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Can Coronary Calcification Define the Warranty Period of a Normal Myocardial Perfusion Study?
EDITORIAL
EDITORIAL
January 2008
Mayo Clinic Proceedings
Volume 83 Number 1
Can Coronary Calcification Define the Warranty Period of a Normal Myocardial Perfusion Study?
M
yocardial perfusion scintigraphy (MPS) has an important role in diagnosis and management of patients presenting with known or suspected coronary artery disease (CAD).1 Moreover, it is the most commonly used and well-documented noninvasive method for risk stratification. In large cohorts of patients, a clear association has been demonstrated between the extent of perfusion abnormalities and risk of coronary events. Alternatively, normal results from MPS define patients at low risk, in general less than 1%, for adverse cardiac events during the next year.2 This observation holds true even among patients with high (ie, >85%) pretest likelihood of CAD.1,3 Accordingly, these patients can be managed medically, and the costs and risks of invasive testing and of revascularization can be avoided. Still, event rates have been reported to increase after both normal and abnormal results from studies in certain subsets of patients. Particularly in the presence of comorbidity, the risk of future adverse cardiac events appears to be in the range of 1% to 3%, even if results of MPS are normal.2,4,5 Moreover, a temporal component of risk has been identified; although risk is initially low, it increases over time after normal results from MPS. Several clinical characteristics, including known CAD or diabetes, have been found to further alter this temporal component of risk.5 These observations have contributed to the notion that a “warranty period” exists for normal results on MPS. As a consequence, repeated testing over time might be appropriate. However, the following questions arise: In which patients should imaging be repeated? If imaging should be repeated, when? To date, the answers to these questions have not been settled. A particularly relevant question is
Address correspondence to Jeroen J. Bax, MD, PhD, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands ([email protected]). © 2008 Mayo Foundation for Medical Education and Research
10
Mayo Clin Proc.
whether patients with evidence of atherosclerosis but initially normal myocardial perfusion will develop perfusion abnormalities over time. The use of coronary calcium scoring has been proposed as an ap- See also proach to study and resolve these questions page 17 because coronary calcifications are a direct marker for coronary atherosclerosis. Moreover, a large body of evidence indicates an association between the presence and extent of calcium and the risk of adverse cardiac events. This prognostic value is independent of baseline characteristics and is superior to the Framingham Risk Score.6.7 Accordingly, it is conceivable that detection of atherosclerosis by means of calcium scoring will allow identification of a high-risk subset within a low-risk population. This concept was tested by Askew et al.8 In a retrospective study, 69 asymptomatic patients with low-risk results on MPS but elevated coronary calcium levels (median calcium score, 443), who remained asymptomatic during follow-up, underwent repeated testing within 4 years (mean ± SD, 1.9±0.8 years) after the initial study. In most patients (65 [94%]), no changes were observed in myocardial perfusion during the repeated MPS study. In only 4 patients (6%), all with a baseline calcium score exceeding 100, progression in MPS risk category was observed. During a mean ± SD follow-up of 4.3±1.6 years after the repeated MPS, only 3 revascularizations occurred, resulting in an event-free survival of 94%. Accordingly, the authors concluded that, in asymptomatic patients with a low-risk MPS study, repeated testing within 4 years is not justified even if coronary calcium is present. Because our understanding of the pathophysiology and course of progression from subclinical coronary atherosclerosis (evidenced by calcification of coronary arteries) to hemodynamically important CAD (evidenced by abnormal MPS data) is currently limited, observations such as those by Askew et al are important and of great value for
• January 2008;83(1):10-12
•
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
EDITORIAL
