Coronary CT Angiography for Acute Chest Pain in the ER

pdf path

Image Gallery

Acute chest pain presents a clinical challenge because of its prevalence, broad differential, and risk of serious morbidity and mortality. The diagnosis is complicated by its spectrum of presentations, including the most severe ST-elevation myocardial infarction (MI) and unstable angina (UA), where biomarker evidence of myocardial damage is lacking. Event prediction remains difficult even if coronary atherosclerotic disease (CAD) can be demonstrated, as the majority of plaque ruptures are—perhaps surprisingly—clinically silent, with acute coronary syndromes (ACS) occurring stochastically in proportion to CAD burden.1 If patients can be determined to be CAD-negative, however, they have essentially zero risk, both in the short and long term.

This review discusses the state of coronary CT angiography (CCTA) for management of acute chest pain in the emergency department (ED). CCTA directly visualizes coronary plaque burden, thereby ruling out a greater proportion of negative patients than any other noninvasive test. Simultaneously, it delivers the best short-term diagnostic accuracy in comparison to existing accelerated diagnostic protocols (Table 1).2 CCTA also provides the best long-term prognosis at the earliest time point, as well as positive effects on downstream morbidity and mortality. Nevertheless, the present level of CCTA utilization does not reflect its superior ability. We will explore the effectiveness of CCTA and advocate for its intelligent use in this patient population.

Non-CCTA Accelerated Diagnostic Protocols

Chest pain places a significant burden on the ED and the health care system as a whole. Standards of care include clinical observation, serial electrocardiograms (ECGs), serial cardiac biomarkers, and provocative functional or imaging tests, with the overall goal of reducing short-term major adverse cardiovascular events (MACE). Several accelerated diagnostic protocols have been developed to reduce ED and total costs without compromising patient safety.

The TIMI (Thrombolysis In Myocardial Infarction) score was initially developed to assess ACS severity in diagnosed patients; it has been used with varying degrees of success to predict ACS itself.3 The ADAPT accelerated diagnostic pathway combines the lowest possible TIMI score of zero with negative conventional troponin-I at 2 hours to reduce the risk of ACS to 0.3%.4 The ADAPT pathway has a specificity of approximately 25%, meaning only approximately a quarter of disease negative patients actually test negative. The remaining three quarters test positive, are not “ruled out,” and are exposed to additional testing. A randomized clinical trial (RCT) employing ADAPT vs. standard of care found that ADAPT doubles the early discharge rate without compromising patient safety.5 The APACE pathway uses high-sensitivity troponin-I at 2 hours with a TIMI score as high as 1 to achieve essentially the same low-risk rate as ADAPT and a specificity proportion of close to 50%.6

The HEART risk score was specifically constructed to predict the risk of ACS and was validated within the ED patient population.7 The HEART pathway successfully combines a low-risk HEART score with a 3-hour conventional troponin-I to reduce the risk of MACE rate to zero with a specificityt proportion of approximately 50%.8 ADAPT and APACE recommend outpatient functional testing following early discharge due to a fatality within the study cohort in which a stress test was performed but incorrectly interpreted. Notably, the HEART pathway investigators suggest that based on their results, low-risk patients require no further outpatient testing. Additional protocols have been suggested (Table 1).

Acute setting accelerated diagnostic pathways must avoid provocative testing because of the real—albeit unlikely—possibility of provoking infarction.9 Functional accelerated protocols must therefore rely on the resting state as a pseudo-stress equivalent. Acute rest single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) demonstrates a 99% negative predictive value (NPV) for acute MI, but examinations must be read critically with a resultant loss of specificity.10,11 Moreover, these findings are for MI only. With respect to all short-term MACE, the miss rate appears closer to 7%.10 In practice, an RCT employing SPECT after negative biomarker testing demonstrated reduced admissions with no change in short-term outcome. However, widespread implementation of this protocol is unlikely due to the practical difficulties surrounding the unscheduled use of radionuclide pharmaceuticals.12

