Review Articles

Arteriosclerosis
Rethinking the Current Classication
Gregory A. Fishbein, BS; Michael C. Fishbein, MD

Context.Arteriosclerosis is the vascular disease that is the leading cause of mortality in industrialized countries. Currently, there are 3 lesions within the broader category of arteriosclerosis: atherosclerosis, Mo nckeberg medial calcic sclerosis, and arteriolosclerosis. Objective.In this review, we discuss the history of the terminology and current classication of arteriosclerosis and problems with the current classication. We also discuss recently described new arterial lesions that are not in the current classication. Data Sources.In spite of the prevalence and importance of arteriosclerotic vascular disease, and the widerteriosclerosis is literally the hardening of an artery. Standard textbooks of pathology and numerous other resources consistently list 3 lesions under the term arteriosclerosis : (1) atherosclerosis, (2) Mo nckeberg medial calcic sclerosis, and (3) arteriolosclerosis.13 These lesions generally share 3 features: (1) they result in stiffening of arterial vessels; (2) they cause thickening of the arterial wall; and (3) in the past, they have been considered degenerative diseases. Herein we review the history of arteriosclerosis nomenclature, the current classication of arteriosclerosis, and the shortcomings of this classication. Finally, we review the subtypes of arteriosclerosis with emphasis on how future classication could more accurately and comprehensively categorize these lesions. This discussion includes examples of lesions that could qualify as arteriosclerosis yet are not currently classied as such. We exclude consideration of vasculitides, malformations, vascular dysplasia, connective tissue disorders, and neoplasms involving arterial vessels; the nomenclature of these lesions is already sufciently complex and confusing. HISTORY OF THE TERMINOLOGY AND CLASSIFICATION OF ARTERIOSCLEROSIS The name arteriosclerosis is a term of Greek origin meaning hardening of the arteries. Though arteriosclerosis is
Accepted for publication October 16, 2008. From the Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California. The authors have no relevant nancial interest in the products or companies described in this article. Reprints: Michael C. Fishbein, MD, Department of Pathology and Laboratory Medicine, Room 13-145H, UCLA Center for the Health Sciences, 10833 Le Conte Ave, Los Angeles, CA 90095 (e-mail: mshbein@mednet.ucla.edu). Arch Pathol Lab MedVol 133, August 2009

spread use of the current terminology, there are major problems with the current classication: (1) the current classication has an inconsistent naming convention, (2) the classication fails to use terms that accurately describe the lesions, and (3) important arterial lesions are absent from the classication. In addition, although the terms arteriosclerosis and atherosclerosis describe different lesions, these terms are often used interchangeably. Conclusion.Consideration should be given for a new more inclusive and accurate classication of arteriosclerotic lesions that more accurately reects the pathology of these important vascular lesions. (Arch Pathol Lab Med. 2009;133:13091316) a phenomenon believed to be prevalent since ancient Egypt,4 it only began to catch the attention of investigators in the latter half of the last millennium. In 1575, Fallopius writes of a degeneration of arteries into bone. These ossied arteries were commonly noted by anatomists of that period. Johann Friedrich Crell, in 1740, elucidated the phenomenon by asserting that the coronary artery hardenings were, in fact, not bony, but derived from pus.5 Fifteen years later, von Haller was rst to identify such a lesion as an atheroma, a term used in Greek literature to describe a space lled with gruellike matter.6 The rst use of the term arteriosclerosis, however, can be attributed to Jean Fre deric Martin Lobstein7 in his critical analysis of the composition of calcied arterial lesions. By the 20th century, the word arteriosclerosis described a disease state of multiple known etiologies. George Johnson8 can be awarded the distinction of being rst to describe noncalcied, nonatheromatous stiffening of small vessels in his review of Bright disease, published in 1868. His contemporaries, Gull and Sutton,9 introduced the term arterio-capillary brosis to characterize this phenomenon, which would soon thereafter be referred to as arteriolosclerosis. In 1903, J. G. Mo nckeberg published a discussion of an arterial lesion he asserted was distinct from the forms of arteriosclerosis mentioned in the previous paragraphs. His name has since been associated with medial calcication, though, it is not clear whether the condition modern pathologists call Mo nckeberg calcic medial sclerosis is the same pathology he described.10 Around the same time, Felix Marchand11 believed arteriosclerosis to be an inadequately general description of a disease that had now become the focus of much attention. He presented the term atherosclerosis, one he believed was more descriptive of
