The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Attilio Maseri - One of the best experts on this subject based on the ideXlab platform.
-
widespread coronary inflammation in Unstable Angina
The New England Journal of Medicine, 2003Co-Authors: Antonino Buffon, Giovanna Liuzzo, Luigi M. Biasucci, Giuseppe Donofrio, Filippo Crea, Attilio MaseriAbstract:Background Inflammation within vulnerable coronary plaques may cause Unstable Angina by promoting rupture and erosion. In Unstable Angina, activated leukocytes may be found in peripheral and coronary-sinus blood, but it is unclear whether they are selectively activated in the vascular bed of the culprit stenosis. Methods We measured the content neutrophil myeloperoxidase content in the cardiac and femoral circulations in five groups of patients: two groups with Unstable Angina and stenosis in either the left anterior descending coronary artery (24 patients) or the right coronary artery (9 patients); 13 with chronic stable Angina; 13 with variant Angina and recurrent ischemia; and 6 controls. Blood samples were taken from the aorta, the femoral vein, and the great cardiac vein, which selectively drains blood from the left but not the right coronary artery. Results The neutrophil myeloperoxidase content of aortic blood was similar in both groups of patients with Unstable Angina (–3.9 and –5.5, with negative...
-
Pathogenic mechanisms in Unstable Angina.
Heart, 1999Co-Authors: Attilio Maseri, Giovanna Liuzzo, Luigi M. BiasucciAbstract:Many theories have been developed to explain the pathogenesis of Unstable Angina, but so far none has adequately explained all the known facts about this disease. Most patients with Unstable Angina have atheromatous deposits in their coronary arteries, and progressive stenosis caused by large atheromatous plaques was once thought to be responsible for the development of ischaemic symptoms. However, a study comparing the coronary arteries of patients who had a history of chronic stable Angina for at least two years with those who had a history of Unstable Angina failed to support this hypothesis.1 The study found that the severity of atheroma varies greatly between individuals and that patients with uncomplicated chronic stable Angina tended to have more severe atheroma than patients who have Unstable Angina as the first clinical manifestation of ischaemic heart disease. An alternative theory that has gained wide acceptance attributes Unstable Angina to the sudden fissure or rupture of an atherosclerotic plaque. This exposes the highly thrombogenic endothelium to the circulation, and a platelet rich thrombus rapidly develops over the site of plaque rupture. The thrombus obstructs but usually does not fully occlude the vessel. Blood flow may be occasionally reduced causing distal ischaemia but the myocardium remains viable. Although thrombosis undoubtedly has a central role in Unstable Angina, recent studies indicate that other mechanisms also play a part in some patients. It is therefore appropriate to reconsider the evidence concerning the aetiology of this condition. The first piece of evidence indicating that other mechanisms are present comes from clinical observations. One would expect that thrombosis over the site of plaque rupture would be an acute event, from which the patient would either recover or die. In either case the time course of the illness would be short, whereas Unstable Angina tends to wax and …
-
elevated levels of interleukin 6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie, <3 pg/mL, in healthy volunteers) was detectable in 23 (61%) of 38 patients with Unstable Angina but in only 6 (21%) of 29 with stable Angina (P<.01). Median interleukin-6 levels were 5.25 pg/m...
-
Elevated Levels of Interleukin-6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie,
Luigi M. Biasucci - One of the best experts on this subject based on the ideXlab platform.
