Vascular Pathophysiological Changes in Patients with COVID-19: A Review Article
-
Mohammad Hassani
,
Peyman Bakhshaei shahrbabaki
,
Seyed Bashir Mirtajani
,
Mohammadreza Moshari
,
Pouya Tayebi
Abstract
In the last days of 2019, a novel strain of coronaviruses reported in Wuhan and spread rapidly all over the world which called 2019 novel coronavirus (2019- nCoV). Almost a few months later in the early 2020 (January 2020), the WHO declared the outbreak of COVID-19 a Public Health Emergency which Compared with the other SARS- CoV, has a stronger transmission capacity.
Although respiratory problems are the main clinical symptoms of COVID-19, some patients also experience other conditions and injuries, such as severe vascular damage. Therefore, it can be said that understanding the damage caused by this infection to the vascular system and its underlying mechanisms is of great importance.
[1] Abedini A, Mirtajani SB, Karimzadeh M, Jahangirifard A, Kiani A. Can Hesperidin be the Key to the Treatment of Severe Acute Respiratory Syndrome COV-2? Biomed Biotechnol Res J. 2020;4(5):108-9.
[2] Pager CT, Dutch RE. Cathepsin L is involved in proteolytic processing of the Hendra virus fusion protein. J Virol. 2005; 79(20):12714-20.
[3] Yuan S, Jiang SC, Li ZL. Analysis of possible intermediate hosts of the new coronavirus SARS-CoV-2. Front Vet Sci. 2020; 7:379.
[4] Zhang T, Wu Q, Zhang Z. Probable pangolin origin of SARS-CoV-2 associated with the COVID-19 outbreak. Curr Biol. 2020; 30(7):1346-1351.e2.
[5] Goh KJ, Choong MC, Cheong EH, Kalimuddin S, Duu Wen S, Phua GC, et al. Rapid progression to acute respiratory distress syndrome: Review of current understanding of critical illness from coronavirus disease 2019 (COVID-19) infection. Ann Acad Med Singapore. 2020; 49:108-18.
[6] Wu Y, Xu X, Chen Z, Duan J, Hashimoto K, Yang L, et al. Nervous system involvement after infection with COVID-19 and other coronaviruses. Brain Behav Immun. 2020; 87:18-22.
[7] Iadecola C, Anrather J, Kamel H. Effects of COVID-19 on the nervous system. Cell. 2020; 183(1):16-27.e1.
[8] Klironomos S, Tzortzakakis A, Kits A, Öhberg C, Kollia E, Ahoromazdae A, et al. Nervous System Involvement in Coronavirus Disease 2019. Results from a Retrospective Consecutive Neuroimaging Cohort. Radiology. 2020; 297(3):E324-34.
[9] Morgello S. Coronaviruses and the central nervous system. J Neurovirol. 2020; 26(4):459-73.
[10] Gavriatopoulou M, Korompoki E, Fotiou D, Ntanasis-Stathopoulos I, Psaltopoulou T, Kastritis E, et al. Organ-specific manifestations of COVID-19 infection. Clin Exp Med. 2020 Nov;20(4):493-506.
[11] Epelman S, Tang WW, Chen SY, Van Lente F, Francis GS, Sen S. Detection of soluble angiotensin-converting enzyme 2 in heart failure: insights into the endogenous counter-regulatory pathway of the renin-angiotensin-aldosterone system. J Am Coll Cardiol. 2008; 52(9):750-4.
[12] Uri K, Fagyas M, Siket IM, Kertesz A, Csanádi Z, Sandorfi G, et al. New perspectives in the renin-angiotensin-aldosterone system (RAAS) IV: circulating ACE2 as a biomarker of systolic dysfunction in human hypertension and heart failure. PLoS One. 2014; 9(4):e87845.
[13] Subramanian A, Vernon K, Slyper M, Waldman J, Luecken MD, Gosik K, et al. RAAS blockade, kidney disease, and expression of ACE2, the entry receptor for SARS-CoV-2, in kidney epithelial and endothelial cells. bioRxiv. 2020.
[14] Young MJ, Clyne CD, Chapman KE. Endocrine aspects of ACE2 regulation: RAAS, steroid hormones and SARS-CoV-2. J Endocrinol. 2020; 247(2):R45-R62.
