Cognitive impairment (CI) shares common cardiovascular risk factors with acute myocardial infarction (AMI), and is increasingly prevalent in our ageing population. Whilst AMI is associated with increased rates of CI, CI remains underreported and infrequently identified in patients with AMI. In this review, we discuss the evidence surrounding AMI and its links to dementia and CI, including pathophysiology, risk factors, management and interventions. Vascular dysregulation plays a major role in CI, with atherosclerosis, platelet activation, microinfarcts and perivascular inflammation resulting in neurovascular unit dysfunction, disordered homeostasis and a dysfunctional neurohormonal response. This subsequently affects perfusion pressure, resulting in enlarged periventricular spaces and hippocampal sclerosis. The increased platelet activation seen in coronary artery disease (CAD) can also result in inflammation and amyloid-β protein deposition which is associated with Alzheimer’s Dementia. Post-AMI, reduced blood pressure and reduced left ventricular ejection fraction can cause chronic cerebral hypoperfusion, cerebral infarction and failure of normal circulatory autoregulatory mechanisms. Patients who undergo coronary revascularization (percutaneous coronary intervention or bypass surgery) are at increased risk for post-procedure cognitive impairment, though whether this is related to the intervention itself or underlying cardiovascular risk factors is debated. Mortality rates are higher in dementia patients with AMI, and post-AMI CI is more prevalent in the elderly and in patients with post-AMI heart failure. Medical management (antiplatelet, statin, renin-angiotensin system inhibitors, cardiac rehabilitation) can reduce the risk of post-AMI CI; however, beta-blockers may be associated with functional decline in patients with existing CI. The early identification of those with dementia or CI who present with AMI is important, as subsequent tailoring of management strategies can potentially improve outcomes as well as guide prognosis.

Introduction: Noninvasive tests, such as Fibrosis-4 (FIB-4), liver-stiffness measurement (LSM) by vibration-controlled transient elastography, and Fibroscan-AST (FAST), are frequently used for risk stratification in NAFLD. The comparative performance of FIB-4 and LSM and FAST to predict clinical outcomes of patients with NAFLD remained unclear. We aim to evaluate the performance of FIB-4, LSM, and FAST scores to predict clinical outcomes in patients with NAFLD. Methods: We included consecutive adult patients with NAFLD with transient elastography performed between 2015 and 2022 from the United States and Singapore. Patients with NAFLD stratified based on baseline FIB-4, LSM, and FAST score were followed up until clinical outcomes notably liver-related events (LREs), LREs or death, death, and major adverse cardiac events. Results: A total of 1262 patients with NAFLD (63% with obesity and 37% with diabetes) with vibration-controlled transient elastography were followed up for median 3.5 years. FIB-4 stratified patients with NAFLD into low-risk (2.67) in 59.4%, 31.5%, and 9.1%, respectively. No LRE occurred with baseline FIB-4 <1.3, regardless of LSM and FAST score. Higher FIB-4 was associated with a higher risk of LREs within each LSM category. FIB-4 had a higher area under the received operating characteristic curve than LSM or FAST score to predict LRE. Conclusions: In this multicenter international study, FIB-4 and LSM synergistically predicted the risk of LRE. In patients with FIB-4 <1.3, vibration-controlled transient elastography may incorrectly classify up to 10% of the patients as high risk. FIB-4 should be incorporated into risk stratification in NAFLD even among patients who underwent VCTE.

Background The role of bridging intravenous thrombolysis (IVT) before endovascular thrombectomy (EVT) in the treatment of acute ischemic stroke (AIS) remains debatable. Atrial fibrillation (AF) associated strokes may be associated with reduced treatment effect from IVT. This study compares the effect of bridging IVT in AF and non-AF patients. Methods This retrospective cohort study comprised anterior circulation large vessel occlusion (LVO) AIS patients receiving EVT alone or bridging IVT plus EVT within 6 hours of symptom onset. Primary outcome was good functional outcome defined as modified Rankin Scale (mRS) 0–2 at 90 days. Secondary outcomes were successful reperfusion defined as expanded Thrombolysis In Cerebral Infarction (eTICI) grading ≥2b flow, symptomatic intracerebral hemorrhage (sICH), and in-hospital mortality. Results We included 705 patients (314 AF and 391 non-AF patients). The mean age was 68.6 years and 53.9% were male. The odds of good functional outcomes with bridging IVT was higher in the non-AF (adjusted odds ratio (aOR) 2.28, 95% CI 1.06 to 4.91, P=0.035) compared with the AF subgroups (aOR 1.89, 95% CI 0.89 to 4.01, P=0.097). However, this did not constitute a significant effect modification by the presence of AF on bridging IVT (interaction aOR 0.12, 95% CI −1.94 to 2.18, P=0.455). The rate of successful reperfusion, sICH, and mortality were similar between bridging IVT and EVT for both AF and non-AF patients. Conclusion The presence of AF did not modify the treatment effect of bridging IVT. Further individual patient data meta-analysis of randomized trials may shed light on the comparative efficacy of bridging IVT in AF versus non-AF LVO strokes.