Allergy and the cardiovascular system

Authors

  • M. Triggiani,

    Corresponding author
    1. Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy,
    2. Center for Basic and Clinical Immunology Research (CISI), Naples, Italy
      M. Triggiani, Division of Clinical Immunology and Allergy, University of Naples Federico II, 80131 Naples, Via S. Pansini 5, Italy.
      E-mail: triggian@unina.it
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  • V. Patella,

    1. Unit of Allergy and Clinical Immunology, Department of Medicine ASL/SA3, General Hospital of Agropoli, Salerno, and
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  • R. I. Staiano,

    1. Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy,
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  • F. Granata,

    1. Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy,
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  • G. Marone

    1. Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy,
    2. Center for Basic and Clinical Immunology Research (CISI), Naples, Italy
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  • Conflicts of interest: The authors have declared that they have no conflict of interest.

M. Triggiani, Division of Clinical Immunology and Allergy, University of Naples Federico II, 80131 Naples, Via S. Pansini 5, Italy.
E-mail: triggian@unina.it

Summary

The 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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