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.

Use of CT coronary angiography (CTCA) to evaluate chest pain has rapidly increased over the recent years. While its utility in the diagnosis of coronary artery disease in stable chest pain syndromes is clear and is strongly endorsed by international guidelines, the role of CTCA in the acute setting is less certain. In the low-risk setting, CTCA has been shown to be accurate, safe and efficient but inherent low rates of adverse events in this population and the advent of high-sensitivity troponin testing have left little room for CTCA to show any short-term clinical benefit.In higher-risk populations, CTCA has potential to fulfil a gatekeeper role to invasive angiography. The high negative predictive value of CTCA is maintained while also identifying non-obstructive coronary disease and alternative diagnoses in the substantial group of patients presenting with chest pain who do not have type 1 myocardial infarction. For those with obstructive coronary disease, CTCA provides accurate assessment of stenosis severity, characterisation of high-risk plaque and findings associated with perivascular inflammation. This may allow more appropriate selection of patients to proceed to invasive management with no disadvantage in outcomes and can provide a more comprehensive risk stratification to guide both acute and long-term management than routine invasive angiography.

Being born preterm (PT, <37 weeks gestation) or at very low birth weight (VLBW, <1500 g) is associated with increased rates of cardiopulmonary disorders in childhood. As survivors age, late cardiac effects, including right ventricular (RV) remodelling and occult pulmonary hypertension are emerging. In this population-based study, we aimed to investigate right heart structure and function in young adults born PT at VLBW compared to normal-weight term-born controls. The New Zealand VLBW Study has followed all infants born in 1986 with birth weight <1500 g. All were born preterm from 24 to 37 weeks. A total of 229 (71% of survivors) had echocardiograms aged 26–30 years which were compared to age-matched, term-born, normal-weight controls (n = 100). Young adults born preterm at very low birth weight exhibited smaller RV dimensions compared to term-born peers. Standard echocardiographic measures of RV function did not differ, but mildly reduced function was detected by RV longitudinal strain. This difference was related to birth weight and gestational age but not lung function or left ventricular function. Echocardiographic strain imaging may be an important tool to detect differences in RV function preterm and VLBW.

Background: The comparison of coronary computed tomography angiography plaques and perivascular adipose tissue (PVAT) between patients with acute myocardial infarction (AMI) posttreatment and patients with stable coronary artery disease is poorly understood. Our objective was to evaluate the differences in coronary computed tomography angiography–quantified plaque and PVAT characteristics in patients post‐AMI and identify signs of residual inflammation. Methods and Results: We analyzed 205 patients (age, 59.77±9.24 years; 92.20% men) with AMI ≤1 month and matched them with 205 patients with stable coronary artery disease (age, 60.52±10.04 years; 90.24% men) based on age, sex, and cardiovascular risk factors. Coronary computed tomography angiography scans were assessed for nonculprit plaque and vessel characteristics, plaque volumes by composition, high‐risk plaques, and PVAT mean attenuation. Both patient groups exhibited similar noncalcified plaque volumes (383.35±313.23 versus 378.63±426.25 mm ³ , P =0.899). However, multivariable analysis revealed that patients post‐AMI had a greater patient‐wise noncalcified plaque volume ratio (estimate, 0.089 [95% CI, 0.053–0.125], P <0.001), largely attributed to a higher fibrofatty and necrotic core volume ratio, along with higher peri‐lesion PVAT mean attenuation (estimate, 3.968 [95% CI, 2.556–5.379], P <0.001). When adjusted for vessel length, patients post‐AMI had more high‐risk plaques (estimate, 0.417 [95% CI, 0.298–0.536], P <0.001) per patient. Conclusions: Patients post‐AMI displayed heightened noncalcified plaque components, largely due to fibrofatty and necrotic core content, more high‐risk plaques, and increased PVAT mean attenuation on a per‐patient level, highlighting the necessity for refined risk assessment in patients with AMI after treatment.

Background: Growth differentiation factor-15 (GDF-15) has been shown to be associated with adverse clinical outcomes in patients after an acute coronary syndrome when measured soon after an event. Although dynamic in the acute phase after myocardial injury, GDF-15 has been shown to remain stable during convalescence. In this study, we aimed to assess the value of GDF-15 as a long-term prognostic marker for clinical outcomes when measured in the convalescent phase following an acute coronary syndrome. Methods: GDF-15 concentrations were measured in 1945 patients who were recruited between 2002 and 2009 to the Coronary Disease Cohort Study. For this analysis, follow-up was curtailed at 10 years and association of GDF-15 with all-cause death, cardiovascular death, recurrent myocardial infarction, and heart failure hospitalizations were assessed with multivariate Cox proportional hazard regression analysis. Results: After 10 years of follow-up, there were 648 deaths (348 from cardiovascular causes), 500 admissions for myocardial infarction, and 436 for heart failure. Four-month convalescent GDF-15 demonstrated a robust independent association with all endpoints, which remained after adjustment for Global Registry of Acute Coronary Events score and other convalescent biomarkers. When compared to the lowest quartile of GDF-15 concentrations, those in the highest quartile had a 3-fold increased risk of all-cause death. Conclusions: Convalescent plasma GDF-15 is a strong and independent predictor of 10-year all-cause death, cardiovascular death, recurrent myocardial infarction, and heart failure admission following an acute coronary syndrome. Australian New Zealand Clinical Trials Registry Trial ID: ACTRN12605000431628.

Aim: The performance of plasma soluble urokinase plasminogen activator receptor (suPAR) for prediction of heart failure (HF) readmission or death within 5 years was assessed in patients incurring (i) initially undifferentiated chest pain and (ii) immediately after diagnosed acute coronary syndromes (ACS), and (iii) in recovery after ACS. Methods: suPAR concentrations were measured at admission for acute chest pain patients (n=917) including confirmed ACS (26.5%), and in an independent 4-6 weeks post-ACS cohort (n=1301). suPAR’s prognostic performance, in comparison, and combination with cTnI or NT-proBNP was evaluated by risk discrimination, hazard ratios (HR) as continuous variables and cut-off concentrations across the three settings in unadjusted and adjusted analyses. Results: In acute undifferentiated chest pain including the subgroup with confirmed ACS and separately post-ACS convalescence, combining suPAR and NT-proBNP yielded the highest discriminatory power for endpoints (c-statistics >0.80, ≥ Δ0.02). suPAR in the acute and post-ACS convalescent conferred additional hazard for the composite endpoint of HF/death (HR>1.4), HF (HR>1.3) and death (HR>1.2) after adjustment for risk factors including circulating cardiac markers. Although suPAR >3.65ng/mL (>83% specificity, >91% NPV) was superior in admission ACS (HR:10.5) for risk of HF/death, independent prediction for the composite endpoint remained consistent across the three settings and in men. Conclusion: Plasma suPAR independently predicted risk of readmissions with HF and death, independent of key clinical indicators and cardiac markers at all points of the patient journey from acute chest pain presentation through to post-ACS convalescence. Its use in acute chest pain and ACS may augment risk stratification strategies.