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A 34-year-old man presented with fatigue for 3 months and fever for the last 1 month. His previous medical history was significant for Marfan syndrome and he had undergone Bentall procedure 10 years ago for type A aortic dissection. Postsurgery, he was lost to follow-up for the next 10 years until

Rheumatic heart disease is an important cause of mortality and morbidity in developing countries, and is the leading cause of triple valve replacement. Myocardial infarction (MI) in such cases can be due to the coronary embolism from the prosthetic valves or due to atherosclerotic vascular disease. Intravascular imaging helps in delineating the cause. We present a case of a 34-year-old premenopausal woman with no conventional cardiovascular risk factors and had triple valve replacement 4 years ago and anterior wall MI with cardiogenic shock and left ventricular failure. She was managed with mechanical ventilation, thrombolysis, diuretics, double antiplatelets and anticoagulation with low molecular weight heparin. Intravascular ultrasound showed a lipid-rich plaque with associated plaque rupture and thrombosis. Intravascular imaging helps in delineating the cause of MI and further management. Atherosclerotic MI in a patient with no conventional risk factors is rare and needs to be considered.

Severe aortic stenosis (AS) may rarely present like acute coronary syndrome with increased cardiac biomarker despite having normal coronaries. Here we describe a case of very severe AS, who presented with exertional and rest angina and a high level of TnI. Angiography revealed normal coronaries. Echocardiography showed very severe AS with peak velocity of 5.08 m/s and maximum and mean gradient of 103 and 54 mm Hg, respectively. The patient subsequently underwent aortic valve replacement (AVR) successfully. Subendocardial ischaemia may occur in patients with severe AS during haemodynamic stress, even in the setting of normal unobstructed coronaries due to supply-demand mismatch. Subsequent degeneration and death of the cardiac myocytes cause cTnI elevation, which anticipates the start of the clinical downhill course in severe AS. Our case highlights the importance of thorough physical examination and early use of echocardiography in patients with angina to detect the presence of severe AS.

Left ventricular (LV) pseudoaneurysm is a rare but potentially fatal complication of myocardial infarction (MI) which needs to be differentiated from true LV aneurysm.[1][1] Most of the LV pseudoaneurysms post MI are located at the inferior and posterolateral wall (82% of all post MI pseudoaneurysms

A 40-year-old woman presented with fever of unknown origin (FUO) for 2 months. Without a definitive diagnosis and having received multiple empirical antibiotics from outside without relief, she was referred to our centre. Cardiac auscultation was remarkable for a grade 3/6 continuous murmur in the upper left sternal border. Echocardiogram revealed a patent ductus arteriosus (PDA) and a 5×7 mm mobile vegetation at the pulmonary artery bifurcation. Blood culture grewStreptococcusmutans. Embolisation of the vegetation to the pulmonary circulation occurred after the start of intravenous antibiotics resulting in fever relapse. Antibiotics were continued for 6 weeks and the fever settled. She underwent device closure of PDA after 12 weeks and is currently doing fine. Infective endocarditis/endarteritis is an important differential in a patient of FUO. A thorough clinical examination is important in every case of FUO, gives an important lead into diagnosis and guides appropriate investigations to confirm it.