Yao Neng Teo

Background: A significant proportion of patients with ST-elevation myocardial infarction (STEMI) present without cardiac symptoms of chest pain. Such presentations potentially affect the care they receive and ultimately affect these patients’ short and long-term outcomes. We analysed a national acute myocardial infarction (AMI) registry to characterise the demographics, processes of care and outcomes of non-chest pain (NCP) STEMI presentations. Methods: Retrospective data for all STEMI cases from 2007 to 2020 were analysed from the Singapore Myocardial Infarction Registry. Cases which happened during inpatient and interfacility transfers were excluded. Univariable and multivariable logistic models were used to identify factors associated with NCP presentation. Cox proportional hazard models were constructed to investigate the prognostic influence of NCP on short-term and long-term mortality outcomes. ORs and HRs were calculated along with their 95% CI. Results: Among 21 858 patients with first-onset STEMI, 12.6% presented with NCP. These patients were older, more likely to be women and Chinese and had never smoked. The prevalence of diabetes and hypertension was also higher. These patients were also less likely to present with other possible cardiac symptoms of AMI, such as dyspnoea and diaphoresis. They were less likely to receive percutaneous coronary intervention (36% vs 77%) and had longer door-to-balloon times (100 min vs 70 min). After adjusting for differences in baseline risk factors and clinical characteristics, NCP presentation was associated with a higher risk of all-cause mortality at 30 days (HR 2.93, 95% CI 2.62 to 3.28), 1 year (HR 2.80, 95% CI 2.56 to 3.06), 5 years (HR 2.47, 95% CI 2.30 to 2.66) and 10 years (HR 2.31, 95% CI 2.16 to 2.46). Conclusion: After adjusting for baseline risk factors and treatments received, NCP presentation was still independently associated with worse survival outcomes. Further research is required to risk-stratify these patients and address the suboptimal treatment rates and outcomes.

Background: Compared with patients who develop ST‐segment–elevation myocardial infarction (STEMI) outside the hospital and present at the emergency department (outpatient‐onset), patients with inpatient‐onset STEMI may paradoxically experience a poorer prognosis due to underlying disease, despite the apparent immediate access to acute health care services. Methods: Patients with first‐onset STEMI who underwent percutaneous coronary intervention ( PCI) in the Singapore Myocardial Infarction Registry (2007–2020) were included. For patients with inpatient‐onset STEMI , the recognition‐to‐balloon time was measured from symptom onset to PCI . For outpatient‐onset STEMI , the recognition‐to‐balloon time was defined as the sum of the symptom‐to‐door and door‐to‐balloon time. Logistic regression was used to identify factors associated with delayed PCI after inpatient‐onset STEMI . Cox regression was used to assess 30‐day, 1‐year, 5‐year, and 10‐year all‐cause and cardiovascular mortality. Results: A total of 19 149 patients, 17 659 (92.2%) outpatient‐onset and 1595 (7.8%) inpatient‐onset, were included. The median follow‐up duration was 6.91 years. Patients with inpatient‐onset STEMI were older, more frequently women, nonsmokers, more likely to have comorbidities, less likely to present with typical STEMI symptoms, and more likely to experience delays in PCI than patients with outpatient‐onset STEMI within the hospital setting. The independent predictors of delayed PCI for inpatient‐onset STEMI were age ≥65 years, diabetes, breathlessness at presentation, and Killip class III. After adjustment for differences in baseline and clinical characteristics, inpatient‐onset STEMI was associated with significantly greater 1‐year, 5‐year, and 10‐year all‐cause mortality (1‐year hazard ratio [HR], 1.27 [95% CI, 1.13–1.43]; 5‐year HR, 1.27 [95% CI, 1.13–1.43]). There was no difference in 30‐day all‐cause or short‐/long‐term cardiovascular mortality. Conclusions: Inpatient‐onset STEMI was linked to an increased long‐term risk of all‐cause mortality compared with outpatient‐onset STEMI despite a shorter recognition‐to‐balloon time.

Background: Cerebral small‐vessel disease encompasses a spectrum of magnetic resonance imaging features reflecting microvascular pathology in ischemic stroke. Among these, white matter hyperintensities (WMHs) and cerebral microbleeds (CMBs) are the most widely studied. While both are well established as risk factors for cognitive decline in patients with acute ischemic stroke (AIS), their prognostic value for vascular events and death after AIS remains unclear. This study aims to evaluate WMH and CMB as predictors of recurrent stroke, cardiovascular death, and all‐cause death in patients with AIS. Methods: We systematically searched PubMed and Embase for longitudinal studies from July 1977 to March 2024 reporting adjusted hazard ratios (HRs) or odds ratios for these outcomes after AIS. Pooled estimates were generated using random‐effects models, and heterogeneity was explored using meta‐regression and prediction intervals. Results: Fifty studies (n=44 140) were included. WMHs were a significant predictor of stroke recurrence (HR,1.72 [95% CI, 1.39–2.13]) and all‐cause death (HR, 1.58 [95% CI, 1.11–2.23]). Similarly, CMBs were associated with stroke recurrence (HR, 1.88 [95% CI, 1.52–2.33]), with lobar and mixed types conferring higher risk than deep CMBs, and predicted cardiovascular death (HR, 1.45 [95% CI, 1.2–1.75]). For stroke recurrence, risk estimates increased in parallel with WMH and CMB burden. Conclusions: This meta‐analysis supports WMHs and CMBs as independent predictors of stroke recurrence and death in AIS. Burden and distribution further refine prognostic accuracy and inform poststroke risk assessment.