[15] Michaud V, Deodhar M, Arwood M, Al Rihani SB, Dow P, Turgeon J. ACE2 as a Therapeutic Target for COVID-19; its Role in Infectious Processes and Regulation by Modulators of the RAAS System. J Clin Med. 2020; 9(7):2096.
[16] Rabelo LA, Alenina N, Bader M. ACE2–angiotensin-(1–7)–Mas axis and oxidative stress in cardiovascular disease. Hypertens Res. 2011; 34(2):154-60.
[17] Vickers C, Hales P, Kaushik V, Dick L, Gavin J, Tang J, et al. Hydrolysis of biological peptides by human angiotensin-converting enzyme-related carboxypeptidase. J Biol Chem. 2002; 277(17):14838-43.
[18] Yamamoto K, Ohishi M, Katsuya T, Ito N, Ikushima M, Kaibe M, et al. Deletion of angiotensin-converting enzyme 2 accelerates pressure overload-induced cardiac dysfunction by increasing local angiotensin II. Hypertension. 2006; 47(4):718-26.
[19] Ferrario CM, Trask AJ, Jessup JA. Advances in biochemical and functional roles of angiotensin-converting enzyme 2 and angiotensin-(1–7) in regulation of cardiovascular function. Am J Physiol Heart Circ Physiol. 2005; 289(6):H2281-90.
[20] Ortega JT, Serrano ML, Pujol FH, Rangel HR. Role of changes in SARS-CoV-2 spike protein in the interaction with the human ACE2 receptor: An in-silico analysis. EXCLI Jl. 2020; 19:410-7.
[21] Rajpal A, Rahimi L, Ismail‐Beigi F. Factors leading to high morbidity and mortality of COVID‐19 in patients with type 2 diabetes. J Diabetes. 2020;12(12):895-908.
[22] Chen L, Li X, Chen M, Feng Y, Xiong C. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res. 2020; 116(6):1097-100.
[23] Devaux CA, Rolain JM, Raoult D. ACE2 receptor polymorphism: Susceptibility to SARS-CoV-2, hypertension, multi-organ failure, and COVID-19 disease outcome. J Microbiol Immunol Infect. 2020; 53(3):425-435.
[24] Bean D, Kraljevic Z, Searle T, Bendayan R, Pickles A, Folarin A, et al. Treatment with ACE-inhibitors is associated with less severe disease with SARS-Covid-19 infection in a multi-site UK acute Hospital Trust. medRxiv. 2020.
[25] Semenza GL. Hypoxia-inducible factor 1 (HIF-1) pathway. Science's STKE. 2007; 2007(407):cm8-.
[26] Ke Q, Costa M. Hypoxia-inducible factor-1 (HIF-1). Mol Pharmacol. 2006; 70(5):1469-80.
[27] Bourgonje AR, Abdulle AE, Timens W, Hillebrands JL, Navis GJ, Gordijn SJ, et al. Angiotensin‐converting enzyme‐2 (ACE2), SARS‐CoV‐2 and pathophysiology of coronavirus disease 2019 (COVID‐19). J Pathol. 2020; 251(3):228-248.
[28] Polak SB, Van Gool IC, Cohen D, Jan H, van Paassen J. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol. 2020; 33(11):2128-2138.
[29] Magro C, Mulvey JJ, Berlin D, Nuovo G, Salvatore S, Harp J, et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases. Transl Res. 2020 220:1-13.
[30] Gąsecka A, Borovac JA, Guerreiro RA, Giustozzi M, Parker W, Caldeira D, et al. Thrombotic Complications in Patients with COVID-19: Pathophysiological Mechanisms, Diagnosis, and Treatment. Cardiovasc Drugs Ther. 2021; 35(2):215-229.
[31] Menter T, Haslbauer JD, Nienhold R, Savic S, Hopfer H, Deigendesch N, et al. Postmortem examination of COVID‐19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction. Histopathology. 2020; 77(2):198-209.
[32] Amezcua JM, Jain R, Kleinman G, Muh CR, Guzzetta M, Folkerth R, et al. COVID-19-Induced Neurovascular Injury: a Case Series with Emphasis on Pathophysiological Mechanisms. SN Compr Clin Med. 2020; 2(11):2109-2125.