CCTA-based Acute Chest Pain Management

CCTA for patients with acute chest pain is more effective at many levels. A systematic review and meta-analysis performed in 2008 yielded an NPV of 100% and specificity of 89% in predicting significant CAD.13 In 2012, a systematic review and meta-analysis concluded that CCTA has an NPV of 99.3% for ACS and a specificity of 87%, meaning only approximately 1 in 10 negative patients are exposed to further testing.14 Three ensuing large multicenter RCTs compared CCTA and functional protocols and demonstrated that CCTA accelerates diagnosis, with twice to quadruple as many direct discharges from the ED, a reduction in ED costs of 18% to 38%, and no increase in short-term MACE.15 An RCT comparing CCTA with the cheapest and most widely used functional test, treadmill exercise stress ECG, shows that costs with CCTA are still lower, primarily driven by decreased length of stay.16 In 2014, the American Heart Association-American College of Cardiology Non-ST Elevation Acute Coronary Syndrome (AHA/ACC NSTE-ACS) guidelines assigned CCTA the highest level of evidence. The 2015 AHA/ACC released appropriate use criteria jointly with the American College of Radiology (ACR) that endorse CCTA as a first-line exam.17

CCTA and High-Sensitivity Troponins

The benefit of CCTA continues in the high-sensitivity troponin era, although its advantages have recently been questioned. A 2016 RCT in the Netherlands comparing CCTA to usual care including high-sensitivity troponins showed a 6% increase in direct ED discharges with CCTA, 65% vs. 59%, although without attaining statistical significance.18 The authors suggest their study was underpowered to show the small CCTA ED discharge rate benefit. They also note that the integrated nature of the Netherlands health system and excellent access to primary care steered a greater proportion of low-risk, CAD-negative and, hence, CCTA-negative patients away from the ED.18 The diagnostic power of CCTA rests in its excellent ability to identify patients without CAD and, therefore, without risk; thus, as CAD burden increases within the test population, the diagnostic accuracy decreases. From RCTs in the United States, it has been calculated that cost savings will occur only in populations where CCTA will show < 50% stenosis in at least 72% of patients, ie, populations with relatively lower risk of ACS.19 The Netherlands study just barely met this quota, with 74% of patients negative for obstructive CAD.18 These caveats suggest that in a U.S. population with lower risk, the ED discharge rate for a combined CCTA and higher-sensitivity troponin strategy might be higher.

Moreover, although the Netherlands study reports that both cohorts demonstrated similar median lengths of stay, 6.3 hours, outcomes within the next quartile of patients dramatically differed. Specifically, 75% of CCTA cohort stays were < 11.1 hours, while 75% of patients within the usual care group were not discharged until >25.5 hours. CCTA also prevented additional downstream testing. It is not surprising that CCTA led to statistically significant lower short-term costs, a savings of approximately one-third, despite the higher prevalence of CAD.18 The different findings from the U.S. studies may reflect a practice pattern emphasizing earlier ED disposition decisions, but certainly do not reduce the central conclusion of shorter stays and lower costs using CCTA.

Technical Improvements in CCTA

The spatial resolution of CCTA is typically 0.35 mm as compared to 0.16 mm for invasive angiography. Whereas a 3-mm coronary lumen is delineated on 18 pixels in fluoroscopy, CCTA displays the same vessel over 9 voxels, limiting determination of the exact degree of CAD.20 CCTA stenosis severity is therefore reported in increments of 25%. While interventional coronary angiography (ICA) outpaces CCTA in differentiating patients with varying degrees of CAD severity, surpassing CCTA’s positive predictive value (PPV), the NPV of CCTA at least equals that of ICA.20,21

CCTA continues to improve technically. Traditionally, CCTA struggled to match the temporal resolution of the invasive exam. Fluoroscopy yields 30 frames per second, corresponding to a resolution of 33 milliseconds, essentially eliminating motion artifact.20 Increased CCTA temporal resolution on an ECG-gated exam is now achieved using multicycle reconstructions, higher gantry rotation speeds, use of multiple x-ray sources, and wider detectors.20

Radiation dose in CCTA initially matched the effective dose of SPECT MPI exams of approximately 12-14 mSv; however, prospective gating, faster scanning, and better reconstruction algorithms have halved the dose, with improvement continuing. By comparison, a noncomplicated diagnostic cardiac catheterization delivers 8-10 mSv. Controversy exists as to whether exposure < 50 mSv imparts any increased risk, with major societies at odds about appropriate recommendations.22 Assuming, for the sake of caution—as the ACR does—the absence of a threshold for radiation-induced damage, the lifetime attributable risk of fatal cancer for a 5 mSv study would be a single additional fatal cancer per 2,000 examinations, undoubtedly a small fraction of the likely study benefit.22 The latest CT scanners deliver diagnostic scans at approximately 1 mSv.20,23 At such doses, radiation is no longer a realistic concern.

