Origin of Elevated Serum Enzyme Activities after Direct-Current Countershock

Konttinen, Aarne; Hupli, Veikko; Louhija, Antti; Härtel, Gottfried

doi:10.1056/nejm196907312810502

Cited by 52 publications

(9 citation statements)

References 32 publications

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“…However, serum total CK activity also increases in some other diseases (Pearce et al, 1964;Dubo et al, 1967;Perkoff, 1968;Konttinen et al, 1969) The MB isoenzyme of CK appears to constitute a quite specific indicator of heart damage, since it has been found outside the myocardium in skeletal muscle only with very slight activity (Somer and Konttinen, 1972a;Takahashi et al, 1972). Other organs that have high CK activities are the brain, though this contains BB isoenzyme, and skeletal muscles, which have MM isoenzyme.…”

Section: Discussionmentioning

confidence: 99%

“…Analyses were made of the following enzymes from unhaemolysed sera taken during the first two hospital days, as reported earlier (Elliot and Wilkinson, 1961;Konttinen et al, 1969): lactate dehydrogenase (LD) and its isoenzymes, a-hydroxybutyrate dehydrogenase (HBD), aspartate aminotransferase BB isoenzyme, which characterizes lung and brain tissues, was not present in any of the sera. Patients with angina pectoris had only muscle-type CK isoenzyme (MM) in their sera., which accords with findings in healthy persons.…”

Section: Methodsmentioning

confidence: 99%

“…Serum CK activity is raised, however, in muslce diseases (Pearce et al, 1964), brain damage (Dubo et al, 1967), alcoholism (Konttinen et al, 1970), and sometimes in pulmonary embolism (Perkoff, 1968) or after electroconversion of heart rhythm (Konttinen et al, 1969). The specificity may be expectedto be improved by serum CK isoenzyme determinations, since the MB isoenzyme of CK is found almost exclusively in the myocardium (Van der Veen and Wilebrands, 1966).…”

Section: Introductionmentioning

confidence: 99%

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Specificity of Serum Creatine Kinase Isoenzymes in Diagnosis of Acute Myocardial Infarction

Konttinen¹,

Somer²

1973

BMJ

102

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Specificity of Serum Creatine Kinase Isoenzymes in Diagnosis of Acute Myocardial Infarction

Konttinen¹,

Somer²

1973

BMJ

102

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“…Intramuscular injections can cause a rise in CPK activity9' 10 but these were avoided in our patients, except in a few instances in which opiates were administered before admission to the coronary care unit. CPK release has also been described after cardiover- 23 in sion and in shock,24 due to poor perfusion of peripheral muscles. No cases of cardiogenic shock were included in our study, and collection of blood specimens was always abandoned following cardioversion.…”

Section: Relation Of Integrated Appearance Function Of Cpk Release Tomentioning

confidence: 99%

Clinical measurement of myocardial infarct size. Modification of a method for the estimation of total creatine phosphokinase release after myocardial infarction.

Norris¹,

Whitlock²,

Barratt-Boyes³

et al. 1975

Circulation

250

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A modified method for the measurement of total creatine phosphokinase release from venous blood samples taken four-hourly after myocardial infarction has been used in 43 patients admitted to a Coronary Care Unit. The fractional decay rate (Kd) of enzyme activity has been measured by a standardized method in each patient, and accuracy of the calculation of total enzyme release has been improved by allowance for individual variations in decay rate, and discarding of data from which decay rates cannot be measured within confidence limits of less than plus or minus 15 per cent. Total enzyme release was greater in cases of transmural infarction than in patients with subendocardial infarction, and showed a good positive correlation with clinical indices of the extent of myocardial damage. As noted by previous workers, this method allows for the measurement of the rate as well as the extent of enzyme release, and so should prove useful in the clinical evaluation of therapeutic agents which might accelerate or retard the rate of myocardial necrosis in patients with acute myocardial infarction.

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“…This observation, along with the electrocardiogram (ECG) changes (repolarisation abnormalities) sometimes seen after dc cardioversion, led to the suggestion that dc cardioversion causes myocardial damage. Most of the creatine kinase released after cardioversion comes from the chest wall skeletal muscles,8 which also liberate the MB subfraction. Therefore, the extent that emergency dc cardioversion contributes to raised creatine kinase or its MB isoenzyme is unclear.…”

mentioning

confidence: 99%

Direct current cardioversion does not cause cardiac damage: evidence from cardiac troponin T estimation

Rao

Naeem

et al. 1998

Heart

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Aim-To determine whether elective direct current (dc) cardioversion of atrial fibrillation/flutter causes myocardial damage. Methods and results-Cardiac troponin T and creatine kinase were estimated 20-28 hours after dc cardioversion in 51 patients who received dc shocks for elective cardioversion of chronic atrial fibrillation/ flutter. Although creatine kinase was raised in 44 patients, cardiac troponin T was undetectable in all patients. Conclusion-Cardiac damage does not occur as a result of cardioversion. (Heart 1998;80:229-230) Keywords: cardioversion; troponin T; creatine kinase; atrial fibrillation Direct current (dc) cardioversion 1 revolutionised the management of cardiac arrhythmias. However, before the standardisation of outputs from external defibrillators there was controversy about the most appropriate strength of current to be used.2 Animal experiments have suggested that repeated high energy dc shocks result in myocardial damage.3 4 In humans, dc cardioversion causes a rise in the concentration of creatine kinase and its MB subfraction. [5][6][7] This observation, along with the electrocardiogram (ECG) changes (repolarisation abnormalities) sometimes seen after dc cardioversion, led to the suggestion that dc cardioversion causes myocardial damage. Most of the creatine kinase released after cardioversion comes from the chest wall skeletal muscles, 8 which also liberate the MB subfraction. Therefore, the extent that emergency dc cardioversion contributes to raised creatine kinase or its MB isoenzyme is unclear. The belief that myocardial damage might result from higher strengths of current may also have influenced recommendations about the choice of current strength. It remains uncertain whether dc cardioversion does actually cause myocardial damage.Cardiac troponin T is a cardiac specific protein component of the troponin/tropomyosin complex. 9 A rise in serum troponin T concentrations is specific for cardiac damage. It remains raised for up to 48 hours after myocardial injury, thus providing a wide time window. 9Currently available data suggest that the kinetics of cardiac troponin T release from acutely damaged myocardium are identical whatever the cause of damage. 10Our study was undertaken to determine whether there was any evidence of myocardial damage after elective dc cardioversion of atrial fibrillation/flutter by measuring concentrations of cardiac troponin T in patients undergoing dc cardioversion. MethodsFifty one consecutive patients undergoing elective dc cardioversion for atrial fibrillation/ flutter were entered into the study. None had chronic renal failure, acute myocardial infarction, or skeletal muscle disease. As described previously, 11 dc shocks were administered in increasing strengths of 100 J, 200 J, 300 J, and 360 J (only one shock of each strength), until either sinus rhythm was restored or 360 J was applied.A blood sample was taken 20-28 hours after dc cardioversion. Samples were centrifuged and analysed or frozen at −70°C until analysis (all analyses were p...

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Origin of Elevated Serum Enzyme Activities after Direct-Current Countershock

Cited by 52 publications

References 32 publications

Specificity of Serum Creatine Kinase Isoenzymes in Diagnosis of Acute Myocardial Infarction

Specificity of Serum Creatine Kinase Isoenzymes in Diagnosis of Acute Myocardial Infarction

Clinical measurement of myocardial infarct size. Modification of a method for the estimation of total creatine phosphokinase release after myocardial infarction.

Direct current cardioversion does not cause cardiac damage: evidence from cardiac troponin T estimation

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