Deans' stroke musings: Echocardiographic correlates of MRI imaging markers of cerebral small-vessel disease in patients with atrial-fibrillation-related ischemic stroke

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, March 30, 2023

Echocardiographic correlates of MRI imaging markers of cerebral small-vessel disease in patients with atrial-fibrillation-related ischemic stroke

I see nothing here that is going to get survivors recovered or EXACTLY prevent dementia. So I would fire everyone involved. Solve the problems of stroke survivors, not just tell us they exist.

Echocardiographic correlates of MRI imaging markers of cerebral small-vessel disease in patients with atrial-fibrillation-related ischemic stroke

Kaili Ye¹^†,

Wendan Tao¹^†,

Zhetao Wang²,

Dayan Li³,

Mangmang Xu¹,

Junfeng Liu¹ and

Ming Liu¹^*

¹Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
²Department of Radiology, West China Hospital, Sichuan University, Chengdu, China
³Cardiac Ultrasound Office, Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China

Background and objectives: Atrial fibrillation (AF) has been linked to dementia risk, partly explained by cerebral small vessel disease (CSVD). Since AF and cardiovascular comorbidities were associated with cardiac dysfunction, we aimed to determine the association between echocardiographic parameters and neuroimaging markers of CSVD in patients with AF-related ischemic stroke.

Methods: This cross-sectional study enrolled patients with AF-related ischemic stroke from March 2013 to December 2019 who underwent transthoracic echocardiography and brain 3T MRI, including T1, T2, Flair, and SWI imaging sequences. We assessed the presence of lacunes and cerebellar microbleeds (CMBs), the severity of white matter hyperintensity (WMH) scored by the Fazekas scale (0-6), and the severity of enlarged perivascular spaces (EPVS) in basal ganglia (BG) and centrum semiovale (CSO) classified into three categories (0–10, 10–25, and >25). CSVD burden was rated on a 0-to-4 ordinal scale. Generalized linear regression analysis and post hoc comparisons with Bonferroni correction were performed to assess the association between various echocardiographic parameters and these lesions, adjusted for demographics and potential confounders.

Results: 119 patients (68.38 ± 12.692 years; male 45.4 %) were included for analysis, of whom 55 (46.2%) had lacunes, 40 (33.6%) had CMBs, and median severity for WMH, BG-EPVS, CSO-EPVS, and CSVD burden were 2 (IQR: 1–3), 1 (IQR: 1–2), 1 (IQR: 0–1), and 1 (IQR: 1–2) respectively. In multivariable, fully adjusted models, left ventricular posterior wall thickness (LVPW) was associated with a higher risk of lacunes (RR 1.899, 95% CI: 1.342–2.686) and CSVD burden (RR = 2.081, 95%CI: 1.562–2.070). Right atrial diameter (RAD) was associated with greater CSO-EPVS (RR = 2.243, 95%CI: 1.234–4.075). No echocardiographic parameters were revealed to be associated with CMBs and WMH.

Conclusion: In patients with AF-related ischemic stroke, LVPW is associated with a higher risk of lacunes and CSVD burden, while RAD was associated with greater CSO-EPVS. Larger studies are required to determine these associations and to elucidate if these associations can help facilitate cognitive evaluation and brain MRI screening.

Introduction

Increasing evidence suggests that atrial fibrillation (AF) appears to be correlated with cognitive decline independent of clinical stroke (1, 2). Cerebral small vessel disease (CSVD) is one of the pathological mechanisms through which AF might lead to cognitive impairment. A more recent large sample of study (3) has demonstrated that nearly 25% of patients with AF-related ischemic stroke or transient ischemic attack have preexisting cognitive impairment. They found imaging markers of CSVD were independently associated with cognitive impairment prior to ischemic events.

There is no complete explanation of the mechanism that links AF and CSVD, but chronic cerebral hypoperfusion, inflammation, and shared vascular risk factors, such as hypertension and diabetes mellitus, may all be involved. Patients with AF are more likely to develop cardiac dysfunction, for example, many patients with AF develop an enlarged left atrium (LA) and enlarged left ventricular (LV), and are also associated with an increased incidence of heart failure. Conversely, patients with cardiac dysfunction are known to contribute to AF development and maintenance (4–6). According to previous studies, some cardiac subclinical indicators, such as left ventricular structure and LV systolic dysfunction, may contribute to greater white matter hyperintensity (WMH) (6), and LA volume, may contribute to silent brain infarcts (7) even in the absence of AF. However, none of them investigated whether cardiac structural or functional abnormalities correlated with neuroimaging markers of CSVD in patients with AF-related ischemic stroke. Thus, we evaluated the cross-sectional association of the echocardiographic parameters of cardiac structure or function with the neuroimaging markers of CSVD on MRI in patients with AF-related ischemic stroke.