A principal technical advantage of CCTA is that the data obtained is intrinsically 3-dimensional. Images from a single acquisition can be viewed from any angle or projection with no vessel overlap, unlike the 2-dimensional data produced by angiography. This benefit partially compensates for CCTA’s lesser spatial and temporal resolution. Commonly used projections and reformations include surface rendering (Figure 1), curved multiplanar reconstructions (Figure 2), and straightened multiplanar reconstructions along the course of the vasculature (Figure 3).

High-risk Coronary Features Indicate Increased Risk

CCTA demonstrates prognostically important pathology not seen on catheter angiography. High-risk CCTA coronary plaque features include positive remodeling (increase in the outside diameter of the vessel, Figure 4), spotty calcium (Figure 5A), low attenuation plaque (Figures 5A-B), and rim-enhancing plaque (the “napkin-ring” sign, Figure 6), the latter likely indicating the presence of a lipid-laden plaque core.24 The relative risk of these high-risk plaque features for short-term MACE within the ED population is comparable to that of obstructive CAD, approximately 30 times.24 This holds true even after controlling for the presence of obstructive disease, thus increasing exam utility. CCTA-positive patients with nonobstructive CAD and without high-risk features could be classified as lower risk, increasing the proportion of patients that CCTA could clear. In patients with obstructive CAD and high-risk features, the PPV of the exam increases.24 High-risk features also serve as a biomarker of functional disease, as both plaque volume and high-risk characteristics correlate with the functional significance of a lesion as determined by invasive measurement of the pressure differential across the lesion, ie, ICA with measurement of the fractional flow reserve (FFR).25

Long-term Prognosis: The 6-Year CCTA Guarantee

In outpatients, a completely negative CCTA provides a virtual guarantee of approximately 6 years of MACE-free survival, while nonobstructive CAD indicates a stable small risk for at least 2 years.26 The risk of MACE is approximately 0.5% per year for limited nonobstructive CAD and between 2-3 times that number with obstructive disease or extensive non-obstructive disease.1 Risk increases with the number of vessels involved. Just as high-risk features affect short-term risk, they also increase risk over the long term.26,27

No stress modality can rival CCTA in detecting nonobstructive disease, since stress testing is blind to disease that is not flow limiting. Thus, only CCTA can provide information about the early CAD stages noninvasively. For this same reason, CCTA provides a longer guarantee if negative, in addition to comparable prognostic information when positive. Comparison between CCTA and exercise ECG actually demonstrates increased long-term risk in CCTA-positive patients irrespective of functional testing results.28 CCTA and SPECT can work synergistically to risk-stratify patients at the cost of increased radiation dose.27

Clinical Benefit to Anatomical over Functional Testing

Long-term studies reveal a clinical benefit to CCTA. Not surprisingly, CCTA outperforms functional tests when anatomical findings on ICA are used as the reference standard. Within a population of 6200 patients undergoing CCTA after a functional test, for example, the relative risk of a false-positive or false-negative stress test as compared to an inaccurate CCTA was 1.4 and 3.1, respectively.29 An analysis of the nationwide elective ICA registry confirms the higher PPV of CCTA vs. all the various stress tests at approximately 70% vs. 46%.30 Newer research, however, suggests that revascularization should be guided by the functional perfusion deficit as measured by FFR during ICA, and a systematic review and meta-analysis demonstrate that SPECT outperforms CCTA in identifying lesions when ICA with FFR is used as the new gold standard.31 One would expect, based on this research, to find clinical benefit for noninvasive functional testing; however, the opposite has been shown.

