Acute Myocardial Infarction With ST Elevation

The goal of this phase IIc clinical trial is to learn if recombinant human thymosin beta 4 injection (NL005) works to treat heart damage in people who have had a serious type of heart attack called ST-segment elevation myocardial infarction (STEMI) and have been treated with emergency percutaneous coronary intervention (PCI, a procedure to open the blocked artery). It will also learn about the safety of NL005. The main questions it aims to answer are: * Does NL005 lower the size of permanent heart muscle damage measured by cardiac magnetic resonance (CMR) scan 90 days after treatment? * What medical problems do participants have when taking NL005? Researchers will compare two different doses of NL005 to a placebo (a look-alike substance that contains no drug) to see if NL005 works better to reduce heart damage caused by the heart attack. Participants will: * Receive NL005 or placebo through a vein within 4 hours after the PCI procedure, then once a day for 7 days * Stay in the hospital for the first week for monitoring, blood draws, and electrocardiograms (heart tracings) * Have a CMR scan on Day 6 and Day 90 to measure the size of the heart injury * Return to the hospital for checkups on Day 30 and Day 90 * Be contacted by the study team (by phone or online) 3 times during the first year and come back to the hospital on Day 360 to check long-term recovery

The primary risk factor for coronary artery disease is atherosclerosis, with inflammation playing a crucial role in the development and progression of this condition. It has now been proven that inflammation is key in the development of complications after an acute myocardial infarction. These complications can be immediate and mechanical, such as ventricular wall rupture and ventricular arrhythmia, or long-term, presenting as major cardiovascular events like heart failure. During acute myocardial infarction (AMI), circulating high-sensitivity CRP levels increase approximately 6 hours after the onset of ischemia. CRP levels measured between 24 and 72 hours after symptom onset are a significant prognostic marker for one-year outcomes. Higher high-sensitivity CRP levels at the time of AMI are linked to more severe coronary atherosclerotic lesions seen on angiography and lower LVEF one month after the event. A serum high-sensitivity CRP concentration greater than 10 mg/L after an AMI indicates inflammation, reflecting myocardial necrosis, plaque rupture, and acute thrombosis. In patients with AMI, persistent or increasing CRP levels are strongly associated with a higher risk of all-cause and non-cardiovascular death, especially when inflammation (CRP \> 2.0 mg/L) continues for a year. Aside from reperfusion therapy, very few pharmacological approaches have been used to reduce inflammation after AMI. One such approach was the use of colchicine in the COVERT-MI randomized, double-blind, multicenter trial. This trial compared five days of oral colchicine with a placebo and found no difference in infarct size between the groups at five days or three months, as measured by cardiac magnetic resonance imaging. SGLT-2 inhibitors are drugs that have revolutionized the management of cardiovascular diseases, offering proven benefits for patients with heart failure and notable nephroprotective effects. However, their use after acute myocardial infarction has not yet been sufficiently established, as the only two published clinical trials so far failed to meet their primary goal of reducing hospitalizations for heart failure. Additionally, evidence of their use in post-AMI inflammation exists only in experimental studies. In experimental studies, SGLT2 global-knockout (KO) mice were used to demonstrate that dapagliflozin significantly influences cardiac fibrosis and inflammation, and markedly alters the gene expression profiles of macrophages and fibroblasts. Moreover, dapagliflozin directly inhibited macrophage-mediated inflammation, thereby suppressing cardiac fibroblast activation. Similarly, only experimental studies have shown that semaglutide decreases elevated levels of TNF-α, IL-6, ROS, and MDA in the serum and cardiac tissues of obese mice. By lowering the expression of Cxcl2, S100a8, and S100a9 in neutrophils, semaglutide may help reduce cardiac inflammation and oxidative stress. Therefore, the objective of this study is to compare the effects of dapagliflozin and semaglutide on inflammatory markers (hs-CRP and IL-6) in patients with acute ST-segment elevation myocardial infarction.

The goal of this observational study is to learn about the effectiveness of an artificial intelligence-based early warning system for predicting adverse events in patients with acute myocardial infarction (AMI). The main question it aims to answer is: Does an AI-based early warning system improve the assessment and prediction of adverse events across the full course of AMI care (from prevention to diagnosis, treatment, and rehabilitation)? Participants who are receiving routine medical care for AMI in tertiary hospitals will have their multimodal medical data (clinical records, diagnostic tests, imaging, treatment pathways) collected and analyzed. Data will be integrated using innovative cross-modal representation methods and predictive models. The study will follow patients during their hospital stay and subsequent clinical follow-up to evaluate the feasibility, accuracy, and clinical value of the AI-based early warning system.

Glucose monitoring after Acute Myocardial infarct in people with diabetes is a Dexcom funded study that is investigating whether the use of continuous glucose monitors (Dexcom ONE model) in people with type 2 diabetes facilitates time in glycaemic range in the 6 months after an acute myocardial infarction. As an exploratory outcome it will investigate whether time in glycaemic range is associated with changes in mortality and major adverse cardiac events in the 6 months after acute myocardial infarct.