The purpose of this study is to estimate the prevalence of allergic diseases and atopy among patients with angiographically confirmed coronary artery disease as well as to assess levels of serum allergic inflammation markers in this population.
Cardiovascular disease (CVD) is one of the leading causes of death, disability and medical resources use worldwide. Atherosclerosis remains the basic pathology found in CVD. Based on theoretical knowledge and animal experimental models it can be hypothesized that allergic inflammation affects atherosclerotic plaque formation/disruption. The exact nature of such interaction remains unknown. The process most probably takes place at the molecular level and involves both: specific interleukin formation and mast cells recruitment. On the one hand some pro-allergic interleukins have been found to inhibit atherosclerotic plaque formation in experimental animal models. However, other hypothesis conclude that mediators released by mast cells might encourage hypoxemia of the heart muscle cells and thus promote their necrosis. Mast cells and eosinophils -typically associated with allergy - are both found in human heart muscle, cross sections of coronary arteries and atherosclerotic plaques. Atopic patients who are prone to IgE-mediated mast cell activation seem to run a lower risk of sudden cardiac death after myocardial infarction. It may be associated with the fact that atopy produces a mild haemostatic imbalance similar to that typical of aspirin - moderately long bleeding time, depressed platelet aggregability and delayed generation of thrombin in clotting blood. Tryptase, one of the mediators released from mast cells widely used marker of anaphylaxis, has recently been shown to be increased in sera of patients with angiographically significant narrowings in coronary arteries. These results are in accordance with the previous finding of increased total IgE (antibody involved in type I allergic reaction) post myocardial infarction. Allergic myocardial infarction (also known as Kounis syndrome) - a condition in which heart muscle ischemia results from allergic insult sometimes even in the absence of permanent coronary artery lesions - is another hint supporting the hypothesis of possible interaction between allergy and cardiovascular diseases. Despite relatively many reports studying the association at molecular, in vitro and clinical level, the research investigating the problem as a whole, connecting laboratory data with clinical picture, is scarce. Our research aims at providing epidemiological evidence on the prevalence of allergy and atopy as well as serum allergy markers profile in subjects with coronary artery disease. Our study is dedicated to post-coronary angiography subjects willing to express informed consent for study participation. Coronarography has been chosen as a verification tool for several reasons: * it gives more accurate diagnosis of clinically relevant coronary narrowings than basic ECG, ECG exercise test or coronary angioCT * it enables the distinction between typical angina pectoris and Prinzmetal's angina * it has become a common procedure in Poland giving a relatively large and diverse cohort of patients undergoing the procedure whom we could address
Study Type
OBSERVATIONAL
Enrollment
300
Clinic of Internal Medicine, Asthma and Allergy
Lodz, Poland
Prevalence of allergic diseases
Asthma, allergic rhinitis, allergic concjunctivitis, atopic dermatitis, contact eczema, drug, food and insect venom allergy will be assessed through a structured questionnaire based on ISAAC and ECRHS questions regarding allergy symptoms. Additionally: Asthma diagnosis is verified through basic spirometry, reversibility test, skin prick tests and/or serum specific IgE. Allergic rhinitis diagnosis is verified through skin prick tests and/or serum specific IgE.
Time frame: Within a month from study recruitment completion.
Serum tryptase
Systemic tryptase will be measured with ImmunoCAP fluorescence enzyme immunoassay in patients sera.
Time frame: Within a month from study recruitment completion.
Serum eosinophil cationic protein
Systemic eosinophil cationic protein (ECP) will be measured with ImmunoCAP fluorescence enzyme immunoassay in patients sera.
Time frame: Within a month from study recruitment completion.
Prevalence of atopy.
Atopy is defined as increased serum total/specific IgE and/or positive skin prick tests in the absence of relevant allergy clinical symptoms.
Time frame: Within a month from study recruitment completion.
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