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
