AHollenhorst plaque (also known as a retinal cholesterol embolus) is a cholesterol embolus that is seen in a blood vessel of the retina. It is usually found when a physician performs ophthalmoscopy, during which a plaque will appear as a small, bright crystal that is refractile (reflects the light from the ophthalmoscope) and yellow.[1] This is a medical exam finding, and is not a medical condition, though it may be related to cardiovascular conditions such as atherosclerosis of the internal carotid artery.[1] It was first described by American ophthalmologist Robert Hollenhorst in 1961.[2]
| Hollenhorst plaque | |
|---|---|
| Specialty | Cardiovascular |
A Hollenhorst plaque is the result of embolization (breaking off) of cholesterol forming an atheromatous plaque. This occurs in a blood vessel that is upstream of the eye, such as the internal carotid artery on the same side as the eye (ipsilateral), or the aorta.[1] This cholesterol embolus is then able to travel via the bloodstream to distal (downstream) vessels.[1] When it reaches the tiny blood vessels in the retina of the eye, the plaque may become lodged, where it is visible on eye exam by a physician as a bright crystal (the Hollenhorst plaque).[1] The plaques most commonly lodge at vessel bifurcations, meaning areas where the blood vessel branches into two or more smaller vessels.[1]
Hollenhorst plaques may cause retinal occlusion, where the plaque blocks blood flow through the retinal vessels, resulting in temporary or permanent vision loss in the affected eye.[1] However, while Hollenhorst plaques do become lodged in retinal arteries, they generally do not fully prevent blood flow so do not cause ischemia.[1] Once a Hollenhorst plaque is discovered in a retinal vessel, it may further migrate and lodge elsewhere, break into smaller pieces, or dissolve and disappear entirely.[1]
While Hollenhorst plaques generally not cause problems with health of the eye, they may be a sign of systemic health issues, particularly of the cardiovascular system.[2] These plaques are more common in men than in women, and are more likely to be present in people who have hypertension, past or current smokers, older patients, and those with history of any vascular disease (including history of transient ischemic attack, stroke, coronary artery disease, and/or peripheral vascular disease).[2] Appearance of retinal plaques is associated with strokes and may be a risk factor for stroke, however because plaques may disappear on their own, discovery of plaques is not predictive of an impending stroke.[2] Risk of death after a stroke may be increased in those who are noted to have Hollenhorst plaques compared to stroke patients who do not.[2] The most common condition associated with appearance of a Hollenhorst plaque is carotid artery disease, including carotid artery stenosis (narrowing of the space inside the vessel).[3]
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Hollenhorst plaques still require more research, and because of this, there is a wide range of testing that a physician may or may not choose to complete. While there are many possible options, the American Academy of Ophthalmology recommends the following steps be taken when an asymptomatic plaque is first noted.[1]
While there is disagreement among medical professionals on what testing is considered necessary, several forms of testing are not shown to be effective in evaluating patients for cardiovascular disease after a retinal cholesterol embolus is found.[1] This recommendation is for patients who do not have any symptoms or concerning past medical history, and testing is ultimately decided by the physician on a case-by-case basis for the individual patient. These include:
The phenomenon is named after the American ophthalmologist Robert Hollenhorst.
The first recorded description of "bright" retinal emboli was made in 1927 by TH Butler. While other retinal emboli had been described, the bright nature of these differentiated them from prior descriptions.[2]
Hollenhorst further described finding bright plaques in 1958, at the same time they were independently described by German researchers R. Witmer and A. Schmid via a case study.[2][5][6] They further hypothesized that these plaques were composed of cholesterol. However, it was Hollenhorst who went on to establish the link between these bright emboli and cerebrovascular disease.[2] He further discovered the relationship between presence of these plaques, and increased mortality from cardiovascular disease. In his study of patients with carotid artery disease, he noticed that the plaques occurred on the same side as the affected artery.[2] In 1960 he expanded his research, and noted that the plaques could be made to move by applying pressure to the eye.[2] Additionally, he found that the plaques often occurred after a patient had had carotid artery surgery.[2]
In 1961, Hollenhorst published “Significance of Bright Plaques in Retinal Arterioles” in the Journal of the American Medical Association and described his findings.[2][6] Besides the previously discussed points, he described that the plaques were able to break into smaller fragments, and generally did not completely block retinal arteries. He also reported an experiment conducted with a neurologist named Jack Whisnant, that verified the idea that the plaques were composed of cholesterol.[2] To do this, they took cholesterol crystals and material from atheromatous plaques in humans, and injected the into the carotids of dogs and Macaca rhesus monkeys. They found development of similar retinal plaques in these animals.[2] In 1963, the cholesterol composition was confirmed by researchers via autopsy of a patient who died during carotid surgery.[2]
Hollenhorst continued to study these plaques, detailing associations with their appearance and cerebral ischemic events. He also noted that survival these patients was decreased compared to those without plaques.[2]
Work continued on this topic, and studies include the 1997 Blue Mountain Eye Study conducted in Australia and the Beaver Dam Eye Study in Wisconsin, of which patients have been followed up for the past 15 years.[1][7][8] In 2005, one study looked at data from both the Atherosclerosis Risk in Communities (ARIC) study, and the Cardiovascular Health Study (CHS) and suggested evaluation composed of cardiovascular workup and smoking cessation.[1][9] Other work continued to build on this and includes 2008 the Los Angeles Latino Eyes Study (LAKES) study,[1][10] and the 2017 Singapore Epidemiology of Eye Disease Study (SEEDS).[1][11]