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COVID-19 DA MIOKARD SHIKASTLANISHINING MORFOLOGIK NAMOYON BO’LISHI

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MAQOLA ANNOTATSIYASI

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Bugungi holatda COVID-19 patogenezi va morfogenezi yetarlicha o’rganilmagan, shuning uchun ushbu maqola COVID-19da miokard parenximatoz-stromal elementlarining shikastlanishini o’rganishga bag’ishlanadi. Tadqiqot materiali bo’lib 28 yoshdan 56 yoshgacha vafot etgan 26 bemorning COVID -19 da oshqozon devorlari miokardidan olingan kesmalar xizmat qiladi. Morfologik tadqiqot natijalari ko’rsatishicha, COVID-19da miokard interstitsial to’qimasining mukoid bo’kishi va shishishi gialuronan to’planishi, distrofiya, disgeneratsiya rivojlanishi hamda biriktiruvchi to’qima tuzilishi va tomirlar yallig’lanishi hisobiga yuz beradi. Miokard parenximasida kontraktli buzilish, kardiomiotsit sitoplazmalarining gomogen zichlashishi (jipslashishi), miofibrill ko’ndalang chizig’ining yo’qolishi, bazofiliyaning o’choqli rivojlanishi, kardiomiotsitlarning ShIK-ijobiy (musbat) metaplaziyasi,mushak tolalarining nekrobiozi va degeneratsiyasi; kardiomiotsitlar yadrosining parchalanishi va jipslashishi aniqlanadi. Shikastlangan kardiomiotsitlar dastlab yadro shakli va bo’yalishining o’zgarishi, sarkoplazma vakulizatsiyasida namoyon bo’ladi, so’ngra displaziya turida yadro giperxromaziyasi va yiriklashishi kuzatiladi, keyinchalik yadro haroratning sekin asta pastlab, bemorning sog’ayishi bilan havo rangda bo’yalishi hamda gomogenizatsiya, metaxromaziya aniqlanadi; keyinchalik metaxromaziya kardiomiotsit barcha sitoplazmasini egallaydi va hujayralar nobud bo’ladi.

MUALIFLAR

Teglar

# inflammation# воспаление# миокард# myocardium# heart# yallig’lanish# кардиомиоциты# сердце# дистрофия# COVID-19# Yurak# miokard# kardiomiotsit# interstitsiya# distrofiya# disregeneratsiya# интерстиций# дисрегенерация# cardiomyocytes# interstitium# dystrophy# dysregeneration

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Maqola idintifikatorlari

Foydalanilgan adabiyotlar

1. Ackermann M., Verleden S. E., Kuehnel M. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020; DOI: 10.1056/NEJMoa2015432. 2. De Rosa S., Spaccarotella C., Basso C. et al.; on behalf of Societa Italiana di Cardiologia and the CCU Academy investigators group. Reduction of hospitalizations for myocardial infarction in Italy in the COVID-19 era. Eur Heart J.2020; doi:10.1093/ eurheartj/ehaa409. 3. Guo T., Fan Y., Chen M. et all. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19) // JAMA Cardiol. 2020; 5 (7): 811-818. 4. Kuster G. M., Pfister O., Burkard T. et al. SARS-CoV2: should inhibitors of the renin -angiotensin system be with drawn in patients with COVID-19? Eur Heart J.2020; 41: 1801-1803. 5. Lax S. F., Skok K., Zechner P. et al.Pulmonary Arterial Thrombosis in COVID-19 With Fatal Outcome: Results From a Prospective, Single-Center, Clinicopathologic Case Series. Ann Intern Med. 2020; https://doi.org/10.7326/M20-2566 6. Shi S., Qin M., Shen B. et all. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China // JAMA Cardiol. 2020; 5 (7): 802-810. 7. Vaduganathan M., Vardeny O., Michel T. et al. Renin -Angiotensin -AldosteroneSystem Inhibitors in Patients with Covid-19. N Engl J Med. 2020; 382: 1653-1659. 8. Varga Z., Flammer A. J., Steiger P. Endothelial cell infection and endotheliitis inCOVID-19. Lancet. 2020; https://doi. org/10.1016/S0140-6736 (20) 30937-5

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