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A 25-year-old male with a background of ulcerative colitis presented with a two-week history of central chest pain. His ECG on presentation showed global T wave inversion with a peak troponin I of 165 ng/mL. Clinical diagnosis of myopericarditis/myocarditis was made. Echocardiography and cardiac magnetic resonance (MR) confirmed the diagnosis. On detailed assessment of his medication history, mesalazine was suspected as an etiological factor, with discontinuation resulting in an improvement in symptoms, inflammatory markers and cardiac enzymes. This is a unique case of mesalazine-induced myopericarditis on a background of inflammatory bowel disease.

76-year-old female presented following an episode of collapse. She was hypotensive with the paramedics and remained refractory despite fluid resuscitation. Her initial baseline tests revealed an elevated troponin; she subsequently underwent a coronary angiogram that showed mild coronary artery disease. Left ventriculogram was performed, which showed abnormal mid-wall ballooning and severely impaired systolic function, characteristic of Takotsubo syndrome. Echocardiogram confirmed the presence of diagnosis and presence of left ventricular outflow tract obstruction with high gradient. She was initiated on medical heart failure therapy and improved. Follow-up investigations after 2 months showed complete resolution of systolic dysfunction and symptoms.

A 73-year-old male was brought into hospital with chest pain and inferior ST elevation on ECG. The patient immediately proceeded to the catheter lab for primary percutaneous coronary intervention. Angiography did not identify any culprit lesions to account for the patient’s electrocardiographic changes and ongoing symptoms of chest pain. Bedside echocardiography revealed critical aortic stenosis. Intra-aortic balloon pump (IABP) was inserted, resulting in resolution of chest pain and ST-segment changes. The patient underwent successful aortic valve (AV) replacement without the need for coronary intervention. This is a rare presentation of critical aortic stenosis (AS) presenting as ST-segment elevation myocardial infarction (STEMI).

The present study sought to identify confounding factors for the interpretation of copeptin levels in healthy individuals. The natriuretic peptides are recognized as diagnostic and prognostic tools in HF (heart failure). Interpretation of BNP (brain natriuretic peptide) and NTproBNP (N-terminal pro-BNP) levels is multifaceted as their secretion is influenced by many variables. A newly identified glycopeptide called copeptin is comparable with the natriuretic peptides in the diagnosis and prognosis of HF and as a prognostic biomarker after AMI (acute myocardial infarction). Copeptin, derived from the C-terminal portion of the precursor to AVP (arginine vasopressin), is secreted stoichiometrically with vasopressin, hence it can be used as a surrogate marker of the AVP system. In the present study, 706 healthy volunteers were recruited from a local HF screening study. Participants with a history of cardiovascular disease and those with echocardiographic abnormalities were excluded from the study. Copeptin and NTproBNP levels were assayed using in-house immunoluminometric assays. Median copeptin levels were significantly higher in the male volunteers compared with the females [median (range): 4.3 (0.4–44.3) compared with 3.2 (1.0–14.8) pmol/l; P<0.001]. In males, copeptin was correlated with eGFR (estimated glomerular filtration rate; rs=−0.186, P<0.001). In females, the correlation of copeptin with eGFR was weak (rs=−0.097, P=0.095). DT (deceleration time) and left atrial size correlated with higher copeptin levels (rs=0.085, P=0.029 and rs=0.206, P<0.001 respectively). Only gender (P<0.001), eGFR (P<0.001), left atrial size (P=0.04) and DT (P=0.02) remained independently predictive of plasma copeptin. The present study suggests that gender and renal function specific partition values should be used to interpret copeptin values in future studies of this biomarker in HF or ischaemic heart disease. [ABSTRACT FROM AUTHOR]