Cardiovascular Risk in Systemic Sclerosis
Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Angeloudi, Eleni [verfasserIn] Pagkopoulou, Eleni [verfasserIn] Arvanitaki, Alexandra [verfasserIn] Soulaidopoulos, Stergios [verfasserIn] Garyfallos, Alexandros [verfasserIn] Kitas, George [verfasserIn] Dimitroulas, Theodoros [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Current treatment options in rheumatology - Berlin [u.a.] : Springer, 2015, 6(2020), 3 vom: 30. Juni, Seite 282-298 |
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| Übergeordnetes Werk: |
volume:6 ; year:2020 ; number:3 ; day:30 ; month:06 ; pages:282-298 |
| Links: |
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| DOI / URN: |
10.1007/s40674-020-00152-z |
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| Katalog-ID: |
SPR040857212 |
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| 520 | |a Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. | ||
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| 650 | 4 | |a Scleroderma |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cardiovascular disease |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Atherosclerosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Macrovascular disease |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Arvanitaki, Alexandra |e verfasserin |4 aut | |
| 700 | 1 | |a Soulaidopoulos, Stergios |e verfasserin |4 aut | |
| 700 | 1 | |a Garyfallos, Alexandros |e verfasserin |4 aut | |
| 700 | 1 | |a Kitas, George |e verfasserin |4 aut | |
| 700 | 1 | |a Dimitroulas, Theodoros |e verfasserin |4 aut | |
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10.1007/s40674-020-00152-z doi (DE-627)SPR040857212 (SPR)s40674-020-00152-z-e DE-627 ger DE-627 rakwb eng 610 ASE Angeloudi, Eleni verfasserin aut Cardiovascular Risk in Systemic Sclerosis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. Systemic sclerosis (dpeaa)DE-He213 Scleroderma (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Atherosclerosis (dpeaa)DE-He213 Macrovascular disease (dpeaa)DE-He213 Pagkopoulou, Eleni verfasserin aut Arvanitaki, Alexandra verfasserin aut Soulaidopoulos, Stergios verfasserin aut Garyfallos, Alexandros verfasserin aut Kitas, George verfasserin aut Dimitroulas, Theodoros verfasserin aut Enthalten in Current treatment options in rheumatology Berlin [u.a.] : Springer, 2015 6(2020), 3 vom: 30. Juni, Seite 282-298 (DE-627)815913990 (DE-600)2806597-9 2198-6002 nnns volume:6 year:2020 number:3 day:30 month:06 pages:282-298 https://dx.doi.org/10.1007/s40674-020-00152-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2020 3 30 06 282-298 |
| spelling |
10.1007/s40674-020-00152-z doi (DE-627)SPR040857212 (SPR)s40674-020-00152-z-e DE-627 ger DE-627 rakwb eng 610 ASE Angeloudi, Eleni verfasserin aut Cardiovascular Risk in Systemic Sclerosis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. Systemic sclerosis (dpeaa)DE-He213 Scleroderma (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Atherosclerosis (dpeaa)DE-He213 Macrovascular disease (dpeaa)DE-He213 Pagkopoulou, Eleni verfasserin aut Arvanitaki, Alexandra verfasserin aut Soulaidopoulos, Stergios verfasserin aut Garyfallos, Alexandros verfasserin aut Kitas, George verfasserin aut Dimitroulas, Theodoros verfasserin aut Enthalten in Current treatment options in rheumatology Berlin [u.a.] : Springer, 2015 6(2020), 3 vom: 30. Juni, Seite 282-298 (DE-627)815913990 (DE-600)2806597-9 2198-6002 nnns volume:6 year:2020 number:3 day:30 month:06 pages:282-298 https://dx.doi.org/10.1007/s40674-020-00152-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2020 3 30 06 282-298 |
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10.1007/s40674-020-00152-z doi (DE-627)SPR040857212 (SPR)s40674-020-00152-z-e DE-627 ger DE-627 rakwb eng 610 ASE Angeloudi, Eleni verfasserin aut Cardiovascular Risk in Systemic Sclerosis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. Systemic sclerosis (dpeaa)DE-He213 Scleroderma (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Atherosclerosis (dpeaa)DE-He213 Macrovascular disease (dpeaa)DE-He213 Pagkopoulou, Eleni verfasserin aut Arvanitaki, Alexandra verfasserin aut Soulaidopoulos, Stergios verfasserin aut Garyfallos, Alexandros verfasserin aut Kitas, George verfasserin aut Dimitroulas, Theodoros verfasserin aut Enthalten in Current treatment options in rheumatology Berlin [u.a.] : Springer, 2015 6(2020), 3 vom: 30. Juni, Seite 282-298 (DE-627)815913990 (DE-600)2806597-9 2198-6002 nnns volume:6 year:2020 number:3 day:30 month:06 pages:282-298 https://dx.doi.org/10.1007/s40674-020-00152-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2020 3 30 06 282-298 |
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10.1007/s40674-020-00152-z doi (DE-627)SPR040857212 (SPR)s40674-020-00152-z-e DE-627 ger DE-627 rakwb eng 610 ASE Angeloudi, Eleni verfasserin aut Cardiovascular Risk in Systemic Sclerosis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. Systemic sclerosis (dpeaa)DE-He213 Scleroderma (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Atherosclerosis (dpeaa)DE-He213 Macrovascular disease (dpeaa)DE-He213 Pagkopoulou, Eleni verfasserin aut Arvanitaki, Alexandra verfasserin aut Soulaidopoulos, Stergios verfasserin aut Garyfallos, Alexandros verfasserin aut Kitas, George verfasserin aut Dimitroulas, Theodoros verfasserin aut Enthalten in Current treatment options in rheumatology Berlin [u.a.] : Springer, 2015 6(2020), 3 vom: 30. Juni, Seite 282-298 (DE-627)815913990 (DE-600)2806597-9 2198-6002 nnns volume:6 year:2020 number:3 day:30 month:06 pages:282-298 https://dx.doi.org/10.1007/s40674-020-00152-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2020 3 30 06 282-298 |
