Troponin Elevation in Supraventricular Tachycardia: Primary Dependence on Heart Rate

Yedder, Naïm Ben; Roux, Jean François; Ayala‐Paredes, F.

doi:10.1016/j.cjca.2010.12.004

Cited by 61 publications

(63 citation statements)

References 10 publications

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“…8,18 In our study, heart rate did not correlate with elevation of hs-cTnT, although the duration of tachycardia had an association. This finding may be explained by these proposed mechanisms for troponin elevation during cardiac stress and tachycardia: troponin is released via integrin-mediated transient membrane leakage 19 or through intact membranes via the formation of blebs that contain nonstructurally bound troponin.…”

Section: Discussioncontrasting

confidence: 63%

“…Although multiple authors of case reports and series have shown that cardiac enzyme levels rise during PSVT, 7,12,13 we found only one study 14 in which the pattern of enzyme elevation was described. Of note, elevated concentrations of serum cTnT are observed in many but not all patients with PSVT, 8 rendering it difficult to explain the mechanism of cTnT elevation. It is argued that transient elevations of cTnT can occur without cardiomyocyte death, and several mechanisms have been proposed to explain this phenomenon.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 This can mislead clinicians in the management of PSVT. Therefore, defining the kinetic effects of troponin elevation, especially high-sensitivity troponin, as well as the predictors of elevation, is important for straightforward clinical diagnosis of a possible underlying ischemic condition.…”

Section: During Calendar Year 2013 We Enrolled 70 Of 72 Consecutive mentioning

confidence: 99%

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Predictors of High-Sensitivity Cardiac Troponin T Elevation in Patients with Acute Paroxysmal Supraventricular Tachycardia and Ischemic Heart Disease

Sayadnik¹,

Shafiee²,

Jenab³

et al. 2017

Texas Heart Institute Journal

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We studied the predictors and patterns of high-sensitivity cardiac troponin T (hs-cTnT) C ardiac troponin T (cTnT) is a highly sensitive and specific biomarker for the diagnosis of acute myocardial infarction (AMI).1 However, elevated cTnT is also seen in other cardiac and noncardiac conditions. 2-5 It has therefore been proposed that the diagnosis of AMI should be made depending on changes in cTnT level in an appropriate clinical situation, to distinguish ischemic from nonischemic causes of cTnT elevation. 6 In addition, recently available high-sensitivity troponin assays can reliably detect much lower concentrations of troponin than older assays could. However, minor changes or elevations in cTnT levels without other evidence for AMI can be confusing.Paroxysmal supraventricular tachycardia (PSVT) has been identified as a probable cause of troponin elevation in the absence of severe ischemic heart disease (IHD). 7,8 This can mislead clinicians in the management of PSVT. Therefore, defining the kinetic effects of troponin elevation, especially high-sensitivity troponin, as well as the predictors of elevation, is important for straightforward clinical diagnosis of a possible underlying ischemic condition.In this study, we had 2 goals: to identify predictors of high-sensitivity cardiac troponin T (hs-cTnT) elevation; and to determine the pattern of changes in hs-cTnT levels in PSVT patients who had elevated hs-cTnT levels (with or without IHD) upon presentation at the emergency department of our tertiary-care cardiovascular center. Patients and MethodsDuring calendar year 2013, we prospectively enrolled consecutive patients (age, >30 yr) who were admitted to the emergency department

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Section: Discussioncontrasting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: During Calendar Year 2013 We Enrolled 70 Of 72 Consecutive mentioning

confidence: 99%

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Predictors of High-Sensitivity Cardiac Troponin T Elevation in Patients with Acute Paroxysmal Supraventricular Tachycardia and Ischemic Heart Disease

Sayadnik¹,

Shafiee²,

Jenab³

et al. 2017

Texas Heart Institute Journal

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“…Rates of cardiac troponin increase ranging from 33% to 37% using conventional assays have been described in smaller cohorts (36,37 ). Increased cardiac troponin was positively associated with the maximum heart rate in these studies and independently predicted 1-year major CV events in 1 of them [HR 3.7 (95% CI 1.2-11.1)] (36 ).…”

Section: Atrial Fibrillation and Supraventricular Arrhythmiamentioning

confidence: 89%

Application of Cardiac Troponin in Cardiovascular Diseases Other Than Acute Coronary Syndrome

