Abstract
Aims
Troponin I (TNI) is an established marker for the diagnosis of acute coronary syndrome (ACS). The study evaluated if (induced) tachycardiac arrhyhthmias within the scope of the electrophysiological studies (EPS) led to elevation of TNI serum levels.
Method
TNI was measured in the serum of 28 patients before and after the EPS. The left ventricular ejection fraction (LV-EF) was investigated by two-dimensional echocardiography. Left ventricle hypertrophy (LVH) was measured according to the recommendations of the American Society of Echocardiography. All patients underwent coronary angiography prior to the EPS, and significant coronary heart disease was defined as stenosis > 50%. The EPS revealed supraventricular and ventricular tachycardias using the 18-step protocol with one, two, and three extrastimuli.
Results
Indications for the EPS were syncope (n = 15), atrioventricular tachycardia (n = 4), non-sustained VT (n = 6), and sustained VT (n = 3). Coronary heart disease (CHD) was detected in 8 patients (1-vessel: n = 3; 2-vessel: n = 4; 3-vessel: n = 1), and 2 patients underwent percutaneous coronary intervention before EPS. Echocardiography revealed normal LV-EF in 18 patients and a reduction in the others (low n = 3, middle n = 5, high n = 2). Thirteen patients suffered from LVH. In 2 patients, external cardioversion was required during the EPS. TNI was elevated over 0.1 ng/ml (risk stratification cut-off for ACS) in 4 patients before and in 12 patients after EPS. There was no relationship between LV-EF, CHD, and the elevation of TNI after the EPS.
Conclusion
TNI can be elevated by (induced) tachycardias within the scope of electrophysiological studies without a relationship to LV-EF, LVH, and CHD.
Zusammenfassung
Ziel
Troponin I (TNI) ist ein etablierter Marker für die Diagnose eines akuten Koronarsyndroms (ACS). In der vorliegenden Studie wurde ermittelt, ob (induzierte) tachykarde Arrhythmien im Rahmen elektrophysiologischer Untersuchungen (EPU) zur Erhöhung des TNI-Serumspiegels führten.
Methode
TNI wurde im Serum von 28 Patienten vor und nach EPU bestimmt. Die linksventrikuläre Ejektionsfraktion (LV-EF) wurde mittels zweidimensionaler Echokardiographie gemessen. Eine linksventrikuläre Hypertrophie (LVH) wurde gemäß den Empfehlungen der American Society of Echocardiography ermittelt. Bei allen Patienten wurde eine Koronarangiographie vor der EPU durchgeführt, eine signifikante koronare Herzkrankheit (KHK) war als Stenose > 50% definiert. Bei der EPU wurde eine Stimulation mittels des 18-Schritt-Schemas mit einem, zwei und drei Extrastimuli durchgeführt.
Ergebnisse
Indikationen für EPU waren Synkope (n = 15), atrioventrikuläre Tachykardien (n = 4), nichtanhaltende VT (n = 6), und anhaltende VT (n = 3). Eine KHK wurde bei 8 Patienten festgestellt (1-Gefäß-Erkrankung: n = 3; 2-Gefäß-Erkr.: n = 4; 3-Gefäß-Erkr.: n = 1), und bei 2 Patienten erfolgte eine perkutane Koronarintervention vor EPU. Die Echokardiographie ergab eine normale LV-EF bei 18 Patienten und eine eingeschränkte LV-EF bei den übrigen (leightgradig: n = 3, mittelgradig: n = 5, hochgradig: n = 2). Eine LVH lag bei 13 Patienten vor. Bei 2 Patienten war eine externe Kardioversion während der EPU erforderlich. Bei 4 Patienten vor und bei 12 Patienten nach EPU war TNI über 0,1 ng/ml erhöht (Risikostratifizierungsgrenzwert für ACS). Es gab keinen Zusammenhang zwischen LV-EF, KHK und TNI-Erhöhung nach EPU.
Fazit
TNI kann durch (induzierte) Tachykardien im Rahmen einer EPU erhöht sein, ohne einen Zusammenhang mit LV-EF, LVH und KHK zu zeigen.
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Bandorski, D., Bogossian, H., Lemke, B. et al. Do induced tachycardias within the scope of electrophysiological studies lead to elevated plasma troponin I levels?. Herzschr. Elektrophys. 22, 214–218 (2011). https://doi.org/10.1007/s00399-011-0151-0
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DOI: https://doi.org/10.1007/s00399-011-0151-0