developing algorithms for sequential testing. However, certain methodologic aspects of their study should be considered when interpreting their results. BASELINE CHARACTERISTICS Baseline characteristics of the study population could have substantially influenced results. The number of study participants was small, making it difficult to draw firm conclusions. Moreover, only 35 patients (51%) had high-risk calcium scores (>400). In contrast, calcium scores of less than 100, which are generally considered low risk, were observed in a substantial proportion of patients. Also of importance is the study’s inclusion of only asymptomatic patients. Patients who experienced angina, myocardial infarction, or revascularization between the 2 MPS studies were excluded. However, changes in clinical status imply progression of subclinical CAD to clinically manifest CAD, and it is conceivable that baseline calcium scores in such patients would be higher than in patients with no adverse cardiac events. Nevertheless, a change in clinical status alone would justify further testing, whereas the relevance of serial testing in patients without changes in clinical status remains debatable. The key finding of the current study is that asymptomatic patients remain at low risk after normal results on a baseline MPS, even if coronary calcification is present. Whether this observation also applies to patients with diabetes remains to be determined. In the current study, diabetes was present in only a small proportion (17%) of patients, of whom only 3 (4%) were insulin dependent. Patients with diabetes, however, are precisely those in whom unexpected clinical events can affect those previously asymptomatic, and it has been established that absence of symptoms in diabetes does not necessarily imply absence of CAD. Further, the presence of diabetes has been identified in several studies as an important predictor of increased risk of cardiac events despite initially normal myocardial perfusion.5,9 This is particularly true for insulin-dependent diabetes.9 Therefore, it is conceivable that sequential MPS testing prompted by coronary calcification will increase recognition of progression to clinically relevant CAD in patients with diabetes. Prospective studies of patients with diabetes are needed to examine whether calcium scoring indeed is useful to identify these high-risk patients. EFFECT OF CLINICAL MANAGEMENT The effect of clinical management is another potential confounding factor in the current study. Calcium scores were higher among patients who were referred for repeated testing than scores among those who were not referred. Clearly, the knowledge that coronary calcium was present could Mayo Clin Proc.
have influenced clinical management. This influence might not only have prompted closer monitoring, including repeated imaging studies, but might also have affected therapy, leading to more intense medical therapy and aggressive modification of risk factors. The effect of medical management decisions based on the known presence of subclinical atherosclerosis could further explain the low rate of progression of CAD (evidenced by the absence of changes on repeated MPS) noted in the current study. Recently, results of the Detection of Ischemia in Asymptomatic Diabetics (DIAD-2) study were reported.10 In the DIAD-2 study, 358 asymptomatic patients with type 2 diabetes underwent repeated MPS imaging 3 years after initial evaluation. Unexpectedly, new ischemia developed in only a small proportion, and perfusion remained normal in 259 (90%) of 287 patients with normal results from baseline imaging studies. Even more striking was the observation that ischemia resolved in 79% of patients with abnormal myocardial perfusion at baseline. Careful inspection of the data suggests intensified treatment as the most probable cause for such improvement. Accordingly, more aggressive medical therapy (including the use of statins, aspirin, and angiotensin-converting enzyme inhibitors) and more aggressive treatment of risk factors could have influenced the findings in the study by Askew et al. RECOGNIZING SUBCLINICAL ATHEROSCLEROSIS Finally, it remains to be determined whether calcium scoring is the most suitable marker for subclinical atherosclerosis in attempts to refine risk stratification among patients with normal results of MPS. Recently, Rozanski et al11 evaluated the association between