomarkers. This study found that the absence of coronary artery plaque or obstructions at MSCT had a high negative predictive value for the subsequent diagnosis of acute coronary syndrome. Moreover, the presence of any plaque or coronary obstruction provided information incremental to conventional risk factors in predicting the risk of acute coronary syndrome.

Pundziute et al22 reported on the prognostic value of MSCT coronary angiography in symptomatic patients with known or suspected CAD and a high prevalence of conventional risk factors. At 16 months, a 100% event-free survival was noted in patients with normal MSCT coronary angiography. Patients with coronary atherosclerosis identified on MSCT had a worse prognosis. In keeping with the previous studies, although the risk of events was the highest in patients with obstructive CAD, the risk associated with nonobstructive CAD (Figure 3) was higher than that associated with a normal MSCT study.

The study by Bugiardini et al shows that low-risk patients might be a heterogeneous group and that risk stratification should be improved in these patients. All three of these studies support the concept that detecting the presence of CAD, whether associated with obstructive lesions or not, may be used for improving risk definition within the low-risk patient category.

More hard data are needed to define the clinical and prognostic value of specific MSCT findings in patients with acute coronary syndrome. Large trials will have to prove the clinical meaning of mixed/noncalcified plaques, plaque location, and plaque distribution in both the short and the long-term.

In spite of tremendous technical developments, the resolution of multislice CT is still far from what is needed to visualize individual structures of the atheroma such as the fibrous cap, which is regarded as the pathological marker of vulnerable plaques. The reproducibility and inter-reader agreement in MSCT coronary plaque imaging will also have to be tested in the real world beyond the academic context.

Nevertheless, the available data consistently support the excellent negative predictive value of a normal multislice CT in patients with suspected acute coronary syndrome. Using these data may consistently reduce the number of unnecessary hospital admissions. The finding that not only obstructive lesions but also nonobstructive CAD and mixed plaques are associated with a worse prognosis22,26 is in keeping with the notion that many patients are entirely asymptomatic up to their first acute event, and that plaque composition, in addition to stenosis severity, contributes to the occurrence of events.

Although the routine use of multislice CT in patients with suspected acute coronary syndrome is not supported yet by practice guidelines, the concepts discussed here lay the foundation for use of MSCT in these patients. In the near future, MSCT might find a role in the diagnostic algorithm of low-risk patients with non-ST-elevation acute coronary syndromes to rule out obstructive CAD, reducing times and costs of care and improving risk stratification.

Dr. Pugliese is a radiologist and Dr. Krestin is the radiology chair, both at Erasmus MC University Medical Centre Rotterdam in the Netherlands.

1. Bertrand ME, Simoons ML, Fox KA, et al. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 2002;23(23):1809-1840.

2. Bassand JP, Hamm CW, Ardissino D, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology. Eur Heart J 2007;28(13):1598-1660.

3. Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA 2000;284(7):835-842.

4. Eagle KA, Lim MJ, Dabbous OH, et al. A validated prediction model for all forms of acute coronary syndrome: estimating the risk of 6-month postdischarge death in an international registry. JAMA 2004;291(22):2727-2733.

5. Lagerqvist B, Diderholm E, Lindahl B, et al. FRISC score for selection of patients for an early invasive treatment strategy in unstable coronary artery disease. Heart 2005;91(8):1047-1052.

6. Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation 2000;101(22):2557-2567.

7. Invasive compared with non-invasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in Coronary artery disease Investigators. Lancet 1999;354(9180):708-715

8. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. NEJM 2001;344(25):1879-1887.

9. Fox KA, Poole-Wilson PA, Henderson RA, et al. Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of unstable Angina. Lancet 2002;360(9335):743-751.

10. Mehta SR, Cannon CP, Fox KA, et al. Routine vs selective invasive strategies in patients with acute coronary syndromes: a collaborative meta-analysis of randomized trials. JAMA 2005;293(23):2908-2917.

11. de Winter RJ, Windhausen F, Cornel JH, et al. Early invasive versus selectively invasive management for acute coronary syndromes. NEJM 2005;353(11):1095-104.