Eggers¹,

Lindahl

2017

Clinical Chemistry

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BACKGROUND Increased cardiac troponin concentrations in acute coronary syndrome (ACS) identify patients with ongoing cardiomyocyte necrosis who are at increased risk. However, with the use of more precise assays, cardiac troponin increases are commonly noted in other cardiovascular conditions as well. This has generated interest in the use of cardiac troponin for prognostic assessment and clinical management of these patients. In this review, we have summarized the data from studies investigating the implications of cardiac troponin concentrations in various acute and chronic conditions beyond ACS, i.e., heart failure, myocarditis, Takotsubo cardiomyopathy, aortic dissection, supraventricular arrhythmias, valve disease, pulmonary arterial hypertension, stroke, and in the perioperative setting. CONTENT Cardiac troponin concentrations are often detectable and frankly increased in non-ACS conditions, in particular when measured with high-sensitivity (hs) assays. With the exception of myocarditis and Takotsubo cardiomyopathy, cardiac troponin concentrations carry strong prognostic information, mainly with respect to mortality, or incipient and/or worsening heart failure. Studies investigating the prognostic benefit associated with cardiac troponin–guided treatments however, are almost lacking and the potential role of cardiac troponin in the management of non-ACS conditions is not defined. SUMMARY Increased cardiac troponin indicates increased risk for adverse outcome in patients with various cardiovascular conditions beyond ACS. Routine measurement of cardiac troponin concentrations can however, not be generally recommended unless there is a suspicion of ACS. Nonetheless, any finding of an increased cardiac troponin concentration in a patient without ACS should at least prompt the search for possible underlying conditions and these should be managed meticulously according to current guidelines to improve outcome.

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“…It may be due to an increase in oxygen consumption by the myocardium during tachycardia. Also, a reduction of the oxygen supply to the myocardium due to the shortened diastole with subsequent subendocardial ischemia during tachycardia is possible [15]. Although cTnI elevation in patients presenting to the hospital with SVT is well recognized, the prevalence, predictors, and prognostic significance of cTnI elevation associated with SVT presentation are not known.…”

Section: Discussionmentioning

confidence: 99%

Myocardial injury in a 41-year-old male treated with methylphenidate: a case report

Hole

Schjøtt

2014

BMC Res Notes

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BackgroundElevated cardiac troponin levels are consistent with the diagnosis of an acute coronary syndrome, but may also represent adverse drug reactions. Psychostimulating drugs raise both blood pressure and heart rate, and case reports of sudden death, stroke, and myocardial infarction have led to regulatory and public concern about the cardiovascular safety of these drugs.Case presentationWe present a case where a 41-year-old Norwegian male with radiating chest pain, elevated troponins, and supraventricular tachycardia was hospitalized. Tentative diagnosis was acute coronary syndrome. Percutaneous coronary angiography, but not cardiac magnetic resonance imaging, was performed and medical antiplatelet treatment started. Because of an attention deficit/hyperactivity disorder the patient had recently increased his dose of methylphenidate, but still within the therapeutic dose range. Apart from venlafaxine, also in a therapeutic dose, the patient took no other drugs. An acute coronary syndrome was excluded during hospitalization, and a drug effect was suspected.ConclusionsWhen interpreting troponin results it is important to take into account the context of the patient’s clinical presentation, including the possibility of adverse drug reactions. The adverse drug reaction could include a combination of vasospasm and/or increased oxygen demand due to tachycardia. This case should be borne in mind before a diagnosis of myocardial infarction is given, or a decision to perform invasive coronary angiography is made in patients that use methylphenidate or related substances. Cardiac magnetic resonance imaging could be of diagnostic value in such cases.

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Troponin Elevation in Supraventricular Tachycardia: Primary Dependence on Heart Rate

Cited by 61 publications

References 10 publications

Predictors of High-Sensitivity Cardiac Troponin T Elevation in Patients with Acute Paroxysmal Supraventricular Tachycardia and Ischemic Heart Disease

Predictors of High-Sensitivity Cardiac Troponin T Elevation in Patients with Acute Paroxysmal Supraventricular Tachycardia and Ischemic Heart Disease

Application of Cardiac Troponin in Cardiovascular Diseases Other Than Acute Coronary Syndrome

Myocardial injury in a 41-year-old male treated with methylphenidate: a case report

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