S Rituximab Myocardial infarction: case reportA 60-year-old man developed an acute myocardial infarction following rituximab administration for testicular cancer.The man had a history of diabetes and a recent diagnosis of testicular cancer for which he received an orchiectomy, but he did not have cardiac symptoms prior to starting antineoplastic therapy. Immediately following an infusion of rituximab [dosage and frequency not stated], he developed fever with rigours. That was managed with a hydrocortisone injection and antihistamines. Fifteen minutes later, he reported severe chest pain and diaphoresis. An ECG showed persistent ST elevation in lateral leads despite drug withdrawal and administration of sublingual nitrates.The patient was in pain for over 30 minutes, and a repeat ECG revealed an extensive anterior-wall myocardial infarction. He was thrombolysed over 45 minutes with streptokinase, and results appeared successful. At the time of discharge, a coronary angiogram showed residual thrombosis with dissection of proximal left anterior descending artery and normal coronary perfusion.Arunprasath P, et al. Rituximab induced myocardial infarction: A fatal drug reaction.

Trans catheter closure is feasible in anatomically complex substrates of Secundum ASD. Careful case selection, scrupulous imaging protocol, and expertise in modified techniques are mandatory for successful outcomes.

Background: Coronary sinus (CS) has been shown to be larger in patients with atrioventricular nodal reentrant tachycardia (AVNRT (AUC 0.89, or tachycardia rate (AUC 0.60,. Conclusions: Echocardiographic measurement of the diameter of CS ostium can help in identifying the mechanism of the tachycardia before the invasive electrophysiology study. (Cardiol J 2014; 21, 3: 273-278)

SummaryA 38-year-old man from a remote tribal area of South India presented with right heart failure. On evaluation, he was found to have untreated Graves' disease (GD) with atrial fibrillation and pulmonary hypertension. The left ventricular function was normal. Secondary causes for pulmonary hypertension were ruled out. He was treated with carbimazole and low-dose propranolol. Post 4 months medical therapy, his pulmonary hypertension completely reversed, thus establishing GD as a reversible cause of pulmonary hypertension and isolated right heart failure. BACKGROUND

A 35 year old female presented with recurrent ventricular tachycardia 5 years after she had undergone surgical repair of double chambered right ventricle. Electroanatomical mapping showed a localised scar in the apex with double potentials and good pace map. Ablation here resulted in non-inducibility of ventricular tachycardia. We hypothesise that the scarring in the apex is the result of sustained pressure overload and becomes arrhythmogenic similar to the apical scar in patients with mid-ventricular hypertrophic cardiomyopathy.