DOI: 10.1111/j.1939-3938.2012.01148.x
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PMID: 23176360
Issn Print: 1556-3693
Publication Date: 2012/12/01
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Excerpt
However, they did not search for mast cells in the post-mortem biopsy and they did not refer to the Kounis hypersensitivity acute coronary syndrome (Kounis, Mazarakis, Tsigkas, Giannopoulos, & Goudevenos, 2011).
Kounis syndrome combines acute coronary syndromes with conditions associated with mast cell activation, involving interrelated and interacting inflammatory cells, and includes anaphylactic or anaphylactoid and allergic or hypersensitivity insults. It is caused by preformed and newly synthesized inflammatory mediators released during the anaphylactic process. A subset of platelets bearing FCεRI and FCεRII receptors are also involved in the activation cascade.
Three variants of Kounis syndrome have been described so far. In type I variant coronary spasm, in normal or nearly normal coronary arteries, associated with anaphylactic reaction can progress to myocardial infarction. In type II variant culprit but quiescent pre-existing atheromatous disease combined with anaphylactic reaction can result in acute myocardial infarction. In type III variant, hypersensitivity to any implanted intracoronary stent components can result in devastating intrastent thrombosis.
Kounis syndrome is a hypersensitivity-induced coronary syndrome that shares nearly similar etiology, symptomatology, cardiac manifestations, and laboratory findings with two other hypersensitivity cardiac diseases including eosinophilic arteritis and hypersensitivity myocarditis (Kounis, Zavras, Soufras, & Kitrou, 1989).
Kounis syndrome can rarely complicate the Churg-Strauss syndrome or allergic granulomatous angiitis (bronchial asthma, eosinophilia, vasculitis affecting medium and small-sized arteries and veins in a variety of organs). Churg-Strauss syndrome is sometimes associated with coronary artery spasm (Buhaescu, Williams, & Yood, 2009) or with acute myocardial injury and repeated angina pectoris-like attacks (Suzuki et al., 1991).
Isolated eosinophilic arteritis is a cryptogenic form of coronary arteritis leading to vasospastic angina, myocardial infarction, coronary artery dissection, and sudden death. This entity can also complicate Churg-Strauss syndrome and seems to share the same pathophysiology with type I variant of Kounis syndrome. It is characterized by eosinophilic infiltration of adventitia, media, and intimal subendthelium together with diffusely distributed mast cells (Arena et al., 2010). Eosinophils are bone marrow-derived granulocytic leukocytes, which normally reside in tissues and express H4 histamine receptors and play an important role in the pathophysiology of coronary spasm. Eosiniphilic receptors facilitate eosinophil chemotaxis toward mast cells, which are the major producers of an array of inflammatory soluble mediators, which can induce Kounis syndrome. Soluble mediators secreted by mast cells and eosinophils also modulate reciprocal interactions between these two cells in the so called "allergic effector unit" (Minai-Fleminger, & Levi-Schaffer, 2009). Eosinophilic coronary arteritis has been reported in association with hypersensitivity myocarditis in a patient suffering from bronchial asthma (Rupani, Amonkar, & Deshpande, 2010). The first report of eosinophilic coronary arteritis manifesting as angina pectoris culminated in fatal unstable angina (Kajihara et al., 1988).
Hypersensitivity myocarditis, on the other hand, is an inflammatory disease affecting the cardiac conduction system and the myocardial tissue manifesting mainly as a complication of drug therapy.
