The Enigmas For Pramipexole

At four-weeks and three Cell Cycle inhibitor months of follow-up, the clinical condition and the ECG of the patient was unremarkable. Discussion Brugada syndrome (BS) was first described as a triad of right bundle branch block pattern, ST-segment elevation and sudden cardiac death (3). With an estimated prevalence of 5 per 10,000 individuals, BS is known to cause sudden cardiac death due to its propensity to cause ventricular arrythmias (5). BS is more common among men, with a mean age at diagnosis of 40-45 years (5). Affected individuals often have a history of sudden cardiac death in the family as the inheritance is autosomal dominant (4). A variety of mutations have been linked with the syndrome; the most common being the SCN5A mutation which encodes the alpha subunit of the human cardiac voltage dependent Na channel found in as many as about 18-30% of affected patients (6). Three distinct types of ECG patterns in the right precordial leads (V1-3) has been described in Brugada syndrome. In the most common type 1, the coved type of ST segment elevation of �� 2mV gradually descends to a negative T wave, as seen in our case (7). Any condition or medication that alters the sodium currents in the heart may unmask the EKG changes in affected individuals Pramipexole (8). These triggers include fever, electrolyte changes, and a variety of drugs (4, 9). Fever has been reported to be an important trigger for unmasking of Brugada syndrome (2, 4, 6, 8, 10, 11). A rise in temperature causes inactivation of the sodium channel in some of these patients, and causes umasking of concealed Brugada syndrome, like in our patient (10). Failure of timely control of temperature can lead to life-threatening arrhythmia and cardiac arrest (11). Anesthetic agents can also unmask BS pattern of ECG primarily due to an effect on autonomic nervous system (12). The exposure to standard anesthetic agents in our patient did not lead to the unmasking of BS pattern of ECG or arrhythmia in our patient. This finding is an addition to a number of case reports of uneventful general anesthesia in patients with BS (-). Definitive diagnosis of BS requires the presence of characteristic type 1 EKG changes with at least one of the following: documented ventricular arrhythmia, family history of SCD Tofacitinib in vitro or nocturnal agonal respiration. Our patient did not have a family history of sudden cardiac death, nor was the family immediately available for ECG analysis (9). We did not perform an electrophysiological study in our patient to document the inducibility of arrythmias. While, ICD implantation is recommended for BS patients with high-risk for the development of ventricular arrhythmia to avert SCD; the management of low risk patients is less clear (2). A previous study suggested that there is a risk of SCDs even in low risk patients with ECG changes alone, as in our case (16).