calcium scoring and MPS in forecasting outcomes for a large cohort of mainly asymptomatic patients (51%) with a low prevalence of diabetes (8%). Among 1089 patients with normal results from MPS who were monitored for an average ± SD time of 32±16 months, the annualized cardiac event rate was less than 1% in all subgroups of coronary calcium quantity, including those with calcium scores greater than 1000. These findings suggest, as do the findings by Askew et al, that the short-term risk in patients with normal results from MPS is low, irrespective of the extent of coronary calcium deposits. The quantity of coronary calcification does not directly reflect total plaque burden, in particular the extent of noncalcified atherosclerosis. Although calcified and noncalcified coronary plaque are associated, the strength of this association appears to be highly dependent on the clinical presentation. In patients with acute coronary syndromes and in patients with diabetes, calcium scores appear to underestimate noncalcified coronary plaque burden.12-15 In fact, extensive calcification could represent a
• January 2008;83(1):10-12
•
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
11
EDITORIAL
more stable stage of CAD, whereas noncalcified and mixed lesions could be early and unstable stages of disease, possibly with a higher prevalence of vulnerable plaque. The inability to assess noncalcified plaque might be an important shortcoming of coronary calcium scoring. Contrastenhanced computed tomographic angiography (CTA) of the coronary arteries might help improve risk stratification in patients with normal results from MPS. With coronary CTA, not only the extent of atherosclerosis but also its severity, location, and plaque composition can be described. Because coronary CTA is a relatively new technique, preliminary data on its prognostic value are only just emerging.16,17 Currently, no evidence shows that detection of high-risk anatomy by coronary CTA will provide incremental prognostic value over MPS. Therefore, large prospective studies are needed to determine whether detailed analysis of subclinical atherosclerosis by coronary CTA in combination with certain clinical characteristics will allow more accurate identification of patients at increased risk for progression of CAD for whom sequential MPS testing is warranted. Certainly, studies to date, including the current report, suggest that calcium scoring alone does not refine risk assessment in asymptomatic patients with normal results from MPS, and serial testing in these patients might not be useful. Jeroen J. Bax, MD, PhD Joanne D. Schuijf, PhD Department of Cardiology Leiden University Medical Center Leiden, the Netherlands
1. Klocke FJ, Baird MG, Lorell BH, et al. ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). J Am Coll Cardiol. 2003;42(7):1318-1333. 2. Shaw LJ, Iskandrian AE. Prognostic value of gated myocardial perfusion SPECT. J Nucl Cardiol. 2004;11(2):171-185. 3. Berman DS, Hachamovitch R, Kiat H, et al. Incremental value of prognostic testing in patients with known or suspected ischemic heart disease: a basis for optimal utilization of exercise technetium-99m sestamibi myocardial perfusion single-photon emission computed tomography [published correction
12
Mayo Clin Proc.
appears in J Am Coll Cardiol. 1996;27(3):756]. J Am Coll Cardiol. 1995;26 (3):639-647. 4. Giri S, Shaw LJ, Murthy DR, et al. Impact of diabetes on the risk stratification using stress single-photon emission computed tomography myocardial perfusion imaging in patients with symptoms suggestive of coronary artery disease. Circulation. 2002;105(1):32-40. 5. Hachamovitch R, Hayes S, Friedman JD, et al. Determinants of risk and its temporal variation in patients with normal stress myocardial perfusion scans: what is the warranty period of a normal scan? J Am Coll Cardiol. 2003;41(8):1329-1340. 6. Greenland P, LaBree L, Azen SP, Doherty TM, Detrano RC. Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals [published correction appears in JAMA. 2004;291 (5):563]. JAMA. 2004;291(2):210-215. 7. Greenland P, Bonow RO, Brundage BH, et al, Society of Atherosclerosis Imaging and Prevention, Society of Cardiovascular Computed Tomography. ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography). J Am Coll Cardiol. 2007;49 (3):378-402. 