12. Hirsch A, Windhausen F, Tijssen JG, et al. Long-term outcome after an early invasive versus selective invasive treatment strategy in patients with non-ST-elevation acute coronary syndrome and elevated cardiac troponin T (the ICTUS trial): a follow-up study. Lancet 2007;369(9564):827-35.

13. Calvin JE, Klein LW, VandenBerg EJ, et al. Validated risk stratification model accurately predicts low risk in patients with unstable angina. J Am Coll Cardiol 2000;36(6):1803-1808.

14. Cohen M, Demers C, Gurfinkel EP, et al. A comparison of low-molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events Study Group. NEJM 1997;337(7):447-452.

15. Meijboom WB, Mollet NR, van Mieghem CA, et al. 64-slice computed tomography coronary angiography in patients with non-ST elevation acute coronary syndrome. Heart 2007 (doi: 10.1136/hrt.2006.112771. Available online at http://heart.bmj.com/cgi/content/abstract/hrt.2006.112771v1).

16. Dorgelo J, Willems TP, Geluk CA, et al. Multidetector computed tomography-guided treatment strategy in patients with non-ST elevation acute coronary syndromes: a pilot study. Eur Radiol 2005;15(4):708-13.

17. Reilly BM, Evans AT, Schaider JJ, et al. Impact of a clinical decision rule on hospital triage of patients with suspected acute cardiac ischemia in the emergency department. JAMA 2002;288(3):342-350.

18. McCarthy BD, Beshansky JR, D'Agostino RB, Selker HP. Missed diagnoses of acute myocardial infarction in the emergency department: results from a multicenter study. Ann Emerg Med 1993;22(3):579-582.

19. Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses of acute cardiac ischemia in the emergency department. NEJM 2000;342(16):1163-1170.

20. Goldstein JA, Gallagher MJ, O'Neill WW, et al. A randomized controlled trial of multi-slice coronary computed tomography for evaluation of acute chest pain. J Am Coll Cardiol 2007;49(8):863-871.

21. Rubinshtein R, Halon DA, Gaspar T, et al. Usefulness of 64-slice cardiac computed tomographic angiography for diagnosing acute coronary syndromes and predicting clinical outcome in emergency department patients with chest pain of uncertain origin. Circulation 2007;115(13):1762-1768.

22. Pundziute G, Schuijf JD, Jukema JW, et al. Prognostic value of multislice computed tomography coronary angiography in patients with known or suspected coronary artery disease. J Am Coll Cardiol 2007;49(1):62-70.

23. Schroeder S, Kopp AF, Baumbach A, et al. Noninvasive detection and evaluation of atherosclerotic coronary plaques with multislice computed tomography. J Am Coll Cardiol 2001;37(5):1430-1435.

24. Schroeder S, Kuettner A, Leitritz M, et al. Reliability of differentiating human coronary plaque morphology using contrast-enhanced multislice spiral computed tomography: a comparison with histology. JCAT 2004;28(4):449-454.

25. Leber AW, Knez A, Becker A, et al. Accuracy of multidetector spiral computed tomography in identifying and differentiating the composition of coronary atherosclerotic plaques: a comparative study with intracoronary ultrasound. J Am Coll Cardiol 2004;43(7):1241-1247.

26. Bugiardini R, Manfrini O, De Ferrari GM. Unanswered questions for management of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. Arch Intern Med 2006;166(13):1391-1395.

27. Antman EM, McCabe CH, Gurfinkel EP, et al. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction. Results of the thrombolysis in myocardial infarction (TIMI) 11B trial. Circulation 1999;100(15):1593-1601.

28. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. NEJM 2004;350(15):1495-1504.

29. Cannon CP, McCabe CH, Wilcox RG, et al. Oral glycoprotein IIb/IIIa inhibition with orbofiban in patients with unstable coronary syndromes (OPUS-TIMI 16) trial. Circulation 2000;102(2):149-156.

30. Lindahl B, Venge P, Wallentin L. Relation between troponin T and the risk of subsequent cardiac events in unstable coronary artery disease. The FRISC study group. Circulation 1996;93(9):1651-1657.

