Percutaneous Coronary Intervention of an Anomalous Left Main Coronary Artery Arising from the Right Sinus of Valsalva.

Anomalous origination of a coronary artery from the opposite sinus of Valsalva is an uncommon congenital anomaly. Intervention for concurrent coronary artery disease is challenging due to the location of the ostia, the takeoff of the vessel as well as the course of the artery in question. It is also important, where possible, to exclude a "malignant" course as the most common adverse outcome from this anomaly is that of sudden cardiac death. Here we present a case of percutaneous coronary intervention in a patient with anomalous left main origination from the right coronary sinus of Valsalva and a brief discussion on the subject.

Spontaneous omental bleeding in the setting of dual anti-platelet therapy with ticagrelor.

A 68 year-old man, initially managed with primary percutaneous coronary intervention (PCI) to the right coronary artery (RCA) for an inferior ST elevation myocardial infarction (STEMI) with residual disease requiring coronary artery bypass graft surgery (CABG), re-presented with chest pain. There were no acute ischaemic changes on ECG and his pain settled with nitrates. A day later, he developed left sided abdominal pain and hypovolaemic shock after straining in the toilet. A subsequent computed tomography (CT) scan of his abdomen revealed an omental bleed. He proceeded to emergency laparotomy, recovered well, and was discharged on aspirin and clopidogrel. Apart from dual antiplatelet therapy with aspirin and ticagrelor, and presumed raised intra-abdominal pressure, there were no other identified risk factors for increased bleeding.

Peripartum cardiomyopathy in a previously asymptomatic carrier of Duchenne muscular dystrophy.

A 40 year-old woman presented to hospital with 12h of progressive shortness of breath. She was 11 days postpartum, having delivered a full-term male infant. She was discharged on antibiotics for presumed pneumonia, but represented two days later with NYHA class IV symptoms and in acute decompensated heart failure confirmed on clinical examination and chest X-ray. Echocardiography showed a left ventricular ejection fraction (LVEF) of 20%. She was treated for peripartum cardiomyopathy (PPCM) with angiotensin converting enzyme inhibitors (ACEi), beta-blockers and diuretics with normalisation of her cardiac function within six months. Four years later, her son was diagnosed with Duchenne muscular dystrophy (DMD) and she tested positive as a carrier of the mutant gene. It is unclear whether the DMD carrier state alone is associated with increased susceptibility to PPCM or if this is merely the first expression of cardiomyopathy in a previously asymptomatic carrier.