Brugada syndrome (BrS) is a rare genetic disease, of which its clinical manifestations include, but not limited to, syncope or sudden cardiac death. A 30-year-old Bangladeshi male patient with a past medical history of epilepsy was admitted following successful resuscitation from an out of hospital cardiac arrest secondary to ventricular fibrillation. Electrocardiogram (ECG) upon admission was suggestive of BrS type I. His old medical record showed similar ECG 2 months earlier when he had presented with syncope and was diagnosed with seizure. The correlation between BrS and epilepsy has been reported in the literature, discussing whether seizure is an uncommon presentation of BrS or whether epilepsy and BrS share similar genetic mutations that have the potential to cause both arrhythmia and seizures in some patients. Patients who present with seizure and ECG suggestive of Brugada pattern should be evaluated to rule out associated or underlying cardiac arrhythmia.
The central location, the size, and instability of saddle pulmonary embolism (PE) have raised considerable concerns regarding its hemodynamic consequences and the optimal management approach. Sparse and conflicting reports have addressed these concerns in the past. We aimed to evaluate the clinical presentation, hemodynamic and echocardiographic effects, as well as the outcomes of saddle PE, and compare the results with those of non-saddle type. This was a retrospective study of 432 adult patients with saddle and non-saddle PE. Overall, 432 patients were diagnosed with PE by computed tomography pulmonary angiography (CTPA). Seventy-three (16.9%) had saddle PE, and 359 had non-saddle PE. Compared to those with non-saddle PE, patients with saddle PE presented more frequently with tachycardia (68.5% vs. 46.2%, P = .001), and tachypnea (58.9% vs. 42.1%, P = .009) on admission, required more frequent intensive care unit (ICU) admissions (45.8% vs. 26.6%, P = .001) and thrombolysis/thrombectomy use (19.1% vs. 6.7%, P = .001), and were at more risk of developing decompensation and cardiac arrest after their initial admission (15.3% vs. 5.9%, P = .006). On echocardiography, right ventricular (RV) enlargement (60% vs. 31.1%, P = .000), RV dysfunction (45.8% vs. 22%, P = .000), and RV systolic pressure (RVSP) of greater than 40 mmHg (61.5% vs. 39.2%, P = .003) were significantly more observed with saddle PE. The two groups did not differ concerning the rates of hypotension (17.8% vs. 18.7%, P = .864) and hypoxemia (41.1% vs. 34.3%, P = .336) on admission and mortality rates. A logistic regression model indicated that the use of oral contraceptive pills (OCP), RVSP > 40 mmHg, and development of hypotension and decompensation following admission were associated with an increased likelihood of having saddle embolus. Saddle PE accounts for a higher proportion among all PE cases than previously reported. Patients with saddle PE tend to present more frequently with adverse hemodynamic and echocardiographic changes and decompensate after their initial presentation. OCP use, development of hypotension, and decompensation following admission and RVSP > 40 mmHg are significant predictors of saddle PE. These characteristics should not be overlooked when managing patients with saddle PE.
In 1992, the Brugada brothers published a patient series of aborted sudden death, who were successfully resuscitated from ventricular fibrillation (VF). These patients had a characteristic coved ST-segment elevation in the right precordial leads on their 12-lead electrocardiogram with no apparent structural heart abnormality. This disease was referred to as “right bundle branch block, persistent ST-segment elevation, and sudden death syndrome.” The term Brugada syndrome (BrS) was first coined for this new arrhythmogenic entity in 1996. BrS is more prevalent in Southeast Asian ethnic groups and was considered a familial disease due to the presence of syncope and/or sudden deaths in several members of the same family, however, the genetic alteration was only noted in 1998. The genetic characterization of BrS has proven to be challenging. The most common and well-established BrS genotype involves loss-of-function mutations in the SCN5A gene, but only represents between 15% and 30% of the diagnosed patients. Patients with BrS can present with a range of symptoms which can include syncope, seizures, and nocturnal agonal breathing due to polymorphic ventricular tachycardia or VF. If these arrhythmias are sustained, sudden cardiac death may result. Despite the significant progress on the understanding of BrS over the last two decades, there remain a number of uncertainties and challenges; we present an update review on the subject.
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