31. Morrow DA, Cannon CP, Rifai N, et al. Ability of minor elevations of troponins I and T to predict benefit from an early invasive strategy in patients with unstable angina and non-ST elevation myocardial infarction: results from a randomized trial. JAMA 2001;286(19):2405-2412.

32. Schwartz GG, Olsson AG, Ezekowitz MD, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA 2001;285(13):1711-1718.

33. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. NEJM 2001;345(7):494-502.

If multislice CT can rule out obstructive coronary artery disease, time and cost of care would be reduced and risk stratification improved

34. Hoffmann U, Nagurney JT, Moselewski F, et al. Coronary multidetector computed tomography in the assessment of patients with acute chest pain. Circulation 2006;114(21):2251-2260.

Treatment options for multivessel coronary artery disease include medical therapy, percutaneous coronary intervention, and, above all, coronary artery bypass grafting. Current U.S. guidelines regard surgery as the treatment of choice for three-vessel disease and/or in cases involving the left main coronary artery.1

Coronary artery bypass grafting (CABG) is the most common major operation in the U.S., where approximately 300,000 such procedures are performed every year. The comparable figure for Europe is 220,000, with Germany accounting for 75,000 of these operations, Italy for 25,000, and the U.K. for 15,000.

Trends in medicine are moving toward minimization of the invasiveness of procedures. Use of "keyhole" techniques, for example, makes it possible to perform safe and effective surgery, while also cutting costs and reducing patient discomfort. Similarly, the advent of multislice CT is enabling coronary artery disease to be detected reliably and noninvasively.2

All grafts, but especially saphenous vein grafts, have a larger diameter and less residual motion than do native coronaries. This makes them better suited to visualization with CT angiography. Patients undergoing CABG are also generally older than the average surgery recipient, present with comorbidities, and are more likely to have conditions such as valvular heart disease or ventricular dysfunction. These factors increase the risk of complications from cardiac catheterization, and this patient group may thus benefit from noninvasive coronary angiography.

We perform noninvasive assessments of CABGs using 64-slice CT. Our state-of-the-art CT scanner provides an isotropic voxel of 0.4 mm3 and a temporal window of 165 msec (using a single 180 degrees algorithm reconstruction). Gantry rotation of 330 msec allows a table feed of 11.84 mm/sec together with a shortened temporal window. The increased number of slices, coupled with increased temporal resolution, means that scan times can be reduced to around 14 to 16 seconds. This is an important factor when seeking patient compliance for breath-hold scanning of large body volumes.

Scanning begins at the level of the aortic arch to depict the entire graft. Satisfactory results are gained when high tube current (850 to 950 mAs) is matched with a properly triggered bolus tracking technique.3

Bypass grafts have a large diameter, are relatively motionless, and tend to have little or no calcified deposits. While these conditions all favor CTA, patient preparation should not be neglected. Image quality can be affected by high and/or irregular heart rates. The best candidate for noninvasive CTA is stable with no contrast allergies, not suffering from severe renal failure, and has a heart beating at less than 70 bpm in sinus rhythm. Administration one hour prior to examination of oral beta blockers and, eventually, benzodiazepines to reduce heart rate is mandatory for a diagnostic result.

Intravenous administration of a 100 mL bolus of nonionic contrast through an antecubital vein allows visualization of the coronary tree. Intravascular enhancement can be maximized by using contrast with a high iodine concentration and/or injection at a high flow rate (320 to 400 mgI/mL injected at 4 to 5 mL/sec). Subsequent administration of a 40 to 50-mL saline bolus at the same flow rate, using a dual-head injector, will push the contrast bolus.4

Proper image reconstruction is another important step. An effective slice thickness of 0.75 mm with an increment interval of 0.4 mm will provide 400 to 500 images. Well-chosen parameters and a good-quality native image data set will allow optimal postprocessing. Volume-rendered reconstructions are often used to show the anatomic configuration of the coronary tree (Figure 1). Such reconstructions can help when following coronary artery bypass conduits and extrapolating the supposed course of an occluded bypass. A focal bump on the ascending aorta, for instance, usually corresponds with the residual anastomosis of the occluded venous graft to the aorta. Similarly, a road map of metallic clips can represent the path of an occluded internal mammary artery.