8. Askew JW, Miller TD, Araoz PA, Breen JF, Hodge DO, Gibbons RJ. Abnormal electron beam computed tomography results: value of repeating myocardial perfusion single-photon emission computed tomography in the ongoing assessment of coronary artery disease. Mayo Clin Proc. 2008;83(1):17-22. 9. Berman DS, Kang X, Hayes SW, et al. Adenosine myocardial perfusion single-photon emission computed tomography in women compared with men: impact of diabetes mellitus on incremental prognostic value and effect on patient management. J Am Coll Cardiol. 2003;41(7):1125-1133. 10. Wackers FJ, Chyun DA, Young LH, et al, Detection of Ischemia in Asymptomatic Diabetics Study Investigators. Resolution of asymptomatic myocardial ischemia in patients with type 2 diabetes in the Detection of Ischemia in Asymptomatic Diabetics (DIAD) study. Diabetes Care. 2007 Nov; 30(11):2892-2898. Epub 2007 Aug 6. 11. Rozanski A, Gransar H, Wong ND, et al. Clinical outcomes after both coronary calcium scanning and exercise myocardial perfusion scintigraphy. J Am Coll Cardiol. 2007 Mar 27;49(12):1352-1361. Epub 2007 Feb 14. 12. Beckman JA, Ganz J, Creager MA, Ganz P, Kinlay S. Relationship of clinical presentation and calcification of culprit coronary artery stenoses. Arterioscler Thromb Vasc Biol. 2001;21(10):1618-1622. 13. Motoyama S, Kondo T, Sarai M, et al. Multislice computed tomographic characteristics of coronary lesions in acute coronary syndromes. J Am Coll Cardiol. 2007 Jul 24;50(4):319-326. Epub 2007 Jul 6. 14. Schuijf JD, Beck T, Burgstahler C, et al. Differences in plaque composition and distribution in stable coronary artery disease versus acute coronary syndromes; non-invasive evaluation with multi-slice computed tomography. Acute Card Care. 2007;9(1):48-53. 15. Raggi P, Shaw LJ, Berman DS, Callister TQ. Prognostic value of coronary artery calcium screening in subjects with and without diabetes. J Am Coll Cardiol. 2004;43(9):1663-1669. 16. Min JK, Shaw LJ, Devereux RB, et al. Prognostic value of multidetector coronary computed tomographic angiography for prediction of all-cause mortality. J Am Coll Cardiol. 2007 Sep 19;50(12):1161-1170. Epub 2007 Sep 4. 17. 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 Jan 2;49(1):6270. Epub 2006 Dec 14.
• January 2008;83(1):10-12
•
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
EDITORIAL
January 2008
Mayo Clinic Proceedings
Volume 83 Number 1
Can Coronary Calcification Define the Warranty Period of a Normal Myocardial Perfusion Study?
M
yocardial perfusion scintigraphy (MPS) has an important role in diagnosis and management of patients presenting with known or suspected coronary artery disease (CAD).1 Moreover, it is the most commonly used and well-documented noninvasive method for risk stratification. In large cohorts of patients, a clear association has been demonstrated between the extent of perfusion abnormalities and risk of coronary events. Alternatively, normal results from MPS define patients at low risk, in general less than 1%, for adverse cardiac events during the next year.2 This observation holds true even among patients with high (ie, >85%) pretest likelihood of CAD.1,3 Accordingly, these patients can be managed medically, and the costs and risks of invasive testing and of revascularization can be avoided. Still, event rates have been reported to increase after both normal and abnormal results from studies in certain subsets of patients. Particularly in the presence of comorbidity, the risk of future adverse cardiac events appears to be in the range of 1% to 3%, even if results of MPS are normal.2,4,5 Moreover, a temporal component of risk has been identified; although risk is initially low, it increases over time after normal results from MPS. Several clinical characteristics, including known CAD or diabetes, have been found to further alter this temporal component of risk.5 These observations have contributed to the notion that a “warranty period” exists for normal results on MPS. As a consequence, repeated testing over time might be appropriate. However, the following questions arise: In which patients should imaging be repeated? If imaging should be repeated, when? To date, the answers to these questions have not been settled. A particularly relevant question is
Address correspondence to Jeroen J. Bax, MD, PhD, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands ([email protected]). © 2008 Mayo Foundation for Medical Education and Research
10
Mayo Clin Proc.
