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Background: The Assessing cardiovascular risk using Scottish Intercollegiate Guidelines Network (ASSIGN) risk score, developed in 2006, is used in Scotland for estimating the 10-year risk of first atherosclerotic cardiovascular disease (ASCVD). Rates of ASCVD are decreasing, and an update is required. This study aimed to recalibrate ASSIGN (V.2.0) using contemporary data and to compare recalibration with other potential approaches for updating the risk score.

Methods: Data from Scotland-resident participants from UK Biobank (2006-2010) and the Generation Scotland Scottish Family Health Study (2006-2010), aged 40-69 and without previous ASCVD, were used for the derivation of scores. External evaluation was conducted on UK Biobank participants who were not residents of Scotland. The original ASSIGN predictor variables and weights formed the basis of the new sex-specific risk equation to predict the 10-year risk of ASCVD. Different approaches for updating ASSIGN (recalibration, rederivation and regression adjustment) were tested in the evaluation cohort.

Results: The original ASSIGN score overestimated ASCVD risk in the evaluation cohort, with median predicted 10-year risks of 10.6% for females and 15.1% for males, compared with observed risks of 6% and 11.4%, respectively. The derivation cohort included 44 947 (57% females and a mean age of 55) participants. The recalibrated score, ASSIGN V.2.0, improved model fit in the evaluation cohort, predicting median 10-year risk of 4% for females and 8.9% for males. Similar improvements were achieved using the regression-adjusted model. Rederivation of ASSIGN using new beta coefficients offered only modest improvements in calibration and discrimination beyond simple recalibration. At the current risk threshold of20% 10-year risk, the original ASSIGN equation yielded a positive predictive value (PPV) of 16.3% and a negative predictive value (NPV) of 94.4%. Recalibrated ASSIGN V.2.0 showed similar performance at a 10% threshold, with a PPV of 16.8% and an NPV of 94.6%.

Conclusions: The recalibrated ASSIGN V.2.0 will give a more accurate estimation of contemporary ASCVD risk in Scotland.

Background: Coronary heart disease (CHD) remains a leading cause of mortality and disability worldwide. Approximately half of the patients who have had a prior hospital admission for CHD will have a recurrent coronary event, with the majority of these occurring within 12 months. Despite well-established evidence-based therapies, medication non-adherence is highly prevalent and reasons for medication non-adherence are poorly understood. This study evaluates factors influencing adherence to secondary prevention medications in people with acute coronary syndrome (ACS).

Methods: We performed a secondary analysis of TEXT messages to improve MEDication adherence and Secondary prevention after ACS (TEXTMEDS), a single-blind randomised clinical trial of 1424 patients with ACS from 18 hospitals across Australia. The primary outcome was self-reported medication adherence to each of up to five classes of guideline-recommended cardioprotective medications indicated for secondary prevention after ACS. Patients were followed up at 6-month and 12-month time points and were defined as adherent if at both time points, the proportion of indicated medications taken was >80% (>24/30 days in the preceding 1 month) for all five classes if not otherwise contraindicated. Logistic regression analysis and the Least Absolute Shrinkage and Selection Operator regularisation technique were used to assess the effect of sociodemographic and clinical factors on medication adherence.

Results: The analyses included 1379 participants with complete adherence data (mean age 58.5±10.7 years; 1095 (79.4%) men). The following variables were associated with adherence to cardiovascular medications at both 6 and 12 months: greater number of total medications taken (OR: 1.33; 95% CI: 1.25 to 1.42) and attending a cardiac rehabilitation programme (1.47; 95% CI: 1.17 to 1.86). In contrast, female sex (0.67; 95% CI: 0.50 to 0.90) and physical disability (0.43; 95% CI: 0.23 to 0.77) were associated with lower likelihood of medication adherence.

Conclusions: Sociodemographic and clinical factors may influence medication adherence. Greater awareness, discussion and monitoring of these factors during patient follow-up may help improve medication adherence.

Trial registration number: Australian New Zealand Clinical Trials Registry; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=364448; registration number: ACTRN12613000793718.

Acute myocardial infarction-related cardiogenic shock (AMI-CS) is a severe, life-threatening condition characterised by inadequate tissue perfusion due to the heart's inability to pump blood effectively. The pathophysiology of AMI-CS usually arises from the sudden loss of myocardial contractility, leading to a decrease in cardiac output and systemic hypoperfusion. In approximately 90% of AMI-CS cases, the left ventricle is the primary site of dysfunction.Despite early recognition and the implementation of strategies such as primary percutaneous coronary intervention, the mortality rate associated with AMI-CS remains alarmingly high, reflecting significant unmet clinical needs. A major challenge lies in identifying the optimal patient population for mechanical circulatory support (MCS) devices, as these interventions are costly and can lead to serious complications.This review provides a comprehensive overview of the pathophysiological mechanisms underlying AMI-CS, explores the current range of MCS devices available and offers an in-depth discussion on the balance of benefits and risks associated with these devices. By highlighting key evidence from recent studies, we aim to shed light on the clinical decision-making process and improve outcomes in this high-risk patient population.