Curved multiplanar reconstructions (C-MPRs) along the lumen center line will detect coronary disease on bypass grafts and native coronary arteries. A multiplanar approach is mandatory for proper evaluation of coronary vessels and grafts. The operator or software should follow the vessel of interest throughout its course and search for abnormalities. Viewing planes should be aligned to the main axis of the vessel, and multiple views with this approach should be taken. C-MPRs along the central lumen line will show the entire vessel within a single image.

Stenosis should be visualized in a plane orthogonal to the main axis of the vessel. When doubtful images are seen on one data set, additional reconstruction at different time intervals during the cardiac cycle should be used. If an image along the vessel or inside the vessel lumen remains the same throughout the cardiac cycle, the chances are good that it is showing a real lesion rather than an artifact.

Evaluation of calcified native vessels can improve by use of a sharper convolution filter. Images will be noisier, but increasing contrast resolution will reduce blooming artifacts from calcium or metallic clips.

Modern CT scanners provide a wide range of options for manipulating raw data. It is possible to obtain any phase of the cardiac cycle and any plane within the scan volume. This freedom and flexibility explain the very high operator dependency for this procedure as well as the extremely long and intensive training required for high diagnostic accuracy.5,6 Results also depend on the care taken during patient selection.

Angina following CABG is caused by graft descent and failure (occlusion), often in combination with progressive atherosclerosis in the native coronaries. Chest pain can arise in the early postoperative phase (within one month of surgery), owing to technical factors and superimposed thrombosis, and in the intermediate phase (within a year), due to intimal hyperplasia and luminal narrowing. Chest pain occurring in the late phase (over a year after surgery) can be caused by lipid-rich atherosclerosis similar to that which affects native coronary vessels.

Progression of atherosclerosis in native coronary arteries is responsible for acute coronary syndrome in up to 47% of patients within five years of surgery and up to 24% of patients within 10 years of surgery.7 CTA evaluation should therefore cover native coronary arteries as well as bypass conduits (Figure 2). Postsurgical patients will have diffuse and advanced atherosclerosis, causing vessels to be diffusely narrowed and extensively calcified. They will often have undergone percutaneous coronary intervention prior to bypass grafting. Detection of significant luminal narrowing can be challenging with such diseased vessels.8

Evaluation of the entire thorax is unnecessary given the rarity of significant stenosis at the ostium of mammary arteries.9 Lengthening the scan

volume means decreasing the tube current intensity. This hampers evaluation of native coronaries and impairs image quality.

We use saphenous vein bypass grafts. It has been demonstrated, however, that atherosclerosis affects all grafts after the early postoperative phase. Occlusion rates are generally 15% to 20% in the first year. A further 2% of grafts then occlude annually for the next five years. The annual occlusion rate rises to 5% six years after surgery and remains at this rate until 10 years postsurgery. By this point, only 35% to 45% of the venous bypass grafts will still be open (Figure 3).10

The left internal mammary artery (LIMA) is used most frequently for CABG. Surgical options include end-to-side, free, sequential, and T or Y grafts. The LIMA graft is the most important graft performed in ischemic patients. The rate of occlusion during the first year after surgery is 5%, and it rises to 10% to 20% at 10 years.11 Numerous studies have shown that this procedure should not be withheld from any group of patients. Contraindications include radiation damage and documented subclavian stenosis.

The radial artery is considered the next best choice for CABG. Its length (greater than or equal to 20 cm) makes it suitable for extensive grafting. Disadvantages include the need to assess ulnar collateral circulation to avoid paresthesia and ischemia. A large number of metallic clips must be used along the vessel, and these can cause streak artifacts. The radial artery is also reportedly liable to spasms after surgical removal.

