СОВРЕМЕННЫЕ АСПЕКТЫ ПАТОГЕНЕЗА КАЛЬЦИНОЗА АОРТАЛЬНЫХ ПОЛУЛУНИЙ (обзор литературы)

  • Николай Иванович Гуляев Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Никита Алексеевич Варавин Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Александр Евгеньевич Коровин Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Валерий Валентинович Кузнецов Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Владимир Валерьевич Яковлев Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Александр Волеславович Гордиенко Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6

Аннотация

Кальцинированный аортальный стеноз (КАС) — основная причина протезирования аортального клапана. Отсутствие медикаментозных методов лечения и высокая распространенность КАС представляют его важной проблемой в кардиологии. Современные результаты исследований клапанов аорты при их кальцификации подтверждают гипотезу, что КАС является результатом активного процесса формирования костной ткани, который может происходить посредством дифференцировки остеобластов. Хотя существуют общие факторы риска с процессом атерогенеза, не у всех пациентов с ишемической болезнью сердца выявляется кальцинированный аортальный стеноз. В статье представлены современные взгляды на патогенез кальцинированного аортального стеноза, приводится его сравнительная характеристика с атеросклерозом. Библиогр. 51 назв. Ил. 3. Табл. 1.

Ключевые слова:

аортальный клапан, аортальный стеноз, кальцификация, остеопротегерин, RANKL, RANK, атеросклероз, эндотелиальная дисфункция, матриксные металлопротеиназы, Wnt-сигнальная система

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Литература

Литература

Шевченко Ю. Л., Матвеев С. А., Рогачев М. В., Добрынин В. М., Гудымович В. Г. Внутрисердечный кальциноз // Клинич. медицина и патофизиология. 1997. № 2. С. 27–30.

Bossé Y., Mathieu P., Pibarot P. The Next Step to Elucidate the Etiology of Calcific Aortic Valve Stenosis // Journal of the American College of Cardiology. 2008. Vol. 51, No 14. P. 1327–1336.

Seth Goldbarg H., Elmariah S., Miller M. A., Fuster V. Insights Into Degenerative Aortic Valve Disease // Journal of the American College of Cardiology. 2007. Vol. 50, No 13. P. 1205–1213.

Carabello B. A., Paulus W. J. Aortic stenosis // Lancet. 2009. Vol. 373. P. 956–966.

Helske S., Lindstedt K. A., Laine M. et al. Induction of local angiotensin II-producing systems in stenoticaortic valves // J. Am. Coll. Cardiol. 2004. No 44. P. 1859–1866.

Shao J., Cai J., Towler D. A. Molecular Mechanisms of Vascular сalcification // Arterioscler. Thromb. Vasc. Biol. 2006. Vol. 26, No 7. P. 1423–1430.

Yetkin E., Waltenberger J. Molecular and cellular mechanisms of aortic stenosis // International Journal of Cardiology. 2009. No 135. P. 4–13.

Dweck M. R., Boon N. A., Newby D. E. Calcific Aortic Stenosis A Disease of the Valve and the Myocardium // Journal of the American College of Cardiology. 2012. Vol. 60, No 19. P. 1854–1863.

Mohler E. R. III. Mechanisms of Aortic Valve Calcification // Jour. of Cardiology. 2004. Vol. 94. P. 1396–1402.

Yin Yipa C. Y., Simmons C. A. The aortic valve microenvironment and its role in calcific aortic valve disease // Cardiovascular Pathology. 2011. No 20. P. 177–182.

Rajamannan N. M., Evans F. J., Aikawa E. et al. Calcific Aortic Valve Disease: Not Simply a Degenerative Process // Circulation. 2011. Vol. 124. P. 1783–1791.

Milin A. C., Vorobiof G., Aksoy O., Ardehali R. Insights Into Aortic Sclerosis and Its Relationship With Coronary Artery Disease // Journal of the American Heart Association. 2014. No 3. P. 1205–1213.

