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Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

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Coronary artery abnormalities in Hyper-IgE syndrome.

Alexandra F Freeman¹, Elizabeth Mannino Avila, Pamela A Shaw

¹Immunopathogenesis Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), 10 Center Drive, Bethesda, MD 20892-1899, USA. freemaal@mail.nih.gov

Journal of Clinical Immunology

|April 16, 2011

Summary

Coronary artery abnormalities like aneurysms and tortuosity are common in Hyper-IgE syndrome (HIES) patients. These findings suggest STAT3 mutations significantly impact vascular remodeling, independent of atherosclerosis.

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Area of Science:

Immunology
Cardiology
Genetics

Background:

Hyper-IgE syndrome (HIES) is a rare primary immunodeficiency.
It stems from autosomal dominant STAT3 mutations, leading to recurrent infections and connective tissue issues.
Coronary artery abnormalities are infrequently reported in HIES.

Purpose of the Study:

To determine the frequency and characteristics of coronary artery abnormalities in STAT3-mutated HIES patients.
To compare these findings with a matched non-HIES control group.
To investigate the association between cardiac risk factors and coronary artery abnormalities in HIES.

Main Methods:

Coronary artery imaging (CT or MRI) was performed on 38 HIES patients (ages 8-57).
Images were assessed for tortuosity, dilation, and aneurysms.
A control group of 33 age- and gender-matched individuals without HIES was also evaluated.

Main Results:

70% of HIES patients exhibited coronary artery tortuosity or dilation; 37% had aneurysms.
These incidences were significantly higher than in the non-HIES group (21% tortuosity/dilation, 3% aneurysms).
Hypertension was more prevalent in HIES and linked to vessel abnormalities; atherosclerosis was minimal.

Conclusions:

Coronary artery aneurysms and tortuosity are common findings in HIES.
The high prevalence of these abnormalities, despite low atherosclerosis, highlights STAT3's role in vascular remodeling.
STAT3 mutations appear to be a significant factor in human vascular remodeling and atherosclerosis development.