Assessing arterial conduits can be more difficult than examinations of venous conduits. Visualization is hindered by the smaller size of vessels and the clips placed to seal collateral arteries and distal anastomosis with the native coronary vessels. Visualization of the graft lumen can be limited by beam-hardening artifacts from metallic sternal wires if the LIMA runs close to the anterior chest wall. The lack of dynamic representation and quantification of blood flow abnormalities on CTA also prevents evaluation of flow competition between grafts and native vessels. This mechanism accounts for a significant number of venous and arterial occlusions.

Evidence from several studies indicates that CT-based CABG evaluation is more accurate when the number of detector rows is increased (see table). Sensitivity and specificity change from 83% to near 100% with the move from four- to 64-slice CT. Faster gantry rotation and decreased individual detector widths have also contributed to this improvement in performance. Very few groups have used CT to evaluate native coronaries in patients who have undergone CABG. Yet 64-slice technology provides sufficient spatial and temporal resolution to evaluate even native vessels reliably.

Noninvasive stress tests, such as exercise electrocardiography, echocardiography, and nuclear imaging, have been used to detect myocardial ischemia during postsurgical coronary evaluation. These tests have shown low accuracy, however, and they have been unable to determine the exact site of stenosis or occlusion. Coronary CTA is the only technique that permits noninvasive visualization of the coronary tree. It is considered the last diagnostic step prior to invasive procedures, though it is possible to consider a future role for this technique both before and after surgery.

Patients with valvular disease should undergo conventional coronary angiography. This will enable performance of coronary stenosis detection, valvular replacement, and bypass grafting (or percutanous interventions) during the same procedure. Patients without significant stenoses could avoid conventional angiography.

The main role of CTA in patients with chronic chest pain (stable angina) is to provide information that angiography cannot. This could include the wall characteristics of the ascending aorta and degree of calcification in the aorta, LIMA, and native vessels. Information on vessels and plaque will influence whether the patient undergoes an endovascular procedure or surgical treatment.

Preoperative planning of mild invasive direct and totally endoscopic CABG can also be carried out with CTA.17 These surgical techniques avoid the need for thoracotomy, cardiopulmonary bypass, or other procedures associated with high morbidity and mortality in older patients. The availability of more accurate anatomic information not provided by traditional angiographic modalities may benefit surgeons. One example is the presence of intramyocardial course and severe calcification of the native coronaries that can affect the endoscopic approach. Another example of this information involves the anatomic relationship between the LIMA and the left anterior descending coronary artery and its branches, which must be clearly shown when CT is performed for the planning of minimally invasive surgery.

Ostial lesions of the left main (LM) artery can be difficult to evaluate with conventional coronary angiography, owing to catheter placement. Intravascular ultrasound and/or wire pressure measurements are often required to better define the degree of stenosis. CTA offers an alternative noninvasive option of evaluating ostial LM disease. CT additionally provides reliable measurements of ventricular wall thickness and volumes prior to ventriculoplasty for postinfarction aneurysmatic left ventricle dilatation. Bypass surgery may be planned together with a ventricular patch.

CT has been proposed as a method of assessing myocardial viability, showing comparable results with MRI.18 MRI and CT can both identify the presence, location, and extent of irreversible myocardial injury correctly, whether acute or chronic. Preoperative CT could assess left myocardial viability that may benefit from revascularization. Follow-up CT at six months could demonstrate midterm response to surgery, especially for patients who suffered severe preoperative severe hypokinesia or akinesia.19

Coronary CTA could have a role in the follow-up of symptomatic patients. It can detect stenoses in CABGs and native vessels (lumen reduction > 50%) and indicate which patients should undergo repeat surgery or percutaneous intervention. Follow-up could be extended to all patients four to six weeks postsurgery. Prompt percutaneous treatment of thrombotic occlusions leads to remarkable outcomes. Efficacy of venous grafts is also improved.

Will noninvasive CT coronary angiography replace conventional coronary angiography? This remains a point for debate.20 Sixty-four-slice CT, and perhaps dual-energy x-ray source technology, will surely have a role in the assessment of CABG patients. This may improve the standing of CT as the cornerstone of clinical coronary imaging in the near future.