Background: IgG4-related disease (IgG4-RD) is a relapsing-remitting, fibroinflammatory, multisystem disorder. Cardiovascular involvement from IgG4-RD has not been systematically characterised. In this study, we sought to evaluate consecutive patients with IgG4-RD using a detailed multiparametric cardiovascular magnetic resonance (CMR) imaging protocol.

Methods: We prospectively enrolled 11 patients with histology-confirmed IgG4-RD; with active disease at time of scan. We undertook a detailed multiparametric CMR imaging protocol at 1.5T including cine imaging, native T1 and T2 mapping, stress perfusion imaging with inline quantitation of myocardial blood flow and late gadolinium enhancement (LGE) imaging.

Results: All patients exhibited at least one abnormality on CMR imaging. Abnormal elevation of global or segmental left ventricular myocardial T1 and T2 values was present in four patients, suggesting myocardial oedema or inflammation. Abnormal LGE, suggesting myocardial scar fibrosis, was present in nine patients, with eight displaying a non-ischaemic pattern, and one showing an ischaemic pattern. Four patients fulfilled both Lake Louise Criteria for active myocardial inflammation, while a further six fulfilled one criterion. Myocardial perfusion reserve was normal in all evaluable patients. Ten patients had normal ventricular volumes, mass and systolic function. In addition, thoracic aortitis was identified in three patients who underwent ¹⁸F-flourodeoxyglucose PET/CT imaging, with resolution following anti-B-cell treatment.

Conclusions: In this cohort of patients with histology-confirmed IgG4-RD, multiparametric CMR revealed no changes in gross cardiac structure and function, but frequent myocardial tissue abnormalities. These data suggest a plausible pathophysiological link between IgG4-RD and cardiovascular involvement.

Objective: To investigate the associations between a comprehensive set of retinal vascular parameters and incident stroke to unveil new associations and explore its predictive power for stroke risk.

Methods: Retinal vascular parameters were extracted from the UK Biobank fundus images using the Retina-based Microvascular Health Assessment System. We used Cox regression analysis, adjusted for traditional risk factors, to examine the associations, with false discovery rate adjustment for multiple comparisons. Receiver operating characteristic (ROC) curves were used to assess their predictive values.

Results: During a median follow-up of 12.5 years, 749 incident strokes occurred among 45 161 participants. The analysis identified 29 significant parameters associated with stroke risk, with a notable dominance of density parameters (over half). Each SD change in these parameters increased stroke risk by 9.8% to 19.0%. For identified calibre parameters, each SD change was associated with an increased risk (ranging from 10.1% to 14.1%). For identified complexity parameters and arterial inflection count tortuosity, each SD decrease was linked to an increased risk (ranging from 10.4% to 19.5%). The introduction of retinal vascular parameters improved the area under the ROC curve to 0.752, significantly outperforming the model using only traditional risk factors (0.739, p<0.001).

Conclusions: Retinal vascular analysis, a non-invasive screening approach for stroke risk assessment, performed better than traditional risk stratification models. The 29 novel retinal indicators identified offer new avenues for stroke pathophysiology research.

Cardiovascular alterations are common in patients who had ischaemic stroke, haemorrhagic stroke and other acute brain disorders such as seizures. These cardiac complications are important drivers of morbidity and mortality and comprise blood-based detection of cardiomyocyte damage, ECG changes, heart failure and arrhythmia. Recently, the concept of a distinct 'stroke-heart syndrome' has been formulated as a pathophysiological framework for poststroke cardiac complications. The concept considers cardiac sequelae after stroke to be the result of a stroke-induced disturbance of the brain-heart axis. In this review, we describe the spectrum of cardiac changes secondary to ischaemic stroke and other acute brain disorders. Furthermore, we focus on Takotsubo syndrome secondary to acute brain disorders as a model disease of disturbed brain-heart interaction. Finally, we aim to provide an overview of the anatomical and functional links between the brain and the heart, with emphasis on the autonomic network and the role of inflammation. Given the clinical relevance of the deleterious impact of acute brain injury on the heart, we call for clinical awareness and for starting joint efforts combining expertise of neurology and cardiology to identify specific therapeutic interventions.