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the lesions of interest. Oskar Klotz12 was quick to point out that, although more specic, Marchands designation was not applicable to all arteriosclerotic lesions, like those described by Mo nckeberg, in which no true atheroma is present. In January of 1954, the American Journal of Clinical Pathology published a letter to the editor, written by S. M. Rabson,3 entitled, Arteriosclerosis: Denitions. In it, Rabson alludes to an article he had recently read featuring arteriosclerosis in its title but nowhere in its text. This prompted Rabson to send letters to various heads of university pathology departments, inquiring as to the meaning of words such as arteriosclerosis and atherosclerosis. The results of his survey were denitions that lacked specicity, uniformity, and consistency, a situation that we feel continues to this day. In his letter, a frustrated Rabson suggests that arteriosclerosis be a generic label used to describe any of the arterial pathologies we have discussed previously. The term atherosclerosis, he asserts, can reasonably be dened as arteriosclerosis with atheromatosis, and its use should be restricted to that specic condition. This denition, provided by Rabson, has persevered and remains the denition pathologists operate with today. CURRENT CLASSIFICATION It appears that Rabsons brief editorial became the foundation of the classication of arteriosclerosis that is used today. Currently, arteriosclerosis is classied into 3 lesions: (1) atherosclerosis, (2) Mo nckeberg medial calcic sclerosis, and (3) arteriolosclerosis. Atherosclerosis is a disease of elastic and large muscular arteries in which the atheroma is the characteristic lesion. The lesions of atherosclerosis enlarge the arterial intima with variable amounts and types of lipids, connective tissues, inammatory cells, and a variety of extracellular components including matrix proteins and enzymes and calcium deposits.6,13,14 As atherosclerosis is the number one killer in industrialized countries, this lesion has been studied extensively, with great progress in understanding its pathogenesis, risk factors, natural history, treatment, and prevention. There are existing subclassications of atherosclerosis, including one adopted by the American Heart Association.15 Although this classication is not without shortcomings,14 it has been generally accepted, so the subcategories of atherosclerosis are not discussed in this article. Mo nckeberg medial calcic sclerosis, as its name implies, is a calcication process that affects the media of large and medium-sized arteries. It is said to be a disease rarely seen in patients younger than 50 years. According to our German translators, Mo nckebergs calcic lesions involve only the tunica media of arteries, without any nckeberg compromise of the arterial lumen.16 However, Mo sclerosis and atherosclerosis may coexist. Arteriolosclerosis, as its name implies, is a lesion of arterioles, small arterial vessels with 1 or 2 layers of smooth muscle cells. Arteriolosclerosis affects arterioles throughout the body and is most typically associated with hypertension and diabetes mellitus. There are 2 undoubtedly related, yet histologically distinct, subtypes of arteriolosclerosis: the hyperplastic type and the hyaline type.17
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PROBLEMS WITH THE CURRENT CLASSIFICATION There are 3 major problems with the current classication: (1) it has an inconsistent naming convention, (2) it fails to use terms that accurately describe the lesions, and (3) major sclerotic arterial lesions are absent from the classication. Another problem is that although the terms arteriosclerosis and atherosclerosis describe different lesions, these terms are used interchangeably. This inappropriate use of these terms has been pointed out by Aschoff18 almost 100 years ago, Rabson3 more than 60 years ago, and by others more recently.6 The rst problem of inconsistent naming is evident by the fact that the rst 2 types of arteriosclerosis, atherosclerosis and Mo nckeberg medial sclerosis, are dened by their gross and histopathologic features. On the other hand, arteriolosclerosis is dened by the size of the involved vessel. The term arteriolosclerosis does not describe any pathologic characteristics. Clearly, a classication should be consistent. That is, the classes should have similar descriptors, either based on the pathology, or based on the anatomic site of the lesion, but not one or the other. Arteriolo is not a pathologic lesion but rather a prex that qualies the lesion to very small arteries. Only the terms for the subtypes of arteriolosclerosis, hyaline arteriosclerosis and hyperplastic arteriolosclerosis, elucidate the histopathology. The second problem is that the current system of naming does not describe these lesions accurately. Even the term arteriosclerosis is perhaps a misnomer; many quintessential arteriosclerotic lesions are not in fact hardened arteries. In recent years, researchers have paid much attention to so-called vulnerable atherosclerotic plaques, or thin brous cap atheromasplaques in which a thin sheath of brous tissue envelops a large lipid core.19 Indeed, these are often soft plaques yet we describe them as sclerotic or hardened. Furthermore, the term Mo nckeberg medial sclerosis is most likely being used incorrectly. The lesion that is generally regarded as Mo nckeberg medial sclerosis, ironically, may not be the lesion that Mo nckeberg himself described. On review of the medical literature, we found 25 articles