Thaden J. J., Nkomo V. T., Enriquez-Sarano M. The Global Burden of Aortic Stenosis // Progressin cardiocascular disease. 2014. No 56. P. 565–571.

Rajamannan N. M. Calcific Aortic Stenosis: Lessons Learned from Experimental and Clinical Studies // Arterioscler. Thromb. Vasc. Biol. 2009. Vol. 29, No 2. P. 162–168.

Towler D. A. Molecular and Cellular Aspects of Calcific Aortic Valve Disease // Circulation Research. 2013. Vol. 113, No 2. P. 198–208.

Otto C. M., Lind B. K., Kitzman D. W. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly // N. Engl. J. Med. 1999. No 341. P. 142–147.

Leggett M., Otto C. M. Aortic valve disease // Curr. Opin. Cardiol. 1996. No 11. P. 120–125.

Митрофанова Л. Б. Клинико-морфологические особенности сердца при клапанных пороках различной этиологии. СПб., 2005. 394 с.

Otto M., Kuusisto J., Reichenbach D. D., Gown A. M., O’Brien K. D. Characterization of the early lesion of ‘degenerative’ valvular aortic stenosis // Circulation. 1994. Vol. 90. P. 844–853.

Yang X., Fullerton D. A., Su X., Lihua Ao, Cleveland J. C., Meng X. Pro-Osteogenic Phenotype of Human Aortic Valve Interstitial Cells Is Associated With Higher Levels of Toll-Like Receptors 2 and 4 and Enhanced Expression of Bone Morphogenetic Protein 2 // J. American College of Cardiology. 2009. Vol. 53, No 6. P. 491–500.

Galante A., Pietroiusti A., Vellini M. et al. C-reactive protein is increased in patients with degenerative aortic valvular stenosis // J. Am. Coll. Cardiol. 2001. No 38. P. 1078–1082.

Garg V., Muth A. N., Ransom J. F. et al. Mutations in Notch1 cause aortic valve disease // Nature. 2005.No 437. P. 270–274.

Miller J. D., Chu, Y. Brooks R. M. et al. Dysregulation of antioxidant mechanisms contributes to increased oxidative stress in calcific aortic valvular stenosis in humans // J. Am. Coll. Cardiol. 2008. No 52.P. 843–850.

Rajamannan N. M. Oxidative-mechanical stress signals stem cell niche mediated Lrp5 osteogenesis in eNOS(-/-) null mice // J. Cell. Biochem. 2012. No 113. P. 1623–1634.

Gong Y., Slee R. B., Fukai N. et al. Oste oporosis-pseudoglioma syndrome collaborative group. LDL receptor-related protein 5 (LRP5) affects bone accrual and eye development // Cell. 2001. No 107. P. 513–523.

Chan K. Is Aortic Stenosis a Preventable Disease? // Journal of the American College of Cardiology.2003. Vol. 42, No 4. P. 593–599.

O’Brien K. D., Shavelle D. M., Caulfield M. T. et al. Association of angiotensin-converting enzyme with low-density lipoprotein in aortic valvular lesions and in human plasma // Circulation. 2002. Vol. 106.P. 2224–2230.

Pinzar E., Wang T., Garrido M. R. Angiotensin II induces tyrosine nitration and activation of ERK1/2 in vascular smooth muscle cells // FEBS Lett. 2005. No 579. P. 5100–5104.

Parisi V., Leosco D., Ferro G. et al. The lipid theory in the pathogenesis of calcific aortic stenosis // Nutrition, Metabolism & Cardiovascular Diseases. 2015. Vol. 25. Is. 6 (June). P. 519–525.

Stewart B. F., Siscovick D., Lind B. K. et al. Clinical factors associated with calcific aortic valve disease.Cardiovascular Health Study // J. Am. Coll. Cardiol. 1997. No 29. P. 630–640.