DR. PALUMBO and DR. CADEMARTIRI are radiologists at the Erasmus Medical Center in Rotterdam, the Netherlands, and at Azienda Ospedaliero-Universitaria in Parma, Italy. PROF. KRESTIN is chair of radiology at Erasmus Medical Center.

1. Eagle KA, Guyon RA, Davidoff R, et al. ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery). Circulation 2004;110(14):e340-437.

2. Mollet NR, Cademartiri F, Van Mieghem CAG, et al. High resolution spiral computed tomography coronary angiography in patients referred for diagnostic conventional coronary angiography. Circulation 2005;112(15):2318-2323.

3. Cademartiri F, Runza G, Belgrano M, et al. Introduction to coronary imaging with 64-slice computed tomography. Radiol Med 2005;110(1-2):16-41.

4. Cademartiri F, de Monye C, Pugliese F, et al. High iodine concentration contrast material for noninvasive multislice computed tomography coronary angiography: iopromide 370 versus iomeprol 400. Invest Radiol 2006;41(3):349-353.

5. Budoff MJ, Cohen MG, Garcia MJ, et al. ACCF/AHA clinical competence statement on cardiac imaging with computed tomography and magnetic resonance. Circulation 2005;112(4):598-617.

6. Budoff MJ, Achenbach S, Fayad Z, et al. Task Force 12: training in advanced cardiovascular imaging (computed tomography); endorsed by the American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Atherosclerosis Imaging and Prevention, and Society of Cardiovascular Computed Tomography. J Am Coll Cardiol 2006;47(4):915-920.

7. Chen L, Theroux P, Lesperance J, et al. Angiographic features of vein grafts versus ungrafted coronary arteries in patients with unstable and previous bypass surgery. J Am Coll Cardiol 1996;28(6):1493-1499.

8. Nieman K, Pattynama PM, Rensing BJ, et al. Evaluation of patients after coronary artery bypass surgery: CT angiographic assessment of grafts and coronary arteries. Radiology 2003;229(3):749-756.

9. Berger PB, Alderman EL, Nadel A, Schaff HV. Frequency of early occlusion and stenosis in a left internal mammary artery to left anterior descending artery bypass graft after surgery through a median sternotomy on conventional bypass: benchmark for minimally invasive direct coronary artery bypass. Circulation 1999;100(23):2353-2358.

10. Campeau L, Enjalbert M, Lesperance J, et al. The relation of risk factors to the development of atherosclerosis in saphenous-vein bypass grafts and the progression of disease in the native circulation. A study 10 years after aortocoronary bypass surgery. NEJM 1984;311(21):1329-1332.

11. Loop FD, Lytle BW, Cosgrove DM, et al. Influence of the internal mammary-artery graft on 10-year survival and other cardiac events. NEJM 1986;314(1):1-6.

12. Ropers D, Ulzheimer S, Wenkel E, et al. Investigation of aortocoronary artery bypass grafts by multislice spiral computed tomography with electrocardiographic-gated image reconstruction. Am J Cardiol 2001;88:792-795.

13. Marano R, Storto ML, Maddestra N, et al. Non invasive assessment of coronary artery bypass graft with retrospectively ECG-gated four row multidetector spiral computed tomography. Eur Radiol 2004;14:1353-1362.

14. Martuscelli E, Romagnoli A, D'Eliseo A, et al. Evaluation of venous and arterial conduit patency by 16-slice spiral computed tomography. Circulation 2004;110:3234-3238.

15. Chiurla E, Menozzi M, Ratti C, et al. Follow-up of coronary artery bypass graft patency by multislice computed tomography. Am J Cardiol 2005;95:1094-1097.

16. Malagutti P, Nieman K, Meijboom WB, et al. Use of 64-slice CT in symptomatic patients after coronary bypass surgery: evaluation of grafts and coronary arteries. Eur Heart J 2006;July 17 [Epub ahead of printed version].

17. Herzog C, Dogan S, Diebold T, et al. Multi-detector row CT versus coronary angiography: preoperative evaluation before totally endoscopic coronary artery bypass grafting. Radiology 2003;229(1):200-208.

