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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]

Sodium‐glucose cotransporter 2 (SGLT2) inhibitors are a unique class of oral anti‐hyperglycaemic medications that act to reduce glucose reabsorption in the renal proximal tubules, thereby enhancing urinary glucose excretion. Large randomized placebo‐controlled trials in people with diabetes at high cardiovascular risk have demonstrated that SGLT2 inhibitors reduce heart failure hospitalization within months of commencing therapy. These findings are of considerable interest, as diabetes is associated with an increased risk of both heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. In addition, left ventricular (LV) hypertrophy and impaired diastolic function is thought to be more prevalent in people with diabetes. Although many hypotheses have been proposed, the underlying mechanisms through which SGLT2 inhibitors reduce the risk of heart failure in people with diabetes are not fully understood. Given the rapid reduction in heart failure hospitalization, it is conceivable that the benefits of SGLT2 inhibitors are due to favourable haemodynamic and metabolic effects on LV function. Several clinical studies have been conducted to investigate the effect of SGLT2 inhibitors on LV structure and function and have found that LV mass index and diastolic function improve following SGLT2 inhibitor therapy in people with type 2 diabetes. If these findings are confirmed in future studies utilizing novel cardiac imaging modalities and large randomized controlled trials, then this will bring new hope for the prevention and management of heart failure with preserved ejection fraction, for which no current treatments have been shown to reduce mortality. At the present time, SGLT2 inhibitors are indicated for the treatment of type 2 diabetes; however, the results of ongoing trials in participants with heart failure but without diabetes are eagerly awaited. The purpose of this review is to summarize current knowledge regarding the effects of SGLT2 inhibitors on LV function, particularly the findings from clinical studies, proposed biological mechanisms, and future directions. [ABSTRACT FROM AUTHOR]

Dyslipidaemia is an important modifiable risk factor contributing to the increased risk of atherosclerotic cardiovascular disease in diabetes. However, determining when to initiate statin therapy in young adults with type 1 diabetes mellitus (T1DM) can often be challenging. This is due to a relative paucity of data in this area to guide management and for developing T1DM-specific risk engines. Current recommendations from international guidelines offer differing approaches to cardiovascular risk stratification and management of dyslipidaemia in T1DM. We present a clinical vignette and comment on the use of nontraditional methods of cardiovascular risk stratification. The strategy for managing dyslipidaemia in young T1DM should be individualized, and recommendations from guidelines should serve to inform clinical judgement. [ABSTRACT FROM AUTHOR]