Sudden Death Documented During 24-Hour Holter Monitoring

A 50-year-old female patient admitted for etiological syncope investigation. A 24-hour Holter was installed where the record showed the mechanism of sudden cardiac death. Sudden bradycardia caused by paroxysmal atrioventricular block led to torsades de pointes, ventricular fibrillation and death. This case shows the importance of Holter in the chronology of arrhythmic events that lead to sudden death and highlights a poorly reported event – the occurrence of cardiac death during 24-hour Holter monitoring.


INTRODUCTION
The prevalence of sudden cardiac death (SCD) in 24-hour Holter monitoring (H24) is not known, but it is estimated to be a rare event. In an unregistered SCD, it is difficult to accurately identify the primary arrhythmia responsible for the event based only on the heart rate obtained by the emergency team, because an arrhythmia can start with one mechanism and degenerate into another 1,2 .

CASE REPORT
Female patient, 50 years old, former smoker, in outpatient follow-up with pneumology due to chronic obstructive pulmonary disease, using tiotropium bromide About 1 min after maintenance of atrial tachycardia rhythm, she showed evolution to torsades de pointes ( Fig. 2b and c) that rapidly evolved to ventricular fibrillation ( Fig. 2d). After recording approximately 1 min of the onset of ventricular fibrillation, the H24 was removed and cardiopulmonary resuscitation maneuvers with defibrillation, cardiac massage and anti-arrhythmic drugs were initiated, however the patient evolved to asystole and after 40 min of resuscitation, she was declared dead.

DISCUSSION
The H24 is a tool that can provide definitive information on electrical events that precede arrhythmias leading to the SCD. It is estimated that the primary event that initiates the events that determine MSC to H24 rarely occurs due to bradyarrhythmias and especially ventricular arrhythmias, which include monomorphic or polymorphic ventricular tachycardia (VT) and ventricular fibrillation 1-3 .
In the largest series of cases, Bayés de Luna et al., in a study with 157 cases of SCD to H24, observed that bradyarrhythmias are responsible for the sequence of events that trigger SCD in less than 20% of the cases, as described in this report. Typically, when they occur, they are associated with advanced age and higher frequency of comorbidities compared to patients with SCD related to ventricular arrhythmias 1 .
Primary ventricular arrhythmias were responsible for 83.4% of the cases of death during monitoring with H24 and the most frequent rhythm was monomorphic VT, followed by torsades of points (TdP) and ventricular fibrillation 1 .
The compensatory mechanisms that occur in a sudden bradycardia can lead to several types of tachyarrhythmias 3-5 . In this report, the AVB led to the episode of atrial Luciano KS, Campane RZ, Sales RL, Kraus A, Pestana ER, Ronsoni RM mechanism with increase of circulating catecholamines and increase of calcium inflow in phase 2 of action potential [3][4][5]

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TdP can be self-limited, however, because it is an arrhythmia with high and disorganized ventricular response, in cases where it occurs in a sustained manner, there is evolution to ventricular fibrillation 1 , as in this report.
Alterations in the ST segment before fatal arrhythmias in H24 can be found in 10 to 30% of cases, mainly when the primary arrhythmia is a polymorphic VT or ventricular fibrillation, suggesting that myocardial ischemia may play a role in the SCD of these patients 1,2 .
The patient in this report presented an unevenness of the ST segment that preceded the AVB appearance, however, despite risk factors for atherosclerotic disease, it was not possible to obtain data proving the ischemic origin of paroxysmal AVB.
Some studies 1,8-10 tried to correlate a circadian periodicity from the time of SCD to H24 and observed a peak incidence  The nocturnal predominance of SCD was observed in a group of patients in which the initial event that triggered the SCD was TdP, possibly linked to some channelopathies that may have the vagal period as trigger 1 .
In this case, the sequence of arrhythmic mechanisms that culminated in SCD during monitoring with H24 was described, an event barely reported in the literature, especially when the initial event is a bradycardia. In this case, atrioventricular block was initially observed followed by atrial tachycardia, TdP and finally ventricular fibrillation with evolution to SCD.