Small vessel disease is one cause of vascular dementia (others being stroke and mini-strokes). It may also be referred to as coronary microvascular disease or small vessel heart disease. It is a disease that causes disability and disorientation in ageing people. It may also be referred to as coronary microvascular disease. (Also see the post entitled coronary microvascular disease.)
In Small Vessel Disease, the small arteries in the heart become narrowed. It causes signs and symptoms of heart disease, such as chest pain (angina).
The brain requires oxygen supplied by blood via the vascular network to function normally. Vascular dementia, the second most common cause of dementia, results from problems with blood supply to the brain. If the vessels are damaged, blood may not be able to reach the brain cells and consequently the cells may die of oxygen starvation triggering the onset of vascular dementia. Increasingly, it seems that one particular type of vascular disease, small vessel disease, may be the major form of vascular dementia.
According to the Mayo Clinic, dietary supplements that may be helpful for people with small vessel disease include (as with any other alternative therapy,consult your doctor before taking any supplements to ensure they won’t interfere with any medications you’re taking):
- Coenzyme Q10. This coenzyme, which is naturally present in your body, can improve blood pressure and circulation when taken as a supplement. Coenzyme Q10, taken in daily doses up to 200 milligrams, may improve small vessel blood flow in people with diabetes and coronary artery disease and could have a similar effect in people with small vessel disease.
- L-arginine. This amino acid that’s normally used by the body to help metabolize protein may help treat symptoms of small vessel disease by relaxing your blood vessels. This therapy shouldn’t be used in anyone who’s already had a heart attack.
Small Vessel Disease is under-diagnosed. It is difficult to detect, therefore many people have the condition and are not aware of it. When it is diagnosed it is usually after a doctor checks for blockages in the main arteries of the heart due to symptoms such as angina, but finds little or no narrowing in the large vessels, even though symptoms persist.
Although anyone can have small vessel disease, it’s more common in women and in people who have diabetes or high blood pressure.
Because small vessel disease can make it harder for the heart to pump blood to the rest of the body, small vessel disease can cause serious problems if left untreated, such as:
- Coronary artery spasm
- Heart attack
- Sudden cardiac death
- Heart failure
- Vascular dementia, when blood and oxygen have trouble reaching the brain.
Small vessel disease is treatable but can be difficult to detect or diagnose.
It is the larger arteries in the heart that are responsible for pumping blood through your heart, but the small vessels expand when you’re active and then contract while you’re at rest.
The large vessels in your heart can become narrowed or blocked through atherosclerosis, a condition in which fatty deposits build up in the arteries. In small vessel disease, the narrowing of the small vessels in the heart makes it so they can’t expand properly when you’re active. As a result, you don’t get an adequate supply of oxygen-rich blood. This inability to expand is called endothelial dysfunction. This problem may cause your small vessels to actually become smaller when you’re active or under emotional stress. The reduced blood flow through the small vessels causes chest pain and other symptoms similar to those you’d have if you were having angina or a heart attack.
Symptoms of Small Vessel Disease
- Chest pain, squeezing or discomfort
- Chest pain associated with discomfort in your left arm or jaw
- Chest pain that worsens with daily activities and at times of emotional stress
- Neck, shoulder, upper back or abdominal discomfort
- Shortness of breath
- Unusual fatigue
- A loss of energy
- Trouble sleeping
If you’re having chest pain along with other signs and symptoms — such as shortness of breath, sweating, nausea, dizziness, or pain that radiates beyond your chest to one or both of your arms or your neck — seek emergency medical care immediately. If you’re having symptoms such as fatigue and abdominal pain, it might be difficult to tell if your signs and symptoms are due to small vessel disease, but anytime there is chest pain, you should see your doctor to find out the cause.
Risk factors for small vessel disease include:
- High cholesterol
- High blood pressure
- Obesity (body mass index of 30 or higher)
- Unhealthy diet
- Inactive lifestyle
- Insulin resistance
- An estrogen deficiency, in women
- Polycystic ovarian syndrome
- Increasing age, older than 45 in men and older than 55 in women
It’s not clear why some people develop small vessel disease and other develop large vessel coronary artery disease even though the risk factors are the same.
More on Small Vessel Disease:
Damage to blood vessels in the brain may come about as a result of a number of conditions including high blood pressure, heart problems, high cholesterol and diabetes. Early recognition and treatment of any of these conditions is very important as they can lead to the onset of vascular dementia, but adequate management of these conditions can prevent the onset of VaD. Vascular dementia can be caused by two events that can occur in blood vessels. The first is stroke and the second is small vessel disease, although many people may have a mixture of causes. Stroke refers to brain damage that is permanent and results from interrupted blood supply to a specific part of the brain. Symptoms vary depending on which brain region has been affected. For example if a motor region of the brain were damaged then the symptom would be paralysis. If a speech centre is affected then communication will be impeded. Damage to other areas of the brain can result in the onset of dementia. Vascular dementia resulting from stroke is categorised in two ways, single-infarct or multi-infarct, depending on whether it was caused by one or several incidences of stroke.