[33] Darwesh AM, Bassiouni W, Sosnowski DK, Seubert JM. Can N-3 polyunsaturated fatty acids be considered a potential adjuvant therapy for COVID-19-associated cardiovascular complications? Pharmacol Ther. 2021; 219:107703.
[34] Sparks MA, South AM, Badley AD, Baker-Smith CM, Batlle D, Bozkurt B, et al. Severe acute respiratory syndrome coronavirus 2, COVID-19, and the renin-angiotensin system: Pressing needs and best research practices. Hypertension. 2020; 76(5):1350-67.
[35] Kempuraj D, Selvakumar GP, Ahmed ME, Raikwar SP, Thangavel R, Khan A, et al. COVID-19, mast cells, cytokine storm, psychological stress, and neuroinflammation. Neuroscientist. 2020; 26(5-6):402-14.
[36] Ross R, Conti P. COVID-19 induced by SARS-CoV-2 causes Kawasaki-like disease in children: role of pro-inflammatory and anti-inflammatory cytokines. J Biol Regul Homeost Agents. 2020; 34(3):767-73.
[37] Harapan H, Itoh N, Yufika A, Winardi W, Keam S, Te H, et al. Coronavirus disease 2019 (COVID-19): A literature review. J Infect Public Health. 2020; 13(5):667-673.
[38] Chau AS, Weber AG, Maria NI, Narain S, Liu A, Hajizadeh N, et al. The Longitudinal Immune Response to Coronavirus Disease 2019: Chasing the Cytokine Storm. Arthritis Rheumatol. 2020; 73(1):23-35.
[39] Azkur AK, Akdis M, Azkur D, Sokolowska M, van de Veen W, Brüggen MC, et al. Immune response to SARS‐CoV‐2 and mechanisms of immunopathological changes in COVID‐19. Allergy. 2020; 75(7):1564-81.
[40] Jiang L, Tang K, Levin M, Irfan O, Morris SK, Wilson K, et al. COVID-19 and multisystem inflammatory syndrome in children and adolescents. Lancet Infect Dis. 2020; 20(11):e276-e288.
[41] Ettman CK, Abdalla SM, Cohen GH, Sampson L, Vivier PM, Galea S. Prevalence of depression symptoms in US adults before and during the COVID-19 pandemic. JAMA Netw Open. 2020; 3(9):e2019686.
[42] Menni C, Valdes AM, Freidin MB, Sudre CH, Nguyen LH, Drew DA, et al. Real-time tracking of self-reported symptoms to predict potential COVID-19. Nat Med. 2020; 1037–1040.
[43] Hassani M, Nozarinia M, Marashi SA. COVID-19 disease, its challenge for Iranian vascular surgeons and our works. Iranian Journal of Vascular Surgery and Endovascular Therapy. 2021; 1(2).
[44] Wu L, O'Kane AM, Peng H, Bi Y, Motriuk-Smith D, Ren J. SARS-CoV-2 and cardiovascular complications: From molecular mechanisms to pharmaceutical management. Biochem Pharmacol. 2020; 178:114114.
[45] Sidarta-Oliveira D, Jara CP, Ferruzzi AJ, Skaf MS, Velander WH, Araujo EP, et al. SARS-CoV-2 receptor is co-expressed with elements of the kinin–kallikrein, renin–angiotensin and coagulation systems in alveolar cells. Sci Rep. 2020; 10(1):1-9.
[46] Griese DP, Achatz S, Batzlsperger CA, Strauch UG, Grumbeck B, Weil J, et al. Vascular gene delivery of anticoagulants by transplantation of retrovirally-transduced endothelial progenitor cells. Cardiovasc Res. 2003; 58(2):469-77.
[47] Schouten M, Wiersinga WJ, Levi M, Van Der Poll T. Inflammation, endothelium, and coagulation in sepsis. J Leukoc Biol. 2008; 83(3):536-45.
[48] Verhamme P, Hoylaerts MF. The pivotal role of the endothelium in haemostasis and thrombosis. Acta Clin Belg. 2006; 61(5):213-9.
[49] Sprague AH, Khalil RA. Inflammatory cytokines in vascular dysfunction and vascular disease. Biochem Pharmacol. 2009; 78(6):539-52.
