Background: The dual antiplatelet therapy (DAPT) score was developed to identify patients undergoing percutaneous coronary intervention (PCI) who are likely to derive benefit (score > 2) or harm (score < 2) from extended DAPT beyond 1 year after PCI in terms of ischemic and bleeding outcomes. We examined the associations between DAPT score at index PCI and long-term mortality from an all-comers PCI registry in patients receiving DAPT according to the standard of care. Methods: We retrospectively examined prospectively collected data from the Melbourne Interventional Group PCI database (2005-2018) and grouped patients as having DAPT score > 2 or < 2. Long-term mortality was assessed from the Australian National Death Index linkage. The primary end point was long-term mortality as determined using survival analysis. Secondary end points included in-hospital events and 30-day major adverse cardiac events (MACE), a composite of death, myocardial infarction, or target vessel revascularisation. Results: Of 27,740 study patients, 9402 (33.9%) had DAPT score > 2. Patients with DAPT score > 2 were younger, included more women, and had a higher prevalence of cardiovascular risk factors. Patients with DAPT score > 2 had higher in-hospital mortality (3.0% vs 1.0%), major bleeding (2.3% vs 1.6%), 30-day MACE (7.1% vs 3.1%), and long-term mortality at a median follow-up of 5.17 years (21.9% vs 16.5%) P < 0.001 for all. Conclusions: One-third of all-comer patients undergoing PCI had a DAPT score > 2 with greater short-term ischemic and bleeding risk, and higher long-term mortality. Risk assessment with the DAPT score may guide the duration and intensity of DAPT beyond the early postPCI period.

Ventricular septal defect (VSD) associated with acute myocardial infarction and cardiogenic shock is a time critical and challenging management dilemma, with a mortality rate approaching 90%. We describe a case of inferior STEMI complicated by an ischaemic VSD and cardiogenic shock successfully stabilised with veno-arterial extracorporeal membrane oxygenation (VA-ECMO) as a bridge to surgical repair and coronary revascularisation.

Previous large multi‐centre randomised controlled trials have not provided clear benefit with routine intracoronary thrombus aspiration (TA) as an adjunct to primary percutaneous coronary intervention (PCI) in patients with ST‐elevation myocardial infarction (STEMI).

In Australia, overall COVID case burden in 2020 was low; however, government mandated lockdown resulted in reduced medical attendances. We assessed for differences in cardiac presentations and 30-day outcomes during the first lockdown period compared with the previous year.

We previously reported that exogenous angiotensin (Ang) 1-7 has adverse cardiac effects in experimental kidney failure due to its action to increase cardiac angiotensin converting enzyme (ACE) activity. This study investigated if the addition of an ACE inhibitor (ACEi) to Ang 1-7 infusion would unmask any beneficial effects of Ang 1-7 on the heart in experimental kidney failure. Male Sprague-Dawley rats underwent subtotal nephrectomy (STNx) and were treated with vehicle, the ACEi ramipril (oral 1mg/kg/day), Ang 1-7 (subcutaneous 24 μg/kg/h) or dual therapy (all groups, n = 12). A control group (n = 10) of sham-operated rats were also studied. STNx led to hypertension, renal impairment, cardiac hypertrophy and fibrosis, and increased both left ventricular ACE2 activity and ACE binding. STNx was not associated with changes in plasma levels of ACE, ACE2 or angiotensin peptides. Ramipril reduced blood pressure, improved cardiac hypertrophy and fibrosis and inhibited cardiac ACE. Ang 1-7 infusion increased blood pressure, cardiac interstitial fibrosis and cardiac ACE binding compared to untreated STNx rats. Although in STNx rats, the addition of ACEi to Ang 1-7 prevented any deleterious cardiac effects of Ang 1-7, a limitation of the study is that the large increase in plasma Ang 1-7 with ramipril may have masked any effect of infused Ang 1-7.

Left ventricular hypertrophy (LVH) increases the risk of death in chronic kidney disease (CKD). The transcription factor Kruppel-like factor 15 (KLF15) is expressed in the heart and regulates cardiac remodelling through inhibition of hypertrophy and fibrosis. It is unknown if KLF15 expression is changed in CKD induced LVH, or whether expression is modulated by blood pressure reduction using angiotensin converting enzyme (ACE) inhibition.