Future cardiology
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Patients who continue to suffer from severe and disabling angina pectoris, despite optimum treatment in terms of conventional pharmacological therapy and/or revascularization procedures, have been termed as having refractory angina pectoris. The future group of patients with refractory angina pectoris will be different from today's patients and represent a 'moving target' as risk factors, efficacy of treatment and indications continue to change. ⋯ There is strong evidence for SCS giving symptomatic benefits (decrease in anginal attacks), improved quality of life and improvement of functional status. In addition, SCS seems to be cost effective with a 'break-even' after approximately 15-16 months.
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Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation, such as allergies or hypersensitivity and anaphylactic or anaphylactoid insults that can involve other interrelated and interacting inflammatory cells behaving as a 'ball of thread'. It is caused by inflammatory mediators such as neutral proteases including tryptase and chymase, arachidonic acid products, histamine, platelet activating factor and a variety of cytokines and chemokines released during the activation process. Platelets with FCεRI and FCεRII receptors also participate in the above cascade. ⋯ Kounis syndrome has revealed that the same mediators released from the same inflammatory cells are present in acute coronary events of nonallergic etiology. These cells are not only present in the culprit region before plaque erosion or rupture but they release their contents just before an actual coronary event. Therefore, does Kounis syndrome represent a magnificent natural paradigm and nature's own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture showing a novel way towards our effort to prevent acute coronary syndromes? Drugs, substances targeting the stem cell factor that is essential for mast cell development, proliferation, survival, adhesion and homing as well as monoclonal antibodies and natural molecules that protect mast cell surface and stabilize mast cell membrane could emerge as novel therapeutic ways capable to prevent acute coronary and acute cerebrovascular events.