-
widespread coronary inflammation in Unstable Angina
The New England Journal of Medicine, 2003Co-Authors: Antonino Buffon, Giovanna Liuzzo, Luigi M. Biasucci, Giuseppe Donofrio, Filippo Crea, Attilio MaseriAbstract:Background Inflammation within vulnerable coronary plaques may cause Unstable Angina by promoting rupture and erosion. In Unstable Angina, activated leukocytes may be found in peripheral and coronary-sinus blood, but it is unclear whether they are selectively activated in the vascular bed of the culprit stenosis. Methods We measured the content neutrophil myeloperoxidase content in the cardiac and femoral circulations in five groups of patients: two groups with Unstable Angina and stenosis in either the left anterior descending coronary artery (24 patients) or the right coronary artery (9 patients); 13 with chronic stable Angina; 13 with variant Angina and recurrent ischemia; and 6 controls. Blood samples were taken from the aorta, the femoral vein, and the great cardiac vein, which selectively drains blood from the left but not the right coronary artery. Results The neutrophil myeloperoxidase content of aortic blood was similar in both groups of patients with Unstable Angina (–3.9 and –5.5, with negative...
-
Pathogenic mechanisms in Unstable Angina.
Heart, 1999Co-Authors: Attilio Maseri, Giovanna Liuzzo, Luigi M. BiasucciAbstract:Many theories have been developed to explain the pathogenesis of Unstable Angina, but so far none has adequately explained all the known facts about this disease. Most patients with Unstable Angina have atheromatous deposits in their coronary arteries, and progressive stenosis caused by large atheromatous plaques was once thought to be responsible for the development of ischaemic symptoms. However, a study comparing the coronary arteries of patients who had a history of chronic stable Angina for at least two years with those who had a history of Unstable Angina failed to support this hypothesis.1 The study found that the severity of atheroma varies greatly between individuals and that patients with uncomplicated chronic stable Angina tended to have more severe atheroma than patients who have Unstable Angina as the first clinical manifestation of ischaemic heart disease. An alternative theory that has gained wide acceptance attributes Unstable Angina to the sudden fissure or rupture of an atherosclerotic plaque. This exposes the highly thrombogenic endothelium to the circulation, and a platelet rich thrombus rapidly develops over the site of plaque rupture. The thrombus obstructs but usually does not fully occlude the vessel. Blood flow may be occasionally reduced causing distal ischaemia but the myocardium remains viable. Although thrombosis undoubtedly has a central role in Unstable Angina, recent studies indicate that other mechanisms also play a part in some patients. It is therefore appropriate to reconsider the evidence concerning the aetiology of this condition. The first piece of evidence indicating that other mechanisms are present comes from clinical observations. One would expect that thrombosis over the site of plaque rupture would be an acute event, from which the patient would either recover or die. In either case the time course of the illness would be short, whereas Unstable Angina tends to wax and …
-
elevated levels of interleukin 6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie, <3 pg/mL, in healthy volunteers) was detectable in 23 (61%) of 38 patients with Unstable Angina but in only 6 (21%) of 29 with stable Angina (P<.01). Median interleukin-6 levels were 5.25 pg/m...
-
Elevated Levels of Interleukin-6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie,
Giovanna Liuzzo - One of the best experts on this subject based on the ideXlab platform.
-
widespread coronary inflammation in Unstable Angina
The New England Journal of Medicine, 2003Co-Authors: Antonino Buffon, Giovanna Liuzzo, Luigi M. Biasucci, Giuseppe Donofrio, Filippo Crea, Attilio MaseriAbstract:Background Inflammation within vulnerable coronary plaques may cause Unstable Angina by promoting rupture and erosion. In Unstable Angina, activated leukocytes may be found in peripheral and coronary-sinus blood, but it is unclear whether they are selectively activated in the vascular bed of the culprit stenosis. Methods We measured the content neutrophil myeloperoxidase content in the cardiac and femoral circulations in five groups of patients: two groups with Unstable Angina and stenosis in either the left anterior descending coronary artery (24 patients) or the right coronary artery (9 patients); 13 with chronic stable Angina; 13 with variant Angina and recurrent ischemia; and 6 controls. Blood samples were taken from the aorta, the femoral vein, and the great cardiac vein, which selectively drains blood from the left but not the right coronary artery. Results The neutrophil myeloperoxidase content of aortic blood was similar in both groups of patients with Unstable Angina (–3.9 and –5.5, with negative...
