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| ORIGINAL ARTICLE |
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| Year : 2021 | Volume
: 22
| Issue : 4 | Page : 249-255 |
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The role of coronary computed tomography angiography in evaluation of high troponin patients with narrow-complex supraventricular tachycardia
Huseyin Ede1, Hosameldin Salah Shabib Sayed Ahmed1, Ahmed Sobhy Hassan Ghonim Mahfouz2, Alaa Abdullah Ali Rahhal1, Shabir Ali Haider1, Naseer Ahmed Madni1, Mohammad Akl Alkhatib1, Hossin Mohamed Elshrif1, Sumaya Mehdar A Al-Saadi Al Yafei2, Jassim Mohd Al Suwaidi1, Awad A Razaq Al-Qahtani1, Nidal Ahmad Asaad1
1 Department of Cardiology, Hamad Medical Corporation Heart Hospital, Doha, Qatar
2 Department of Pharmacology, Hamad Medical Corporation Heart Hospital, Doha, Qatar
| Date of Submission | 28-Jan-2021 |
| Date of Acceptance | 13-Dec-2021 |
| Date of Web Publication | 11-Feb-2022 |
Correspondence Address:
Dr. Huseyin Ede
Department of Cardiology, Hamad Medical Corporation Heart Hospital, Doha
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/HEARTVIEWS.HEARTVIEWS_10_21
 Abstract | | |
Aim: The aim of this study was to investigate the relation of high-sensitive cardiac troponin T (hs-cTnT) elevation with characteristics of supraventricular tachycardia (SVT) episode (duration and maximum heart rate) and coronary computed tomography angiography (CCTA) findings in patients with SVT who presented to the emergency room with palpitation.
Methods: This retrospective, single-center, noninvasive study included all patients aged between 18 years and 65 years who presented to the emergency department due to narrow-complex SVT and underwent CCTA to rule out coronary artery disease (CAD) due to elevation of hs-cTnT and reverted back to sinus rhythm after intravenous adenosine. The first, second, and the maximum hs-cTnT levels were obtained from the database. The patients were classified into normal coronaries, nonobstructive CAD, and obstructive CAD according to findings of the CCTA. The findings of the groups were compared.
Results: Eighty-five patients were enrolled in the study. Of them, 21 (26%) patients were female. Sixty-three patients (74%) had normal coronary arteries as per CCTA results, whereas 22 patients (22%) had nonobstructive CAD and two patients (2%) had obstructive CAD. The groups did not differ statistically in respect to hs-cTnT measurements, duration of the arrhythmia, and maximum heart rate at SVT episode. There was no significant statistical correlation between hs-cTnT and the study parameters except the maximum heart rate.
Conclusion: Cardiac troponins may increase in patients with paroxysmal SVT irrespective of the presence of coronary lesions, and the CCTA may not be an appropriate investigation in the differential diagnosis of paroxysmal SVT with elevated hs-cTnT.
Keywords: Coronary artery disease, coronary computed tomography angiography, high-sensitive cardiac troponin, supraventricular tachycardia
How to cite this article:
Ede H, Ahmed HS, Mahfouz AS, Rahhal AA, Haider SA, Madni NA, Alkhatib MA, Elshrif HM, Al Yafei SM, Al Suwaidi JM, Al-Qahtani AA, Asaad NA. The role of coronary computed tomography angiography in evaluation of high troponin patients with narrow-complex supraventricular tachycardia. Heart Views 2021;22:249-55 |
How to cite this URL:
Ede H, Ahmed HS, Mahfouz AS, Rahhal AA, Haider SA, Madni NA, Alkhatib MA, Elshrif HM, Al Yafei SM, Al Suwaidi JM, Al-Qahtani AA, Asaad NA. The role of coronary computed tomography angiography in evaluation of high troponin patients with narrow-complex supraventricular tachycardia. Heart Views [serial online] 2021 [cited 2023 Mar 23];22:249-55. Available from: https://www.heartviews.org/text.asp?2021/22/4/249/337535 |
| Introduction | |  |
Cardiac biomarkers have been used very frequently in the daily practice of cardiology. They are very helpful in diagnosis and follow-up of the patients, especially when they are used in the acute setting.[1] High-sensitive troponin T is one of the most frequently used cardiac biomarkers in the world. It is the preferred serologic test for the evaluation of patients with suspected acute coronary syndrome (ACS).[2]
