Background: Low voltage areas (LVAs) on left atrial (LA) voltage mapping correlate with atrial fibrosis. However, there is no uniform standard for the definition of LVAs, or mapping techniques and mapping rhythms, so that the predictive value of left atrial LVAs for recurrence of atrial fibrillation (AF) is uncertain. This study aimed to explore the relationship between the presence of pre-ablation left atrial LVAs and the risk of recurrent AF after catheter ablation. Methods: The databases of PubMed, Embase, Web of science, Cochrane library, Scopus, Wanfang Datebase, China National Knowledge Infrastructure, China Biology Medicine and China Scientific Journal Datebase were searched from inception to 31 July 2023. Relevant studies regarding left atrial LVAs prior to ablation to predict postoperative recurrence of AF were identified and analyzed. The efficacy endpoints were defined as the recurrence of atrial arrhythmia lasting over 30 s. Results: A total of 12 studies with 1070 patients were included. We found the presence of pre-ablation left atrial LVAs correlated with the risk of recurrent AF after ablation (hazard ratio (HR) = 2.87, 95% confidence interval (CI): 2.33–3.52). The presence of pre-ablation left atrial LVAs can predict the risk of recurrent AF after ablation both in the follow-up duration ≤12 months group and follow-up duration >12 months group (follow-up duration ≤12 months: HR = 2.93, 95% CI: 2.20–3.90; follow-up duration >12 months: HR = 2.80, 95% CI: 2.09–3.77). The presence of pre-ablation left atrial LVAs correlated with the risk of recurrent AF after ablation in paroxysmal AF (HR = 2.89, 95% CI: 1.97–4.24). Conclusions: The presence of pre-ablation left atrial LVAs correlate with the risk of recurrent AF after catheter ablation.

Background: Tobacco use disorder (TUD) adversely impacts older patients with established cardiovascular disease (CVD) risk. However, CVD risk in chronic habitual cannabis users without the confounding impact of TUD hasn’t been explored. We aimed to determine the risk of major adverse cardiac and cerebrovascular events (MACCE) in older non-tobacco smokers with established CVD risk with vs. without cannabis use disorder (CUD). Methods: We queried the 2019 National Inpatient Sample for hospitalized non-tobacco smokers with established traditional CVD risk factors aged ≥65 years. Relevant ICD-10 codes were used to identify patients with vs. without CUD. Using multivariable logistic regression, we evaluated the odds of MACCE in CUD cohorts compared to non-CUD cohorts. Results: Prevalence of CUD in the sample was 0.3% (28,535/10,708,815, median age 69), predominantly male, black, and non-electively admitted from urban teaching hospitals. Of the older patients with CVD risk with CUD, 13.9% reported MACCE. The CUD cohort reported higher odds of MACCE (OR 1.20, 95% CI 1.11–1.29, p < 0.001) compared to the non-CUD cohort. Comorbidities such as hypertension (OR 1.9) and hyperlipidemia (OR 1.3) predicted a higher risk of MACCE in the CUD cohort. The CUD cohort also had higher unadjusted rates of acute myocardial infarction (7.6% vs. 6%) and stroke (5.2% vs. 4.8%). Conclusions: Among older non tobacco smokers with known CVD risk, chronic cannabis use had a 20% higher likelihood of MACCE compared to those who did not use cannabis.

The restriction of normal blood flow is the cause of many diseases including stroke and coronary artery diseases. To study the consequences of vessel blockade, previous models mainly focused on major arteries and have been well studied. However, the sequela from interruption of capillary vessels by microemboli was less well characterized. In this study, we exploited polystyrene microspheres as a mimicry of microemboli and found that microspheres of this size can be trapped in capillary vessels of all organs without causing apparent acute morbidities of the host. Interestingly, we accidentally found significantly increased recruitment of monocyte to the brain vasculature expressing low levels of Ly6C expression, but not to other organs. Further study revealed the spleen is the major origin of the recruited monocyte. Most importantly, VCAM-1 which is constitutively expressed on mouse brain vasculature orchestrates the recruitment of monocyte. Blockade of VCAM-1 in mice can substantially reduce monocyte recruitment. Interestingly, monocytes get activated through TNF- signaling which likely happens in the spleen instead of the brain. Collectively, we found a unique monocyte recruitment strategy in the brain comparing to other orangs, in response to capillary blockade induced by polystyrene microspheres.