Five days after this injury, he presented with a sudden onset chest pain. He did not have any history of cardiac disease previously. On physical examination, blood pressure was 110/80 mm Hg, and cardiac pulse was 70 beats per minute. Cardiovascular and other system examination results were normal. There were no ST-T changes on ECG. The troponin level was 2.31 ng/mL (reference, 0.005-0.065 ng/mL), CK-MB was 10.6 ng/mL. Because of the presence of chest pain complaint with elevated cardiac enzymes, Transthoracic echocardiography was performed. On TTE, there was chordae rupture on the anterior leaftet of the mitral valve (Fig. 1). There was no mitral insufficiency. For detailed assessment, transesophageal echocardiography was performed; chordae rupture on the mitral valve’s anterior leaftet was observed (Fig. 2). Absence of mitral insufficiency and mitral valve prolapsus and observation of smaller chordae than primary chordae directed the diagnosis to secondary chordae rupture. After 24 hours, the patient’s cardiac enzymes

Fig. 1 Transthoracic Parasternal long axis view shows mitral cordae rupture (arrow). LA, left atrium; LV, left ventricle; RV, right ventricle.

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260.e2 Case Report

Rhythm disorders. However, there is no agreement on how to follow patients for probable cardiac mechanical complications. The CK-MB fraction may increase by 25% secondary to muscle trauma induced by EC [6]. There is no information about troponin changes after EI [1].

In conclusion, cardiac mechanical complications after EI are not only caused by the high-tension EC, but it may also develop by low-tension EC exposure as in our case. In the assessment of patients presenting with cardiac symptoms and high enzyme levels after EI, TTE is the most appropriate initial method that may be selected.

Fig. 2 Transesophageal echocardiogram demonstrates secondary chordae rupture on the mitral valve’s anterior leaftet (arrow). AO, aorta; LA; left atrium; LV, left ventricle; RV, right ventricle.

decreased to normal. acetylsalicylic acid was administered, and the patient was then taken to follow-up. In the 1-year follow-up, no cardiac symptoms were observed.

Asystole and ventricular fibrillation are the most severe rhythm disorders developing after EI [4]. In a study of Bailey et al [5], these were assessed with regard to EI patients to assess the path for follow-up of the patients’ rhythm disorders. In this study, it was emphasized that asymptomatic patients without loss of consciousness and with EI lower than 1000 V and normal initial ECG required no cardiac monitorization [5].

The other pathologies that electrical trauma causes in the heart are Myocardial necrosis and consequent mechanical complications. The first report of such case in the literature belongs to Guler et al [2]. They reported aortic valve rupture 2 weeks after high-tension EI. The second case was a stroke case after mitral valve chordae rupture reported by Fluery et al [3]. In this case, the clinical picture appeared 2 weeks after the EC exposure. Fluery et al [3] made no comment with regard to the type of ruptured chordae.

Different from the aforementioned 2 cases, our case was exposed to low-tension EC. Because the patient had no previous cardiac disease symptoms and his admission with chest pain and elevated cardiac enzymes was 5 days after low-tension EI, it was thought that EI was the most probable cause of secondary chordae rupture.

There is a consensus related with the use of ECG and telemetry in the follow-up of patients exposed to EI for

Hakan Akilli MD Alpay Aribas MD cardiology department Meram School of Medicine

Konya University, Konya, Turkey E-mail address: [email protected]

Nazire Belgin Akilli MD Emergency Medicine Department Konya Training and Research Hospital

Konya, Turkey

Mehmet Kayrak

Hasan Gok Cardiology Department Meram School of Medicine

Konya University, Konya, Turkey

http://dx.doi.org/10.1016/j.ajem.2012.03.012

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