Although troponins are highly sensitive and useful in the diagnosis of acute myocardial infarction and several protocols have been suggested using it for the screening of patients in an emergency department to rule in or rule out the diagnosis of acute myocardial infarction, these protocols cannot be applied for all clinical settings. There are, however, several false-positive troponin findings in different clinical settings that may lead to unnecessary cardiac investigations and treatments.[3],[4],[5]
Additionally, these false-positive non-ACS clinical states may result in longer length of hospital stay, social and financial burden in addition to the psychological effect on the patients.[6],[7]
These non-ACS troponin elevations can be related to cardiac causes (such as acute myocarditis, stress (Takotsubo) cardiomyopathy, tachycardia, or dilated cardiomyopathy) or due to noncardiac causes (such as trauma, exertion, chronic kidney disease, anemia, sepsis, or pulmonary embolism).[2],[8],[9]
Paroxysmal supraventricular tachycardia (SVT) is one of the most common tachyarrhythmias.[10] It can cause palpitations, syncope or presyncope, lightheadedness or dizziness, diaphoresis, chest pain, or shortness of breath. The diagnosis is usually made by 12-lead ECG. Guideline-based treatments include vasovagal maneuvers, cardioversion, intravenous adenosine, beta-blockers, or calcium channel blockers.[10]
Troponin elevations in the setting of SVT is very frequently seen in an emergency department, and most of the time, the pattern of troponin rise and decrease can mimic ACS pattern.[11] Troponin elevations in the setting of SVT episode always create clinical confusion due to the possibility of concurrent acute ischemia although the possibility of ACS is very low. Additionally, the patients may undergo noninvasive assessment to rule out obstructive coronary artery disease (CAD).
Currently, it is not known what is the amount of troponin that would indicate the presence of a significant CAD. The relation of troponin elevation with characteristics of SVT episode (such as maximum heart rate during the SVT episode and duration of SVT), demographic characteristics of the patients, and coronary anatomy of the patients has not been clearly documented in the literature.
In this study, we aimed to investigate the relation of troponin elevation with characteristics of SVT episode and coronary computed tomography angiography (CCTA) findings in patients with narrow-complex SVT. We sought to find out the relation in this study.
| Materials and Methods | | |
This is a retrospective, single-center, nationwide, noninvasive study which included patients aged between 18 years and 65 years and who presented to the emergency departments of the hospital due to SVT. These patients had undergone CCTA to rule out CAD due to elevation of high-sensitive cardiac troponin T (hs-cTnT). For this purpose, all patients who came to our institution due to SVT between January 2015 and August 2020 were reviewed through our centralized database and the patients fulfilling the inclusion criteria were enrolled in the study.
SVT was defined as any sustained narrow-QRS (<120 ms in duration) tachyarrhythmia of supraventricular origin. The study included only those patients with SVT who reverted to sinus rhythm with intravenous adenosine. Thus, any patient who received direct current cardioversion was excluded. The patients with ventricular tachycardia, atrial flutter, atrial fibrillation, or atrial tachycardia at the time of index admission were excluded. The diagnosis of SVT was confirmed by the cardiologist who was blinded to the study protocol after reviewing the 12-lead electrocardiography (ECG) of the patients in the database.
The exclusion criteria for the study were as follows: hemodynamic instability (blood pressure of <90/60 mmHg for more than 30 min, angina, decreased level of consciousness, hypotension, or acute pulmonary edema) at index admission, acute myocardial infarction at index admission, history of CAD or angina, the left ventricular ejection fraction (LVEF) of <50%, history of congestive heart failure, history of moderate or severe valvular disease, history of congenital heart disease or previous cardiac surgery, any cardiomyopathies or pericardial diseases, chronic kidney disease (glomerular filtration rate below 90 ml/min/1.73 m2), liver disease (defined as blood transaminase levels of more than three times above the upper normal limit), hemoglobin level of <10 g/dl, history of stroke, malignancy, hypo- or hyperthyroidism, active infection, or trauma at index admission.
Ethical and institutional approval for the study was obtained accordingly (MRC-01-20-789 dated on September 24, 2020).
