Pathophysiology of Atherosclerosis Plaque Progression
Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterise...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sakakura, Kenichi [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
13 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape - Eggertsen, L. ELSEVIER, 2017, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:22 ; year:2013 ; number:6 ; pages:399-411 ; extent:13 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.hlc.2013.03.001 |
|---|
| Katalog-ID: |
ELV021683530 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV021683530 | ||
| 003 | DE-627 | ||
| 005 | 20230625134021.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2013 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.hlc.2013.03.001 |2 doi | |
| 028 | 5 | 2 | |a GBVA2013003000012.pica |
| 035 | |a (DE-627)ELV021683530 | ||
| 035 | |a (ELSEVIER)S1443-9506(13)00071-1 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 550 |q VZ |
| 084 | |a 38.48 |2 bkl | ||
| 084 | |a 38.90 |2 bkl | ||
| 084 | |a 42.94 |2 bkl | ||
| 100 | 1 | |a Sakakura, Kenichi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Pathophysiology of Atherosclerosis Plaque Progression |
| 264 | 1 | |c 2013transfer abstract | |
| 300 | |a 13 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. | ||
| 520 | |a Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. | ||
| 650 | 7 | |a Plaque rupture |2 Elsevier | |
| 650 | 7 | |a Remodelling |2 Elsevier | |
| 650 | 7 | |a Plaque progression |2 Elsevier | |
| 650 | 7 | |a Pathophysiology |2 Elsevier | |
| 650 | 7 | |a Atherosclerosis |2 Elsevier | |
| 650 | 7 | |a Thin cap fibroatheroma |2 Elsevier | |
| 700 | 1 | |a Nakano, Masataka |4 oth | |
| 700 | 1 | |a Otsuka, Fumiyuki |4 oth | |
| 700 | 1 | |a Ladich, Elena |4 oth | |
| 700 | 1 | |a Kolodgie, Frank D. |4 oth | |
| 700 | 1 | |a Virmani, Renu |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Eggertsen, L. ELSEVIER |t Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape |d 2017 |g Amsterdam [u.a.] |w (DE-627)ELV000398209 |
| 773 | 1 | 8 | |g volume:22 |g year:2013 |g number:6 |g pages:399-411 |g extent:13 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.hlc.2013.03.001 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OPC-GGO | ||
| 936 | b | k | |a 38.48 |j Marine Geologie |q VZ |
| 936 | b | k | |a 38.90 |j Ozeanologie |j Ozeanographie |q VZ |
| 936 | b | k | |a 42.94 |j Meeresbiologie |q VZ |
| 951 | |a AR | ||
| 952 | |d 22 |j 2013 |e 6 |h 399-411 |g 13 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
k s ks |
|---|---|
| matchkey_str |
sakakurakenichinakanomasatakaotsukafumiy:2013----:ahpyilgoahrslrsslq |
| hierarchy_sort_str |
2013transfer abstract |
| bklnumber |
38.48 38.90 42.94 |
| publishDate |
2013 |
| allfields |
10.1016/j.hlc.2013.03.001 doi GBVA2013003000012.pica (DE-627)ELV021683530 (ELSEVIER)S1443-9506(13)00071-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Sakakura, Kenichi verfasserin aut Pathophysiology of Atherosclerosis Plaque Progression 2013transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Elsevier Nakano, Masataka oth Otsuka, Fumiyuki oth Ladich, Elena oth Kolodgie, Frank D. oth Virmani, Renu oth Enthalten in Elsevier Eggertsen, L. ELSEVIER Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape 2017 Amsterdam [u.a.] (DE-627)ELV000398209 volume:22 year:2013 number:6 pages:399-411 extent:13 https://doi.org/10.1016/j.hlc.2013.03.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 22 2013 6 399-411 13 045F 610 |
| spelling |
10.1016/j.hlc.2013.03.001 doi GBVA2013003000012.pica (DE-627)ELV021683530 (ELSEVIER)S1443-9506(13)00071-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Sakakura, Kenichi verfasserin aut Pathophysiology of Atherosclerosis Plaque Progression 2013transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Elsevier Nakano, Masataka oth Otsuka, Fumiyuki oth Ladich, Elena oth Kolodgie, Frank D. oth Virmani, Renu oth Enthalten in Elsevier Eggertsen, L. ELSEVIER Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape 2017 Amsterdam [u.a.] (DE-627)ELV000398209 volume:22 year:2013 number:6 pages:399-411 extent:13 https://doi.org/10.1016/j.hlc.2013.03.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 22 2013 6 399-411 13 045F 610 |
| allfields_unstemmed |
10.1016/j.hlc.2013.03.001 doi GBVA2013003000012.pica (DE-627)ELV021683530 (ELSEVIER)S1443-9506(13)00071-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Sakakura, Kenichi verfasserin aut Pathophysiology of Atherosclerosis Plaque Progression 2013transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Elsevier Nakano, Masataka oth Otsuka, Fumiyuki oth Ladich, Elena oth Kolodgie, Frank D. oth Virmani, Renu oth Enthalten in Elsevier Eggertsen, L. ELSEVIER Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape 2017 Amsterdam [u.a.] (DE-627)ELV000398209 volume:22 year:2013 number:6 pages:399-411 extent:13 https://doi.org/10.1016/j.hlc.2013.03.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 22 2013 6 399-411 13 045F 610 |
| allfieldsGer |
10.1016/j.hlc.2013.03.001 doi GBVA2013003000012.pica (DE-627)ELV021683530 (ELSEVIER)S1443-9506(13)00071-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Sakakura, Kenichi verfasserin aut Pathophysiology of Atherosclerosis Plaque Progression 2013transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Elsevier Nakano, Masataka oth Otsuka, Fumiyuki oth Ladich, Elena oth Kolodgie, Frank D. oth Virmani, Renu oth Enthalten in Elsevier Eggertsen, L. ELSEVIER Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape 2017 Amsterdam [u.a.] (DE-627)ELV000398209 volume:22 year:2013 number:6 pages:399-411 extent:13 https://doi.org/10.1016/j.hlc.2013.03.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 22 2013 6 399-411 13 045F 610 |
| allfieldsSound |