-
Pathogenic mechanisms in Unstable Angina.
Heart, 1999Co-Authors: Attilio Maseri, Giovanna Liuzzo, Luigi M. BiasucciAbstract:Many theories have been developed to explain the pathogenesis of Unstable Angina, but so far none has adequately explained all the known facts about this disease. Most patients with Unstable Angina have atheromatous deposits in their coronary arteries, and progressive stenosis caused by large atheromatous plaques was once thought to be responsible for the development of ischaemic symptoms. However, a study comparing the coronary arteries of patients who had a history of chronic stable Angina for at least two years with those who had a history of Unstable Angina failed to support this hypothesis.1 The study found that the severity of atheroma varies greatly between individuals and that patients with uncomplicated chronic stable Angina tended to have more severe atheroma than patients who have Unstable Angina as the first clinical manifestation of ischaemic heart disease. An alternative theory that has gained wide acceptance attributes Unstable Angina to the sudden fissure or rupture of an atherosclerotic plaque. This exposes the highly thrombogenic endothelium to the circulation, and a platelet rich thrombus rapidly develops over the site of plaque rupture. The thrombus obstructs but usually does not fully occlude the vessel. Blood flow may be occasionally reduced causing distal ischaemia but the myocardium remains viable. Although thrombosis undoubtedly has a central role in Unstable Angina, recent studies indicate that other mechanisms also play a part in some patients. It is therefore appropriate to reconsider the evidence concerning the aetiology of this condition. The first piece of evidence indicating that other mechanisms are present comes from clinical observations. One would expect that thrombosis over the site of plaque rupture would be an acute event, from which the patient would either recover or die. In either case the time course of the illness would be short, whereas Unstable Angina tends to wax and …
-
elevated levels of interleukin 6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie, <3 pg/mL, in healthy volunteers) was detectable in 23 (61%) of 38 patients with Unstable Angina but in only 6 (21%) of 29 with stable Angina (P<.01). Median interleukin-6 levels were 5.25 pg/m...
-
Elevated Levels of Interleukin-6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie,
Antonio Giuseppe Rebuzzi - One of the best experts on this subject based on the ideXlab platform.
-
elevated levels of interleukin 6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie, <3 pg/mL, in healthy volunteers) was detectable in 23 (61%) of 38 patients with Unstable Angina but in only 6 (21%) of 29 with stable Angina (P<.01). Median interleukin-6 levels were 5.25 pg/m...
-
Elevated Levels of Interleukin-6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie,
Sergio Altamura - One of the best experts on this subject based on the ideXlab platform.
-
elevated levels of interleukin 6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie, <3 pg/mL, in healthy volunteers) was detectable in 23 (61%) of 38 patients with Unstable Angina but in only 6 (21%) of 29 with stable Angina (P<.01). Median interleukin-6 levels were 5.25 pg/m...
-
Elevated Levels of Interleukin-6 in Unstable Angina
Circulation, 1996Co-Authors: Luigi M. Biasucci, Giovanna Liuzzo, Alessandra Vitelli, Antonio Giuseppe Rebuzzi, Sergio Altamura, Giuseppina Caligiuri, Gennaro Ciliberto, Claudia Monaco, Attilio MaseriAbstract:Background Elevated plasma levels of C-reactive protein have been found in the majority of patients with Unstable Angina. The evidence of elevated levels of acute-phase proteins in Unstable Angina is in line with a growing body of evidence that suggests that inflammation plays a role in this syndrome and is an indirect sign of increased production of interleukin-6, which is the major determinant of acute-phase–protein production by the liver. However, in Unstable Angina, there is no direct proof of the role played by interleukin-6. Methods and Results We measured levels of interleukin-6 in 38 patients with Unstable Angina at the time of their admission to the coronary care unit and in 29 patients with stable Angina. In the same groups of patients, we also measured C-reactive protein. Interleukin-6 (undetectable, ie,