or texts that described Mo nckeberg medial sclerosis. In 10 of these publications the authors state that Mo nckeberg sclerosis involves the internal elastic lamina (IEL); in the other 15 publications the authors stated that the IEL is free of calcication.10 In our own experience, and formal review of 14 specimens with calcication of the arterial media, all cases also had calcication of the IEL. Often there were portions of the artery with only IEL calcication.20 Thus, the weight of evidence indicates that the lesion inaptly regarded as medial sclerosis actually involves the IELregarded by anatomy textbooks as intima2123and may or may not involve the media. The third, and perhaps the most important, problem is that there are important arterial lesions of which everyone is aware that are not yet part of the current classication. These include transplant arteriopathy, restenosis lesions after balloon angioplasty and stenting, intimal nonatherosclerotic proliferative lesions in arterial vessels larger than arterioles, and a variety of disorders associated with vascular calcication, not generally regarded as Mo nckeberg sclerosis. Transplant arteriopathy, generally a nonatherosclerotic hyperplastic bromuscular intimal proliferation, occurs in
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Figure 1. Terminology of arteriosclerosis. The current classication of arteriosclerotic lesions organized categorically. Abbreviation: IEL, internal elastic lamina.

virtually all types of solid organ transplants. Transplant arteriopathy affects large and small muscular arteries and veins as well. Early on, there is inammation in the vessel that can be mild or marked which may involve 1 or more of the 3 layers. Usually, the intima is affected more than the media or adventitia, but sometimes even a transmural, necrotizing arteritis may occur. Following the inammatory stage is the typical intimal bromuscular proliferation. With time, the lesions become less cellular and more brotic. Calcication, thrombosis, and atheroma formation can also occur in the setting of transplant arteriopathy. In the heart, where this lesion is most damaging, transplant coronary artery disease affects large and small epicardial coronary arteries and intramyocardial arteries. Another now common iatrogenic form of intimal hyperplasia is that associated with restenosis after balloon angioplasty24 or after intravascular stent placement.25 The intimal proliferation in restenosis lesions is histologically the same as in transplant arteriopathy and the hyperplastic form of arteriolosclerosis. There are a number of other situations in which arteries, not arterioles, show lesions histologically similar to those seen in the hyperplastic type of arteriolosclerosis lesions. One commonly encountered site for such lesions is the temporal artery. In elderly patients in whom biopsy is negative for temporal arteritis, these intimal lesions are often observed.26 Indeed, in the American Heart Association classication of atherosclerosis, the atheroma-prone lesion is not the fatty streak but rather a region of intimal bromuscular hyperplasia, referred to as adaptive intimal thickening.13 Identical lesions may be seen throughout the body as a nonspecic nding in muscular arteries. Although the term intimal hyperplasia is often used to describe intimal thickening with smooth muscle cells, collagen, and other components present, we recognize that
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this phrase may not be completely accurate. Because smooth muscle cells in the intima may have migrated from the media or adventitia, or have been deposited from circulating progenitor cells, the process in the intima is not simply hyperplasia. Furthermore, there are a variety of other terms used synonymously to describe intimal thickening, such as neointima, bromuscular hyperplasia, adaptive intimal thickening, hypertrophy, and broplasia, just to name some. Whether or not these are appropriate for specic lesions, or truly synonymous, requires additional study. In addition to what Mo nckeberg described, there are a number of other patterns of arterial calcication. We recently reported calcication limited to the IEL observed in the coronary arteries of human immunodeciency virus (HIV)positive patients and HIV-negative elderly patients with a variety of chronic diseases.27 These patients had normal renal function. In patients who do have renal dysfunction, alterations in calcium metabolism may cause widespread tissue calcication that affects the arterial bed, so-called vascular tachyphylaxis.28 Renal failure can also result in more extensive calcication within atherosclerotic plaques and/or extensive medial calcication that affect arteries throughout the body. In patients with secondary hyperparathyroidism, x-rays of the hands may reveal such calcication in digital arteries. In diabetic patients with severe peripheral vascular disease, arteries in amputated limbs frequently show heavily calcied atherosclerotic plaques and marked medial calcication. Importantly, electron beam computed tomography of coronary arteries in patients with chronic renal disease yields higher calcium scores than in individuals with normal renal function.29 Whether this calcication is in the atherosclerotic lesions or the arterial media has not been addressed.