10.1016/j.hlc.2013.03.001 doi GBVA2013003000012.pica (DE-627)ELV021683530 (ELSEVIER)S1443-9506(13)00071-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Sakakura, Kenichi verfasserin aut Pathophysiology of Atherosclerosis Plaque Progression 2013transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Elsevier Nakano, Masataka oth Otsuka, Fumiyuki oth Ladich, Elena oth Kolodgie, Frank D. oth Virmani, Renu oth Enthalten in Elsevier Eggertsen, L. ELSEVIER Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape 2017 Amsterdam [u.a.] (DE-627)ELV000398209 volume:22 year:2013 number:6 pages:399-411 extent:13 https://doi.org/10.1016/j.hlc.2013.03.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO 38.48 Marine Geologie VZ 38.90 Ozeanologie Ozeanographie VZ 42.94 Meeresbiologie VZ AR 22 2013 6 399-411 13 045F 610 |
| language |
English |
| source |
Enthalten in Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape Amsterdam [u.a.] volume:22 year:2013 number:6 pages:399-411 extent:13 |
| sourceStr |
Enthalten in Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape Amsterdam [u.a.] volume:22 year:2013 number:6 pages:399-411 extent:13 |
| format_phy_str_mv |
Article |
| bklname |
Marine Geologie Ozeanologie Ozeanographie Meeresbiologie |
| institution |
findex.gbv.de |
| topic_facet |
Plaque rupture Remodelling Plaque progression Pathophysiology Atherosclerosis Thin cap fibroatheroma |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape |
| authorswithroles_txt_mv |
Sakakura, Kenichi @@aut@@ Nakano, Masataka @@oth@@ Otsuka, Fumiyuki @@oth@@ Ladich, Elena @@oth@@ Kolodgie, Frank D. @@oth@@ Virmani, Renu @@oth@@ |
| publishDateDaySort_date |
2013-01-01T00:00:00Z |
| hierarchy_top_id |
ELV000398209 |
| dewey-sort |
3610 |
| id |
ELV021683530 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV021683530</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625134021.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.hlc.2013.03.001</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013003000012.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV021683530</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1443-9506(13)00071-1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">550</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">38.48</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">38.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">42.94</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Sakakura, Kenichi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Pathophysiology of Atherosclerosis Plaque Progression</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">13</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Plaque rupture</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Remodelling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Plaque progression</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Pathophysiology</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Atherosclerosis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Thin cap fibroatheroma</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nakano, Masataka</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Otsuka, Fumiyuki</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ladich, Elena</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kolodgie, Frank D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Virmani, Renu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Eggertsen, L. ELSEVIER</subfield><subfield code="t">Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape</subfield><subfield code="d">2017</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV000398209</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:22</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:399-411</subfield><subfield code="g">extent:13</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.hlc.2013.03.001</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">38.48</subfield><subfield code="j">Marine Geologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">38.90</subfield><subfield code="j">Ozeanologie</subfield><subfield code="j">Ozeanographie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">42.94</subfield><subfield code="j">Meeresbiologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">22</subfield><subfield code="j">2013</subfield><subfield code="e">6</subfield><subfield code="h">399-411</subfield><subfield code="g">13</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Sakakura, Kenichi |
| spellingShingle |
Sakakura, Kenichi ddc 610 ddc 550 bkl 38.48 bkl 38.90 bkl 42.94 Elsevier Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Pathophysiology of Atherosclerosis Plaque Progression |
| authorStr |
Sakakura, Kenichi |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV000398209 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 550 - Earth sciences |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl Pathophysiology of Atherosclerosis Plaque Progression Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma Elsevier |
| topic |
ddc 610 ddc 550 bkl 38.48 bkl 38.90 bkl 42.94 Elsevier Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma |
| topic_unstemmed |
ddc 610 ddc 550 bkl 38.48 bkl 38.90 bkl 42.94 Elsevier Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma |
| topic_browse |
ddc 610 ddc 550 bkl 38.48 bkl 38.90 bkl 42.94 Elsevier Plaque rupture Elsevier Remodelling Elsevier Plaque progression Elsevier Pathophysiology Elsevier Atherosclerosis Elsevier Thin cap fibroatheroma |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
m n mn f o fo e l el f d k fd fdk r v rv |
| hierarchy_parent_title |
Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape |
| hierarchy_parent_id |
ELV000398209 |
| dewey-tens |
610 - Medicine & health 550 - Earth sciences & geology |
| hierarchy_top_title |
Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV000398209 |
| title |
Pathophysiology of Atherosclerosis Plaque Progression |
| ctrlnum |
(DE-627)ELV021683530 (ELSEVIER)S1443-9506(13)00071-1 |
| title_full |
Pathophysiology of Atherosclerosis Plaque Progression |
| author_sort |
