Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: Insights from a coronary sinus sampling study

Aslan T Turer, Tayo A Addo, Justin L. Martin, Marc S. Sabatine, Gregory D. Lewis, Robert E. Gerszten, Ellen C. Keeley, Joaquin E. Cigarroa, Richard A. Lange, L. David Hillis, James A de Lemos

Research output: Contribution to journalArticle

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Abstract

Objectives: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release. Background: A new hs-cTnT assay offers greater sensitivity than current assays. Methods: Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. Results: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups. Conclusions: Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

Original languageEnglish (US)
Pages (from-to)2398-2405
Number of pages8
JournalJournal of the American College of Cardiology
Volume57
Issue number24
DOIs
StatePublished - Jun 14 2011

Fingerprint

Sampling Studies
Troponin T
Coronary Sinus
Myocardial Ischemia
Ischemia
Coronary Artery Disease
Catheterization
Lactic Acid
Chest Pain
Infarction
Necrosis

Keywords

  • cardiac biomarkers
  • coronary artery disease
  • ischemia
  • rapid pacing
  • troponin T

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay : Insights from a coronary sinus sampling study. / Turer, Aslan T; Addo, Tayo A; Martin, Justin L.; Sabatine, Marc S.; Lewis, Gregory D.; Gerszten, Robert E.; Keeley, Ellen C.; Cigarroa, Joaquin E.; Lange, Richard A.; Hillis, L. David; de Lemos, James A.

In: Journal of the American College of Cardiology, Vol. 57, No. 24, 14.06.2011, p. 2398-2405.

Research output: Contribution to journalArticle

Turer, Aslan T ; Addo, Tayo A ; Martin, Justin L. ; Sabatine, Marc S. ; Lewis, Gregory D. ; Gerszten, Robert E. ; Keeley, Ellen C. ; Cigarroa, Joaquin E. ; Lange, Richard A. ; Hillis, L. David ; de Lemos, James A. / Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay : Insights from a coronary sinus sampling study. In: Journal of the American College of Cardiology. 2011 ; Vol. 57, No. 24. pp. 2398-2405.
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abstract = "Objectives: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release. Background: A new hs-cTnT assay offers greater sensitivity than current assays. Methods: Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. Results: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups. Conclusions: Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.",
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T2 - Insights from a coronary sinus sampling study

AU - Turer, Aslan T

AU - Addo, Tayo A

AU - Martin, Justin L.

AU - Sabatine, Marc S.

AU - Lewis, Gregory D.

AU - Gerszten, Robert E.

AU - Keeley, Ellen C.

AU - Cigarroa, Joaquin E.

AU - Lange, Richard A.

AU - Hillis, L. David

AU - de Lemos, James A

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N2 - Objectives: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release. Background: A new hs-cTnT assay offers greater sensitivity than current assays. Methods: Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. Results: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups. Conclusions: Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

AB - Objectives: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release. Background: A new hs-cTnT assay offers greater sensitivity than current assays. Methods: Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. Results: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups. Conclusions: Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

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KW - rapid pacing

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