whether patients with evidence of atherosclerosis but initially normal myocardial perfusion will develop perfusion abnormalities over time. The use of coronary calcium scoring has been proposed as an ap- See also proach to study and resolve these questions page 17 because coronary calcifications are a direct marker for coronary atherosclerosis. Moreover, a large body of evidence indicates an association between the presence and extent of calcium and the risk of adverse cardiac events. This prognostic value is independent of baseline characteristics and is superior to the Framingham Risk Score.6.7 Accordingly, it is conceivable that detection of atherosclerosis by means of calcium scoring will allow identification of a high-risk subset within a low-risk population. This concept was tested by Askew et al.8 In a retrospective study, 69 asymptomatic patients with low-risk results on MPS but elevated coronary calcium levels (median calcium score, 443), who remained asymptomatic during follow-up, underwent repeated testing within 4 years (mean ± SD, 1.9±0.8 years) after the initial study. In most patients (65 [94%]), no changes were observed in myocardial perfusion during the repeated MPS study. In only 4 patients (6%), all with a baseline calcium score exceeding 100, progression in MPS risk category was observed. During a mean ± SD follow-up of 4.3±1.6 years after the repeated MPS, only 3 revascularizations occurred, resulting in an event-free survival of 94%. Accordingly, the authors concluded that, in asymptomatic patients with a low-risk MPS study, repeated testing within 4 years is not justified even if coronary calcium is present. Because our understanding of the pathophysiology and course of progression from subclinical coronary atherosclerosis (evidenced by calcification of coronary arteries) to hemodynamically important CAD (evidenced by abnormal MPS data) is currently limited, observations such as those by Askew et al are important and of great value for
• January 2008;83(1):10-12
•
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
EDITORIAL
developing algorithms for sequential testing. However, certain methodologic aspects of their study should be considered when interpreting their results. BASELINE CHARACTERISTICS Baseline characteristics of the study population could have substantially influenced results. The number of study participants was small, making it difficult to draw firm conclusions. Moreover, only 35 patients (51%) had high-risk calcium scores (>400). In contrast, calcium scores of less than 100, which are generally considered low risk, were observed in a substantial proportion of patients. Also of importance is the study’s inclusion of only asymptomatic patients. Patients who experienced angina, myocardial infarction, or revascularization between the 2 MPS studies were excluded. However, changes in clinical status imply progression of subclinical CAD to clinically manifest CAD, and it is conceivable that baseline calcium scores in such patients would be higher than in patients with no adverse cardiac events. Nevertheless, a change in clinical status alone would justify further testing, whereas the relevance of serial testing in patients without changes in clinical status remains debatable. The key finding of the current study is that asymptomatic patients remain at low risk after normal results on a baseline MPS, even if coronary calcification is present. Whether this observation also applies to patients with diabetes remains to be determined. In the current study, diabetes was present in only a small proportion (17%) of patients, of whom only 3 (4%) were insulin dependent. Patients with diabetes, however, are precisely those in whom unexpected clinical events can affect those previously asymptomatic, and it has been established that absence of symptoms in diabetes does not necessarily imply absence of CAD. Further, the presence of diabetes has been identified in several studies as an important predictor of increased risk of cardiac events despite initially normal myocardial perfusion.5,9 This is particularly true for insulin-dependent diabetes.9 Therefore, it is conceivable that sequential MPS testing prompted by coronary calcification will increase recognition of progression to clinically relevant CAD in patients with diabetes. Prospective studies of patients with diabetes are needed to examine whether calcium scoring indeed is useful to identify these high-risk patients. EFFECT OF CLINICAL MANAGEMENT The effect of clinical management is another potential confounding factor in the current study. Calcium scores were higher among patients who were referred for repeated testing than scores among those who were not referred. Clearly, the knowledge that coronary calcium was present could Mayo Clin Proc.