Sakakura, Kenichi |
| journal |
Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape |
| journalStr |
Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology 500 - Science |
| recordtype |
marc |
| publishDateSort |
2013 |
| contenttype_str_mv |
zzz |
| container_start_page |
399 |
| author_browse |
Sakakura, Kenichi |
| container_volume |
22 |
| physical |
13 |
| class |
610 610 DE-600 550 VZ 38.48 bkl 38.90 bkl 42.94 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Sakakura, Kenichi |
| doi_str_mv |
10.1016/j.hlc.2013.03.001 |
| dewey-full |
610 550 |
| title_sort |
pathophysiology of atherosclerosis plaque progression |
| title_auth |
Pathophysiology of Atherosclerosis Plaque Progression |
| abstract |
Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. |
| abstractGer |
Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. |
| abstract_unstemmed |
Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO |
| container_issue |
6 |
| title_short |
Pathophysiology of Atherosclerosis Plaque Progression |
| url |
https://doi.org/10.1016/j.hlc.2013.03.001 |
| remote_bool |
true |
| author2 |
Nakano, Masataka Otsuka, Fumiyuki Ladich, Elena Kolodgie, Frank D. Virmani, Renu |
| author2Str |
Nakano, Masataka Otsuka, Fumiyuki Ladich, Elena Kolodgie, Frank D. Virmani, Renu |
| ppnlink |
ELV000398209 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth |
| doi_str |
10.1016/j.hlc.2013.03.001 |
| up_date |
2024-07-06T20:13:35.618Z |
| _version_ |
1803861953734508544 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV021683530</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625134021.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.hlc.2013.03.001</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013003000012.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV021683530</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1443-9506(13)00071-1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">550</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">38.48</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">38.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">42.94</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Sakakura, Kenichi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Pathophysiology of Atherosclerosis Plaque Progression</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">13</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Atherosclerotic plaque rupture with luminal thrombosis is the most common mechanism responsible for the majority of acute coronary syndromes and sudden coronary death. The precursor lesion of plaque rupture is thought to be a thin cap fibroatheroma (TCFA) or “vulnerable plaque”. TCFA is characterised by a necrotic core with an overlying thin fibrous cap (≤65μm) that is infiltrated by macrophages and T-lymphocytes. Intraplaque haemorrhage is a major contributor to the enlargement of the necrotic core. Haemorrhage is thought to occur from leaky vasa vasorum that invades the intima from the adventitia as the intima enlarges. The early atherosclerotic plaque progression from pathologic intimal thickening (PIT) to a fibroatheroma is thought to be the result of macrophage infiltration. PIT is characterised by the presence of lipid pools which consist of proteoglycan with lipid insudation. The conversion of the lipid pool to a necrotic core is poorly understood but is thought to occur as a result of macrophage infiltration which releases matrix metalloproteinase (MMPs) along with macrophage apoptosis that leads to the formation of a acellular necrotic core. The fibroatheroma has a thick fibrous cap that begins to thin over time through macrophage MMP release and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA. Other causes of thrombosis include plaque erosion which is less frequent than plaque rupture but is a common cause of thrombosis in young individuals especially women <50 years of age. The underlying lesion morphology in plaque erosion consists of PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortious arteries.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Plaque rupture</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Remodelling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Plaque progression</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Pathophysiology</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Atherosclerosis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Thin cap fibroatheroma</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nakano, Masataka</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Otsuka, Fumiyuki</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ladich, Elena</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kolodgie, Frank D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Virmani, Renu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Eggertsen, L. ELSEVIER</subfield><subfield code="t">Seaweed beds support more juvenile reef fish than seagrass beds in a south-western Atlantic tropical seascape</subfield><subfield code="d">2017</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV000398209</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:22</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:399-411</subfield><subfield code="g">extent:13</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.hlc.2013.03.001</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">38.48</subfield><subfield code="j">Marine Geologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">38.90</subfield><subfield code="j">Ozeanologie</subfield><subfield code="j">Ozeanographie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">42.94</subfield><subfield code="j">Meeresbiologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">22</subfield><subfield code="j">2013</subfield><subfield code="e">6</subfield><subfield code="h">399-411</subfield><subfield code="g">13</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4018974 |