Introduction Sarcopenia is an emerging marker of biological health and is associated with poor outcomes in many disease states. In this study, we aimed to evaluate the utility of muscle biomarkers in predicting clinical outcomes for patients with large vessel occlusion (LVO) acute ischemic stroke (AIS). Methods This was a single-center observational cohort study of consecutive patients that underwent endovascular thrombectomy (EVT) for LVO AIS. A deep-learning model was employed to segment and measure the volume, surface area, and maximum thickness of temporalis and sternocleidomastoid (SCM) muscles. The primary outcome was poor functional outcome, defined by an mRS of 3-6 at 3 months post-stroke. Univariable and multivariable logistic regression models were performed to evaluate associations between the muscle biomarkers and outcome measures after adjusting for clinical variables of age, sex, and NIHSS. Results A total of 297 patients were included. 175 (58.9%) had poor functional outcomes at 3 months post-stroke. For each 10cm³ decrease in SCM volume (SV) and temporalis volume (TV), the odds of poor functional outcome at 3 months post-stroke increased by 34% (OR 0.66, 95% CI 0.52-0.84, p < 0.001) and 18% (OR 0.82, 95% CI 0.73-0.91, p < 0.001), respectively. After adjusting for age, sex and NIHSS, our baseline outcome model yielded an AUC of 0.716. Including sarcopenia biomarkers in the model improved discrimination: SV dichotomized (adjusted OR (aOR) 0.39, 95% CI 0.20-0.74, p-value <0.01, AUC: 0.731), TV dichotomized (aOR 0.51, 95% CI 0.30-0.86, p-value 0.012, AUC: 0.724). Conclusion Our study identified that temporalis and SCM muscle volumes were independently associated with functional outcomes after EVT for LVO AIS.

Background Current guidelines on the management strategy for patients with asymptomatic severe aortic stenosis (AS) remain unclear. This uncertainty stems from the lack of data regarding the natural history of these patients. To address this gap, we performed a systematic review and meta-analysis examining the natural history of asymptomatic severe AS patients receiving conservative treatment. Methods The PubMed, Cochrane, and Embase databases were searched from inception to 24 January 2024 using the keywords “asymptomatic” AND “aortic” AND “stenosis”. We included studies examining patients with asymptomatic severe AS. In interventional trials, only data from conservatively managed arms were collected. A one-stage meta-analysis was conducted using individual patient data reconstructed from published Kaplan–Meier curves. Sensitivity analysis was performed for major adverse cardiovascular outcomes in patients who remained asymptomatic throughout follow-up. Results A total of 46 studies were included (n = 9545). The median time to the development of symptoms was 1.11 years (95% CI 0.90–1.53). 49.36% (40.85–58.59) of patients who were asymptomatic had suffered a major adverse cardiovascular event by 5 years. The median event-free time for heart failure hospitalization (HFH) was 5.50 years (95% CI 5.14–5.91) with 36.34% (95% CI 33.34–39.41) of patients experiencing an HFH by year 5. By 5 years, 79.81% (95% CI 69.26–88.58) of patients developed symptoms (angina, dyspnoea, syncope and others) and 12.36% (95% CI 10.01–15.22) of patients died of cardiovascular causes. For all-cause mortality, the median survival time was 9.15 years (95% CI 8.50–9.96) with 39.43% (CI 33.41–36.40) of patients dying by 5 years. The median time to AVR was 4.77 years (95% CI 4.39–5.17), with 52.64% (95% CI 49.85–55.48) of patients requiring an AVR by 5 years. Conclusion Our results reveal poor cardiovascular outcomes for patients with asymptomatic severe AS on conservative treatment. A significant proportion eventually requires an AVR. Further research is needed to determine if early intervention with AVR is more effective than conservative treatment.

Background: In patients with embolic stroke of undetermined source (ESUS), occult atrial fibrillation (AF) has been implicated as a key source of cardioembolism. However, only a minority acquire implantable cardiac loop recorders (ILRs) to detect occult paroxysmal AF, partly due to financial cost and procedural inconvenience. Without the initiation of appropriate anticoagulation, these patients are at risk of increased ischemic stroke recurrence. Hence, cost-effective and accurate methods of predicting AF in ESUS patients are highly sought after. Objective: We aimed to incorporate clinical and echocardiography data into machine learning (ML) algorithms for AF prediction on ILRs in ESUS. Methods: This was a single-center cohort study that included 157 consecutive patients diagnosed with ESUS from October 2014 to October 2017 who had ILR evaluation. We developed four ML models, with hyperparameters tuned, to predict AF detection on an ILR. Results: The median age of the cohort was 67 (IQR 59–74) years old and the median monitoring duration was 1051 (IQR 478–1287) days. Of the 157 patients, 32 (20.4%) had occult AF detected on the ILR. Support vector machine predicted for AF with a 95% confidence interval area under the receiver operating characteristic curve (AUC) of 0.736–0.737, multilayer perceptron with an AUC of 0.697–0.708, XGBoost with an AUC of 0.697–0.697, and random forest with an AUC of 0.663–0.674. ML feature importance found that age, HDL-C, and admitting heart rate were important non-echocardiography variables, while peak mitral A-wave velocity and left atrial volume were important echocardiography parameters aiding this prediction. Conclusion: Machine learning modeling incorporating clinical and echocardiographic variables predicted AF in ESUS patients with moderate accuracy.

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.