Oggianti E., Venneri R. N. L., Chubuchny V. et al. Aortic Valve Sclerosis Is Associated With Systemic Endothelial Dysfunction // Journal of the American College of Cardiology. 2003. Vol. 41, No 1. Р. 136–141.

Novaro G. M., Katz R., Aviles R. J. et al. Clinical factors, but not C-reactive protein, predict progression of calcific aortic-valve disease: the Cardiovascular Health Study // J. Am. Coll. Cardiol. 2007. No 50. P. 8.

Graham L. S., Tintut Y., Parhami F. et al. Bone density and hyperlipidemia: the T-lymphocyte connection // J. B one Miner. Res. 2010. No 25. P. 2460–2469.

Mohler E. R. III. Aortic Valve Calcification: How and Why? // ACC current journal review. 2001. P. 84–85.

Соловьева Н. И. Матриксные металлопротеиназы и их биологические функции // Биоорганическая химия. 1998. № 24. С. 217–226.

Nagase H. Zinc metalloproteinases in health and disease / ed. N. M. Ноoper. London: Taylor & Francis Ltd., 1996. 153 р.

Scott J. E. Structure and function in extracellular matrices depend on interactions between anionic glycosaminoglycans // Pathol. Biol. (Paris). 2001. Vol. 49, No 4 (May). P. 284–289.

Rajamannan N. M., Subramaniam M., Stock S. R. et al. Atorvastatin inhibits calcification and enhancesnitric oxide synthase production in the hypercholesterolaemic aortic valve // Heart. 2005. No 91. P. 806–810.

Holmen S. L., Giambernardi T. A., Zylstra C. R. et al. Decreased BMD and limb deformities in mice carrying mutations in both Lrp5 and Lrp6 // J. B one Miner. Res. 2004. No 19. P. 2033–2040.

Westendorf J. J., Kahler R. A., Schroeder T. M. Wnt signaling in osteoblasts and bone diseases // Gene. 2004. No 341. P. 19–39.

Nakagawa N., Kinosaki M., Yamaguchi K., Shima N. RANK is the essential signaling receptor for
osteoclast differentiation factor in osteoclastogenesis // Biochem. Biophys. Res. Commun. 1998. No 253. P. 395–400.

Orita Y., Yamamoto H., Kohno N. et al. Role of osteoprotegerin in arterial calcification: development of new animal model // Arterioscler. Thromb. Vasc. Biol. 2007. No 27. P. 2058–2064.

Persy V., D’Haese P. Vascular calcification and bone disease: the calcification paradox // Trends Mol. Med. 2009. No 15. P. 405–416.

Graham, L. S. Parhami F., Tintut Y. et al. Oxidized lipids enhance RANKL production by T lymphocytes: implications for lipid-induced bone loss // Clin. Immunol. 2009. No 133. P. 265–275.

Weiss R. M., Miller J. D., Heistad D. D. Fibrocalcific aortic valve disease: Opportunity to understand disease mechanisms using mouse models // Circ. Res. 2013. Vol. 113, No 2. P. 209–222.

Аничков Н. Н. Современное состояние вопроса об этиологии и патогенезе атеросклероза// Клиническая медицина. 1937. Т. 15, № 3. С. 347–356.

Цукерман Г. И., Бураковский В. И., Голиков Г. Т., Семеновский М. Л. Пороки аортального клапана. М.: Медицина. 1972. 240 c.

Вальтер А. В. Хронические пороки аортальных клапанов. Л.: ВММА, 1948. 158 с.

Егоров И. В.Сенильный аортальный стеноз: век изучения// Современная ревматология. 2007.№ 1. С. 20–25.

Edwards J. E. Calcific aortic stenosis // Circulation. 1963. Vol. 28. P. 817–823.

Chan K. L., Teo K., Dumesnil J. G. et al. Effect of Lipid Lowering With Rosuvastatin on Progression of Aortic Stenosis. Results of the Aortic Stenosis Progression Observation: Measuring Effects of Rosuvastatin (ASTRONOMER) // Trial. Circulation. 2010. Vol. 121, No 2. P. 306–314.