Demographic characteristics of the patients (age, gender, weight, height, race (as African, European, Central/North Asian, South Asian, European, Middle Eastern, North American, South American, and Australian) were obtained. Body mass index of each subject was calculated by a formula (weight in kilogram divided by square of height in meter). Concomitant morbidities (hypertension and diabetes) were recorded. Duration of SVT was the time from the onset of the palpitation till the time that sinus rhythm was established. Maximum heart rate was obtained from 12-lead ECG showing SVT in the database. In this study, we defined a new parameter to assess the effect of SVT on the heart: duration heart rate product (DHRP). This was calculated by the formula as follows: DHRP = duration of SVT in minutes multiplied by maximum heart rate (in beats/minute).
Blood hemoglobin, neutrophil count, lymphocyte count, and thyroid-stimulating hormone values at the time of SVT episode were recorded. Neutrophil-to-lymphocyte ratio was calculated as neutrophil count divided by lymphocyte count. During the index admission due to SVT episode, hs-cTnT value (normal range in our laboratory was 0–15 ng/L), the second set of hs-cTnT that was taken 3 h after the first set, and the maximum troponin value were obtained from the database. Delta hs-cTnT was defined as a difference between the first and the second sets of hs-cTnT.
Transthoracic echocardiography images of all patients in the database were reviewed by the cardiologist blinded to the study results. The left atrial diameter and volume, LVEF, and grade of the left ventricular diastolic dysfunction were obtained as per the recommendations of the American Society of Echocardiography.[12]
Computed tomography coronary angiography was performed via a 128-row, multi-detector Siemens Somatom Definition Flash device using 128 mm × 0.6 mm collimation, prospective scan technique with iohexol 350. The images of the patients were reviewed by the radiologist blinded to the data of the patients. Main vessels were defined as follows: the left main coronary artery, the left anterior descending artery, the left circumflex artery, the right coronary artery, the diagonal, and the obtuse marginal branches.
Quantitative coronary calcium scores of each patient were measured by using the method previously described by Agatston et al.[13]
Coronary lesion was defined as any level of stenosis at main vessels. Coronary lesion that resulted in stenosis of more than moderate degree by CCTA was defined as obstructive CAD. The subjects were divided into three groups as per CCTA results: the patients without CAD (defined as patients without coronary lesion), the patients with nonobstructive CAD (defined as patients with stenosis of mild or moderate degree), and the patients with obstructive CAD (defined as patients with stenosis of more than moderate degree).
Correlation analyses of demographic characteristics, echocardiographic findings, maximum heart rate at SVT episode, duration of SVT, DHRP values, and CCTA findings with hs-cTnT measurements were performed. Additionally, these findings were compared among different groups.
Statistical analysis
Version 24 SPSS analysis program (Statistical Package for Social Sciences-SPSS, Inc., Chicago, Illinois) for Windows was used for statistical analysis. The distribution of the data was analyzed by using the Kolmogorov–Smirnov test. Descriptive variables were presented as mean ± standard deviation for normally distributed continuous variables, median (interquartile difference) for nonnormally distributed continuous variables, shown as a number (percent) for categorical variables. Interquartile difference is the difference between the 75th and 25th percentiles.
One-way ANOVA test was used for comparison of normally distributed parametric variables of the groups in respect to their averages and “Tukey's honestly significant difference” test was employed in determining the group causing the difference; the Kruskal–Wallis test was used for nonparametric variables, and the Mann–Whitney U-test was used to determine the group that caused the difference. The Chi-square test was used to analyze the relationship among categorical variables of the groups. The direction of the relationship among the groups was examined with the Spearman correlation test for nonparametric variables and Pearson correlation test for parametric variables. In the analyses, P < 0.05 value was considered statistically significant.
| Results | | |
The study included 85 patients who fulfilled the inclusion criteria. Of them, 21 (26%) patients were female. The average age of the study population was 44.3 ± 10.4 years. With respect to the geographical origin of the patients, 43 (51%) were from South Asia, 39 (46%) from the Middle East, one patient from Europe, one patient from Africa, and one patient from Australia.
