INTRODUCTION: Brugada Syndrome (BrS) is one of the most studied channelopathies, with more than 100 different identified gene mutations, and accounts for 20% of sudden deaths in individuals with a structurally intact heart. The associated pattern of BrS is presumed to be due to action potential duration mismatch between epicardium and endocardium, predominantly involving the right ventricle. It can be unmasked by medications, electrolyte abnormalities and chest trauma [2]. Medications that can unmask the Brugada pattern (BrP) on an electrocardiogram (ECG) include Flecainide, ajmaline and procainamide [2]. In addition, there have been reports of tricyclic antidepressants (TCAs) and lithium associated with unmasking of BrP. CASE PRESENTATION:A 66-year-old male with major depressive disorder, and incomplete right bundle branch block (RBBB) on prior ECG presented to the emergency department reporting a sudden onset of non-exertional lightheadedness and recurrent falls preceded by blurry vision in the absence of loss of consciousness, chest pain, diaphoresis or palpitations. Ischemic evaluation four months prior was unremarkable. At this presentation, he was normotensive with a heart rate of 88 beats per minute. Review of medical records revealed he has been on concomitant therapy with lithium and amitriptyline for the past two years secondary to poorly controlled depression and labile mood. Labs showed normal electrolytes and kidney function. ECG showed RBBB and ST-segment elevation in leads V1 and V2 consistent with type1 BrP (Figure 1). He was later discharged after placement of a cardiac event monitor, with a plan for gradual discontinuation of lithium.DISCUSSION: Amongst the cases of sudden cardiac death BrS is one of the most studied. The mismatch between action potential duration of epicardium and endocardium of right ventricle has been an underlying etiology of this channelopathy that can remain hidden for years. Risk stratification of patients for secondary prevention of adverse effects associated with BrP has been extensively studied. Survivors of cardiac arrest are considered the highest risk patients with class 1A recommendation to undergo implantable cardiovascular defibrillator placement (ICD) placement [3]. Asymptomatic patients at the time of diagnosis are considered low risk and do not require any intervention. However, management of patients who present with syncope is controversial and may require electrophysiological (EP) study to assess for inducible ventricular arrhythmias.CONCLUSIONS: When a patient presents with an ECG consistent with brugada pattern, a thorough history is essential. Information in regard to syncope, presyncope, family history of premature death, and a detailed medication list is critical in risk stratification. Based on this information, a decision about ICD implantation, loop recorder placement, EP study or close follow up is determined.

INTRODUCTION:As a relatively new entity that has come into the literature, BRASH syndrome is an acronym for a collection of objective findings inclusive of bradycardia, renal failure, atrioventricular (AV) nodal block, shock, and hyperkalemia. It is a distinct process arising from the synergistic effects of hyperkalemia and an AV-nodal blocker in the setting of renal insufficiency. Patients often are treated as isolated hyperkalemia or AV-node blocker overdose. Hereby, we present a case of BRASH syndrome and aim to point out the importance of initial workup and management of this syndrome. CASE PRESENTATION:A 66-year-old male with a history of hypertension, presented to the emergency room with altered mental status. His was bradycardic to 47 with a blood pressure of 101/67 mmHg. Initial laboratory work noted a serum potassium level of 6.3 mEq/L, sodium of 138 mEq/L, creatinine of 1.7 mg/L, serum bicarbonate of 18 mEq/L and corrected calcium level of 8.8 mEq/L. Electrocardiogram (ECG) demonstrated sinus bradycardia without hyperacute T-waves (figure1). Patient's home medication regimen review revealed he had been started on metoprolol tartrate 50 mg twice daily about a week prior to presentation. Beta blocker was held, and IV calcium gluconate was administered with resolution of bradycardia.DISCUSSION: Initial presentation of BRASH syndrome varies from mild hyperkalemia to hemodynamic compromise. Bradycardia directly reduces the cardiac output, which worsens the renal perfusion with activation of the RAAS system resulting in hyperkalemia. Furthermore, hyperkalemia affects the repolarization phase of action potential in cardiac pacemaker cells inducing more bradycardia by decreasing the potassium gradient across sinoatrial nodal cell membranes. Isolated hyperkalemia usually does not result in bradycardia until serum potassium level reach 7 mEq/L (1). However, with concurrent use of AV node blockers, bradycardia can occur in patients with a lower serum potassium level. Evidence of supratherapeutic levels of AV blockers is not a part of diagnosing BRASH syndrome (2). Isolated AV blockade intoxication can be differentiated from BRASH syndrome by normal serum level of the medication. Bradycardia related to BRASH syndrome is often resistant to atropine and should be addressed with intravenous calcium. Intravenous insulin and dextrose or epinephrine infusion can prevent the need for invasive measures such as intravenous pacing or dialysis (3). Fluid resuscitation should be individually evaluated for each patient to avoid volume overload. CONCLUSIONS:The vicious cycle of bradycardia, hyperkalemia and renal insufficiency can lead to hemodynamic compromise and shock. The geriatric population is on the rise in the United States and is considered high risk for BRASH syndrome due to chronic kidney disease. It is important for clinicians to be cautious with use of AV nodal blockers in this patient population.

INTRODUCTION: Abiotrophia stands for "life nutrition deficiency," indicating that the species needs supplemented media for growth and survival. This bacteria requires Vitamin B6 and L-cysteine to grow and it is unable to in regular blood agar. This creates difficulty in detection of this pathogen. Abiotrophia defectiva has been shown to reside in the oral, upper respiratory flora, and intestinal mucosa and is implicated in culture-negative endocarditis. This case report highlights the complex presentation, management, and complications of a rare cause of a common disease. CASE PRESENTATION:A 66 year old male member of Jehovah's Witness with a history of bicuspid aortic valve presented with a 3 month history of substernal chest pain, palpitations, productive cough, dyspnea and fever. Physical examination was remarkable for grade III systolic murmur at right 2nd intercostal space. Transthoracic echocardiogram showed an ejection fraction of 40-45% with a bicuspid aortic valve. Blood cultures grew Abiotrophia defectiva in 4/4 bottles and TEE confirmed a 1.8 cm x 0.5 cm vegetation on the aortic valve cusp. The patient started an empiric regimen of Vancomycin and Gentamicin for at least 6 weeks after negative blood cultures. The patient declined aortic valve replacement. Subsequently, MRI imaging displayed findings of L4-5 disciits without epidural extension. His clinical course further deteriorated with atrial fibrillation and acute kidney injury which rapidly progressed to acute tubular necrosis. He was transferred to a new tertiary hospital where he underwent a bloodless aortic valve replacement without any complications. DISCUSSION: A. defectiva is an aggressive multidrug resistant organism with a poor prognosis. This unique case highlights the unpredictable nature of A. defectiva endocarditis, propensity for devastating complications, and the role of surgical management. A. defectiva's ability to produce an exopolysaccharide and bind to fibronectin in the extracellular matrix contribute to its virulence. The American Heart Association guidelines recommend the treatment regimen used for Enterococcus endocarditis: Penicillin and Gentamicin for 4-6 weeks. However, 90% of the isolates are resistant to penicillin. This patient was started on the alternative regimen with Vancomycin and Gentamicin with limited benefit. Future studies can explore whether A. defectiva endocarditis warrants triple antibiotic therapy.CONCLUSIONS: Infectious endocarditis caused by A. defectiva is extremely rare but not infrequent. The clinical course of endocarditis should always be monitored in an intensive and thorough manner, but one's guard needs to be even higher with A. defectiva endocarditis. Early suspicion, diagnosis, and aggressive management of this fastidious microorganism is vital to prevent grave complications and create a better prognosis for patients.