[50] Smith RS, Zhang Z, Bouchard M, Li J, Lapp HS, Brotske GR, et al. Vascular catheters with a nonleaching poly-sulfobetaine surface modification reduce thrombus formation and microbial attachment. Sci Transl Med. 2012; 4(153):153ra132.
[51] Vazquez-Garza E, Jerjes-Sanchez C, Navarrete A, Joya-Harrison J, Rodriguez D. Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians. J Thromb Thrombolysis. 2017; 44(3):377-85.
[52] Panigada M, Bottino N, Tagliabue P, Grasselli G, Novembrino C, Chantarangkul V, et al. Hypercoagulability of COVID‐19 patients in intensive care unit. A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost. 2020; 18(7):1738-1742.
[53] Grobler C, Maphumulo SC, Grobbelaar LM, Bredenkamp JC, Laubscher GJ, Lourens PJ, et al. Covid-19: The rollercoaster of fibrin (ogen), d-dimer, von willebrand factor, p-selectin and their interactions with endothelial cells, platelets and erythrocytes. Int J Mol Sci. 2020; 21(14):5168.
[54] Colmenero I, Santonja C, Alonso‐Riaño M, Noguera‐Morel L, Hernández‐Martín A, Andina D, et al. SARS‐CoV‐2 endothelial infection causes COVID‐19 chilblains: histopathological, immunohistochemical and ultrastructural study of seven paediatric cases. Br J Dermatol. 2020; 183(4):729-37.
[55] Bikdeli B, Madhavan MV, Jimenez D, Chuich T, Dreyfus I, Driggin E, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020; 75(23):2950-2973.
[56] Robertson M. Fgl2: link between hepatitis B and SARS? Drug Discov Today. 2003; 8(17):768-70.
[57] Marsden PA, Ning Q, Fung LS, Luo X, Chen Y, Mendicino M, et al. The Fgl2/fibroleukin prothrombinase contributes to immunologically mediated thrombosis in experimental and human viral hepatitis. J Clin Invest. 2003; 112(1):58-66.
[58] Liu Y, Gao W, Guo W, Guo Y, Shi M, Dong G, et al. Prominent coagulation disorder is closely related to inflammatory response and could be as a prognostic indicator for ICU patients with COVID-19. J Thromb Thrombolysis. 2020; 50(4):825-32.
[2] Pager CT, Dutch RE. Cathepsin L is involved in proteolytic processing of the Hendra virus fusion protein. J Virol. 2005; 79(20):12714-20.
[3] Yuan S, Jiang SC, Li ZL. Analysis of possible intermediate hosts of the new coronavirus SARS-CoV-2. Front Vet Sci. 2020; 7:379.
[4] Zhang T, Wu Q, Zhang Z. Probable pangolin origin of SARS-CoV-2 associated with the COVID-19 outbreak. Curr Biol. 2020; 30(7):1346-1351.e2.
[5] Goh KJ, Choong MC, Cheong EH, Kalimuddin S, Duu Wen S, Phua GC, et al. Rapid progression to acute respiratory distress syndrome: Review of current understanding of critical illness from coronavirus disease 2019 (COVID-19) infection. Ann Acad Med Singapore. 2020; 49:108-18.
[6] Wu Y, Xu X, Chen Z, Duan J, Hashimoto K, Yang L, et al. Nervous system involvement after infection with COVID-19 and other coronaviruses. Brain Behav Immun. 2020; 87:18-22.
[7] Iadecola C, Anrather J, Kamel H. Effects of COVID-19 on the nervous system. Cell. 2020; 183(1):16-27.e1.
[8] Klironomos S, Tzortzakakis A, Kits A, Öhberg C, Kollia E, Ahoromazdae A, et al. Nervous System Involvement in Coronavirus Disease 2019. Results from a Retrospective Consecutive Neuroimaging Cohort. Radiology. 2020; 297(3):E324-34.
[9] Morgello S. Coronaviruses and the central nervous system. J Neurovirol. 2020; 26(4):459-73.