have influenced clinical management. This influence might not only have prompted closer monitoring, including repeated imaging studies, but might also have affected therapy, leading to more intense medical therapy and aggressive modification of risk factors. The effect of medical management decisions based on the known presence of subclinical atherosclerosis could further explain the low rate of progression of CAD (evidenced by the absence of changes on repeated MPS) noted in the current study. Recently, results of the Detection of Ischemia in Asymptomatic Diabetics (DIAD-2) study were reported.10 In the DIAD-2 study, 358 asymptomatic patients with type 2 diabetes underwent repeated MPS imaging 3 years after initial evaluation. Unexpectedly, new ischemia developed in only a small proportion, and perfusion remained normal in 259 (90%) of 287 patients with normal results from baseline imaging studies. Even more striking was the observation that ischemia resolved in 79% of patients with abnormal myocardial perfusion at baseline. Careful inspection of the data suggests intensified treatment as the most probable cause for such improvement. Accordingly, more aggressive medical therapy (including the use of statins, aspirin, and angiotensin-converting enzyme inhibitors) and more aggressive treatment of risk factors could have influenced the findings in the study by Askew et al. RECOGNIZING SUBCLINICAL ATHEROSCLEROSIS Finally, it remains to be determined whether calcium scoring is the most suitable marker for subclinical atherosclerosis in attempts to refine risk stratification among patients with normal results of MPS. Recently, Rozanski et al11 evaluated the association between calcium scoring and MPS in forecasting outcomes for a large cohort of mainly asymptomatic patients (51%) with a low prevalence of diabetes (8%). Among 1089 patients with normal results from MPS who were monitored for an average ± SD time of 32±16 months, the annualized cardiac event rate was less than 1% in all subgroups of coronary calcium quantity, including those with calcium scores greater than 1000. These findings suggest, as do the findings by Askew et al, that the short-term risk in patients with normal results from MPS is low, irrespective of the extent of coronary calcium deposits. The quantity of coronary calcification does not directly reflect total plaque burden, in particular the extent of noncalcified atherosclerosis. Although calcified and noncalcified coronary plaque are associated, the strength of this association appears to be highly dependent on the clinical presentation. In patients with acute coronary syndromes and in patients with diabetes, calcium scores appear to underestimate noncalcified coronary plaque burden.12-15 In fact, extensive calcification could represent a
• January 2008;83(1):10-12
•
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
11
EDITORIAL
more stable stage of CAD, whereas noncalcified and mixed lesions could be early and unstable stages of disease, possibly with a higher prevalence of vulnerable plaque. The inability to assess noncalcified plaque might be an important shortcoming of coronary calcium scoring. Contrastenhanced computed tomographic angiography (CTA) of the coronary arteries might help improve risk stratification in patients with normal results from MPS. With coronary CTA, not only the extent of atherosclerosis but also its severity, location, and plaque composition can be described. Because coronary CTA is a relatively new technique, preliminary data on its prognostic value are only just emerging.16,17 Currently, no evidence shows that detection of high-risk anatomy by coronary CTA will provide incremental prognostic value over MPS. Therefore, large prospective studies are needed to determine whether detailed analysis of subclinical atherosclerosis by coronary CTA in combination with certain clinical characteristics will allow more accurate identification of patients at increased risk for progression of CAD for whom sequential MPS testing is warranted. Certainly, studies to date, including the current report, suggest that calcium scoring alone does not refine risk assessment in asymptomatic patients with normal results from MPS, and serial testing in these patients might not be useful. Jeroen J. Bax, MD, PhD Joanne D. Schuijf, PhD Department of Cardiology Leiden University Medical Center Leiden, the Netherlands
1. Klocke FJ, Baird MG, Lorell BH, et al. ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). J Am Coll Cardiol. 2003;42(7):1318-1333. 2. Shaw LJ, Iskandrian AE. Prognostic value of gated myocardial perfusion SPECT. J Nucl Cardiol. 2004;11(2):171-185. 3. Berman DS, Hachamovitch R, Kiat H, et al. Incremental value of prognostic testing in patients with known or suspected ischemic heart disease: a basis for optimal utilization of exercise technetium-99m sestamibi myocardial perfusion single-photon emission computed tomography [published correction
12
Mayo Clin Proc.
