Serum immunoglobulin E response to myocardial infarction.

Szczeklik, Andrzej; Sładek, Krzysztof; Szczerba, Andrzej; Dropiński, Jerzy

doi:10.1161/01.cir.77.6.1245

Cited by 49 publications

(39 citation statements)

References 26 publications

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“…17 Several clinically relevant stimuli activate HHMC isolated from DCM, ICM, and control subjects. Serum IgE levels are increased in patients with several cardiovascular diseases, 13,14 and anti-IgE induces the release of preformed (histamine and tryptase) and de novo synthesized (LTC 4 ) mediators from cardiac mast cells. Moreover, SCF, a cytokine synthesized by fibroblasts 46 that induces mast cell growth in vitro 25,27 and in vivo, 28 activates HHMC.…”

Section: Discussionmentioning

confidence: 99%

“…Serum levels of IgE antibodies are increased in the circulation of patients with cardiovascular diseases. 13,14 A polyclonal antibody against the Fc⑀ portion of IgE cased a concentration-related (3ϫ10 -1 to 5 g/mL) histamine release from HHMC from control subjects and DCM and ICM patients. In these experiments, the percent histamine did not vary among three groups examined; however, when the absolute level of release was correlated per gram of wet tissue, the difference was highly significant (Fig 7).…”

Section: Mediator Release From Isolated Cardiac Mast Cells Induced Bymentioning

confidence: 99%

“…10 -12 Finally, serum IgE levels are increased in patients with coronary artery disease. 13,14 Taken together, these observations raise the possibility that local activation of cardiac mast cells might contribute, through the release of vasoactive mediators, to certain cardiovascular diseases. 15,16 Fibrosis is a hallmark of failing hearts in DCM and ICM.…”

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confidence: 95%

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Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

et al. 1998

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Background-We compared cardiac mast cell (HHMC) density and the immunological and nonimmunological release of mediators from mast cells isolated from heart tissue of patients with idiopathic dilated (DCM) (nϭ24) and ischemic cardiomyopathy (ICM) (nϭ10) undergoing heart transplantation and from control subjects (nϭ10) without cardiovascular disease. Methods and Results-HHMC density in DCM (18.4Ϯ1.6 cells/mm 2 ) and ICM (18.4Ϯ1.5 cells/mm 2 ) was higher than that in control hearts (5.3Ϯ0.7 cells/mm 2 ; PϽ.01). The histamine and tryptase contents of DCM and ICM hearts were higher than those of control hearts. The histamine content of the hearts was correlated with mast cell density (r s ϭ.91; PϽ.001). Protein A/gold staining of heart tissue revealed stem cell factor (SCF), the principal growth, differentiating, and activating factor of human mast cells, in HHMC secretory granules. Histamine release from cardiac mast cells caused by immunological (anti-IgE and rhSCF) and nonimmunological stimuli (Ca 2ϩ ionophore A23187) was higher in patients with DCM and ICM compared with control subjects. Immunological activation of HHMC induced a significantly greater release of tryptase and LTC 4 in patients with DCM and ICM compared with control subjects. Conclusions-Histamine and tryptase content and mast cell density are higher in failing hearts than in control hearts. SCF, present in secretory granules of HHMC, might represent an autocrine factor sustaining mast cell hyperplasia in heart tissue in these patients. The increased local release of fibrogenic factors (eg, histamine, tryptase, and leukotriene C 4 ) might contribute to collagen accumulation in the hearts of patients with cardiomyopathy. 1 Mast cells are present in human heart tissue 2,3 and in adventia and intima of coronary arteries of patients with coronary artery disease. [4][5][6] Moreover, the in vitro immunological activation of human heart tissue with anti-IgE induces the release of histamine and prostaglandin D 2 . 7,8 The concentration of histamine and the density of mast cells are increased in the arteries of cardiac patients, 4,5,9 and coronary arteries from cardiac patients are hyperresponsive in vitro to histamine. 4 Furthermore, in vivo administration of histamine and other mast cell-derived mediators (peptide LTC 4 ) in humans causes significant cardiovascular effects. 10 -12 Finally, serum IgE levels are increased in patients with coronary artery disease. 13,14 Taken together, these observations raise the possibility that local activation of cardiac mast cells might contribute, through the release of vasoactive mediators, to certain cardiovascular diseases. 15,16 Fibrosis is a hallmark of failing hearts in DCM and ICM. 17 The cells and the mediators responsible for fibroblast proliferation and collagen accumulation in failing hearts in DCM and ICM are largely unknown. Mast cells are involved in many types of inflammation and repair processes and are found in increased numbers in fibrotic tissues. For example, increased mast cell density has be...

