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Dyslipidemia and capillary rarefaction. A new relationship?
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Abstracts / Atherosclerosis 241 (2015) e32ee71
Aim. To assess whether lipoprotein(a) (Lp(a)) apheresis influences the severity of the angina and exercise tolerance in stable coronary heart disease (CHD) patients immediately after the 18-month treatment period and at long-term follow-up within the conventional guideline-driven therapy. Methods. The initial and 18 and 42-month follow-up analysis was done on 30 CHD patients with Lp(a) levels 50 mg/dL included in the Specific Lp(a) Apheresis for the Regression of Coronary and Carotid Atherosclerosis (LaRCA) study. On the atorvastatin background, Lp(a) immunoadsorption procedures (POCARD Ltd., Russia) were carried out on a weekly basis in 15 patients while the rest formed the control group. Results. After 18-month period, in the main group among patients with Canadian Cardiovascular Society class III-IV angina six out of seven improved in symptoms within the first several months, whereas in the control group some worsening of angina was observed in three patients (Table). Stress-test results positive for myocardial ischemia decreased to 40% in the main and remained unchanged in the control group. After 2 years, exercise tolerance was still significantly greater in the Lp(a) apheresis group (P¼0.01). Conclusion. Specific Lp(a) apheresis during 18 months resulted in the reduction of angina symptoms and exercise capacity improvement in comparison with the traditional approach. Lp(a) lowering strategy led to stabilization of the CHD course within two years of terminating immunoadsorption.
mulation, and lipid modification in sIA pathobiology. Methods: We analyzed 20 ruptured and 16 unruptured intraoperatively resected sIA walls using immunohistochemistry, and compared the results with the previously published data on Oil Red O -positive lipid accumulation, neovascularization, microhemorrhages, mast cells, and macrophages. Results: Apolipoprotein B-100 (apoB-100) was present in 36, apolipoprotein A-I (apoA-I) and hydroxynonenal-7 (oxidized LDL) in 35, and adipophilin in 32 sIAs. The accumulations were located mainly within the extracellular matrix. The median positively stained area of the total sIA wall surface area was 56% for apoA-I, 16% for apoB-100, 10% for hydroxynonenal-7, and 13% for adipophilin. According to our preliminary results, the expressions of these markers associated with the number of CD68- and CD163-positive macrophages, neovascularization, and wall degeneration. The apoB-100-positive staining associated with the lack of intact CD31positive endothelium. Both apolipoproteins showed increased amounts when mast cells and microhemorrhages were present. Accumulation of oxidized LDL associated with the presence of microhemorrhages. The adipophilin-positive wall area was largest in ruptured sIAs. Conclusions: Macrophages and mast cells may promote lipid accumulation in degenerated sIAs by degrading apolipoproteins and luminal endothelium. Inflammation and microhemorrhages may induce oxidation of the accumulated lipids. Lipid accumulation may promote remodeling, degeneration and rupture of the sIA wall.
EAS-0865. DYSLIPIDEMIA AND CAPILLARY RAREFACTION. A NEW RELATIONSHIP? A. Triantafyllou 1, P. Anyfanti 1, G. Triantafyllou 1, V. Gkolias 1, M. Mantzouranis 1, A. Pyrpasopoulou 2, X. Zabulis 3, E. Gavriilaki 1, S. Aslanidis 2, S. Douma 1. 1 3rd Dep. of Internal Medicine Papageorgiou GH Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, Greece; 2 2nd Propedeutic Dep. of Internal Medicine of Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, Greece; 3 Institute of Computer Science, Foundation for Research and Technology e Hellas, Heraklion, Greece Aim: Dyslipidemia is a well-established cardiovascular risk factor bearing a strong and indisputable correlation with cardiovascular morbidity and mortality. Capillary rarefaction, on the other hand, represents a forthcoming promising but rather understudied estimate of microvascular impairment in cardiovascular diseases. The aim of this study was to investigate the association between the lipid profile and capillaroscopy findings of the skin, in a population of normotensive individuals and hypertensive patients.