[10] Gavriatopoulou M, Korompoki E, Fotiou D, Ntanasis-Stathopoulos I, Psaltopoulou T, Kastritis E, et al. Organ-specific manifestations of COVID-19 infection. Clin Exp Med. 2020 Nov;20(4):493-506.
[11] Epelman S, Tang WW, Chen SY, Van Lente F, Francis GS, Sen S. Detection of soluble angiotensin-converting enzyme 2 in heart failure: insights into the endogenous counter-regulatory pathway of the renin-angiotensin-aldosterone system. J Am Coll Cardiol. 2008; 52(9):750-4.
[12] Uri K, Fagyas M, Siket IM, Kertesz A, Csanádi Z, Sandorfi G, et al. New perspectives in the renin-angiotensin-aldosterone system (RAAS) IV: circulating ACE2 as a biomarker of systolic dysfunction in human hypertension and heart failure. PLoS One. 2014; 9(4):e87845.
[13] Subramanian A, Vernon K, Slyper M, Waldman J, Luecken MD, Gosik K, et al. RAAS blockade, kidney disease, and expression of ACE2, the entry receptor for SARS-CoV-2, in kidney epithelial and endothelial cells. bioRxiv. 2020.
[14] Young MJ, Clyne CD, Chapman KE. Endocrine aspects of ACE2 regulation: RAAS, steroid hormones and SARS-CoV-2. J Endocrinol. 2020; 247(2):R45-R62.
[15] Michaud V, Deodhar M, Arwood M, Al Rihani SB, Dow P, Turgeon J. ACE2 as a Therapeutic Target for COVID-19; its Role in Infectious Processes and Regulation by Modulators of the RAAS System. J Clin Med. 2020; 9(7):2096.
[16] Rabelo LA, Alenina N, Bader M. ACE2–angiotensin-(1–7)–Mas axis and oxidative stress in cardiovascular disease. Hypertens Res. 2011; 34(2):154-60.
[17] Vickers C, Hales P, Kaushik V, Dick L, Gavin J, Tang J, et al. Hydrolysis of biological peptides by human angiotensin-converting enzyme-related carboxypeptidase. J Biol Chem. 2002; 277(17):14838-43.
[18] Yamamoto K, Ohishi M, Katsuya T, Ito N, Ikushima M, Kaibe M, et al. Deletion of angiotensin-converting enzyme 2 accelerates pressure overload-induced cardiac dysfunction by increasing local angiotensin II. Hypertension. 2006; 47(4):718-26.
[19] Ferrario CM, Trask AJ, Jessup JA. Advances in biochemical and functional roles of angiotensin-converting enzyme 2 and angiotensin-(1–7) in regulation of cardiovascular function. Am J Physiol Heart Circ Physiol. 2005; 289(6):H2281-90.
[20] Ortega JT, Serrano ML, Pujol FH, Rangel HR. Role of changes in SARS-CoV-2 spike protein in the interaction with the human ACE2 receptor: An in-silico analysis. EXCLI Jl. 2020; 19:410-7.
[21] Rajpal A, Rahimi L, Ismail‐Beigi F. Factors leading to high morbidity and mortality of COVID‐19 in patients with type 2 diabetes. J Diabetes. 2020;12(12):895-908.
[22] Chen L, Li X, Chen M, Feng Y, Xiong C. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res. 2020; 116(6):1097-100.
[23] Devaux CA, Rolain JM, Raoult D. ACE2 receptor polymorphism: Susceptibility to SARS-CoV-2, hypertension, multi-organ failure, and COVID-19 disease outcome. J Microbiol Immunol Infect. 2020; 53(3):425-435.
[24] Bean D, Kraljevic Z, Searle T, Bendayan R, Pickles A, Folarin A, et al. Treatment with ACE-inhibitors is associated with less severe disease with SARS-Covid-19 infection in a multi-site UK acute Hospital Trust. medRxiv. 2020.
[25] Semenza GL. Hypoxia-inducible factor 1 (HIF-1) pathway. Science's STKE. 2007; 2007(407):cm8-.
[26] Ke Q, Costa M. Hypoxia-inducible factor-1 (HIF-1). Mol Pharmacol. 2006; 70(5):1469-80.
