Stroke: What is the relationship between coronary atherosclerosis and white matter lesions?

Coronary artery disease (CAD) is related to white matter disease, but the extent of the common mechanism remains unclear
.
Possible common risk factors for atherosclerosis, genetic susceptibility, and unidentified new risk factors are all contributing factors to heart and brain diseases

Early-onset clinical CAD events are strongly clustered in families
.
In addition, among healthy family members who had significant CAD at a young age, a high incidence of calcified and non-calcified coronary plaques was found

In addition to the causal relationship with CAD, there is evidence that traditional vascular risk factors, such as hypertension, are related to white matter hyperplasia (WMHs).
Some people believe that through targeted treatment of these risk factors, the development of WMH may be delayed Even reversed
.

Studies have shown that genetic analysis of patients with deep WMH (DWMH) and periventricular WMH (PVWMH) shows that PVWMH and DWMH have independent genetic basis, suggesting an independent cause
.
Although WMH has reduced cerebral blood flow compared with normal white matter, the average cerebral blood flow between DWMH and PVWMH also seems to be different.

For example, DWMH is more related to arteriosclerosis, while PVWMH is related to chronic hemodynamic insufficiency, for example, leading to the occurrence of watershed infarction
.

In view of these data, and considering that the caliber of the cerebrovascular and the anastomosis are different due to different positions
.

Therefore, certain areas of the brain may be more susceptible to vascular disease than other areas
.

Michelle C.
Johansen and others of Hopkins University previously discovered that among the healthy relatives of early-onset CAD patients, there is an association between the total volume of coronary plaques and the total volume of WMH, which is associated with known vascular risk factors.
Irrelevant
.

Given that this cohort has a strong family history of early-onset coronary heart disease, it is possible that there is a genetic susceptibility to systemic vascular disease in multiple vascular beds at a young age
.

Therefore, they tested the relationship between the existence and burden of subclinical CAD in a high-risk population and the WMH volume of WMH (DWMH, PVWMH, and border zone (cuff)) globally and in 3 different locations, regardless of vascular risk factors

Specifically: They analyzed 782 asymptomatic first-degree relatives of GeneSTAR (the genetic study of atherosclerosis risk).
These patients had early-onset coronary artery disease (<60 years old) and had coronary arteries in the same period.
Computed tomography angiography and brain magnetic resonance imaging
.
Taking into account the multi-level mixed-effect linear regression model of family structure, the relationship between total WMH and 3 regions (deep WMH, periventricular WMH [PVWMH] or border zone [cuff]) and coronary artery disease markers were evaluated

The average age of these patients was 51 ± 10 years, 58% of them were women and 39% were African Americans
.

Participants with any coronary plaques had 52% larger WMH volumes than those without plaques (95% CI, 0.
24-0.
59)
.
For every 1% increase in coronary plaque volume, the total WMH volume increases by 0.

For every 1% increase in total coronary plaque, the volume of deep WMH increases by 5.
03% (95% CI, 4.
67-5.
38), the volume of PVWMH increases by 5.
10% (95% CI, 4.
72-5.
48), and the volume of cuff increases by 2.
74% (95% CI, 4.
72-5.
48).
%CI, 2.
38-3.
09), when comparing deep WMH and PVWMH (P interaction = 0.
001) or cuff (P ​​interaction <0.
001), this association is different
.

The important significance of this study lies in the discovery: in healthy high-risk populations, the presence and volume of coronary plaques are related to the larger WMH volume, which is the most intense in PVWMH
.
These findings in high-risk families indicate that there is a disease relationship in two different vascular beds, beyond traditional risk factors, and may be due to genetic predispositions