Sixty-three patients (74%) had normal coronary arteries as per CCTA results, whereas 22 patients (22%) had nonobstructive CAD and 2 patients (2%) had obstructive CAD. The demographic, laboratory, and echocardiographic findings of the groups are expressed in [Table 1]. The average age of the patients with nonobstructive CAD was significantly higher than that of the patients with normal coronaries (P < 0.01), but there was no difference between the average age of the patients with nonobstructive CAD and the patients with obstructive CAD (P = 0.052). The difference between the groups in respect to diastolic dysfunction grade was due to the patients with obstructive CAD because these patients had worse diastolic dysfunction compared to the patients with normal coronaries and with nonobstructive CAD (P < 0.001 and < 0.005, respectively). Additionally, the diastolic grade of both the patients with normal coronaries and nonobstructive CAD was similar (P = 0.226). There was no significant difference with respect to other demographic, laboratory, and echocardiographic parameters among the groups [Table 1]. | Table 1: Baseline demographic, laboratory, and clinical characteristics of patients with supraventricular tachycardia according to coronary artery disease status (n=85)
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The average calcium score of the study population was 10.2 ± 40.4 Hounsfield units. The maximum heart rate during SVT episode was 185 ± 31 bpm, and the median duration of SVT episode from the onset of palpitation to the termination of the tachyarrhythmia was 77 min. The median hs-cTnT value of the study population was 36.7 ng/L. The SVT characteristics, hs-cTnT values, and CCTA findings of the groups are shown in [Table 2]. As per CCTA results, one patient was with obstructive two-vessel CAD and one patient with obstructive three-vessel CAD. The coronary calcium score of the patients with obstructive CAD was significantly higher than the patients of nonobstructive CAD (P < 0.05). Other variables related to SVT characteristics and hs-cTnT were similar in all groups [Table 2]. | Table 2: Supraventricular tachycardia characteristics and coronary computed tomography findings of the groups (n=85)
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Additional analyses showed that none of the other factors, such as gender, smoking status, presence of diabetes mellitus, or hypertension, had any significant relation with hs-cTnT or duration or maximum heart rate of the SVT episode (for all comparisons, P > 0.05).
In correlation analyses, there was no significant correlation between hs-cTnT-related parameters and demographic, laboratory, and echocardiographic parameters except neutrophil count. First hs-cTnT (r = 0.291; P < 0.05), second hs-cTnT (r = 0.428; P < 0.005), delta hs-cTnT (r = 0.360; P < 0.005), and maximum hs-cTnT (r = 0.381; P < 0.001) levels at admission were significantly correlated with neutrophil count. A similar correlation was found between neutrophil-to-lymphocyte ratio with second hs-cTnT (r = 0.366; P < 0.005) and maximum hs-cTnT (r = 0.256; P < 0.05) levels.
There was a significant correlation between all hs-cTnT parameters with maximum heart rate measured during SVT episode [Table 3]. There was no statistical correlation between hs-cTnT parameters with coronary calcium score and the other SVT characteristics [Table 3]. | Table 3: The correlation analyses of the high-sensitive cardiac troponin T with other parameters (n=85)
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| Discussion | | |
In this retrospective, single-center study, we found that there was no statistical relation between troponin rise and CCTA findings in patients with narrow-complex SVT terminated by intravenous adenosine. In other words, almost all the narrow-complex SVT patients with high hs-cTnT values had normal or nonobstructive CAD and there is no relation of the severity of CAD with level of hs-cTnT during SVT episode irrespective of the presence of major cardiovascular risk factors. Furthermore, we found that hs-cTnT correlated only with maximum heart rate at SVT episode and not with SVT duration or DHRP.
Cardiac troponins are frequently used biomarkers to detect myocardial injury in different clinical settings.[14] The value of hs-cTnT in detection of acute myocardial infarction has been well known. However, because of its high sensitivity in such a way that very low concentrations easily be measured with the newest technologies, their presence can result in clinical confusion or lead the physicians to perform further clinical investigations, especially in non-ACS setting.[15],[16] An example to such clinical circumstance is SVT-induced hs-cTnT positivity.[2] In the literature, there is no study searching clinical importance of hs-cTnT at this clinical setting. Thus, our study is unique in this aspect. We found that there is no relation of serum hs-cTnT levels with severity of CAD in patients with narrow-complex SVT irrespective of the presence of cardiovascular risk factors.
Only 2.4% of the patients with SVT had obstructive CAD among all the patients that was far less than the prevalence of CAD in the general population.[17] This result is expected due to younger age and low prevalence of cardiovascular risk factors in the study population. Additionally, there was no statistical difference between patients with obstructive CAD and the other groups with respect to hs-cTnT levels. Thus, it may provide clinical proof not to perform routine troponin follow-up in this setting unless there are concomitant ACS findings such as chest pain, dyspnea, and/or ECG changes in sinus rhythm suggestive of coronary ischemia.
