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Ann Allergy Asthma Immunol. 2014 Apr;112(4):309-16. doi: 10.1016/j.anai.2013.09.017. Epub 2013 Oct 10.

Stress triggers coronary mast cells leading to cardiac events.

Author information

1
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Present address: Department of Internal Medicine, Jacoby Medical Center, New York, New York.
2
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Present address: Department of Psychiatry, Westchester Hospital, Mt Kisco, New York.
3
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts.
4
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Department of Internal Medicine, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Department of Biochemistry, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Department of Psychiatry, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts. Electronic address: theoharis.theoharides@tufts.edu.

Abstract

OBJECTIVE:

Stress precipitates and worsens not only asthma and atopic dermatitis but also acute coronary syndromes (ACSs), which are associated with coronary inflammation. Evidence linking stress to ACS was reviewed and indicated that activation of coronary mast cells (MCs) by stress, through corticotropin-releasing hormone (CRH) and other neuropeptides, contributes to coronary inflammation and coronary artery disease.

DATA SOURCES:

PubMed was searched (2005-2013) for articles using the following keywords: allergies, anaphylaxis, anxiety, coronary arteries, coronary artery disease, C-reactive protein, cytokines, chymase, histamine, hypersensitivity, interleukin-6 (IL-6), inflammation, mast cells, myocardial ischemia, niacin, platelet-activating factor, rupture, spasm, statins, stress, treatment, tryptase, and uroctortin.

STUDY SELECTIONS:

Articles were selected based on their relevance to how stress affects ACS and how it activates coronary MCs, leading to coronary hypersensitivity, inflammation, and coronary artery disease.

RESULTS:

Stress can precipitate allergies and ACS. Stress stimulates MCs through the activation of high-affinity surface receptors for CRH, leading to a CRH-dependent increase in serum IL-6. Moreover, neurotensin secreted with CRH from peripheral nerves augments the effect of CRH and stimulates cardiac MCs to release IL-6, which is elevated in ACS and is an independent risk factor for myocardial ischemia. MCs also secrete CRH and uroctortin, which induces IL-6 release from cardiomyocytes. The presence of atherosclerosis increases the risk of cardiac MC activation owing to the stimulatory effect of lipoproteins and adipocytokines. Conditions such as Kounis syndrome, mastocytosis, and myalgic encephalopathy/chronic fatigue syndrome are particularly prone to coronary hypersensitivity reactions.

CONCLUSION:

Inhibition of cardiac MCs may be a novel treatment approach.

PMID:
24428962
PMCID:
PMC4288814
DOI:
10.1016/j.anai.2013.09.017
[Indexed for MEDLINE]
Free PMC Article
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