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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 6  |  Issue : 2  |  Page : 104-107

Significantly high serum cardiac troponin level with supraventricular tachyarrhythmia in the absence of coronary artery disease


1 Department of Cardiology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China
2 Department of Cardiology, The Third People's Hospital of Yuhang District of Hangzhou, Hangzhou, Zhejiang Province, China

Date of Submission27-Oct-2021
Date of Decision02-Dec-2021
Date of Acceptance06-Dec-2021
Date of Web Publication28-Dec-2021

Correspondence Address:
Dr. Yigang Zhong
Department of Cardiology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, No. 261, Huansha Road, Shangcheng District, Hangzhou 310006, Zhejiang Province
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijhr.ijhr_14_21

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  Abstract 


Although elevated cardiac troponin is considered to be the gold standard biomarker for the identification of acute coronary syndrome, it may also occur in other clinical situations as supraventricular tachyarrhythmia (SVT) and acute coronary syndrome. We reported the case of a 77-year-old patient with a highly elevated cTn after the onset of SVT. Normal coronary arteries were detected through coronary angiography and intravenous ultrasound. It seems that the association of the cardiac troponin elevation in SVT patients with future cardiovascular events is very low. Meanwhile, more attention should be paid to those patients with high cardiovascular risk factors.

Keywords: Acute coronary syndrome, cardiac troponin, coronary artery disease, supraventricular tachyarrhythmia


How to cite this article:
Chen L, Zhong Y, Xu Y, Chen L, Yu F. Significantly high serum cardiac troponin level with supraventricular tachyarrhythmia in the absence of coronary artery disease. Int J Heart Rhythm 2021;6:104-7

How to cite this URL:
Chen L, Zhong Y, Xu Y, Chen L, Yu F. Significantly high serum cardiac troponin level with supraventricular tachyarrhythmia in the absence of coronary artery disease. Int J Heart Rhythm [serial online] 2021 [cited 2022 Jul 2];6:104-7. Available from: https://www.ijhronline.org/text.asp?2021/6/2/104/334129




  Introduction Top


Cardiac troponin (cTn) has currently been regarded as a sensitive and specific biomarker for the diagnosis of acute myocardial infarction and has a well-defined prognostic value.[1] However, it is well known that cTn is also commonly elevated in other nonacute coronary syndrome conditions including chronic heart failure, diabetes, pulmonary arterial hypertension, and chronic kidney disease.[2] It is unclear why these elevations occur, yet cTn elevations in many of these noncoronary disease patients cannot be ignored for they are directly correlated to a worse prognosis. Since the improvements in troponin assay sensitivity, minor changes, or elevations in cTn can be detected, which means more differential diagnoses have to be considered.

Several small case series has confirmed that supraventricular tachyarrhythmia (SVT) are associated with cTn elevation.[3],[4],[5],[6],[7],[8],[9],[10],[11],[12] However, the mechanisms and kinetic patterns of cTn elevation, as well as the prevalence, predictors, and prognostics of SVT-associated cTn elevation remain unclear. Furthermore, to rule out acute coronary syndrome, an invasive cardiac evaluation such as coronary angiography is often performed in SVT patients with chest pain as well as elevated cTn, but the result generally turns out to be normal. Previous studies have shown that cTnI could be mildly elevated in SVT patients. We present a case of significantly high level of serum cTn with SVT and review the available literature concerning SVT-related cTn elevation to a better understanding.


  Case Report Top


A 77-year-old male patient was admitted to the local hospital with a chief complaint of sharp chest pain and palpitation for 3 h on June 10, 2019. He had histories of hypertension, tobacco smoking, and alcohol consumption for the decades of years. The electrocardiogram showed SVT and ST-segment elevation in lead V3R-V4R [Figure 1]a and [Figure 1]b. No segmental wall motion abnormality was shown through echocardiography. The level of cTnI was 0.12 ng/mL on admission. However, 3 h later, the level of cTnI was up to 12.09 ng/mL and then to 14.3 ng/mL after 6 h. He was diagnosed with acute myocardial infarction. Intravenous thrombolysis with recombinant tissue plasminogen activator was applied within 2 h after admission, the symptoms were relieved, and electrocardiography returned to normal [Figure 1]c. The following days, he was treated with aspirin, clopidogrel, low-molecular-weight-heparin, and atorvastatin. After 6-day treatment, the cTnI level was declined to 2.45 ng/mL. To assess the severity of coronary artery disease (CAD), he was transferred to our hospital on June 17, 2019. Coronary angiography was immediately performed after admission. No functional significance of coronary artery stenosis was detected, and no vulnerable plaque or thrombosis was observed by intravenous ultrasound [Figure 2]a, [Figure 2]b, [Figure 2]c. The day before he was prepared to be discharged, the same sharp chest pain and palpitation recurred. Moreover, the electrocardiogram showed SVT as before. Sinus rhythm was restored after amiodarone (300 mg) intravenous administration. Two days later, we performed an intracardiac electrophysiological examination with typical atrioventricular nodal reentrant tachycardia. Moreover, slow pathway ablation was successfully performed. Thus, this diagnosis was revised as paroxysmal SVT. Moreover, then he was discharged from our hospital with no further treatments. During 1-month follow-up, he had no symptoms.
Figure 1: The 12-lead electrocardiographic images on admission (a). ST-segment elevation in lead V3R-V4R on admission (b). Electrocardiographic images after symptoms resolved (c)