A meta-analysis of recent clinical trials in outpatients with CAD (PROMISE, SCOT-HEART, and two smaller RCTs) shows a statistically significant reduction of annual MI in patients who underwent CCTA, to approximately 0.7 times the rate of patients with functional exams.32 Three-year follow-up of SCOT-HEART similarly demonstrates a statistically significant cardiac fatality and MI risk ratio of 0.5. This benefit is attributed to statistically significant changes in medical and invasive management.33 CCTA is already a first-line test for outpatient CAD in Europe, and these results suggest it should be first-line in the United States as well.34

Undoubtedly, CCTA could be improved if functional data could be derived from the exam. CT-FFR is a computational technique that noninvasively calculates the pressure gradient across lesions using the 3-dimensional coronary anatomy, without catheterization, without adenosine administration, and with no increase in contrast material injected or in radiation dose. A meta-analysis with invasive FFR as the reference standard validates its accuracy; CT-FFR improves both the sensitivity and specificity of the CCTA exam.35 However, the PLATFORM RCT showed no downstream clinical benefits of CT-FFR compared to CCTA.36,37 Although the rate of future clinical deterioration may depend on the functional deficit, it likely primarily flows from the background clinical and anatomical risk, especially if assessed earlier and/or in a lower-risk population.

Finally, the CATCH trial directly elucidates the long-term impact of CCTA use within the ED population, despite the difficulty in assembling enough patients and events to power a study of this kind.38 In CATCH, patients with potential ACS admitted for less than 24 hours underwent both functional testing and CCTA prior to discharge, but the CCTA data was reported to the referring physician in only half of the patients. After 18 months, the CCTA cohort demonstrated a 2% reduction in cardiac death or MI. This difference was just shy of statistical significance, with p-value of 0.06. The usual care cohort, in contrast, had a statistically significant increased risk of all MACE, 5% vs. 2%, and when including readmission, had a statistically significant higher risk of adverse outcomes, 16% to 11%. Complementing these findings, retrospective analysis of CCTA patients shows five-fold lower odds of recidivism.39 These results demonstrate a morbidity and mortality benefit to early use of CCTA in the ED population, just as in outpatients.

In the long term, CCTA leads to an increase in downstream procedures, which degrades the initial cost-savings.14 However, a meta-analysis of the ED RCTs, which suggests a relatively matched increase of 2% in the patients who undergo ICA and revascularization after CCTA, also suggest that these major procedures are performed appropriately.40 These increased revascularizations may drive the clinical benefits discussed above. Impressively, retrospective analysis found a seven-fold lower likelihood of undergoing ICA without revascularization in ED patients triaged by CCTA.39 ED providers and radiologists should be aware that patients who receive early testing with CCTA rather than downstream functional tests are well-served clinically.

CCTA includes a final ancillary benefit: The most common incidental finding on CCTA is a pulmonary nodule, occurring at approximately the same rate as the general population, one in five. One in 10 nodules may represent a neoplasm, with a potential morbidity and mortality benefit of 1% if just half can be detected. Further work is necessary, but recent studies suggest additional downstream costs are minimal.41

Suggestions for Management

The CAD-RADS (Reporting and Data System) has been introduced to standardize CCTA reporting and guide further research and management.21 Highlights are as follows: Patients with left main coronary stenosis of > 50%, any vessel stenosis of 70%, or 3-vessel disease are described as CAD-RADS-4 and may be candidates for revascularization. In the acute setting, this score indicates that ACS is at least likely. CAD-RADS-3 includes any other stenosis > 50% where ACS is possible and where admission and at least a functional test for further risk stratification would be considered appropriate. CAD-RADS-2 includes stenoses between 25% and 49%, where ACS is unlikely despite the presence of CAD, although high-risk plaque features would lead to a CAD-RADS-2/V designation and should escalate level of concern and further care.

Conclusion

CCTA for acute chest pain provides powerful diagnostic and prognostic information, decreases ED length of stay, reduces ED costs, and provides tangible clinical benefits. The latest biomarkers do not alter these findings. Accelerated diagnostic pathways that encourage early discharge without objective anatomic testing deny patients the proven benefits of CCTA. Further trials will hopefully lead to varied high-sensitivity troponins or integrated risk score cutoffs that stratify patients even better. Until that time, the use of early CCTA to further guide care represents the evidence-based strategy of maximal benefit and least harm, as is strongly supported by data.