References

Shevchenko Yu. L., Matveev S. A., Rogachev M. V., Dobrynin V. M., Gudymovich V. G . Vnutriserdechnyikal’tsinoz [Intracardiac calcification]. Clinical. medicine and pathophysiology, 1997, no. 2, pp. 27–30 (In Russian).

Bossé Y., Mathieu P., Pibarot P. The Next Step to Elucidate the Etiology of Calcific Aortic Valve Stenosis.Journal of the American College of Cardiology, 2008, vol. 51, no. 14, pp. 1327–1336.

Seth Goldbarg H., Elmariah S., Miller M. A., Fuster V. Insights Into Degenerative Aortic Valve Disease.Journal of the American College of Cardiology, 2007, vol. 50, no. 13, pp. 1205–1213.

Carabello B. A., Paulus W. J. Aortic stenosis. Lancet, 2009, vol. 373, pp. 956–966.

Helske S., Lindstedt K. A., Laine M. et al. Induction of local angiotensin II-producing systems in stenotic aortic valves. J. Am. Coll. Cardiol., 2004, no. 44, pp. 1859–1866.

Shao J., Cai J., Towler D. A. Molecular Mechanisms of Vascular сalcification. Arterioscler. Thromb. Vasc. Biol., 2006, vol. 26, no. 7, pp. 1423–1430.

Yetkin E., Waltenberger J. Molecular and cellular mechanisms of aortic stenosis. International Journal of Cardiology, 2009, no. 135, pp. 4–13.

Dweck M. R., Boon N. A., Newby D. E. Calcific Aortic Stenosis A Disease of the Valve and the Myocardium.Journal of the American College of Cardiology, 2012, vol. 60, no. 19, pp. 1854–1863.

Mohler E. R. III. Mechanisms of Aortic Valve Calcification. Jour. of Cardiology, 2004, vol. 94,pp. 1396–1402.

Yin Yipa C. Y ., Simmons C. A. The aortic valve microenvironment and its role in calcific aortic valve disease. Cardiovascular Pathology, 2011, no. 20, pp. 177–182.

Rajamannan N. M., Evans F. J., Aikawa E. et al. Calcific Aortic Valve Disease: Not Simply a Degenerative Process. Circulation, 2011, vol. 124, pp. 1783–1791.

Milin A. C., Vorobiof G., Aksoy O., Ardehali R. Insights Into Aortic Sclerosis and Its Relationship With Coronary Artery Disease. Journal of the American Heart Association, 2014, no. 3, pp. 1205–1213.

Thaden J. J., Nkomo V. T., Enriquez-Sarano M. The Global Burden of Aortic Stenosis. Progressin cardiocascular disease, 2014, no. 56, pp. 565–571.

Rajamannan N. M. Calcific Aortic Stenosis: Lessons Learned from Experimental and Clinical Studies. Arterioscler. Thromb. Vasc. Biol., 2009, vol. 29, no. 2, pp. 162–168.

Towler D. A. Molecular and Cellular Aspects of Calcific Aortic Valve Disease. Circulation Research, 2013, vol. 113, no. 2, pp. 198–208.

Otto C. M., Lind B. K., Kitzman D. W. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N. Engl. J. Med., 1999, no. 341, pp. 142–147.

Leggett M., Otto C. M. Aortic valve disease. Curr. Opin. Cardiol., 1996, no. 11, pp. 120–125.

Mitrofanova L. B. Kliniko-morfologicheskie osobennosti serdtsa pri klapannykh porokakh razlichnoi etiologii [Kliniko-morfologichesky features of heart at valvate defects of various etiology]. St. Petersburg, 2005.394 p. (In Russian).

Otto M., Kuusisto J., Reichenbach D. D., Gown A. M., O’Brien K. D. Characterization of the early lesion of ‘degenerative’ valvular aortic stenosis. Circulation, 1994, vol. 90, pp. 844–853.

