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Learning objectives Aortic stenosis is the archetypal heart valve disease with which many doctors, cardiologists or otherwise, retain the most familiarity. The global healthcare burden of aortic stenosis continues to rise, yet it remains one of the last major cardiovascular diseases for which we have no preventative or disease-modifying medical therapy. Aortic valve replacement is the only ‘curative’ intervention and carries attendant risks, both peri-procedural and remote. Thus, the decision to offer intervention must be carefully considered and taken with the final objective that governs most treatments in mind: to improve symptoms or prognosis. There is also substantial debate surrounding the optimal timing of intervention. Intervene too early and patients may be unnecessarily exposed to the risks of valve replacement. Intervene too late and some patients may sustain irreversible cardiac damage that is associated with an increased risk of heart failure and death. Valve replacement in symptomatic patients with severe aortic stenosis is usually uncontroversial, given their poor prognosis and the strong probability of improving their quality of life. Decisions regarding the management of patients with asymptomatic, isolated, severe aortic stenosis, however, are more complex. In this group, the predominant purpose of intervention would be to improve prognosis. In the absence of robust data, standard care in most cases has remained close observation, usually until symptoms develop.1–3 Implicit in this strategy is the concept that patients with asymptomatic severe aortic stenosis have a very good prognosis, and that there is consequently no net benefit to aortic valve replacement. However, this paradigm has latterly become the subject of scrutiny for several reasons. Symptom assessment is frequently challenging in elderly, …

A 38-year-old man presented with 4 weeks of exertional dyspnoea and abdominal bloating, culminating in an acute episode of paroxysmal nocturnal dyspnoea. He was known to have a cardiomyopathy based on history and echocardiography but had been lost to follow-up before further investigations were completed. There was no chest pain, infective prodrome or recent travel. He smoked tobacco occasionally and drank approximately 50 units of alcohol per week. On examination, blood pressure was 110/80 and heart rate was 90. The jugular venous pressure was elevated. An S3 was heard but lungs were clear to auscultation. The abdomen was soft and mildly tender. Inflammatory markers and renal function were normal and high-sensitivity troponin I was 14 ng/L. Soon after …

A 38-year-old Caucasian man presented with central chest heaviness at rest. There was a history of mild abdominal discomfort but no infective prodrome. There was no antecedent exertional or nocturnal chest pain. The patient had a 26-pack-year history of tobacco smoking and no known comorbidities. Recent social history was unremarkable. Examination and vital signs were normal. An ECG taken with mild residual chest discomfort is shown in figure 1A. High-sensitivity troponin I was 74 ng/L, peaking at 1405 ng/L. Echocardiography demonstrated a structurally normal heart with normal biventricular function. Medical therapy for an acute coronary syndrome was commenced and invasive coronary angiography was performed (figure 1B,C). Figure 1 Index presentation. (A) ECG and (B) coronary angiography: right anterior oblique–caudal view. (C) Coronary angiography: anterior–posterior cranial view. Insets show the proximal …

ObjectiveTroponin and B-type natriuretic peptide (BNP) concentrations are associated with cardiovascular risk in stable patients. Understanding their determinants and identifying modifiable clinical targets may improve outcomes. We aimed to establish clinical and cardiac determinants of these biomarkers.MethodsThis was a prespecified substudy from the randomised Scottish Computed Tomography of the Heart trial, which enrolled patients 18–75 years with suspected stable angina between 2010 and 2014 (NCT01149590). We included patients from six centres in whom high-sensitivity troponin I and BNP were measured (Singulex Erenna). Patients with troponin >99th centile upper reference limit (10.2 ng/L) or BNP ≥400 ng/L were excluded to avoid inclusion of patients with myocardial injury or heart failure. Multivariable linear regression models were constructed with troponin and BNP as dependent variables.ResultsIn total, 885 patients were included; 881 (99%) and 847 (96%) had troponin and BNP concentrations above the limit of detection, respectively. Participants had a slight male preponderance (n=513; 56.1%), and the median age was 59.0 (IQR 51.0–65.0) years. The median troponin and BNP concentrations were 1.4 (IQR 0.90–2.1) ng/L and 29.1 (IQR 14.0–54.0) ng/L, respectively. Age and atherosclerotic burden were independent predictors of both biomarkers. Male sex, left ventricular mass and systolic blood pressure were independent predictors of increased troponin. In contrast, female sex and left ventricular volume were independent predictors of increased BNP.ConclusionsTroponin and BNP are associated with coronary atherosclerosis but have important sex differences and distinct and contrasting associations with CT-determined left ventricular mass and volume.Clinical Trial registrationNCT01149590; Post-results.