ABSTRACT
BACKGROUND: Paroxysmal atrial fibrillation (PAF) is strongly associated with ischemic stroke. Continuous cardiac implantable electronic devices (CIEDs) can assess PAF episodes over prolonged periods. Studies that attempted to find a temporal association between PAF and ischemic stroke were inconclusive. Thus, we performed a systematic review and meta-analysis to assess this relationship. AIMS: This study aimed to assess the temporal association between AF episodes and stroke within 30 days of the arrhythmic episode. The secondary outcome is a temporal association within a 90-day period. SUMMARY OF REVIEW: A total of 2804 studies that discussed the temporal relationship between PAF and ischemic stroke were screened, and 7 studies were included in the meta-analysis. Among the 4041 patients included in these studies, there were 138 patients with device detected PAF episodes and stroke. Four studies used a 30-day window for temporality and the pooled odds ratio (OR) showed a significant association (OR 4.11 (95% CI 1.03-16.40)). The three studies reporting on AF and stroke within a 90-day window did not find a significant temporal relationship (OR 0.43 (95% CI 0.13-1.41)). Finally, the pooled result of those seven studies did not show a significant association (OR 1.51 (95% CI 0.44-5.17)). CONCLUSION: This meta-analysis supports a temporal relationship between PAF and ischemic stroke within a 30-day window. Establishing this relationship is important for individualized risk prediction and targeted anticoagulation treatment. DATA ACCESS STATEMENT: The data will be made available upon reasonable request.
ABSTRACT
Background: SARS-CoV-2 infection and perinatal neurologic outcomes are still not fully understood. However, there is recent evidence of white matter disease and impaired neurodevelopment in newborns following maternal SARS-CoV-2 infection. These appear to occur as a consequence of both direct viral effects and a systemic inflammatory response, with glial cell/myelin involvement and regional hypoxia/microvascular dysfunction. We sought to characterize the consequences of maternal and fetal inflammatory states in the central nervous system of newborns following maternal SARS-CoV-2 infection. Methods: We conducted a longitudinal prospective cohort study from June 2020 to December 2021, with follow-up of newborns born to mothers exposed or not exposed to SARS-CoV-2 infection during pregnancy. Brain analysis included data from cranial ultrasound scans (CUS) with grayscale, Doppler studies (color and spectral), and ultrasound-based brain elastography (shear-wave mode) in specific regions of interest (ROIs): deep white matter, superficial white matter, corpus callosum, basal ganglia, and cortical gray matter. Brain elastography was used to estimate brain parenchymal stiffness, which is an indirect quantifier of cerebral myelin tissue content. Results: A total of 219 single-pregnancy children were enrolled, including 201 born to mothers exposed to SARS-CoV-2 infection and 18 from unexposed controls. A neuroimaging evaluation was performed at 6 months of adjusted chronological age and revealed 18 grayscale and 21 Doppler abnormalities. Predominant findings were hyperechogenicity of deep brain white matter and basal ganglia (caudate nuclei/thalamus) and a reduction in the resistance and pulsatility indices of intracranial arterial flow. The anterior brain circulation (middle cerebral and pericallosal arteries) displayed a wider range of flow variation than the posterior circulation (basilar artery). Shear-wave US elastography analysis showed a reduction in stiffness values in the SARS-CoV-2 exposed group in all analyzed regions of interest, especially in the deep white matter elasticity coefficients (3.98 ± 0.62) compared to the control group (7.76 ± 0.77); p-value < 0.001. Conclusion: This study further characterizes pediatric structural encephalic changes associated with SARS-CoV-2 infection during pregnancy. The maternal infection has been shown to be related to cerebral deep white matter predominant involvement, with regional hyperechogenicity and reduction of elasticity coefficients, suggesting zonal impairment of myelin content. Morphologic findings may be subtle, and functional studies such as Doppler and elastography may be valuable tools to more accurately identify infants at risk of neurologic damage.
ABSTRACT
AIMS: To investigate the incidence of cardiac implantable electronic devices (CIED) malfunction with radiotherapy (RT) treatment and assess predictors of CIED malfunction. METHODS: A 6-year retrospective analysis of patients who underwent RT with CIED identified through the radiation oncology electronic database. Clinical, RT (cumulative dose, dose per fraction, beam energy, beam energy dose, and anatomical area of RT) and CIED details (type, manufacturer, and device malfunction) were collected from electronic medical records. RESULTS: We identified 441 patients with CIED who underwent RT. CIED encountered a permanent pacemaker (PPM) (78%), cardiac resynchronization therapy-pacing (CRT-P) (2%), an implantable cardioverter defibrillator (ICD) (10%), and a CRT-defibrillator (CRT-D) (10%). The mean cumulative dose of RT was 36 gray (Gy) (IQR 1.8-80 Gy) and the most common beam energy used was photon ≥10 megavolt (MV) with a median dose of 7 MV (IQR 5-18 MV). We further identified 17 patients who had CIED malfunction with RT. This group had a higher cumulative RT dose of 42.5 Gy (20-77 Gy) and a photon dose of 14 MV (12-18 MV). None of the malfunctions resulted in clinical symptoms. Using logistic regression, the predictors of CIED malfunction were photon beam energy use ≥10 MV (OR 5.73; 95% CI, 1.58-10.76), anatomical location of RT above the diaphragm (OR 5.2, 95% CI, 1.82-15.2), and having a CIED from the ICD group (OR 4.6, 95% CI, 0.75-10.2). CONCLUSION: Clinicians should be aware of predictors of CIED malfunction with RT to ensure the safety of patients.
ABSTRACT
BACKGROUND & AIMS: Cardiovascular disease remains a leading cause of mortality following liver transplantation (LT). Whether it may be partially attributable to accelerated development of subclinical coronary artery disease is unclear. We sought to assess the longitudinal effect of LT on coronary plaque burden. METHODS: A prospective observational study was conducted in 30 asymptomatic patients who underwent computed tomographic coronary angiography (CTCA) pre- and a median 4-years following LT. Serial changes were quantified using coronary artery calcium score (CACS) and semi-quantitative CTCA scores, in a blinded fashion. High-risk plaque (HRP) characteristics were also assessed. Plaque progression was defined using prognostically significant cut-offs. RESULTS: In the study population (age 59.8 ± 8 years, 80% male), 93 of 459 coronary segments had plaque at baseline. On follow-up CTCA, 68 (+73.1%) new lesions appeared in segments without plaque initially. Nineteen (63.3%) patients demonstrated a clinically significant rise in plaque burden on CACS and semi-quantitative indices on CTCA (all p<0.001). CAD-RADS score rose to ≥4 (≥70% stenosis) in 9 (30%) patients, necessitating ischemia-guided revascularization in 3 (10%) patients. While the absence of coronary calcification or plaque pre-LT was protective, presence of HRP and development of post-transplant metabolic syndrome were both strong independent predictors of atherosclerosis progression. CONCLUSIONS: Our findings suggest that LT is associated with early progression of coronary atherosclerosis. Accelerated progression was noted particularly in those with HRP and post-transplant metabolic syndrome. Understanding the mechanisms of this novel observation and the potential role of preventive cardiovascular therapies in this population merit further study.