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Figure 2. A and B, Atherosclerosis. A, Characteristic eccentric lesion with large lipid-rich (necrotic) core covered by a brous cap (F) (hematoxylineosin, original magnication 2). B, Oil red O stain showing lipid (L-red) within the lipid-rich core (original magnication 40). Smaller darker red dots are lipid-laden macrophages. C, So-called Mo nckeberg medial calcic sclerosis. Note that although there is prominent medial calcication the internal elastic lamina is also involved (arrow) (hematoxylin-eosin, original magnication 40). D through F, Primary arterial calcication. D, Early lesion with interrupted linear calcication limited to the internal elastic lamina (hematoxylin-eosin, original magnication 100). E, von Kossa stain of early lesion with interrupted linear calcication limited to the internal elastic lamina (original magnication 100). F, Linear and nodular calcication of the internal elastic lamina (arrows) (hematoxylin-eosin, original magnication 20).

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Figure 3. A through D, Fibromuscular intimal thickening. A, Adaptive intimal thickening in proximal coronary artery (trichrome, original magnication 40). B, Transplant coronary artery disease (trichrome, original magnication 40). C, Intimal hyperplasia in temporal artery (hematoxylin-eosin, original magnication 40). D, Arteriolonephrosclerosis, hyperplastic type (hematoxylin-eosin, original magnication 200). E and F, Hyalinosis (hematoxylin-eosin, original magnication 200 [E] and periodic acidSchiff, original magnication 200 [F]).

CATEGORIES OF ARTERIOSCLEROSIS Figure 1 shows the subtypes of arteriosclerosis organized into what we believe are the various categories based on the major light-microscopic pathology of the lesions. In the following we describe each subtype in greater
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detail and explain, in our opinion, how each could be represented in future classications of arteriosclerosis. Atherosclerosis Atherosclerosis (Figure 2, A and B) is clearly the most important arteriopathy. Although the sufx sclerosis is
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Figure 4. A and B, Vascular amyloidosis causing stenosis of intramyocardial arteries from a patient who died suddenly (hematoxylin-eosin, original magnication 100 [A] and Congo red, original magnication 100 [B]). C and D, Coronary artery of a patient with oxalosis; crystal deposits are subtle by routine light microscopy but prominent under polarized light (hematoxylin-eosin, original magnications 100 [C and D]). E, Oxalate was also present within a calcied (C) atherosclerotic plaque (hematoxylin-eosin, original magnication 40).