CCTA has been increasingly used in the cardiology practice. CCTA is highly recommended to rule out ACS if hs-cTnT levels and/or ECG findings are inconclusive.[2] This approach is suggested, especially for the low-to-intermediate-risk patients applied to emergency facility due to acute chest pain.[2],[18],[19] Its use in nonacute chest pain setting such as in patients with elevated hs-cTnT is not clear. Additionally, contrast exposure, severe calcifications (high calcium score), availability, lack of experience to assess the images, and elevated or irregular heart rate are some drawbacks of the CCTA.[20]
In our study, only two patients were found to have obstructive CAD as per CCTA among all SVT patients with elevated hs-cTnT within 5 years. Both patients were over 60 years old and with high-risk pretest probability for CAD. Thus, considering the demographic and clinic characteristics of the SVT population (relatively younger age and low-risk cardiovascular profile with a concrete reason to explain hs-cTnT), it may not be helpful to perform the CTCA in low-risk-profile patients with SVT and elevated hs-cTnT but without other findings suggestive of ACS.
Cardiac troponin elevation in paroxysmal SVT has been reported in the literature.[21],[22],[23] Possible mechanism for this may be due to increased myocardial oxygen demand and reduced myocardial oxygen delivery due to short diastole during which myocardial perfusion takes place. Overall impact of tachycardia on heart is the reduced myocardial perfusion which causes the release of cardiac troponins into the circulation.[24],[25]
Additionally, the maximum heart rate during SVT rather than duration of arrhythmia was found to be related to elevated troponin.[21],[22] In our study, we also found that hs-cTnT elevation was correlated with maximum heart rate but not with duration of arrhythmia.
Paroxysmal SVT is a relatively stable rhythm. Thus, in this study, we calculated DHRP for each patient to assess the heart rate burden on heart and effect on hs-cTnT elevation. We could not find any significant correlation between DHRP and hs-cTnT. It may be due to short duration of SVT episodes to create further hs-cTnT elevations. It needs further clarification.
In our study, we did not evaluate only single hs-cTnT value, but we measured the first hs-cTnT, second set of hs-cTnT, delta hs-cTnT, and maximum hs-cTnT measurements during the index event. Thus, we assessed not only the effect of SVT on heart at an instant time but at a period (at least 3 h after termination of the arrhythmia). Maximum heart rate was correlated at the highest level to maximum hs-cTnT (P < 0.005).
Limitations of the study
In the study, we used the CTCA to evaluate the coronary anatomy rather than invasive conventional coronary angiography. The blood samples to test hs-cTnT were collected within the first 10 min after the arrival of the patients to the hospital. However, the duration from the onset of palpitation to the time of blood sample collection was not homogeneous for all subjects. Another limitation to the study was duration of SVT episode. Onset of palpitation (subjective) was considered the beginning of SVT. However, paroxysmal SVT is relatively stable in respect to heart rate. Thus, palpitation will not be resolved unless the arrhythmia is terminated. Another limitation of the study is its retrospective design.
| Conclusion | | |
Hs-cTnT may increase in patients with paroxysmal SVT irrespective of the presence of coronary lesions and CCTA may not be the proper clinical test in the differential diagnosis of paroxysmal SVT with elevated hs-cTnT if there are no other risk factors or ECG findings to suggest myocardial ischemia. The degree of hs-cTnT elevation was found to be related to maximum heart rate rather than duration of arrhythmia, the CCTA findings, or cardiovascular risk factors.
Acknowledgment
Ethical and institutional approval of the study was obtained from the Corporation MRC Department accordingly (MRC-01-20-789 dated on September 24, 2020).
