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Objective: International guidelines provide increasing support for computed tomography coronary angiography (CTCA) in investigating chest pain. A pathway utilising CTCA first‐line for outpatient stable chest pain evaluation was implemented in an Australian ED. Methods: In pre‐post design, the impact of the pathway was prospectively assessed over 6 months (August 2021 to January 2022) and compared with a 6‐month pre‐implementation group (February 2021 to July 2021). CTCA was recommended first‐line in suspected stable cardiac chest pain, followed by chest pain clinic review. Predefined criteria were provided recommending functional testing in select patients. The impact of CTCA versus functional testing was evaluated. Data were obtained from digital medical records. Results: Three hundred and fifteen patients were included, 143 pre‐implementation and 172 post‐implementation. Characteristics were similar except age (pre‐implementation: 58.9 ± 12.0 vs post‐implementation: 62.8 ± 12.3 years, P = 0.004). Pathway‐guided management resulted in higher first‐line CTCA (73.3% vs 46.2%, P < 0.001), lower functional testing (30.2% vs 56.6%, P < 0.001) and lower proportion undergoing two non‐invasive tests (4.7% vs 10.5%, P = 0.047), without increasing investigation costs or invasive coronary angiography (ICA) (pre‐implementation: 13.3% vs post‐implementation: 9.3%, P = 0.263). In patients undergoing CTCA, 40.7% had normal coronaries and 36.2% minimal/mild disease, with no difference in disease burden post‐implementation. More medication changes occurred following CTCA compared with functional testing (aspirin: P = 0.005, statin: P < 0.001). In patients undergoing ICA, revascularisation to ICA ratio was higher following CTCA compared with functional testing (91.7% vs 18.2%, P < 0.001). No 30‐day myocardial infarction or death occurred. Conclusions: The pathway increased CTCA utilisation and reduced downstream investigations. CTCA was associated with medication changes and improved ICA efficiency. [ABSTRACT FROM AUTHOR]

Computed tomography coronary angiography (CTCA) is a non-invasive diagnostic modality that provides a comprehensive anatomical assessment of the coronary arteries and coronary atherosclerosis, including plaque burden, composition and morphology. The past decade has witnessed an increase in the role of CTCA for evaluating patients with both stable and acute chest pain, and recent international guidelines have provided increasing support for a first line CTCA diagnostic strategy in select patients. CTCA offers some advantages over current functional tests in the detection of obstructive and non-obstructive coronary artery disease, as well as for ruling out obstructive coronary artery disease. Recent randomised trials have also shown that CTCA improves prognostication and guides the use of guideline-directed preventive therapies, leading to improved clinical outcomes. CTCA technology advances such as fractional flow reserve, plaque quantification and perivascular fat inflammation potentially allow for more personalised risk assessment and targeted therapies. Further studies evaluating demand, supply, and cost-effectiveness of CTCA for evaluating chest pain are required in Australia. This discussion paper revisits the evidence supporting the use of CTCA, provides an overview of its implications and limitations, and considers its potential role for chest pain evaluation pathways in Australia. [ABSTRACT FROM AUTHOR]

Background: Lipoprotein(a) (Lp[a]) is a risk factor for cardiovascular disease. The burden of thrombus in ST-segment elevation myocardial infarction (STEMI) has implications on treatment and outcomes. However, the association between Lp(a) and atherothrombosis in STEMI remains unclear. Objectives: The aim of the study was to determine the association between Lp(a) and culprit artery thrombus burden in younger patients with STEMI. Methods: This was a single-center study of 83 patients aged <65 years with STEMI between 2016–2018 who underwent percutaneous coronary intervention and measurement of Lp(a); those receiving thrombolytic therapy were excluded. Thrombus burden in the culprit artery was determined angiographically using the Thrombolysis In Myocardial Infarction score and classified as absent-to-small, moderate, or large. Elevated Lp(a) was defined as plasma mass concentration >30 mg/dL. Multivariate analysis was performed adjusting for cardiovascular risk factors. Results: The mean age was 48.0 ± 8.4 years, and 78.3% were male. Thirteen (16%), 9 (11%), and 61 (73%) patients had small, moderate, or large thrombus burden, respectively, and 34 (41%) had elevated Lp(a). Elevated Lp(a) was associated with greater thrombus burden compared to normal Lp(a) (large burden 85% vs. 65%; p = 0.024). Elevated Lp(a) was associated with moderate or large thrombus in univariate (OR 10.70 [95% CI 1.32–86.82]; p = 0.026) and multivariate analysis (OR 10.33 [95% CI 1.19–89.52]; p = 0.034). Lp(a) was not associated with culprit artery or stenosis location according to culprit artery. Conclusions: Elevated Lp(a) is associated with greater thrombus burden in younger patients with STEMI. The finding of this observational study accords with the thrombotic and anti-fibrinolytic properties of Lp(a). A causal relationship requires verification. [ABSTRACT FROM AUTHOR]