[27] Bourgonje AR, Abdulle AE, Timens W, Hillebrands JL, Navis GJ, Gordijn SJ, et al. Angiotensin‐converting enzyme‐2 (ACE2), SARS‐CoV‐2 and pathophysiology of coronavirus disease 2019 (COVID‐19). J Pathol. 2020; 251(3):228-248.
[28] Polak SB, Van Gool IC, Cohen D, Jan H, van Paassen J. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol. 2020; 33(11):2128-2138.
[29] Magro C, Mulvey JJ, Berlin D, Nuovo G, Salvatore S, Harp J, et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases. Transl Res. 2020 220:1-13.
[30] Gąsecka A, Borovac JA, Guerreiro RA, Giustozzi M, Parker W, Caldeira D, et al. Thrombotic Complications in Patients with COVID-19: Pathophysiological Mechanisms, Diagnosis, and Treatment. Cardiovasc Drugs Ther. 2021; 35(2):215-229.
[31] Menter T, Haslbauer JD, Nienhold R, Savic S, Hopfer H, Deigendesch N, et al. Postmortem examination of COVID‐19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction. Histopathology. 2020; 77(2):198-209.
[32] Amezcua JM, Jain R, Kleinman G, Muh CR, Guzzetta M, Folkerth R, et al. COVID-19-Induced Neurovascular Injury: a Case Series with Emphasis on Pathophysiological Mechanisms. SN Compr Clin Med. 2020; 2(11):2109-2125.
[33] Darwesh AM, Bassiouni W, Sosnowski DK, Seubert JM. Can N-3 polyunsaturated fatty acids be considered a potential adjuvant therapy for COVID-19-associated cardiovascular complications? Pharmacol Ther. 2021; 219:107703.
[34] Sparks MA, South AM, Badley AD, Baker-Smith CM, Batlle D, Bozkurt B, et al. Severe acute respiratory syndrome coronavirus 2, COVID-19, and the renin-angiotensin system: Pressing needs and best research practices. Hypertension. 2020; 76(5):1350-67.
[35] Kempuraj D, Selvakumar GP, Ahmed ME, Raikwar SP, Thangavel R, Khan A, et al. COVID-19, mast cells, cytokine storm, psychological stress, and neuroinflammation. Neuroscientist. 2020; 26(5-6):402-14.
[36] Ross R, Conti P. COVID-19 induced by SARS-CoV-2 causes Kawasaki-like disease in children: role of pro-inflammatory and anti-inflammatory cytokines. J Biol Regul Homeost Agents. 2020; 34(3):767-73.
[37] Harapan H, Itoh N, Yufika A, Winardi W, Keam S, Te H, et al. Coronavirus disease 2019 (COVID-19): A literature review. J Infect Public Health. 2020; 13(5):667-673.
[38] Chau AS, Weber AG, Maria NI, Narain S, Liu A, Hajizadeh N, et al. The Longitudinal Immune Response to Coronavirus Disease 2019: Chasing the Cytokine Storm. Arthritis Rheumatol. 2020; 73(1):23-35.
[39] Azkur AK, Akdis M, Azkur D, Sokolowska M, van de Veen W, Brüggen MC, et al. Immune response to SARS‐CoV‐2 and mechanisms of immunopathological changes in COVID‐19. Allergy. 2020; 75(7):1564-81.
[40] Jiang L, Tang K, Levin M, Irfan O, Morris SK, Wilson K, et al. COVID-19 and multisystem inflammatory syndrome in children and adolescents. Lancet Infect Dis. 2020; 20(11):e276-e288.
[41] Ettman CK, Abdalla SM, Cohen GH, Sampson L, Vivier PM, Galea S. Prevalence of depression symptoms in US adults before and during the COVID-19 pandemic. JAMA Netw Open. 2020; 3(9):e2019686.
[42] Menni C, Valdes AM, Freidin MB, Sudre CH, Nguyen LH, Drew DA, et al. Real-time tracking of self-reported symptoms to predict potential COVID-19. Nat Med. 2020; 1037–1040.
[43] Hassani M, Nozarinia M, Marashi SA. COVID-19 disease, its challenge for Iranian vascular surgeons and our works. Iranian Journal of Vascular Surgery and Endovascular Therapy. 2021; 1(2).