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Giannitsis E, Gopi V. Biomarkers for infarct diagnosis and rapid rule-out/rule-in of acute myocardial infarction. Herz 2020;45:509-19.  |
| 2. | Collet JP, Thiele H, Barbato E, Barthélémy O, Bauersachs J, Bhatt DL; ESC Scientific Document Group, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J 2020;42:1289-367. |
| 3. | Twerenbold R, Boeddinghaus J, Nestelberger T, Wildi K, Rubini Gimenez M, Badertscher P, et al. Clinical use of high-sensitivity cardiac troponin in patients with suspected myocardial infarction. J Am Coll Cardiol 2017;70:996-1012. |
| 4. | Body R, Carlton E. Understanding cardiac troponin part 1: Avoiding troponinitis. Emerg Med J 2018;35:120-5. |
| 5. | Park KC, Gaze DC, Collinson PO, Marber MS. Cardiac troponins: From myocardial infarction to chronic disease. Cardiovasc Res 2017;113:1708-18. |
| 6. | Mair J, Lindahl B, Müller C, Giannitsis E, Huber K, Möckel M, et al. What to do when you question cardiac troponin values. Eur Heart J Acute Cardiovasc Care 2018;7:577-86. |
| 7. | Egholm G, Pareek M. Drug-induced rhabdomyolysis with elevated cardiac troponin T. Case Rep Med 2015;2015:270204. |
| 8. | Pirlet C, Pierard L, Legrand V, Gach O. Ratio of high-sensitivity troponin to creatine kinase-MB in takotsubo syndrome. Int J Cardiol 2017;243:300-5. |
| 9. | Berger M, Emir M, Brünnler T, Rockmann F, Lehmann R. Non-coronary predictors of elevated high-sensitive cardiac troponin T (hs-cTnT) levels in an unselected emergency patient cohort. Clin Cardiol 2018;41:1055-61. |
| 10. | Brugada J, Katritsis DG, Arbelo E, Arribas F, Bax JJ, Blomström-Lundqvist C; ESC Scientific Document Group, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J 2020;41:655-720. |
| 11. | Sayadnik M, Shafiee A, Jenab Y, Jalali A, Sadeghian S. Predictors of high-sensitivity cardiac troponin T elevation in patients with acute paroxysmal supraventricular tachycardia and ischemic heart disease. Tex Heart Inst J 2017;44:306-11. |
| 12. | Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015;28:1-39.e14. |
| 13. | Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr., Detrano R. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol 1990;15:827-32. |
| 14. | Yoo SM, Jang S, Kim JA, Chun EJ. Troponin-positive non-obstructive coronary arteries and myocardial infarction with non-obstructive coronary arteries: Definition, etiologies, and role of CT and MR imaging. Korean J Radiol 2020;21:1305-16. |
| 15. | Eggers KM, Jernberg T, Lindahl B. Cardiac troponin elevation in patients without a specific diagnosis. J Am Coll Cardiol 2019;73:1-9. |
| 16. | Giannitsis E, Katus HA. Cardiac troponin level elevations not related to acute coronary syndromes. Nat Rev Cardiol 2013;10:623-34. |
| 17. | Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, et al. American Heart Association Statistics Committee; Stroke Statistics Subcommittee. Heart disease and stroke statistics-2016 update: A report from the American Heart Association. Circulation 2016;133:e38-360. |
| 18. | Smulders MW, Kietselaer BL, Wildberger JE, Dagnelie PC, Brunner-La Rocca HP, Mingels AM, et al. Initial imaging-guided strategy versus routine care in patients with non-ST-segment elevation myocardial infarction. J Am Coll Cardiol 2019;74:2466-77. |
| 19. | Dedic A, Lubbers MM, Schaap J, Lammers J, Lamfers EJ, Rensing BJ, et al. Coronary CT angiography for suspected ACS in the era of high-sensitivity troponins: Randomized multicenter study. J Am Coll Cardiol 2016;67:16-26. |
| 20. | Goldstein JA, Chinnaiyan KM, Abidov A, Achenbach S, Berman DS, Hayes SW, et al. The CT-STAT (Coronary Computed Tomographic Angiography for Systematic Triage of Acute Chest Pain Patients to Treatment) trial. J Am Coll Cardiol 2011;58:1414-22. |
| 21. | Ben Yedder N, Roux JF, Paredes FA. Troponin elevation in supraventricular tachycardia: Primary dependence on heart rate. Can J Cardiol 2011;27:105-9. |
| 22. | Redfearn DP, Ratib K, Marshall HJ, Griffith MJ. Supraventricular tachycardia promotes release of troponin I in patients with normal coronary arteries. Int J Cardiol 2005;102:521-2. |
| 23. | Chow GV, Hirsch GA, Spragg DD, Cai JX, Cheng A, Ziegelstein RC, et al. Prognostic significance of cardiac troponin I levels in hospitalized patients presenting with supraventricular tachycardia. Medicine (Baltimore) 2010;89:141-8. |
| 24. | Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: Outcome after ED care. Am J Emerg Med 2011;29:545-8. |
| 25. | Patanè S, Marte F, Di Bella G. Abnormal troponin I levels after supraventricular tachycardia. Int J Cardiol 2009;132:e57-9. |
[Table 1], [Table 2], [Table 3]
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