Introduction: Lipoprotein(a) [Lp(a)] and diabetes are independently associated with premature coronary artery disease (pCAD). However, there is an inverse relationship between Lp(a) concentration and type 2 diabetes (T2D) risk. We examine whether Lp(a) distribution in patients with pCAD differs between those with or without T2D, and whether elevated Lp(a) is associated with pCAD in patients with T2D.Methods: Lp(a) concentration was measured in consecutive acute coronary syndrome (ACS) patients in two coronary care units (study one: ACS with or without diabetes, study two: ACS and diabetes). Elevated Lp(a) mass concentration was defined as ≥0.5 g/L and pCAD where CAD was diagnosed age <60 years. The association between elevated Lp(a) and pCAD was assessed using logistic regression.Results: Of 449 patients, 233 (51.9%) had pCAD and 278 (61.9%) had T2D. In patients with pCAD, those with T2D had a significantly lower median Lp(a) concentration (0.13 g/L versus 0.27 g/L, p=0.004). In patients with T2D, elevated Lp(a) was significantly associated with pCAD (OR 2.419, 95% CI 1.513-3.867, p<0.001). After adjusting for gender, smoking, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides, elevated Lp(a) remained significantly associated with pCAD (OR 2.895, 95% CI 1.427-5.876, p=0.003) in patients with T2D.Conclusions: In coronary care patients with pCAD, patients with T2D had lower Lp(a) concentrations than those without T2D. Despite this, elevated Lp(a) remained predictive of pCAD in patients with T2D. Measurement of Lp(a) should be considered in younger adults with T2D to identify who may benefit from earlier preventative therapies to reduce pCAD burden. [ABSTRACT FROM AUTHOR]

Hepatic steatosis has been associated with increased risk of coronary artery disease. Individuals with familial hypercholesterolaemia have accelerated but variable progression of coronary artery disease. We investigated whether hepatic steatosis is associated with novel coronary atherosclerosis biomarkers in adults with heterozygous familial hypercholesterolaemia, using comprehensive coronary computed tomographic angiography. We conducted a cross-sectional study of 213 asymptomatic patients with familial hypercholesterolaemia (median age 54.0 years, 59 % female) who underwent coronary computed tomographic angiography for cardiovascular risk assessment in an outpatient clinic. High-risk plaque features, plaque volume and pericoronary adipose tissue attenuation were assessed. From concurrently captured upper abdominal images, severity of hepatic steatosis was computed, as liver minus spleen computed tomography attenuation and stratified into quartiles. Of 213 familial hypercholesterolaemia patients, 59 % had coronary artery calcium, 36 % obstructive coronary artery disease (≥50 % stenosis) and 77 % high-risk plaque features. Increasing hepatic steatosis was associated with higher calcium scores, more high-risk plaque features and presence of obstructive coronary artery disease. Hepatic steatosis was associated with the presence of high-risk plaque features (OR: 1.48; 95 % CI: 1.09–2.00; p = 0.01), particularly in the proximal coronary segments (OR: 1.52; 95 % CI: 1.18–1.96; p = 0.001). Associations persisted on multivariable logistic regression analysis adjusting for cardiometabolic factors, obstructive coronary artery disease and calcium score. Hepatic steatosis was associated with higher plaque volumes (Q4: 499 mm3 vs Q1: 414 mm3, p = 0.02), involving mainly low attenuation and noncalcified plaques (both p = 0.03). No differences in pericoronary adipose tissue attenuation were observed. Hepatic steatosis is associated with multiple indices of advanced coronary atherosclerosis in familial hypercholesterolaemia patients, particularly high-risk plaque features, independent of conventional cardiovascular risk factors and markers. This may involve specific mechanisms related to hepatic steatosis. Clinical trial number: N/A. [Display omitted] • Hepatic fat independently predicts high-risk coronary artery plaque features in FH. • Hepatic fat associates with higher low attenuation and non-calcified plaque volumes. • CT assessment of hepatic fat may add incremental value to CVD risk stratification. [ABSTRACT FROM AUTHOR]

Aims: This study explored characteristics and outcomes of patients with type 1 diabetes mellitus (T1DM) and acute coronary syndromes (ACS).Methods: A retrospective analysis of patients with T1DM admitted with ACS to an Australian hospital was conducted. Risk factor targets were defined by 2021 European Society of Cardiology Guidelines. Outcomes were defined as an adverse cardiovascular event (ACS, unplanned revascularisation, heart failure, stroke, or cardiovascular death) or all-cause mortality within six-months after discharge.Results: 61 patients were included [age 58.5 ± 12.8 years, 39 % female]. Dyslipidaemia (85 %), hypertension (75 %), smoking (28 %), prior coronary artery disease (CAD) (44 %), and microvascular complications (62 %) were common. HbA1c, low-density lipoprotein cholesterol, and blood pressure targets were attained in 12 %, 36 % and 47 %, respectively. ST-elevation myocardial infarction (65 % versus 7 %, p < 0.001) and revascularisation (77 % versus 41 %, p = 0.008) were more common in those without prior CAD. Peak inpatient blood glucose correlated directly with peak troponin (p = 0.011) and inversely with left ventricular ejection fraction (p = 0.027). Nineteen patients experienced an adverse six-month outcome, with peripheral neuropathy (p = 0.039) and in-hospital hypoglycaemia (p = 0.012) being independent predictors.Conclusions: Patients with T1DM and ACS often do not meet guideline targets for cardiovascular risk factors, and frequently present with transmural infarctions. Dysglycemia and microvascular complications predict poorer outcomes. [ABSTRACT FROM AUTHOR]