Small vessel disease results from damage to blod vessels that sit deep in the brain matter and is the most frequent subtype of vascular cognitive impairment (VCI). SVD causes psychological symptoms as well as neurological symptoms concomitant with cognitive deficits. SVD can however be present in the absence of any cognitive impairment as well as varying levels of cognitive impairment ranging from mild cognitive impairment (MCI) to dementia.
In small vessel disease there is thickening of vessel walls, blood-brain barrier disturbance, demyelination and axon loss amongst other problems. The mechanism of SVD development is not clear, although there are two main pathological features. These are lesions of the subcortical, deep and periventricular white matter, generally referred to as white matter lesions (WML) and lacunes of the central grey matter, including the thalamus and basal ganglia.
The thickening of the blood vessel walls, atherosclerosis, is accompanied by hardening of the vessel walls. Risk factors contributing to this phenomenon are hypertension and diabetes mellitus.. The small arterioles are more susceptible to atherosclerosis as they are less elastic than the larger blood vessels. The thickening and hardening of vessel walls result in narrowing of the lumen of the vessel, twisting the vessel itself and thereby creating two conditions.  The first is hypoperfusion whereby the supply of oxygen and nutrients to the brain tissue is slowly cut. The second condition is occlusion where blood supply to a particular part of the brain ceases. These conditions result in ischemic brain tissue.
Arterioles are found mostly in the subcortical region of the brain, close to the frontal lobe, these areas are where vascular damage is likeliest to occur [1, 2] .Extensive damage can lead to dementia which is signified by changes in behaviour that coincides with damage to ischemic regions of the brain. The changes may be either gradual or sudden followed by predictive progression of disease. Changes that are observed affect speech patterns, problem solving ability and a sense of social judgement. Damage to the circuit between the basal ganglia and frontal cortex results in slowness of motor skills, emotional numbness and lack of initiation giving the impression of depression.  SVD is mostly identified in groups where hypertension and diabetes mellitus are most prevalent.
Age and high blood pressure appear to be good predictors of WML. The occurrence of SVD is frequent with age, although elderly individuals with hypertension develop clinically relevant SVD. There is however a great deal of variability, which remains unexplained, among patients with WML. The twin study  suggests that unknown genetic factors are important in the expression of WML. Association between the level of WML and cognitive impairment has been shown to be minimal or absent by several MRI studies   , supporting the experience of clinicians that many patients with noticeable WML have no significant level of cognitive impairment. This makes it questionable as to whether WML are in fact a reliable indicator of the severity of SVD.
Evidence suggests that the progression of white matter hyperintensities (WMH) is dependent upon on the blood pressure and degree of WMH at the start of any given study. This was shown in an Austrian study over 3 years where blood pressure and initial level of WMH were strong predictors of disease progression. The same was evident after 6 years in the same group  . Repeat MRI scans in patients with high levels of WML over 2 years showed significant increase in WML from a mean of 6 to 7 on a 16 point scale with the increase being associated with high blood pressure at baseline. Another study looked at patients with SVD measuring parameters such as WML, atrophy, cognitive ability and cerebral metabolism. Following one year there was no significant change observed using imaging and cognitive measurements  .
Only a few studies have looked at the link between SVD progression and cognitive decline, and in most cases in people who had no cognitive impairment at the start of the studies. One study examined cognitive decline in people between ages 50-80 without dementia or known strokes. MRI scans at age 80 showed correlation of WML with cognitive decline. A longitudinal study in 563 people with dementia exhibited no relation between WML and cognitive decline  until further variables such as depression, atrophy and infarcts were taken into consideration, resulting in a more significant decline in people with WML, a drop of 0.28 MMSE vs. 0.1 MMSE points per year.
One previously mentioned study showed no correlation of occurrence of WML with cognitive change  , although the power to detect these changes was low, while a further study shows that the degree of WMH at baseline did not predict cognitive decline after 4years .
Evidence of disease progression from drug trials
Most drug trials of VaD were not designed to examine different types of vascular dementia. Analysis of subgroups in a trial of galantamine in probable VaD or AD with VaD showed that VaD patients treated with placebo showed no cognitive decline but AD patients treated with placebo did decline  . 46% of the VaD patients had SVD only. Further to this, VaD patients given medication were stable for 3 years . A double blind trial of donepezil, patients with mix VaD treated with placebo were also stable with respect to cognitive ability [21, 22]. A further study of the effects of memantine on VaD showed that placebo groups of SVD patients declined in cognitive ability while stroke patients were stable .
Another study of rivastigmine vs. cardiospirine, a drug with no known effects in VaD, showed no change after 22 months in the cardiospirine and improvement in 30% of the rivastigmine group . In further work after 12 months a 4-point decrease in MMSE score was observed in the cardispirine group and 2.2 point decline in the rivastigmine group.
Management of hypertension has been observed to improve cognitive functioning and prevents dementia [21, 25, 26]. Primary prevention through education and checks on factors such as blood pressure and diabetes is invaluable. Use of MRI screening for dementia could be used as a routine method for identification of SVD. Although AD is progressive and at present not controllable, SVD can be slowed and stabilised by management of risk factors.