appears in J Am Coll Cardiol. 1996;27(3):756]. J Am Coll Cardiol. 1995;26 (3):639-647. 4. Giri S, Shaw LJ, Murthy DR, et al. Impact of diabetes on the risk stratification using stress single-photon emission computed tomography myocardial perfusion imaging in patients with symptoms suggestive of coronary artery disease. Circulation. 2002;105(1):32-40. 5. Hachamovitch R, Hayes S, Friedman JD, et al. Determinants of risk and its temporal variation in patients with normal stress myocardial perfusion scans: what is the warranty period of a normal scan? J Am Coll Cardiol. 2003;41(8):1329-1340. 6. Greenland P, LaBree L, Azen SP, Doherty TM, Detrano RC. Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals [published correction appears in JAMA. 2004;291 (5):563]. JAMA. 2004;291(2):210-215. 7. Greenland P, Bonow RO, Brundage BH, et al, Society of Atherosclerosis Imaging and Prevention, Society of Cardiovascular Computed Tomography. ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography). J Am Coll Cardiol. 2007;49 (3):378-402. 8. Askew JW, Miller TD, Araoz PA, Breen JF, Hodge DO, Gibbons RJ. Abnormal electron beam computed tomography results: value of repeating myocardial perfusion single-photon emission computed tomography in the ongoing assessment of coronary artery disease. Mayo Clin Proc. 2008;83(1):17-22. 9. Berman DS, Kang X, Hayes SW, et al. Adenosine myocardial perfusion single-photon emission computed tomography in women compared with men: impact of diabetes mellitus on incremental prognostic value and effect on patient management. J Am Coll Cardiol. 2003;41(7):1125-1133. 10. Wackers FJ, Chyun DA, Young LH, et al, Detection of Ischemia in Asymptomatic Diabetics Study Investigators. Resolution of asymptomatic myocardial ischemia in patients with type 2 diabetes in the Detection of Ischemia in Asymptomatic Diabetics (DIAD) study. Diabetes Care. 2007 Nov; 30(11):2892-2898. Epub 2007 Aug 6. 11. Rozanski A, Gransar H, Wong ND, et al. Clinical outcomes after both coronary calcium scanning and exercise myocardial perfusion scintigraphy. J Am Coll Cardiol. 2007 Mar 27;49(12):1352-1361. Epub 2007 Feb 14. 12. Beckman JA, Ganz J, Creager MA, Ganz P, Kinlay S. Relationship of clinical presentation and calcification of culprit coronary artery stenoses. Arterioscler Thromb Vasc Biol. 2001;21(10):1618-1622. 13. Motoyama S, Kondo T, Sarai M, et al. Multislice computed tomographic characteristics of coronary lesions in acute coronary syndromes. J Am Coll Cardiol. 2007 Jul 24;50(4):319-326. Epub 2007 Jul 6. 14. Schuijf JD, Beck T, Burgstahler C, et al. Differences in plaque composition and distribution in stable coronary artery disease versus acute coronary syndromes; non-invasive evaluation with multi-slice computed tomography. Acute Card Care. 2007;9(1):48-53. 15. Raggi P, Shaw LJ, Berman DS, Callister TQ. Prognostic value of coronary artery calcium screening in subjects with and without diabetes. J Am Coll Cardiol. 2004;43(9):1663-1669. 16. Min JK, Shaw LJ, Devereux RB, et al. Prognostic value of multidetector coronary computed tomographic angiography for prediction of all-cause mortality. J Am Coll Cardiol. 2007 Sep 19;50(12):1161-1170. Epub 2007 Sep 4. 17. 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 Jan 2;49(1):6270. Epub 2006 Dec 14.
• January 2008;83(1):10-12
•
www.mayoclinicproceedings.com
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.