References

  1. Arbab-Zadeh A, Fuster V. The myth of the “vulnerable plaque”: transitioning from a focus on individual lesions to atherosclerotic disease burden for coronary artery disease risk assessment. J Am Coll Cardiol 2015;65(8):846-855. doi:10.1016/j.jacc.2014.11.041.
  2. Romero J, Husain SA, Holmes AA, et al. Non-invasive assessment of low risk acute chest pain in the emergency department: a comparative meta-analysis of prospective studies. Int J Cardiol 2015. doi:10.1016/j.ijcard.2015.01.032.
  3. Hess EP, Agarwal D, Chandra S, et al. Diagnostic accuracy of the TIMI risk score in patients with chest pain in the emergency department: a meta-analysis. CMAJ 2010;182(10):1039-1044. doi:10.1503/cmaj.092119.
  4. Than M, Cullen L, Aldous S, et al. 2-Hour accelerated diagnostic protocol to assess patients with chest pain symptoms using contemporary troponins as the only biomarker: the ADAPT trial. J Am Coll Cardiol 2012;59(23):2091-2098. doi:10.1016/j.jacc.2012.02.035.
  5. Than M, Aldous S, Lord SJ, et al. A 2-hour diagnostic protocol for possible cardiac chest pain in the emergency department: a randomized clinical trial. JAMA Intern Med 2014;174(1):51-58. doi:10.1001/jamainternmed.2013.11362.
  6. Cullen L, Mueller C, Parsonage WA, et al. Validation of high-sensitivity troponin I in a 2-hour diagnostic strategy to assess 30-day outcomes in emergency department patients with possible acute coronary syndrome. J Am Coll Cardiol 2013;62(14):1242-1249. doi:10.1016/j.jacc.2013.02.078.
  7. Backus BE, Six AJ, Kelder JC, et al. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol 2013;168(3):2153-2158. doi:10.1016/j.ijcard.2013.01.255.
  8. Mahler SA, Riley RF, Hiestand BC, et al. The HEART pathway randomized trial: identifying emergency department patients with acute chest pain for early discharge. Circ Cardiovasc Qual Outcomes 2015;8(2):195-203. doi:10.1161/CIRCOUTCOMES.114.001384.
  9. Amsterdam EA, Kirk JD, Diercks DB, Lewis WR, Turnipseed SD. Immediate exercise testing to evaluate low-risk patients presenting to the emergency department with chest pain. J Am Coll Cardiol 2002;40(2):251-256. doi:10.1016/S0735-1097(02)01968-X.
  10. Shaw LJ, Iskandrian AE. Prognostic value of gated myocardial perfusion SPECT. J Nucl Cardiol 2004;11(2):171-185. doi:10.1016/j.nuclcard.2003.12.004.
  11. Heller G V, Stowers SA, Hendel RC, et al. Clinical value of acute rest technetium-99m tetrofosmin tomographic myocardial perfusion imaging in patients with acute chest pain and nondiagnostic electrocardiograms. J Am Coll Cardiol 1998;31(5):1011-1017. doi:10.1016/S0735-1097(98)00057-6.
  12. Udelson JE, Beshansky JR, Ballin DS, et al. Myocardial perfusion imaging for evaluation and triage of patients with suspected acute cardiac ischemia: a randomized controlled trial. JAMA 2002;288(21):2693-2700. http://www.ncbi.nlm.nih.gov/pubmed/12460092.
  13. Mowatt G, Cook JA, Hillis GS, et al. 64-Slice computed tomography angiography in the diagnosis and assessment of coronary artery disease: systematic review and meta-analysis. Heart 2008;94(11):1386-1393. doi:10.1136/hrt.2008.145292.
  14. Samad Z, Hakeem A, Mahmood SS, et al. A meta-analysis and systematic review of computed tomography angiography as a diagnostic triage tool for patients with chest pain presenting to the emergency department. J Nucl Cardiol 2012;19(2):364-376. doi:10.1007/s12350-012-9520-2.
  15. Schlett CL, Hoffmann U, Geisler T, Nikolaou K, Bamberg F. Cardiac computed tomography for the evaluation of the acute chest pain syndrome: state of the art. Radiol Clin North Am 2015;53(2):297-305. doi:10.1016/j.rcl.2014.11.007.
  16. Hamilton-Craig C, Fifoot A, Hansen M, et al. Diagnostic performance and cost of CT angiography versus stress ECG — A randomized prospective study of suspected acute coronary syndrome chest pain in the emergency department (CT-COMPARE). Int J Cardiol 2014;177:867-873. doi:10.1016/j.ijcard.2014.10.090.
