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AIMS Molecular Science

2020, Volume 7, Issue 3: 183-210. doi: 10.3934/molsci.2020009
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Calcification in human vessels and valves: from pathological point of view

  • 1.
    CVPath Institute, Gaithersburg, MD
  • 2.
    University of Maryland, School of Medicine, Baltimore, MD, USA
  • Received: 27 March 2020 Accepted: 29 May 2020 Published: 02 June 2020

  • Vascular and valvular calcification are commonly encountered in clinical medicine and a greater understanding of their significance and pathophysiology remain a subject of immense importance. In the coronary arteries, vascular calcification burden correlates with the severity of luminal stenosis and atherosclerotic plaque burden. While in progressive lesions, the presence of coronary calcification is not binary but rather depends on the type of calcification. Racial and gender differences, and comorbidities like diabetes mellitus and chronic kidney disease, all affect the presence and severity of calcification. The peripheral arteries of the lower extremities are affected by both medial calcification and intimal calcification, and the former barely contributes to luminal stenosis. The character of atherosclerosis differs between above-knee and below-knee lesions. Valvular calcification generally occurs on the aortic valve leaflets, and pathologic findings range from minimal fibrocalcific changes in early disease to end-stage lesions characterized by fibrotic thickening and nodular calcification. Valvular calcification is similar to atherosclerotic changes, in terms of lipid deposition, inflammation, osteogenic differentiation of valvular interstitial cells, and oxidative stress. However, the mechanisms of vascular and valvular calcification are still not well understood. A deeper understanding of vascular and valvular calcification is needed in order to develop effective anti-calcification therapies and to improve outcomes in these patients.

    Citation: Yu Sato, Hiroyuki Jinnouchi, Atsushi Sakamoto, Anne Cornelissen, Masayuki Mori, Rika Kawakami, Kenji Kawai, Renu Virmani, Aloke V. Finn. Calcification in human vessels and valves: from pathological point of view[J]. AIMS Molecular Science, 2020, 7(3): 183-210. doi: 10.3934/molsci.2020009

    Related Papers:

  • Vascular and valvular calcification are commonly encountered in clinical medicine and a greater understanding of their significance and pathophysiology remain a subject of immense importance. In the coronary arteries, vascular calcification burden correlates with the severity of luminal stenosis and atherosclerotic plaque burden. While in progressive lesions, the presence of coronary calcification is not binary but rather depends on the type of calcification. Racial and gender differences, and comorbidities like diabetes mellitus and chronic kidney disease, all affect the presence and severity of calcification. The peripheral arteries of the lower extremities are affected by both medial calcification and intimal calcification, and the former barely contributes to luminal stenosis. The character of atherosclerosis differs between above-knee and below-knee lesions. Valvular calcification generally occurs on the aortic valve leaflets, and pathologic findings range from minimal fibrocalcific changes in early disease to end-stage lesions characterized by fibrotic thickening and nodular calcification. Valvular calcification is similar to atherosclerotic changes, in terms of lipid deposition, inflammation, osteogenic differentiation of valvular interstitial cells, and oxidative stress. However, the mechanisms of vascular and valvular calcification are still not well understood. A deeper understanding of vascular and valvular calcification is needed in order to develop effective anti-calcification therapies and to improve outcomes in these patients.


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    Abbreviation AV: Aortic valve; CAD: Coronary artery disease; CFA: Common femoral artery; CKD: Chronic kidney disease; CLI: Critical limb ischemia; DM: Diabetes mellitus; FEM-POP: Femoral and popliteal arteries; HbA1c: Hemoglobin A1c; INFRA-POP: Infrapopliteal arteries; MGP: Matrix Gla protein; NF-kB: Nuclear factor kappa beta; OPN: Osteopontin; OPG: Osteoprotegerin; PAD: Peripheral artery disease; RANKL: Receptor activator of NF-B ligand; SFA: Superficial femoral artery; VIC: Valvular interstitial cells; VSMC: Vascular smooth muscle cell;

    Conflict of interest


    CVPath Institute has received institutional research support from R01 HL141425 Leducq Foundation Grant; 480 Biomedical; 4C Medical; 4Tech; Abbott; Accumedical; Amgen; Biosensors; Boston Scientific; Cardiac Implants; Celonova; Claret Medical; Concept Medical; Cook; CSI; DuNing, Inc; Edwards LifeSciences; Emboline; Endotronix; Envision Scientific; Lutonix/Bard; Gateway; Lifetech; Limflo; MedAlliance; Medtronic; Mercator; Merill; Microport Medical; Microvention; Mitraalign; Mitra assist; NAMSA; Nanova; Neovasc; NIPRO; Novogate; Occulotech; OrbusNeich Medical; Phenox; Profusa; Protembis; Qool; Recor; Senseonics; Shockwave; Sinomed; Spectranetics; Surmodics; Symic; Vesper; W.L. Gore; Xeltis. A.V. F. has received honoraria from Abbott Vascular; Biosensors; Boston Scientific; Celonova; Cook Medical; CSI; Lutonix Bard; Sinomed; Terumo Corporation; and is a consultant to Amgen; Abbott Vascular; Boston Scientific; Celonova; Cook Medical; Lutonix Bard; Sinomed. Anne Cornelissen receives research grants from University Hospital RWTH Aachen. R.V. has received honoraria from Abbott Vascular; Biosensors; Boston Scientific; Celonova; Cook Medical; Cordis; CSI; Lutonix Bard; Medtronic; OrbusNeich Medical; CeloNova; SINO Medical Technology; ReCore; Terumo Corporation; W. L. Gore; Spectranetics; and is a consultant Abbott Vascular; Boston Scientific; Celonova; Cook Medical; Cordis; CSI; Edwards Lifescience; Lutonix Bard; Medtronic; OrbusNeich Medical; ReCore; Sinomededical Technology; Spectranetics; Surmodics; Terumo Corporation; W. L. Gore; Xeltis. The other authors declare no competing interests.

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