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EAS-0839. APOLIPOPROTEINS AND LIPIDS ACCUMULATE, BECOME OXIDATIVELY MODIFIED, AND ASSOCIATE WITH INFLAMMATION AND DEGENERATIVE CHANGES OF INTRACRANIAL ARTERY ANEURYSM WALLS € sen 2, S. Lehti 3, J. Hernesniemi 1, M. E. Ollikainen 1, R. Tulamo 1, J. Fro € 1, P.T. Kovanen 3. 1 Neurosurgery, Celsinki University Central Niemela Hospital, Helsinki, Finland; 2 Neurosurgery, Kuopio University Hospital, Kuopio, Finland; 3 Wihuri Research Institute, Wihuri Research Institute, Helsinki, Finland Aim: Saccular intracranial artery aneurysm (sIA) rupture causes subarachnoidal hemorrhage with 50% mortality. Chronic inflammation and vascular wall remodeling associate with sIA degeneration and rupture. The histopathological changes observed in sIA walls are also hallmarks of atherosclerotic plaques. We studied the role of lipoproteins, lipid accu-
Methods: We studied 2 groups of participants, one consisting of naïve, never-treated hypertensive patients with recent onset of hypertension and one of normotensive healthy volunteers. All participants underwent capillaroscopy examination in the dorsum of the upper limb fingers. Capillary density was estimated with the use of semi-automated software, specifically constructed for this purpose. Results: In total, 172 persons were included, 124 hypertensives and 48 normotensives, aged 43.4±11.9 years, 62 presenting with newly diagnosed dyslipidemia. Univariate analysis showed significant correlation between capillary density and HDL levels (r¼0.192, p¼0.015). In group analysis, the correlation remained statistically significant only for the normotensive group, in univariate (r¼0.474, p¼0.001) as well as in multivariate analysis after adjustment for other risk factors (p¼0.034). The patients diagnosed with dyslipidemia exhibited lower number of capillaries compared to controls (141.82 vs 154.9, p¼0.005), likewise independently of blood pressure levels (p¼0.009). Conclusions: This is the first study investigating the relationship between capillary density and dyslipidemia. Capillary rarefaction is more pronounced in individuals with dyslipidemia. The clinical significance and possible underlying pathophysiological mechanisms remain to be further investigated.
Abstracts / Atherosclerosis 241 (2015) e32ee71
Aim. To assess whether lipoprotein(a) (Lp(a)) apheresis influences the severity of the angina and exercise tolerance in stable coronary heart disease (CHD) patients immediately after the 18-month treatment period and at long-term follow-up within the conventional guideline-driven therapy. Methods. The initial and 18 and 42-month follow-up analysis was done on 30 CHD patients with Lp(a) levels 50 mg/dL included in the Specific Lp(a) Apheresis for the Regression of Coronary and Carotid Atherosclerosis (LaRCA) study. On the atorvastatin background, Lp(a) immunoadsorption procedures (POCARD Ltd., Russia) were carried out on a weekly basis in 15 patients while the rest formed the control group. Results. After 18-month period, in the main group among patients with Canadian Cardiovascular Society class III-IV angina six out of seven improved in symptoms within the first several months, whereas in the control group some worsening of angina was observed in three patients (Table). Stress-test results positive for myocardial ischemia decreased to 40% in the main and remained unchanged in the control group. After 2 years, exercise tolerance was still significantly greater in the Lp(a) apheresis group (P¼0.01). Conclusion. Specific Lp(a) apheresis during 18 months resulted in the reduction of angina symptoms and exercise capacity improvement in comparison with the traditional approach. Lp(a) lowering strategy led to stabilization of the CHD course within two years of terminating immunoadsorption.
