The Human Heart As a Shock Organ in Anaphylaxis

Marone, Gianni; Bova, María; Detoraki, Aikaterini; Onorati, Anna Maria; Rossi, Francesca Wanda; Spadaro, Giuseppe

doi:10.1002/0470861193.ch11

Cited by 58 publications

(17 citation statements)

References 53 publications

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“…Activation of these critically positioned mast cells may directly contribute to cardiopulmonary failure. Cardiac mast cells in vitro release many of the classic mast cell mediators of anaphylaxis including PAF [100,101]. PAF is thought to be a critical factor in the development of anaphylactic shock through its ability to induce hypotension and cardiac dysfunction [102].…”

Section: Anaphylaxismentioning

confidence: 99%

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

Brown

Wilson

Metcalfe

2007

Clin Experimental Allergy

242

184

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SummaryMast cells have long been recognized for their role in the genesis of allergic inflammation; and more recently for their participation in innate and acquired immune responses. Mast cells reside within tissues including the skin and mucosal membranes, which interface with the external environment; as well as being found within vascularized tissues next to nerves, blood vessels and glandular structures. Mast cells have the capability of reacting both within minutes and over hours to specific stimuli, with local and systemic effects. Mast cells express the high affinity IgE receptor (FceRI) and upon aggregation of FceRI by allergen-specific IgE, mast cells release and generate biologically active preformed and newly synthesized mediators which are involved in many aspects of allergic inflammation. While mast cells have been well documented to be essential for acute allergic reactions, more recently the importance of mast cells in reacting through pattern recognition receptors in innate immune responses has become recognized. Moreover, as our molecular understanding of the mast cell has evolved, novel targets for modulation have been identified with promising therapeutic potential.

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Section: Anaphylaxismentioning

confidence: 99%

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

Brown

Wilson

Metcalfe

2007

Clin Experimental Allergy

242

184

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“…Cardiac and peripheral vascular symptoms dominate the clinical picture and are often the leading cause of death [5]. While the skin (urticaria and angioedema) and the respiratory tract (laryngeal oedema and bronchospasm) are the main organs involved in the early stages of anaphylaxis, dysfunction of the central and peripheral cardiovascular systems usually dictates the outcome of anaphylactic events [6]. Cardiovascular manifestations of anaphylaxis include hypotension and shock, cardiac arrhythmias, ventricular dysfunction and cardiac arrest [7].…”

Section: Introductionmentioning

confidence: 99%

Allergy and the cardiovascular system

Triggiani

Patella²,

Staiano

et al. 2008

Clinical and Experimental Immunology

155

147

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SummaryThe most dangerous and life-threatening manifestation of allergic diseases is anaphylaxis, a condition in which the cardiovascular system is responsible for the majority of clinical symptoms and for potentially fatal outcome. The heart is both a source and a target of chemical mediators released during allergic reactions. Mast cells are abundant in the human heart, where they are located predominantly around the adventitia of large coronary arteries and in close contact with the small intramural vessels. Cardiac mast cells can be activated by a variety of stimuli including allergens, complement factors, general anesthetics and muscle relaxants. Mediators released from immunologically activated human heart mast cells strongly influence ventricular function, cardiac rhythm and coronary artery tone. Histamine, cysteinyl leukotrienes and platelet-activating factor (PAF) exert negative inotropic effects and induce myocardial depression that contribute significantly to the pathogenesis of anaphylactic shock. Moreover, cardiac mast cells release chymase and renin that activates the angiotensin system locally, which further induces arteriolar vasoconstriction. The number and density of cardiac mast cells is increased in patients with ischaemic heart disease and dilated cardiomyopathies. This observation may help explain why these conditions are major risk factors for fatal anaphylaxis. A better understanding of the mechanisms involved in cardiac mast cell activation may lead to an improvement in prevention and treatment of systemic anaphylaxis.

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“…47 Activated mast cells degranulate and release an array of vasoactive and pro-inflammatory mediators, namely (1) preformed granule associated mediators, (2) newly generated lipid-derived mediators plus (3) cytokines and chemokines (Table 1). [48][49][50][51] Mast cells are widely distributed in tissues, particularly those with external environment contact (i.e. skin, gastrointestinal system, lung) but also in other organs such as the heart.…”

Section: Pathophysiologymentioning

confidence: 99%

“…49 In the heart they are located mainly between myocardial fibres (in close proximity to myocytes), around both large coronary vessels and small intramural coronary arteries, and in the arterial intima and adventitia. 49,51,52 Uniquely, heart mast cells can be directly activated by nonallergenic stimuli (e.g. anaphylatoxins C3a and C5a and substance P), 49,53 as well as by drugs such as muscle relaxants, protamine and radio-contrast media.…”

Section: Pathophysiologymentioning

confidence: 99%

Kounis syndrome: a narrative review

Fourie

2016

Southern African Journal of Anaesthesia and Analgesia

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Inflammatory mediators released from activated mast cells and basophils during hypersensitivity reactions have direct pathological effects on the myocardium and coronary vasculature. It was traditionally thought that cardiovascular signs and symptoms in anaphylaxis are largely due to peripheral vasodilation and increased vascular permeability. However, there is extensive evidence of primary cardiac involvement during hypersensitivity reactions, most notably coronary vasoconstriction as well as atherosclerotic plaque erosion and rupture, leading to angina pectoris and acute coronary syndromes. Furthermore, mast cells are well established as effector cells in atherosclerosis, through their effects on atherosclerotic plaque progression and destabilisation. It was noted over 30 years ago that cardiac patients have a markedly higher concentration of biologic amines (especially histamine) in their coronary vasculature, and, additionally, are hyper-reactive to the effects thereof. This is borne out by the disproportionate mortality rate of those with cardiac disease that suffer a hypersensitivity reaction. Kounis syndrome refers to angina pectoris or an acute coronary syndrome secondary to a hypersensitivity reaction, with the subtypes dependent on the underlying state of the coronaries and presence of a drug-eluting stent or not. This review will focus mainly on the aetiology, pathophysiology, diagnoses and treatment of this important syndrome.

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The Human Heart As a Shock Organ in Anaphylaxis

Cited by 58 publications

References 53 publications

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

Allergy and the cardiovascular system

Kounis syndrome: a narrative review

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