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It acts by blocking the voltage-gated sodium channels, inhibiting the development of a new action potential.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">It can produce hematological adverse events in the form of cytopenias, and in the liver function due to its metabolism at that level. This is why its reactions at the cardiovascular level have been relegated to the background. It can cause negative chronotropic effects, triggering bradycardias of different types. Elderly and female patients are the main risk groups for this complication,<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">1,2</span></a> where a sick sinus syndrome is presupposed. Likewise, it can affect patients with no electrophysiological alterations, as reported in the following case report.</p><p id="par0015" class="elsevierStylePara elsevierViewall">This is a 75-year-old man, with no cardiovascular risk factors. His only medical history is the diagnosis of secondarily generalized focal seizures, following a traumatic brain injury in 1986 due to a traffic collision. The patient was treated with levetiracetam (1500<span class="elsevierStyleHsp" style=""></span>mg/12<span class="elsevierStyleHsp" style=""></span>h) and carbamazepine (300<span class="elsevierStyleHsp" style=""></span>mg/8<span class="elsevierStyleHsp" style=""></span>h). The patient went to the emergency room for a sudden-onset blurred vision and intense dizziness, with no syncope or loss of postural tone. On arrival, in a first electrocardiogram (ECG), the nodal rhythm was 35<span class="elsevierStyleHsp" style=""></span>bpm, without identifying any atrial activity (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A). The blood test showed no ionic, biochemical or metabolic changes that justify the symptomatology. Carbamazepine levels were 12.60<span class="elsevierStyleHsp" style=""></span>μg/ml (therapeutic range: 5.0–10.0).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">The administration of carbamazepine was withdrawn due to the suspicion of intoxication. After continuous ECG monitoring during a washout period, 20<span class="elsevierStyleHsp" style=""></span>h later, a second ECG showed a sinus rhythm 70<span class="elsevierStyleHsp" style=""></span>bpm with electrical axis 60°, normal PR interval and narrow QRS wave (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>B). At this time, the patient was asymptomatic. The carbamazepine levels were 5.20<span class="elsevierStyleHsp" style=""></span>μg/ml. After adjustment of carbamazepine dose, the patient was discharged without any new bradycardia episodes in a 24<span class="elsevierStyleHsp" style=""></span>h Holter-ECG at month 2 of follow-up. The adverse reaction was reported to the Spanish Pharmacovigilance System by electronic form.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Previous studies have shown a negative chronotropic effect of carbamazepine. It acts by blocking sodium channels, interfering with phases 1 and 3 of the cardiac action potential, a mechanism similar to that of class 1a antiarrhythmic agents.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> Furthermore, in experimental animal models it has been proven that carbamazepine may prolong the atrioventricular conduction and slow phase 4 of the action potential in the autonomic nerve fibers.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">It has been suggested that this drug might unmask some latent conduction disturbances. The main risk group would be elderly women,<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">2,4</span></a> particularly those under treatment with other drugs that alter conduction.</p><p id="par0035" class="elsevierStylePara elsevierViewall">This explains the development of bradycardia and advanced atrioventricular block (potentially lethal arrhythmias) in hearts with underlying conduction disorders, but also in patients with structurally and electrophysiologically normal hearts.<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3,4</span></a> This is what happens in this case report, where bradyarrhythmia is directly related to the carbamazepine levels, being resolved when reaching levels within the therapeutic range despite continuing administration, as evidenced by the Holter-ECG without any new events. Considering the causality algorithm of the Spanish Pharmacovigilance System, this case report meets the causal relationship criteria by adding 8 points when analyzing the 7 questions included in the algorhythm.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">The main reports in the literature mention its interference at the atrio-ventricular node and His-Purkinje system due to its action in the sodium channel.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> Few reports are available on carbamazepine interactions in sinoatrial activity,<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> and they involve elderly patients with altered baseline ECG. This case report is about a patient who develops sinus node dysfunction without a conduction disorder.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Therefore, an ECG is recommended systematically before using carbamazepine, as well as during clinical follow-up. Its use should be reconsidered in patients with bundle branch block or conduction alterations, evaluating other alternatives. Another point of interest is to clinically differentiate a new crisis from the manifestations of a bradycardia triggered by antiepileptic treatment. We should be extremely cautious in patients with predisposition to electrolyte disorders, and under treatment with other agents that interfere with the cardiac conduction system.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Gómez-Polo JC, de la Cruz Berlanga E, Cadenas Chamorro R. Disfunción sinusal secundaria a intoxicación por carbamazepina. Med Clin (Barc). 2019;152:e51–e52.</p>" ] ] "multimedia" => array:1 [ 0 => array:6 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 898 "Ancho" => 2500 "Tamanyo" => 657775 ] ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0030" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Advanced heart block aggravated by carbamazepine" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "B. Beermann" 1 => "O. Edhag" 2 => "H. 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Journal Information
Vol. 152. Issue 9.
Pages e51-e52 (May 2019)
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Vol. 152. Issue 9.
Pages e51-e52 (May 2019)
Letter to the Editor
Sinus dysfunction due to carbamazepine intoxication
Disfunción sinusal secundaria a intoxicación por carbamazepina
Juan Carlos Gómez-Polo
, Elena de la Cruz Berlanga, Rosalía Cadenas Chamorro
Corresponding author
Servicio de Cardiología, Hospital Universitario Infanta Sofía, San Sebastián de los Reyes, Madrid, Spain
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