Letters to the Editor
393
Ajmaline challenge in Brugada syndrome Sir, In their report on the ECG findings in a case of Brugada syndrome, Turley and Adams draw atten-
tion to a syndrome that causes sudden unexpected cardiac death in apparently healthy individuals.1 In the reported case the diagnosis was possible from the typical electrocardiogram. As an amendment, we would like to draw attention to those
Figure 1 ECG before giving ajmaline in a survivor from sudden death.
Figure 2 Giving ajmaline unmasks the underlying Brugada syndrome.
394
Letters to the Editor
patients where the diagnosis is not as easy because the ECG is not typical. We report the case of a 60-year-old male, who was resuscitated successfully in our CCU. The ECG was not characteristic of a Brugada syndrome after CPR (Figure 1). After giving ajmaline following the recommended protocol of the European Society of Cardiology the typical pattern appeared (Figure 2).2 The patient reported recurrent syncopes in his medical history. A cardioverter-defibrillator was implanted; the patient’s further history was uneventful up to now.
References
with high levels of circulating catecholamines. In our practice, we observed this pattern in patients with septic shock treated with noradrenaline (norepinephrine), in one patient with delirium tremens, and in one patient with the Guillaume-Barr` e syndrome in acute respiratory distress. In patients with septic shock ventricular dysfunction rapidly recovered after reducing noradrenaline and starting dobutamine. We think it is interesting to point out that only one patient developed ECG abnormalities (deep negative T waves in precordial leads).
References
1. Turley AJ, Adams PC. ECG for physicians: Brugada syndrome. Resuscitation 2007;73:4—5. 2. Rolf S, Bruns HJ, Wichter T, et al. The ajmaline challenge in Brugada syndrome: diagnostic impact, safety, and recommended protocol. Eur Heart J 2003;24:1104—12.
Daniela Mandelburger Department of Internal Medicine, General Hospital of Neunkirchen, Austria Alexander Teubl Department of Internal Medicine II, General Hospital of Wiener Neustadt, Austria Georg R¨ oggla ∗ Department of Internal Medicine, General Hospital of Neunkirchen, Peischingerstrasse 19, A-2620 Neunkirchen, Austria
1. Ennezat PV, Pesenti-Rossi D, Aubert JM, et al. Transient left ventricular basal dysfunction without coronary stenosis in acute cerebral disorders: a novel heart syndrome (inverted Takotsubo). Echocardiography 2005;22(7):599— 602. 2. Van de Walle SO, Gevaert SA, Gheeraert PJ, et al. Transient stress-induced cardiomyopathy with an ‘‘inverted takotsubo’’ contractile pattern. Mayo Clin Proc 2006;81(11):1499—502. 3. Sanchez-Recalde A, Costero O, Oliver JM, Iborra C, Ruiz E, Sobrino JA. Images in cardiovascular medicine. Pheochromocytoma-related cardiomyopathy: inverted Takotsubo contractile pattern. Circulation 2006;113(17): e738—9.
Roberto Copetti ∗ Cristina Gonano Tullio Colombo Luigi Cattarossi San Antonio Abate Hospital, Emergency Department, Tolmezzo (Udine), Italy
∗ Corresponding
author. Tel.: +43 2635 602 2319; fax: +43 2635 602 3559. E-mail address:
[email protected] (G. R¨ oggla)
∗ Corresponding
author. Tel.: +39 0433488428. E-mail address:
[email protected] (R. Copetti)
4 April 2007
5 April 2007 doi: 10.1016/j.resuscitation.2007.04.008 doi: 10.1016/j.resuscitation.2007.04.009
‘‘Inverted Takotsubo’’ pattern Sir, In reference to the paper ‘‘The Artichoke Heart: The inverse counterpart of left ventricular apical ballooning’’ published in Resuscitation 2007;72:342—3, we would like to mention that the particular contractility pattern presented has been already described by Ennezat et al. and named the ‘‘Inverted Takotsubo’’ pattern.1 After this description other papers have appeared describing the same abnormalities of contractility which has always been called the ‘‘Inverted Takotsubo’’.2,3 This pattern probably presents in several patients
Combined flow rates of venous access devices and attachments Sir, A growing variety of non-return, needle free and Y-connector attachments for peripheral and central venous cannulae are available. These devices represent an additional resistance to flow in series with the cannula and may therefore seriously degrade the maximum flow rate obtainable under certain circumstances. Whilst the combined resistance to flow can be measured experimentally (for example1 ) a method for calculating the perfor-