18. Baks T, Cademartiri F, Moelker A, et al. MSCT and MRI for the assessment of reperfused acute myocardial infarction. J Am College Cardiol 2006;48:144-152.

19. Selvanayagam JB, Kardos A, Francis JM, et al. Value of delayed enhancement cardiovascular magnetic resonance imaging in predicting myocardial viability post surgical revascularization. Circulation 2004;110(12):1535-1541.

20. Gibbons RJ, Eckel RH, Jacobs AK. The utilization of cardiac imaging. Circulation 2006;113(13):1715-1716.

State-of-the-art scanners enable noninvasive assessment of bypass grafts and native vasculature for patency and arterial disease

64-slice CT monitors coronary artery health

The strength of radiology is only as great as the strength of the specialty's innovations. That principle underlies an ambitious long-term plan to create a new pan-European institute for top-quality fundamental and applied biomedical imaging research.

Planners are dreaming of an institute at a large physical base somewhere in Europe. This body will house hundreds of researchers, wield a substantial budget, and allocate funding, as well as conduct its own cutting-edge studies. Funding would come from European Union bodies and industry. There is much momentum and support behind the project, and hopes are high that the institute will become a reality within five to 10 years.

Plans for the organization are modeled after the U.S. National Institute for Biomedical Imaging and Bioengineering (NIBIB), which was launched relatively recently under the umbrella of the National Institutes of Health (NIH). The creation of a NIBIB-type of body is a primary goal of a new research committee set up in March 2004 by the European Association of Radiology (EAR). The committee is charged with developing strategies for strengthening infrastructure, advancing imaging as a science in European institutions, stimulating interest in academic radiology as a career option, and generally encouraging excellence in research.

Biomedical imaging is growing in importance in relation to research in fundamental areas such as molecular and genetic processes. Biomedical imaging research is a "translational research" in that it helps to bring laboratory discoveries into the clinic. The field of molecular imaging builds a bridge between fundamental research and clinical applications.

The EAR research committee has developed an action plan to ensure that the development of biomedical imaging research stays on the agenda for the EAR and its members, politicians, and industrial partners. Because it is likely to take many years to get a physical institute up and running in Europe, the EAR committee intends to start with the establishment of an extensive network that will coordinate European centers of excellence for imaging research projects. The network would consist of a number of core institutions and affiliated institutions and could be launched as early as the next European Congress of Radiology in March 2005.

One of the committee's first steps is to conduct an extensive survey among European institutions and organizations to determine potential participation in a network of excellence. Endorsement of European specialist imaging associations will help foster the network's development and broaden the scope of the whole enterprise.

A network of excellence has many potential benefits for participants, including shared organizational and communication systems as well as, ultimately, provision of additional funding and grants.

There will, of course, be challenges. Europe has no equivalent of the NIH to coordinate networks and operate institutes. The political environment and healthcare structures that currently serve Europe as a whole are less developed than in the U.S., where lobbying by radiologists led to the launch of NIBIB. But most politicians in Europe are already convinced that if we are not investing in R&D and innovation, we will lose in the long run. The European Commission's Sixth Framework Programme for Research and Technological Development underscores the importance of innovation and fosters the development of networking initiatives.

Currently, research institutes in Europe backed by national funding organizations work to provide results for individual countries. To bring them together in cooperative efforts, incentives such as additional funding and better coordination of some services will be offered. Help with human resources is also likely.

A network of excellence could help meet their needs by organizing an exchange of personnel between countries. It could also play a training role in countries where programs are less developed.

In the U.S., the funding of healthcare research is highly centralized. Much of the funding for the NIBIB is used to support research performed at institutions throughout the country.

Would that model work in Europe? If the decision is up to the scientific and professional communities, the answer is yes. We are optimistic about gaining support from politicians, industrial partners, and the public as we build a more cooperative, structured environment for biomedical imaging research.

PROF. KRESTIN is chair of radiology at Erasmus MC, University Medical Center at Rotterdam, the Netherlands. He is also chair of the EAR's committee on research. This column reflects the author's personal opinions.

Gabriel P. Krestin, MD, PhD

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