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Figure 2: Angiographic images of the left coronary (a) and right coronary (b) and intravenous ultrasound image (c) show no vulnerable plaque or thrombosis

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  Discussion Top


SVT is generally considered to be a benign arrhythmia, which often has a favorable prognosis. Currently, SVT has been regarded as a probable cause of cTn elevation in patients with normal coronary arteries.[3],[4],[10],[11],[13] Previous studies have reported the prevalence of cTn elevation in SVT patients in the range of 29%–74.3%.[4],[6],[8],[9],[14]

Mechanisms, predictors, and kinetic pattern of cardiac troponin elevation

The mechanism responsible for elevated cTn in noncoronary syndrome SVT patients has not been fully elucidated, but two main hypotheses have been proposed. Many authors believed that cTn elevation during SVT is secondary to “demand ischemia.” High heart rate increases myocardial oxygen demand, decreases oxygen delivery, and subsequently leads to myocardial perfusion reduction during diastole.[3],[11] Another explanation is that “myocardia stretch.” In SVT patients, as the myocardial stretch, more intact cytosolic troponin molecules were released by sarcolemmal.[15]

The main predictors of SVT-related cTn elevation were older age, lower diastolic blood pressure, the presence of impaired left ventricular systolic function, and chest pain.[4],[6],[9],[10],[14] It has been reported that heart rate during the episode of SVT is an independent predictor of cTn elevation.[4],[9],[13],[16],[17] Costabel et al.[7] made a prospective study of 100 SVT patients including atrial fibrillation, atrial flutter, and reentrant tachycardias with or without CAD, the investigators observed that the greatest cTn values occurred in reentrant tachycardias, which could be related to a higher heart rate, regardless of the presence or absence of CAD. These results are similar to those published by Schueler et al.[14] In addition, many authors, such as Redfearn et al.[13] believed that the duration of arrhythmia was not associated with cTn elevation. However, these results were quite different from those in the study by Sayadnik et al.[6] In their findings, heart rate showed no correlation to cTn elevation, while the duration of tachycardia had a close association.

Since cTn is now more easily detected in those nonischemic conditions, it has been emphasized that cTn is more like an organ-specific instead of a disease-specific biomarker.[2],[18] Then, how do the clinicians distinguish acute ischemic heart disease (IHD) from SVT with cTn elevation? In ST-segment-elevation myocardial infarction patients, a study has shown the pattern of cTn elevation, especially high-sensitivity cTn, that is cTn level increased in the 1st day and reached maximal after the 1st day.[5] It is noteworthy that previous studies rarely described the kinetic effects of cTn elevation in SVT patients were rarely described in the past. A recent study by Sayadnik et al.[6] investigated changes in high-sensitivity cTnT between 70 SVT patients with and without underlying IHD and found that compared with 36 h reaching maximal levels in IHD-positive patients, high-sensitivity cTnT peaked within 8 h to 16 h after the onset of SVT in IHD-negative patients. This observation of the kinetic pattern was in accordance with the findings in our case. In addition, both Sayadnik et al.[6] and Costabel et al.[7] noted that IHD seems to only contribute to a higher level of cTn for a longer duration than SVT alone.

Prognosis

Costabel et al.[7] made a 30-day follow-up of the SVT-related cTn elevation patients and found that the association of this elevation with poor cardiovascular outcomes seems to be very low. In their study, only four events were reported and all these patients presented with atrial fibrillation. Similarly, based on the 30-day outcome data, Carlberg et al.[8] concluded that there were no correlations between cTn elevation and cardiovascular events in SVT patients. While the observations by Chow et al.[9] are different from the previous studies. They described that increased risk of future cardiovascular morbidity and/or mortality was associated with the presence of elevated cTnI in the context of SVT (hazard ratio 3.67; 95% confidence interval 1.22–11.1; P = 0.02), and the mean follow-up period was 2.2 ± 1.7 years. Unfortunately, these studies were retrospective in nature and did not allow the investigators to make a most appropriate evaluation in such patients. Further risk stratification was not made, which may affect the results.[8],[9] Hence, in clinical practice, more attention should be paid to the cardiovascular risk factors when we confront an SVT patient with elevated cTn and chest pain to make better evaluation choices and closer follow-up.