derived from the Greek word meaning hardening, atherosclerotic vessels may not be harder than normal and, indeed, may even be softer. One might even consider atherosclerosis an oxymoron. Although sclerosis denotes hardening, athero literally means gruellike. Atherosclerosis is therefore literally, and rather unintuitively, dened as arteries hardened by a thin chunky liquid. Alternate
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terms for some of the lesions might include atheromatous arteriomalacia or atheromatous arteriopathy. However, historically these are referred to as sclerotic lesions, not hard lesions, as they have become semantically distinct terms. In addition, it is quite common for the denition of a term to semantically deviate from its Greek derivation. Indeed, though hippocampus literally means sea horse,
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we accept that this historical nomenclature is not to be taken literally. Furthermore, the word sclerosis is commonly applied in other pathologies in which hardening is not the characteristic change, such as multiple sclerosis and hippocampal sclerosis. Therefore, it is not difcult to accept atherosclerosis as a worthy subtype of arteriosclerosis. Mo nckeberg Medial Calcic Sclerosis Because the term Mo nckeberg medial calcic sclerosis (Figure 2, C) is probably only partially accurate and because there are other forms of arterial calcication, we feel this and other nonatherosclerotic forms of arterial calcication are better described as primary arterial calcication. We have observed primary arterial calcication in 3 patterns. Calcication limited to the IEL is a common phenomenon in temporal arteries.26 Internal elastic lamina calcication occurs infrequently in coronary arteries20 (Figure 2, D through F). We described 19 cases of coronary artery IEL calcication; 10 patients were HIV-positive patients and 9 HIV-negative patients had a variety of chronic illnesses. Sometimes, calcication encroached on adjacent intimal or medial tissue and was associated with mild brosis. There was frequent disruption of the IEL but no inammation. von Kossa, alizarin red S, and trichrome/ elastic stains conrmed the ndings. Patients with IEL calcication often had complex medical histories but did not suffer from chronic renal failure or other conditions known to cause calcium dysregulation. The pathogenesis and clinical signicance of this nding are unknown. However, this mysterious calcication could lead to arterial stiffening and increased pulse pressure and could be mistaken for intimal calcication on coronary imaging. IEL calcication may result from premature aging due to HIV disease and chronic illness or from metabolic disorders in HIV-positive patients. Because IEL calcication is not part of any classication, IEL calcication is probably underreported. Although Mo nckeberg medial calcic sclerosis is not entirely medial and probably begins in the IEL, it is not our intention to rob Mo nckeberg of his namesake. Given the historical context, we feel Mo nckeberg will continue to be associated with calcication limited to the arterial media.16 Incidentally, however, this pattern of calcication may be exceedingly rare or simply may not occur at all. We encourage others to conrm our observations suggesting that medial calcication is virtually always associated with calcication of the IEL.10 The third pattern of primary arterial calcication would be a combination of the rst two; that is, calcication of both the IEL and the media. We believe this will eventually prove to be the primary pattern of calcication in which the arterial media is involved. Arteriolosclerosis We feel the third category, arteriolosclerosis, which distinguishes small artery sclerosis from large artery sclerosis, is an unnecessary distinction. The subtype bromuscular intimal thickening (Figure 3, A through D) would include the hyperplastic form of arteriolosclerosis but would similarly include bromuscular hyperplasia in arteries, as seen in transplant vasculopathy, restenosis lesions after balloon angioplasty or stenting, and nonspecic intimal thickening as occurs in temporal arteries with
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aging. Although hyalinosis typically occurs in arterioles, similar changes can be seen in arteries. Thus, simply describing these lesions as intimal hyalinosis would include such changes in arteries as well as arterioles (Figure 3, E and F).30,31 Finally, there are those miscellaneous entities that share features of the lesions discussed so far in that they cause thickening and stiffening of arteries. Two recent examples we have encountered that are not included in existing categories of vascular diseases are amyloidosis, which can involve arteries and arterioles, and vascular oxalosis (Figure 4, A through E). Vascular involvement by amyloid deposits is a wellknown phenomenon. Amyloid deposits in large and small arteries can cause ischemia and even sudden death when either the epicardial or intramyocardial coronary arteries are involved.32 Oxalosis is a relatively rare metabolic abnormality that may be hereditary or acquired. Oxalate deposits most often occur in the media of elastic and muscular arteries in patients with chronic renal failure. However, we recently reported, for the rst time, intimal deposition of oxalates in atherosclerotic plaques, so-called atherosclerotic oxalosis.33 In a review of coronary arteries from 80 patients, we found 4 cases in which there were prominent oxalate deposits within the atherosclerotic plaques in coronary arteries. Oxalate deposits were also present in the media of arteries, the thyroid gland, and other organs, but not the kidneys, and the patients surprisingly did not have renal failure. Another group of disorders that are associated with vascular lesions that could qualify as arteriosclerosis are systemic genetic disorders such as the mucopolysaccharidoses (Hunter and Hurler syndromes) and Alagille syndrome. These might also be included in a miscellaneous category along with other vascular lesions. As mentioned, there are other categories of arterial diseases: vasculitides, neoplasms, malformations, angiodysplasias, and inheritable disorders of connective tissue. Whether or not these should be incorporated into an allinclusive classication is beyond the scope of our editorial.
This work was supported in part by the generous endowment provided by the Piansky Family Trust. The authors have no potential conicts of interest related to this work.
References
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