Yang X., Fullerton D. A., Su X., Lihua Ao, Cleveland J. C., Meng X. Pro-Osteogenic Phenotype of Human Aortic Valve Interstitial Cells Is Associated With Higher Levels of Toll-Like Receptors 2 and 4 and Enhanced Expression of Bone Morphogenetic Protein 2. J. American College of Cardiology, 2009, vol. 53,no. 6, pp. 491–500.

Galante A., Pietroiusti A., Vellini M. et al. C-reactive protein is increased in patients with degenerative aortic valvular stenosis. J. Am. Coll. Cardiol., 2001, no. 38, pp. 1078–1082.

Garg V., Muth A. N., Ransom J. F . et al. Mutations in Notch1 cause aortic valve disease. Nature, 2005,no. 437, pp. 270–274.

Miller J. D., Chu, Y. B rooks R. M. et al. Dysregulation of antioxidant mechanisms contributes to increased oxidative stress in calcific aortic valvular stenosis in humans. J. Am. Coll. Cardiol., 2008, no. 52, pp. 843–850.

Rajamannan N. M. Oxidative-mechanical stress signals stem cell niche mediated Lrp5 osteogenesis in eNOS(-/-) null mice. J. Cell. Biochem., 2012, no. 113, pp. 1623–1634.

Gong Y., Slee R. B ., Fukai N. et al. Oste oporosis-pseudoglioma syndrome collaborative group. LDL receptor-related protein 5 (LRP5) affects bone accrual and eye development. Cell., 2001, no. 107, pp. 513–523.

Chan K. Is Aortic Stenosis a Preventable Disease? Journal of the American College of Cardiology, 2003,vol. 42, no. 4, pp. 593–599.

O’Brien K. D., Shavelle D. M., Caulfield M. T. et al. Association of angiotensin-converting enzyme with low-density lipoprotein in aortic valvular lesions and in human plasma. Circulation, 2002, vol. 106, pp. 2224–2230.

Pinzar E., Wang T., Garrido M. R. Angiotensin II induces tyrosine nitration and activation of ERK1/2 in vascular smooth muscle cells. FEBS Lett., 2005, no. 579, pp. 5100–5104.

Parisi V., Leosco D., Ferro G. et al. The lipid theory in the pathogenesis of calcific aortic stenosis. Nutrition, Metabolism & Cardiovascular Diseases, 2015, vol. 25, issue 6 (June), pp. 519–525.

Stewart B. F ., Siscovick D., Lind B. K. et al. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J. Am. Coll. Cardiol., 1997, no. 29, pp. 630–640.

Oggianti E., Venneri R. N. L., Chubuchny V. et al. Aortic Valve Sclerosis Is Associated With Systemic Endothelial Dysfunction. Journal of the American College of Cardiology, 2003, vol. 41, no. 1, pp. 136–141.

Novaro G. M., Katz R., Aviles R. J. et al. Clinical factors, but not C-reactive protein, predict progression of calcific aortic-valve disease: the Cardiovascular Health Study. J. Am. Coll. Cardiol., 2007, no. 50, p. 8.

Graham L. S., Tintut Y., Parhami F. et al. Bone density and hyperlipidemia: the T-lymphocyte connection.J. Bone Miner. Res., 2010, no. 25, pp. 2460–2469.

Mohler E. R. III. Aortic Valve Calcification: How and Why? ACC current journal review, 2001, pp. 84–85.

Solovyeva N. I. Matriksnye metalloproteinazy i ikh biologicheskie funktsii [Matrix metalloproteinases and their biological functions]. Journal of Biorganic chemistry, 1998, no. 24, pp. 217–226. (In Russian)

Nagase H. Zinc metalloproteinases in health and disease. Ed. by N. M. Ноoper. London, Taylor & Francis Ltd., 1996. 153 р.