Limitations of the previous case series included a small sample size and missing information from the previous studies. Larger prospective or retrospective studies with careful risk stratification are needed in future.


  Conclusions Top


cTn elevation could be seen in a significant number of SVT patients with normal coronary arteries. This case described a situation that cTn increased significantly almost leading to a misdiagnosis. Cautions should be taken that abnormal cTn levels should be interpreted more carefully and invasive coronary angiography for differential diagnosis should be chosen more carefully in SVT patients with elevated cTn.

Institutional review board statement

The study was approved by the Ethics Committee of Hangzhou First People's Hospital (approval No. (2019) Scientific Research Medical Review No. (014)-01) on April 12, 2019.

Declaration of patient consent

The authors certify that they have obtained the appropriate patient consent form. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published, and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rubini Gimenez M, Twerenbold R, Jaeger C, Schindler C, Puelacher C, Wildi K, et al. One-hour rule-in and rule-out of acute myocardial infarction using high-sensitivity cardiac troponin I. Am J Med 2015;128:861-70.e4.  Back to cited text no. 1
    
2.
Park KC, Gaze DC, Collinson PO, Marber MS. Cardiac troponins: From myocardial infarction to chronic disease. Cardiovasc Res 2017;113:1708-18.  Back to cited text no. 2
    
3.
Zellweger MJ, Schaer BA, Cron TA, Pfisterer ME, Osswald S. Elevated troponin levels in absence of coronary artery disease after supraventricular tachycardia. Swiss Med Wkly 2003;133:439-41.  Back to cited text no. 3
    
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Ben Yedder N, Roux JF, Paredes FA. Troponin elevation in supraventricular tachycardia: Primary dependence on heart rate. Can J Cardiol 2011;27:105-9.  Back to cited text no. 4
    
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Antman EM. Decision making with cardiac troponin tests. N Engl J Med 2002;346:2079-82.  Back to cited text no. 5
    
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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.  Back to cited text no. 6
    
7.
Costabel JP, Urdapilleta M, Lambardi F, Campos R, Vergara JM, Ariznavarreta P, et al. High-sensitivity cardiac troponin levels in supraventricular tachyarrhythmias. Pacing Clin Electrophysiol 2016;39:588-91.  Back to cited text no. 7
    
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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.  Back to cited text no. 8
    
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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.  Back to cited text no. 9
    
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Moore JP, Arcilla L, Wang S, Lee MS, Shannon KM. Characterization of cardiac troponin elevation in the setting of pediatric supraventricular tachycardia. Pediatr Cardiol 2016;37:392-8.  Back to cited text no. 10
    
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Xue F, Jiang TB, Jiang B, Cheng XJ, He YM, Li X, et al. Cardiac troponin I elevation with supraventricular tachycardia: Two case reports and review of the literature. BMC Res Notes 2014;7:136.  Back to cited text no. 11
    
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Bukkapatnam RN, Robinson M, Turnipseed S, Tancredi D, Amsterdam E, Srivatsa UN. Relationship of myocardial ischemia and injury to coronary artery disease in patients with supraventricular tachycardia. Am J Cardiol 2010;106:374-7.  Back to cited text no. 12
    
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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.  Back to cited text no. 13
    
14.
Schueler M, Vafaie M, Becker R, Biener M, Thomas D, Mueller M, et al. Prevalence, kinetic changes and possible reasons of elevated cardiac troponin T in patients with AV nodal re-entrant tachycardia. Acute Card Care 2012;14:131-7.  Back to cited text no. 14
    
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Hessel MH, Atsma DE, van der Valk EJ, Bax WH, Schalij MJ, van der Laarse A. Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation. Pflugers Arch 2008;455:979-86.  Back to cited text no. 15
    
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Turer AT, Addo TA, Martin JL, Sabatine MS, Lewis GD, Gerszten RE, et al. Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: Insights from a coronary sinus sampling study. J Am Coll Cardiol 2011;57:2398-405.  Back to cited text no. 16
    
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Goette A, Bukowska A, Dobrev D, Pfeiffenberger J, Morawietz H, Strugala D, et al. Acute atrial tachyarrhythmia induces angiotensin II type 1 receptor-mediated oxidative stress and microvascular flow abnormalities in the ventricles. Eur Heart J 2009;30:1411-20.  Back to cited text no. 17
    
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Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined – A consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959-69.  Back to cited text no. 18
    


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