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Section: Discussionmentioning

confidence: 99%

Section: Mediator Release From Isolated Cardiac Mast Cells Induced Bymentioning

confidence: 99%

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Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

et al. 1998

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“…20) Secreted IgE molecules bind to mast cells and stimulate them to release histamine, leukotrienes, and cytokines which further play major roles in perpetuating the inflammatory response and contraction of vascular smooth muscle cells. 20,21) We suggested that if mast cells contribute to the pathophysiological process of atherosclerotic plaques, stretching and tearing of the plaque as well as the involved vessel segment by stenting will be responsible for mast cell activation and kindling of an intense inflammatory reaction. A simple way to detect a mast cell-mediated reaction is possible by demonstrating an increased level of IgE which is the signal turning the mast cells on.…”

Section: Discussionmentioning

confidence: 99%

C-Reactive Protein and Immunoglobulin-E Response to Coronary Artery Stenting in Patients with Stable Angina

et al. 2003

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SUMMARYRecent reports indicate that inflammatory mechanisms play a crucial role in the pathogenesis of atherosclerosis and neointimal proliferation as well as coronary restenosis. To provide baseline data for further studies regarding stenting, restenosis and inflammatory response, we prospectively conducted a clinical study to investigate the time related response of plasma levels of immunoglobulin-E (IgE) and C-reactive protein (CRP) which are two different inflammatory markers mediated by different cytokines in stable patients who underwent elective coronary artery stenting. Thirteen consecutive stable patients who underwent coronary artery stenting were included in the study. Levels of IgE and CRP were determined pre-and poststent implantation on four consecutive days and at the end of the first as well as third month. Levels of these two markers were gradually elevated on postprocedure days while reaching peak values on the second and third days for IgE (initial 278 ± 335 IU/mL vs peak 350 ± 489 IU/mL, P = 0.01) and CRP (initial 0.5 ± 0 mg/dL vs peak 2.7 ± 3 mg/dL, P = 0.002), respectively. High levels gradually returned to baseline values determined at the end of the first and even third months after stent implantation implying an acute inflammatory reaction. Stent implantation seems not to cause any persistent and ongoing inflammatory response in the long term. (Jpn Heart J 2003; 44: 593-600)

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“…[4][5][6][7][8] Elevated immunoglobulin E (IgE) levels in particular have been suggested to protect patients with acute myocardial infraction (AMI) from its complications 9,10) . Brief periods of myocardial ischemia before the onset of an acute myocardial infarction have been indicated to improve left ventricular function and shortterm outcomes.…”

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confidence: 99%

Is the Beneficial Effect of Preinfarction Angina Related to an Immune Response?

et al. 2004

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SUMMARYImmune-mediated mechanisms are thought to play a key role in the development of coronary artery disease and its thrombotic complications. Preinfarction angina has been suggested to improve left ventricular function and short-term outcomes.The purpose of the present study was to investigate the relation between the immune response and in-hospital clinical course in preinfarction angina.We prospectively evaluated 93 patients. Forty-three patients exhibited preinfarction angina within 24 hours before the onset of acute myocardial infarction (AMI) (preinfarction angina group) and 50 patients were free from preinfarction angina (sudden onset group). The incidence of complications (heart failure, recurrent angina, arrhythmia and coronary interventions) and in-hospital mortality were assessed in the two study groups. We detected some immune markers, including white blood cells, C-reactive protein, immunoglobulins, and complement.White blood cells and CRP were significantly lower in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.005, respectively). Conversely, IgE and C 4 were significantly higher in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.001, respectively). The incidences of heart failure and severe arrhythmias were lower in the preinfarction group than in the sudden onset group (P < 0.005, P < 0.05 respectively).The beneficial effect of preinfarction angina may be associated with an immuneinflammatory response modified by a brief ischemic episode. (Jpn Heart J 2004; 45: 205-215)

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Serum immunoglobulin E response to myocardial infarction.

Cited by 49 publications

References 26 publications

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

C-Reactive Protein and Immunoglobulin-E Response to Coronary Artery Stenting in Patients with Stable Angina

Is the Beneficial Effect of Preinfarction Angina Related to an Immune Response?

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