  17. Rybicki FJ, Udelson JE, Peacock WF, et al. 2015 ACR/ACC/AHA/AATS/ACEP/ASNC/NASCI/SAEM/SCCT/SCMR/SCPC/SNMMI/STR/STS Appropriate utilization of cardiovascular imaging in emergency department patients with chest pain. J Am Coll Cardiol 2016;67(212):853-879. doi:10.1016/j.jacc.2015.09.011.
  18. Dedic A, Lubbers MM, Schaap J, et al. Coronary CT angiography for suspected ACS in the era of high-sensitivity troponins randomized multicenter study. J Am Coll Cardiol 2016. doi:10.1016/j.jacc.2015.10.045.
  19. Hulten E, Goehler A, Bittencourt MS, et al. Cost and resource utilization associated with use of computed tomography to evaluate chest pain in the emergency department: the Rule Out Myocardial Infarction Using Computer Assisted Tomography (ROMICAT) study. Circ Cardiovasc Qual Outcomes 2013. doi:10.1161/CIRCOUTCOMES.113.000244.
  20. Otero HJ, Steigner ML, Rybicki FJ. The “post-64” era of coronary CT angiography: understanding new technology from physical principles. Radiol Clin North Am 2009;47(1):79-90. doi:10.1016/j.rcl.2008.11.001.
  21. Cury RC, Abbara S, Achenbach S, et al. CAD-RADSTM Coronary Artery Disease – Reporting and Data System. An expert consensus document of the Society of Cardiovascular Computed Tomography (SCCT), the American College of Radiology (ACR) and the North American Society for Cardiovascular Imaging (NASCI). J Cardiovasc Comput Tomogr 2016;10(4):269-281. doi:10.1016/j.jcct.2016.04.005.
  22. Costello JE, Cecava ND, Tucker JE, Bau JL. CT radiation dose: current controversies and dose reduction strategies. Am J Roentgenol 2013;201(6):1283-1290. doi:10.2214/AJR.12.9720.
  23. Ghekiere O, Nchimi A, Djekic J, et al. Coronary computed tomography angiography: patient-related factors determining image quality using a second-generation 320-slice CT scanner. Int J Cardiol 2016;221:970-976. doi:10.1016/j.ijcard.2016.07.141.
  24. Puchner SB, Liu T, Mayrhofer T, et al. High-risk plaque detected on coronary CT angiography predicts acute coronary syndromes independent of significant stenosis in acute chest pain: results from the ROMICAT-II trial. J Am Coll Cardiol 2014;64(7):684-692. doi:10.1016/j.jacc.2014.05.039.
  25. Park H-B, Heo R, ó Hartaigh B, et al. Atherosclerotic plaque characteristics by CT angiography identify coronary lesions that cause ischemia. JACC Cardiovasc Imaging 2015;8(1):1-10. doi:10.1016/j.jcmg.2014.11.002.
  26. Nakazato R, Arsanjani R, Achenbach S, et al. Age-related risk of major adverse cardiac event risk and coronary artery disease extent and severity by coronary CT angiography: results from 15 187 patients from the international multisite CONFIRM study. Eur Heart J Cardiovasc Imaging 2014. doi:10.1093/ehjci/jet132.
  27. Lee H, Yoon YE, Park J-B, et al. The incremental prognostic value of cardiac computed tomography in comparison with single-photon emission computed tomography in patients with suspected coronary artery disease. PLoS One 2016;11(8):e0160188. doi:10.1371/journal.pone.0160188.
  28. Cheezum MK, Subramaniyam PS, Bittencourt MS, et al. Prognostic value of coronary CTA vs. exercise treadmill testing: results from the Partners registry.
  29. Chinnaiyan KM, Raff GL, Goraya T, et al. Coronary computed tomography angiography after stress testing: results from a multicenter, statewide registry, ACIC (Advanced Cardiovascular Imaging Consortium). J Am Coll Cardiol 2012;59(7):688-695. doi:10.1016/j.jacc.2011.10.886.
  30. Patel MR, Dai D, Hernandez AF, et al. Prevalence and predictors of nonobstructive coronary artery disease identified with coronary angiography in contemporary clinical practice. Am Heart J 2014;167(6):846-852.e2. doi:10.1016/j.ahj.2014.03.001.
  31. Danad I, Szymonifka J, Twisk JWR, et al. Diagnostic performance of cardiac imaging methods to diagnose ischaemia-causing coronary artery disease when directly compared with fractional flow reserve as a reference standard: a meta-analysis. Eur Heart J May 2016. doi:10.1093/eurheartj/ehw095.