Scott J. E. Structure and function in extracellular matrices depend on interactions between anionic glycosaminoglycans. Pathol. Biol. (Paris), 2001, vol. 49, no. 4 (May), pp. 284–289.

Rajamannan N. M., Subramaniam M., Stock S. R. et al. Atorvastatin inhibits calcification and enhances nitric oxide synthase production in the hypercholesterolaemic aortic valve. Heart, 2005, no. 91, pp. 806–810.

Holmen S. L., Giambernardi T. A., Zylstra C. R. et al. Decreased BMD and limb deformities in mice carrying mutations in both Lrp5 and Lrp6. J. Bone Miner. Res., 2004, no. 19, pp. 2033–2040.

Westendorf J. J., Kahler R. A., Schroeder T. M. Wnt signaling in osteoblasts and bone diseases. Gene,2004, no. 341, pp. 19–39.

Nakagawa N., Kinosaki M., Yamaguchi K., Shima N. RANK is the essential signaling receptor for osteoclast differentiation factor in osteoclastogenesis. Biochem. Biophys. Res. Commun., 1998, no. 253,pp. 395–400.

Orita Y., Yamamoto H., Kohno N. et al. Role of osteoprotegerin in arterial calcification: development of new animal model. Arterioscler. Thromb. Vasc. Biol., 2007, no. 27, pp. 2058–2064.

Persy V., D’Haese P. Vascular calcification and bone disease: the calcification paradox. Trends Mol. Med., 2009, no. 15, pp. 405–416.

Graham L. S., Parhami F., Tintut Y. et al. Oxidized lipids enhance RANKL production by T
lymphocytes: implications for lipid-induced bone loss. Clin. Immunol., 2009, no. 133, pp. 265–275.

Weiss R. M., Miller J. D., Heistad D. D. Fibrocalcific aortic valve disease: Opportunity to understand disease mechanisms using mouse models. Circ. Res., 2013, vol. 113, no. 2, pp. 209–222.

Anichkov N. N. Sovremennoe sostoianie voprosa ob etiologii i patogeneza ateroskleroza [Current state of a question of an etiology and pathogenesis of atherosclerosis]. Klinich. medicine, 1937, vol. 15, no. 3,pp. 347–356. (In Russian)

Zuckerman G. I., Burakovsky V. I., Golikov G. T., Semenovskiy M. L. Poroki aortal’nogo klapana [Defects of the aortal valve]. Moscow, Meditsina, 1972. 240 p. (In Russian)

Walther A. W. Khronicheskie poroki aortal’nykh klapanov [Chronic defects of aortal valves]. Leningrad,VMMA, 1948, pp. 23–28. (In Russian)

Egorov I. V. [Senile aortal stenosis: century of studying]. Modern rheumatology, 2007, no. 1, pp. 20–25.(In Russian)

Edwards J. E. Calcific aortic stenosis. Circulation, 1963, vol. 28, pp. 817–823.

Chan K. L., Teo K., Dumesnil J. G . et al. Effect of Lipid Lowering With Rosuvastatin on Progression of Aortic Stenosis. Results of the Aortic Stenosis Progression Observation: Measuring Effects of Rosuvastatin (ASTRONOMER). Trial. Circulation, 2010, vol. 121, no. 2, pp. 306–314.
Опубликован
2017-01-16
Как цитировать
Гуляев, Н. И., Варавин, Н. А., Коровин, А. Е., Кузнецов, В. В., Яковлев, В. В., & Гордиенко, А. В. (2017). СОВРЕМЕННЫЕ АСПЕКТЫ ПАТОГЕНЕЗА КАЛЬЦИНОЗА АОРТАЛЬНЫХ ПОЛУЛУНИЙ (обзор литературы). Вестник Санкт-Петербургского университета. Медицина, 11(3), 20–34. https://doi.org/10.21638/11701/spbu11.2016.302.
Раздел
Внутренние болезни