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‘First, do no harm’ are oft misquoted words from Hippocrates’ 2500-year-old work Epidemics . A more complete and accurate translation of his exhortation reads: > The physician must be able to tell the antecedents, know the present, and foretell the future — must mediate these things, and have two special objects in view with regard to disease, namely, to do good or to do no harm.1 This is laudable sentiment but is it realistic for a diagnosis surrounding which much uncertainty remains? Looking back only 20 years, a case report in this publication described spontaneous coronary artery dissection (SCAD) as ‘an extremely rare cause of unstable angina and acute myocardial infarction’.2 That is no longer the case. There has been a surge in the recognition of the condition. One recent study found 33 (2.4%) cases of SCAD among 1375 patients who underwent invasive coronary angiography for acute coronary syndrome in 2019.3 This represents a 10-fold increase in relative diagnostic frequency since an earlier registry (1999–2007) identified only 22 (0.2%) cases from 11 175 patients.4 Presuming that the true incidence is unchanged, this growth reflects a remarkable ‘paradigm shift in clinical appreciation’.5 In contrast to many cardiovascular disorders, SCAD is predominantly a disease affecting middle-aged women with comparatively few traditional atherosclerotic risk factors. The epidemiology, pathophysiology and approach to diagnosis of SCAD have been informed by retrospective observational cohort studies but optimal management remains unclear. Invasive coronary angiography represents the primary imaging modality for identifying the condition, meaning definitive treatment decisions are commonly made in the catheter laboratory and herein lies the challenge. In contrast with atherosclerotic disease, percutaneous coronary intervention (PCI) is associated with less predictable outcomes in …

Preterm birth affects 1 in 10 pregnancies worldwide, with increasing survival rates over the last 30 years. However, as this new generation of long-term survivors approaches middle age, recent studies have revealed increased cardiovascular risk factors and higher rates of ischaemic heart disease and heart failure. Cardiovascular imaging has identified smaller cardiac chamber size, changes in myocardial mass and impaired ventricular function, particularly under physiological stress. Accordingly, this population should be recognised as having a higher risk of heart failure as they age. In this review, we present current evidence for increased rates of heart failure and evidence of alterations in cardiac structure and function in those born preterm. We discuss potential mechanisms to explain this risk including greater frequency of co-morbidities known to be associated with heart failure. We also explore potential mechanistic links specific to the preterm-born population, including the impact of premature birth on myocardial and vascular development and the effects of perinatal haemodynamic changes and chronic lung disease on the developing heart. We highlight gaps in our knowledge and consider implications for patient management relevant to the adult physician.

The Authors’ reply: We thank the author for their interest in our report documenting the long-term prognostic importance of convalescent cardiac troponin concentrations.1 First, we agree that when used for risk stratification low cardiac troponin concentrations miss fewer events than applying the sex-specific 99th centile upper reference limit as a single threshold, and indeed we identified the lower troponin threshold of 5 ng/L to be associated with a 5-year negative predictive value for cardiovascular death of 97.1% (95% CI 95.5 to …

To the Editor , Goorden et al aim to establish the optimal threshold to rule out myocardial infarction using a high-sensitivity cardiac troponin I assay. They report that a cardiac troponin I concentration