Deglutition induced supraventricular tachycardia is an uncommon condition postulated to be a vagally mediated phenomenon due to mechanical stimulation. Patients usually present with mild symptoms or may have severe debilitating symptoms. Treatment with Class I agents, beta blockers, calcium channel blockers, amiodarone and radiofrquency catheter ablation has shown to be successful in the majority of reported cases. We report the case of a 46-year-old healthy woman presenting with palpitations on swallowing that was documented to be transient atrial tachycardia with aberrant ventricular conduction as well as transient atrial fibrillation. She was successfully treated with propafenone with no induction of swallowing-induced tachycardia after treatment. This is also the first case to show swallowing-induced atrial tachycardia and atrial fibrillation in the same patient.

One-fourth of patients with LVSD who undergo CABG do not have LVEF reassessed postoperatively which may lead to underutilization of ICDs.

Background: Due to the rise in the number of reports of stress cardiomyopathy in the literature, awareness of this condition is increasing. Although different names have been used to describe this condition, the similarities in clinical, electrocardiographic, echocardiographic, and angiographic features suggest that they represent the same spectrum of diseases with different underlying causes. The pathophysiology of stress cardiomyopathy remains controversial. Methods:We describe a series of four cases of stress cardiomyopathy admitted to our institution over a period of six months with different presentations, but similar clinical course, EKG, echocardiographic, and catheterization findings. The ages ranged from 22 to 81 years; all four females. All showed characteristic wall motion abnormalities by imaging in the absence of significant coronary artery disease, with spontaneous recovery of left ventricular function with conservative therapy.Results: Although the patients presented with different clinical scenarios, all four showed characteristic features of stress cardiomyopathy suggesting that the pathophysiology affecting the myocardium was the same. We present a review of the literature with a discussion of the history of this condition, characteristic clinical features, and diagnostic criteria used in the past as well as the suggested pathophysiology of this condition. Conclusion:Stress cardiomyopathy is an underdiagnosed reversible cardiomyopathy triggered by severe emotional or physical stress. It represents a spectrum of conditions with reversible severe left ventricular systolic dysfunction that includes neurogenic cardiomyopathy. It is not confined to the Japanese population and can affect people of any ethnic background or nationality.

Persistent left superior vena cava (SVC) is an uncommon condition, usually encountered during cannulation of the left subclavian vein. We describe a patient who required a cardiac device upgrade to cardiac resynchronization implantable cardioverter defibrillator for biventricular failure. The presence of a persistent left SVC proved to be a blessing in disguise in this patient as he had since developed total occlusion of the left subclavian-innominate system.

Brugada syndrome is one of the important causes of sudden cardiac death in young adults. The condition is associated with typical electrocardiogram (ECG) changes in anteroseptal leads V1 and V2 that can be unmasked by various medications, electrolyte disturbances, and even by the febrile state in susceptible individuals. The case history is reported of a patient with atrial flutter and atrial fibrillation who developed Brugada-like ECG changes when treated with propafenone. He was mistakenly diagnosed as having acute myocardial infarction when he presented to the emergency room with acute precordial chest pain. Cardiac catheterisation revealed normal coronary arteries and normal left ventricular systolic function. A review of previous ECGs showed the temporal relationship of ECG changes to initiation of propafenone a few years earlier. The ECG changes resolved with discontinuation of propafenone and re-emerged when he was rechallenged with oral propafenone. This case highlights the importance of recognising the characteristic ECG changes of Brugada syndrome and being able to differentiate them from those of acute myocardial infarction and other conditions manifesting with similar changes.