[44] Wu L, O'Kane AM, Peng H, Bi Y, Motriuk-Smith D, Ren J. SARS-CoV-2 and cardiovascular complications: From molecular mechanisms to pharmaceutical management. Biochem Pharmacol. 2020; 178:114114.
[45] Sidarta-Oliveira D, Jara CP, Ferruzzi AJ, Skaf MS, Velander WH, Araujo EP, et al. SARS-CoV-2 receptor is co-expressed with elements of the kinin–kallikrein, renin–angiotensin and coagulation systems in alveolar cells. Sci Rep. 2020; 10(1):1-9.
[46] Griese DP, Achatz S, Batzlsperger CA, Strauch UG, Grumbeck B, Weil J, et al. Vascular gene delivery of anticoagulants by transplantation of retrovirally-transduced endothelial progenitor cells. Cardiovasc Res. 2003; 58(2):469-77.
[47] Schouten M, Wiersinga WJ, Levi M, Van Der Poll T. Inflammation, endothelium, and coagulation in sepsis. J Leukoc Biol. 2008; 83(3):536-45.
[48] Verhamme P, Hoylaerts MF. The pivotal role of the endothelium in haemostasis and thrombosis. Acta Clin Belg. 2006; 61(5):213-9.
[49] Sprague AH, Khalil RA. Inflammatory cytokines in vascular dysfunction and vascular disease. Biochem Pharmacol. 2009; 78(6):539-52.
[50] Smith RS, Zhang Z, Bouchard M, Li J, Lapp HS, Brotske GR, et al. Vascular catheters with a nonleaching poly-sulfobetaine surface modification reduce thrombus formation and microbial attachment. Sci Transl Med. 2012; 4(153):153ra132.
[51] Vazquez-Garza E, Jerjes-Sanchez C, Navarrete A, Joya-Harrison J, Rodriguez D. Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians. J Thromb Thrombolysis. 2017; 44(3):377-85.
[52] Panigada M, Bottino N, Tagliabue P, Grasselli G, Novembrino C, Chantarangkul V, et al. Hypercoagulability of COVID‐19 patients in intensive care unit. A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost. 2020; 18(7):1738-1742.
[53] Grobler C, Maphumulo SC, Grobbelaar LM, Bredenkamp JC, Laubscher GJ, Lourens PJ, et al. Covid-19: The rollercoaster of fibrin (ogen), d-dimer, von willebrand factor, p-selectin and their interactions with endothelial cells, platelets and erythrocytes. Int J Mol Sci. 2020; 21(14):5168.
[54] Colmenero I, Santonja C, Alonso‐Riaño M, Noguera‐Morel L, Hernández‐Martín A, Andina D, et al. SARS‐CoV‐2 endothelial infection causes COVID‐19 chilblains: histopathological, immunohistochemical and ultrastructural study of seven paediatric cases. Br J Dermatol. 2020; 183(4):729-37.
[55] Bikdeli B, Madhavan MV, Jimenez D, Chuich T, Dreyfus I, Driggin E, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020; 75(23):2950-2973.
[56] Robertson M. Fgl2: link between hepatitis B and SARS? Drug Discov Today. 2003; 8(17):768-70.
[57] Marsden PA, Ning Q, Fung LS, Luo X, Chen Y, Mendicino M, et al. The Fgl2/fibroleukin prothrombinase contributes to immunologically mediated thrombosis in experimental and human viral hepatitis. J Clin Invest. 2003; 112(1):58-66.
[58] Liu Y, Gao W, Guo W, Guo Y, Shi M, Dong G, et al. Prominent coagulation disorder is closely related to inflammatory response and could be as a prognostic indicator for ICU patients with COVID-19. J Thromb Thrombolysis. 2020; 50(4):825-32.
| Files | ||
| Issue | Vol 8 No 2 (2022): Spring |
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| Section | Review Article(s) | |
| DOI | https://doi.org/10.18502/aacc.v8i2.9156 | |
| Keywords | ||
| COVID-19 vascular injury pathophysiological changes | ||
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How to Cite
1.
Hassani M, Bakhshaei shahrbabaki P, Mirtajani SB, Moshari M, Tayebi P. Vascular Pathophysiological Changes in Patients with COVID-19: A Review Article. Arch Anesth & Crit Care. 2022;8(2):144-150.