mulation, and lipid modification in sIA pathobiology. Methods: We analyzed 20 ruptured and 16 unruptured intraoperatively resected sIA walls using immunohistochemistry, and compared the results with the previously published data on Oil Red O -positive lipid accumulation, neovascularization, microhemorrhages, mast cells, and macrophages. Results: Apolipoprotein B-100 (apoB-100) was present in 36, apolipoprotein A-I (apoA-I) and hydroxynonenal-7 (oxidized LDL) in 35, and adipophilin in 32 sIAs. The accumulations were located mainly within the extracellular matrix. The median positively stained area of the total sIA wall surface area was 56% for apoA-I, 16% for apoB-100, 10% for hydroxynonenal-7, and 13% for adipophilin. According to our preliminary results, the expressions of these markers associated with the number of CD68- and CD163-positive macrophages, neovascularization, and wall degeneration. The apoB-100-positive staining associated with the lack of intact CD31positive endothelium. Both apolipoproteins showed increased amounts when mast cells and microhemorrhages were present. Accumulation of oxidized LDL associated with the presence of microhemorrhages. The adipophilin-positive wall area was largest in ruptured sIAs. Conclusions: Macrophages and mast cells may promote lipid accumulation in degenerated sIAs by degrading apolipoproteins and luminal endothelium. Inflammation and microhemorrhages may induce oxidation of the accumulated lipids. Lipid accumulation may promote remodeling, degeneration and rupture of the sIA wall.
EAS-0865. DYSLIPIDEMIA AND CAPILLARY RAREFACTION. A NEW RELATIONSHIP? A. Triantafyllou 1, P. Anyfanti 1, G. Triantafyllou 1, V. Gkolias 1, M. Mantzouranis 1, A. Pyrpasopoulou 2, X. Zabulis 3, E. Gavriilaki 1, S. Aslanidis 2, S. Douma 1. 1 3rd Dep. of Internal Medicine Papageorgiou GH Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, Greece; 2 2nd Propedeutic Dep. of Internal Medicine of Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, Greece; 3 Institute of Computer Science, Foundation for Research and Technology e Hellas, Heraklion, Greece Aim: Dyslipidemia is a well-established cardiovascular risk factor bearing a strong and indisputable correlation with cardiovascular morbidity and mortality. Capillary rarefaction, on the other hand, represents a forthcoming promising but rather understudied estimate of microvascular impairment in cardiovascular diseases. The aim of this study was to investigate the association between the lipid profile and capillaroscopy findings of the skin, in a population of normotensive individuals and hypertensive patients.
Ă
EAS-0839. APOLIPOPROTEINS AND LIPIDS ACCUMULATE, BECOME OXIDATIVELY MODIFIED, AND ASSOCIATE WITH INFLAMMATION AND DEGENERATIVE CHANGES OF INTRACRANIAL ARTERY ANEURYSM WALLS € sen 2, S. Lehti 3, J. Hernesniemi 1, M. E. Ollikainen 1, R. Tulamo 1, J. Fro € 1, P.T. Kovanen 3. 1 Neurosurgery, Celsinki University Central Niemela Hospital, Helsinki, Finland; 2 Neurosurgery, Kuopio University Hospital, Kuopio, Finland; 3 Wihuri Research Institute, Wihuri Research Institute, Helsinki, Finland Aim: Saccular intracranial artery aneurysm (sIA) rupture causes subarachnoidal hemorrhage with 50% mortality. Chronic inflammation and vascular wall remodeling associate with sIA degeneration and rupture. The histopathological changes observed in sIA walls are also hallmarks of atherosclerotic plaques. We studied the role of lipoproteins, lipid accu-
Methods: We studied 2 groups of participants, one consisting of naïve, never-treated hypertensive patients with recent onset of hypertension and one of normotensive healthy volunteers. All participants underwent capillaroscopy examination in the dorsum of the upper limb fingers. Capillary density was estimated with the use of semi-automated software, specifically constructed for this purpose. Results: In total, 172 persons were included, 124 hypertensives and 48 normotensives, aged 43.4±11.9 years, 62 presenting with newly diagnosed dyslipidemia. Univariate analysis showed significant correlation between capillary density and HDL levels (r¼0.192, p¼0.015). In group analysis, the correlation remained statistically significant only for the normotensive group, in univariate (r¼0.474, p¼0.001) as well as in multivariate analysis after adjustment for other risk factors (p¼0.034). The patients diagnosed with dyslipidemia exhibited lower number of capillaries compared to controls (141.82 vs 154.9, p¼0.005), likewise independently of blood pressure levels (p¼0.009). Conclusions: This is the first study investigating the relationship between capillary density and dyslipidemia. Capillary rarefaction is more pronounced in individuals with dyslipidemia. The clinical significance and possible underlying pathophysiological mechanisms remain to be further investigated.