  32. Bittencourt MS, Hulten EA, Murthy VL, et al. Clinical outcomes after evaluation of stable chest pain by coronary computed tomographic angiography versus usual care: a meta-analysis. Circ Cardiovasc Imaging 2016;9(4):e004419. doi:10.1161/CIRCIMAGING.115.004419.
  33. Williams MC, Hunter A, Shah AS V, et al. Use of coronary computed tomographic angiography to guide management of patients with coronary disease. J Am Coll Cardiol 2016;67(15):1759-1768. doi:10.1016/j.jacc.2016.02.026.
  34. Douglas PS. Achieving the full “PROMISE” of imaging outcomes research. Circulation 2016;134(5):359-361. doi:10.1161/CIRCULATIONAHA.116.022876.
  35. Gonzalez JA, Lipinski MJ, Flors L, Shaw PW, Kramer CM, Salerno M. Meta-analysis of diagnostic performance of coronary computed tomography angiography, computed tomography perfusion, and computed tomography-fractional flow reserve in functional myocardial ischemia assessment versus invasive fractional flow reserve. Am J Cardiol 2015;116(9):1469-1478. doi:10.1016/j.amjcard.2015.07.078.
  36. Douglas PS, Pontone G, Hlatky MA, et al. Clinical outcomes of fractional flow reserve by computed tomographic angiography-guided diagnostic strategies vs. usual care in patients with suspected coronary artery disease: the prospective longitudinal trial of FFRct: outcome and resource impacts stud. Eur Heart J 2015;36(47):3359-3367. doi:10.1093/eurheartj/ehv444.
  37. Labounty TM, Nallamothu BK. FFRCT: A new technology in search of a clinical application. Eur Heart J 2015;36(47):3368-3369. doi:10.1093/eurheartj/ehv534.
  38. Linde JJ, Hove JD, Sørgaard M, et al. Long-term clinical impact of coronary CT angiography in patients with recent acute-onset chest pain: the randomized controlled CATCH trial. JACC Cardiovasc Imaging 2015. doi:10.1016/j.jcmg.2015.07.015.
  39. Poon M, Cortegiano M, Abramowicz AJ, et al. Associations between routine coronary computed tomographic angiography and reduced unnecessary hospital admissions, length of stay, recidivism rates, and invasive coronary angiography in the emergency department triage of chest pain. J Am Coll Cardiol 2013;62(6):543-552. doi:10.1016/j.jacc.2013.04.040.
  40. Hulten E, Pickett C, Bittencourt MS, et al. Outcomes after coronary computed tomography angiography in the emergency department: a systematic review and meta-analysis of randomized, controlled trials. J Am Coll Cardiol 2013;61(8):880-892. doi:10.1016/j.jacc.2012.11.061.
  41. Lee CI, Tsai EB, Sigal BM, Plevritis SK, Garber AM, Rubin GD. Incidental extracardiac findings at coronary CT: clinical and economic impact. Am J Roentgenol. 2010;194(6):1531-1538. doi:10.2214/AJR.09.3587.
  42. Mitchell AM, Garvey JL, Chandra A, et al. Prospective Multicenter Study of Quantitative Pretest Probability Assessment to Exclude Acute Coronary Syndrome for Patients Evaluated in Emergency Department Chest Pain Units. Ann Emerg Med 2006;47(5). doi:10.1016/j.annemergmed.2005.10.013.
  43. Body R, Cook G, Burrows G, Carley S, Lewis PS. Can emergency physicians “rule in” and “rule out” acute myocardial infarction with clinical judgement? Emerg Med J 2014;31(11):872-876. doi:10.1136/emermed-2014-203832.
  44. Shah AS, Anand A, Sandoval Y, et al. High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study. Lancet 2015;386(10012):2481-2488. doi:10.1016/S0140-6736(15)00391-8.
Back To Top

Rydzinski Y, Weg N.  Coronary CT Angiography for Acute Chest Pain in the ER.  J Am Osteopath Coll Radiol.  2017;6(2):15-21.

About the Author

Yaacov Rydzinski, MD and Noah Weg, MD

Yaacov Rydzinski, MD and Noah Weg, MD

Dr. Rydzinski and Dr. Weg are with the Department of Radiology, Jacobi Medical Center, Albert Einstein College of Medicine, Bronx, NY.


 

Copyright © The American College of Osteopathic Radiology 2017