Advertisement

The development of calcium deposits in atherosclerotic lesions and their persistence after lipid regression

  • Herbert C Stary
    Correspondence
    Address for correspondence: Herbert C. Stary, MD, Louisiana State University Health Sciences Center, 1901 Perdido Street, New Orleans, Louisiana 70112
    Affiliations
    Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA
    Search for articles by this author

      Abstract

      Children have both macrophages and macrophages that are filled with lipid droplets (foam cells) at susceptible sites of arteries. Such changes are minimal and may not develop further. However, in some adolescents, small pools of dead foam cell remnants and lipid droplets (extracellular lipid) are added to the foam-cell accumulations at the susceptible sites. The pools are the precursor of a much larger confluent accumulation of extracellular lipids (the lipid core)—the hallmark of the atheromas of young adults. As soon as a lesion with a lipid core is present, calcium granules of microscopic size are found among the packed extracellular particles and droplets and in smooth-muscle cells isolated among them. Disintegration of arterial structure at the core facilitates tears at the surface, hematoma, and thrombosis. As a response, layers of reparative fibromuscular tissue are added and may predominate in a lesion. Over time, calcium lumps and plates form through accretion of adjacent extracellular calcium granules. In adults past the fourth decade of life, the greater part of the former lipid core of a lesion may be calcified and there may be osseous metaplasia. The effect of therapeutic reduction of high levels of blood cholesterol on lesions was studied in rhesus monkeys. Drastic reduction of blood cholesterol levels for 3Math Eq years resulted in the disappearance of macrophages, macrophage foam cells and lymphocytes, and reduction of extracellular lipid from advanced lesions. Calcium deposits remained in the arterial wall and were not visibly changed.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to American Journal of Cardiology
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

        • Stary H.C.
        The sequence of cell and matrix changes in atherosclerotic lesions of coronary arteries in the first forty years of life.
        Eur Heart J. 1990; 11: 3-19
        • Stary H.C.
        Atlas of Atherosclerosis Progression and Regression. Parthenon Publishing, London and New York1999
        • Stary H.C.
        • Blankenhorn D.H.
        • Chandler A.B.
        • Glagov S.
        • Insull Jr, W.
        • Richardson M.
        • Rosenfeld M.E.
        • Schaffer S.A.
        • Schwartz C.J.
        • Wagner W.D.
        • et al.
        A definition of the intima of human arteries and of its atherosclerosis-prone regions.
        Circulation. 1992; 85: 391-405
        • Stary H.C.
        Natural history of calcium deposits in atherosclerosis progression and regression.
        Z Kardiol. 2000; 89: 28-35
        • Ghadially F.N.
        Ultrastructural Pathology of the Cell and Matrix. Butterworth-Heinemann, Boston1997
        • Anderson H.C.
        Molecular biology of matrix vesicles.
        Clin Orthop Related Res. 1995; 314: 266-280
        • Wexler L.
        • Brundage B.
        • Crouse J.
        • Detrano R.
        • Fuster V.
        • Maddahi J.
        • Rumberger J.
        • Stanford W.
        • White R.
        • Taubert K.
        Coronary artery calcification.
        Circulation. 1996; 94: 1175-1192
        • Fuster V.
        Mechanisms leading to myocardial infarction.
        Circulation. 1994; 90: 2126-2146
        • Schmid K.
        • McSharry W.O.
        • Pameijer C.H.
        • Binette J.P.
        Chemical and physicochemical studies on the mineral deposits of the human atherosclerotic aorta.
        Atherosclerosis. 1980; 37: 199-210
        • Armstrong M.L.
        Connective tissue in regression.
        Atheroscler Rev. 1978; 3: 147-168
        • Daoud A.S.
        • Jarmolych J.
        • Augustyn J.M.
        • Fritz K.E.
        Sequential morphologic studies of regression of advanced atherosclerosis.
        Arch Pathol. 1981; 105: 233-239
        • Clarkson T.B.
        • Bond M.G.
        • Bullock B.C.
        • Marzetta C.A.
        A study of atherosclerosis regression in maccaca mulatta. IV. Changes in coronary arteries from animals with atherosclerosis induced for 19 months and then regressed for 24 or 48 months at plasma cholesterol concentrations of 300 or 200 mg/dL.
        Exp Mol Pathol. 1981; 34: 345-368
        • Takeo S.
        • Anan M.
        • Fujioka K.
        Functional changes of aorta with massive accumulation of calcium.
        Atherosclerosis. 1989; 77: 175-181
        • Glagov S.
        • Weisenberg E.
        • Zarins C.K.
        • Stankunavicius R.
        • Kolettis G.J.
        Compensatory enlargement of human atherosclerotic coronary arteries.
        N Engl J Med. 1987; 316: 1371-1375
        • Clarkson T.B.
        • Prichard R.W.
        • Morgan T.M.
        • Petrick G.S.
        • Klein K.P.
        Remodeling of coronary arteries in human and nonhuman primates.
        JAMA. 1994; 271: 289-294