Cardiac troponin I levels are normal or minimally elevated after transthoracic cardioversion

John J. Allan, Ronald D. Feld, Arthur A. Russell, Jack H. Ladenson, Mary A M Rogers, Richard E. Kerber, Allan S Jaffe

Research output: Contribution to journalArticle

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Abstract

Objectives. The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury. Background. Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB). Methods. We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated. Results. Patients received a mean (±SD) of 2.1 ± 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal ≤0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal <6.7) in only one patient after cardioversion. Conclusions. Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.

Original languageEnglish (US)
Pages (from-to)1052-1056
Number of pages5
JournalJournal of the American College of Cardiology
Volume30
Issue number4
DOIs
StatePublished - Oct 1997
Externally publishedYes

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Electric Countershock
Troponin I
MB Form Creatine Kinase
Shock
Creatine Kinase
Wounds and Injuries
Electric Impedance
Echocardiography
Sensitivity and Specificity

ASJC Scopus subject areas

  • Nursing(all)

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Cardiac troponin I levels are normal or minimally elevated after transthoracic cardioversion. / Allan, John J.; Feld, Ronald D.; Russell, Arthur A.; Ladenson, Jack H.; Rogers, Mary A M; Kerber, Richard E.; Jaffe, Allan S.

In: Journal of the American College of Cardiology, Vol. 30, No. 4, 10.1997, p. 1052-1056.

Research output: Contribution to journalArticle

Allan, John J. ; Feld, Ronald D. ; Russell, Arthur A. ; Ladenson, Jack H. ; Rogers, Mary A M ; Kerber, Richard E. ; Jaffe, Allan S. / Cardiac troponin I levels are normal or minimally elevated after transthoracic cardioversion. In: Journal of the American College of Cardiology. 1997 ; Vol. 30, No. 4. pp. 1052-1056.
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abstract = "Objectives. The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury. Background. Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB). Methods. We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated. Results. Patients received a mean (±SD) of 2.1 ± 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal ≤0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal <6.7) in only one patient after cardioversion. Conclusions. Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.",
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AU - Allan, John J.

AU - Feld, Ronald D.

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AU - Ladenson, Jack H.

AU - Rogers, Mary A M

AU - Kerber, Richard E.

AU - Jaffe, Allan S

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N2 - Objectives. The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury. Background. Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB). Methods. We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated. Results. Patients received a mean (±SD) of 2.1 ± 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal ≤0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal <6.7) in only one patient after cardioversion. Conclusions. Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.

AB - Objectives. The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury. Background. Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB). Methods. We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated. Results. Patients received a mean (±SD) of 2.1 ± 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal ≤0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal <6.7) in only one patient after cardioversion. Conclusions. Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.

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