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10.1007/s40674-020-00152-z doi (DE-627)SPR040857212 (SPR)s40674-020-00152-z-e DE-627 ger DE-627 rakwb eng 610 ASE Angeloudi, Eleni verfasserin aut Cardiovascular Risk in Systemic Sclerosis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. Systemic sclerosis (dpeaa)DE-He213 Scleroderma (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Atherosclerosis (dpeaa)DE-He213 Macrovascular disease (dpeaa)DE-He213 Pagkopoulou, Eleni verfasserin aut Arvanitaki, Alexandra verfasserin aut Soulaidopoulos, Stergios verfasserin aut Garyfallos, Alexandros verfasserin aut Kitas, George verfasserin aut Dimitroulas, Theodoros verfasserin aut Enthalten in Current treatment options in rheumatology Berlin [u.a.] : Springer, 2015 6(2020), 3 vom: 30. Juni, Seite 282-298 (DE-627)815913990 (DE-600)2806597-9 2198-6002 nnns volume:6 year:2020 number:3 day:30 month:06 pages:282-298 https://dx.doi.org/10.1007/s40674-020-00152-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2020 3 30 06 282-298 |
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Enthalten in Current treatment options in rheumatology 6(2020), 3 vom: 30. Juni, Seite 282-298 volume:6 year:2020 number:3 day:30 month:06 pages:282-298 |
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Enthalten in Current treatment options in rheumatology 6(2020), 3 vom: 30. Juni, Seite 282-298 volume:6 year:2020 number:3 day:30 month:06 pages:282-298 |
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Systemic sclerosis Scleroderma Cardiovascular disease Atherosclerosis Macrovascular disease |
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Current treatment options in rheumatology |
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Angeloudi, Eleni @@aut@@ Pagkopoulou, Eleni @@aut@@ Arvanitaki, Alexandra @@aut@@ Soulaidopoulos, Stergios @@aut@@ Garyfallos, Alexandros @@aut@@ Kitas, George @@aut@@ Dimitroulas, Theodoros @@aut@@ |
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2020-06-30T00:00:00Z |
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Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. 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Angeloudi, Eleni |
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610 ASE Cardiovascular Risk in Systemic Sclerosis Systemic sclerosis (dpeaa)DE-He213 Scleroderma (dpeaa)DE-He213 Cardiovascular disease (dpeaa)DE-He213 Atherosclerosis (dpeaa)DE-He213 Macrovascular disease (dpeaa)DE-He213 |
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Angeloudi, Eleni Pagkopoulou, Eleni Arvanitaki, Alexandra Soulaidopoulos, Stergios Garyfallos, Alexandros Kitas, George Dimitroulas, Theodoros |
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Cardiovascular Risk in Systemic Sclerosis |
| abstract |
Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. |
| abstractGer |
Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. |
| abstract_unstemmed |
Purpose of review Systemic sclerosis (SSc) is a systemic inflammatory, autoimmune disorder characterized by diffuse fibrosis of the skin and visceral organ involvement. Endothelial dysfunction and microvascular injury dominate the pathophysiology and clinical manifestations of the disease, while the impact of macrovascular atherosclerotic disease on cardiovascular (CVD) morbidity and mortality is yet to be established. In this article, we aim to review current knowledge about CVD as well as cardiac complications in SSc and discuss the potentially implicated pathogenetic mechanisms. Recent findings Systemic inflammation has been identified as an important trigger and contributor for the development and progression of atherosclerosis, closely associated with high cardiovascular mortality in patients with autoimmune disorders, such as rheumatoid arthritis. A close interplay between traditional risk factors and factors related to the disease, including inflammation, endothelial injury, and immune-mediated cytotoxicity, sharing common pathogenetic features with microvasculopathy, may be responsible for large-vessel involvement and promotion of atherosclerosis in SSc. Cardiac complications, including heart failure due to impairment of coronary microcirculation and myocardial fibrosis, are listed among the primary cause of death in SSc. Evaluation of indirect surrogate markers of CVD, namely, arterial stiffness, carotid media thickness, and flow-mediated dilation, in small studies has provided inconsistent results regarding the association between SSc and atherosclerosis, highlighting the need for further research on this field. In this article, we aim to review current knowledge about large-vessel involvement and CVD in SSc and discuss the potentially implicated pathogenetic mechanisms. Summary SSc conveys a higher risk for CVD associated with both vascular and fibrotic complications during the course of the disease. Increasing attention is given on the use of vasodilators, immunosuppressants, and more recently antifibrotic drugs that potentially improve myocardial function and reduce atherosclerotic disease burden. |
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| title_short |
Cardiovascular Risk in Systemic Sclerosis |
| url |
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| author2 |
Pagkopoulou, Eleni Arvanitaki, Alexandra Soulaidopoulos, Stergios Garyfallos, Alexandros Kitas, George Dimitroulas, Theodoros |
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Pagkopoulou, Eleni Arvanitaki, Alexandra Soulaidopoulos, Stergios Garyfallos, Alexandros Kitas, George Dimitroulas, Theodoros |
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| doi_str |
10.1007/s40674-020-00152-z |
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2024-07-03T18:42:22.546Z |
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| score |
7.401745 |