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Ischemic heart disease develops as a consequence of a number of etiological risk factors and always coexists with other disease states. These include systemic arterial hypertension and related left ventricular hypertrophy, hyperlipidemia, and atherosclerosis, diabetes and insulin resistance, heart failure, as well as aging. These systemic diseases with aging as a modifying condition, exert multiple biochemical effects on the heart that can potentially affect the development of ischemia/ reperfusion injury per se and interfere with responses to cardioprotective interventions.

Several traditional vascular risk factors are associated with proinflammatory alterations, including leukocyte activation, and predispose cerebral vasculature to thrombogenesis on inflammatory stimulation. Furthermore, accumulation of inflammatory cells, mainly monocytes/macrophages, within the vascular wall starts early during atherogenesis. During later disease stages, their activation can lead to plaque rupture and thrombus formation, increasing stroke risk. Chronic infections (eg, infection with Chlamydia pneumoniae or Helicobacter pylori) were found to increase the risk of stroke. In case-control studies, acute infection within the preceding week was a trigger factor for ischemic stroke. Acute and exacerbating chronic infection may act by activating coagulation and chronic infections and may contribute to atherogenesis.

The endothelium, the single layer of cells on the luminal surface of an artery, is a metabolically active interface between blood and tissue that modulates blood flow and nutrient delivery as well as regulating blood coagulation and thrombosis.4 The endothelium is also responsible for synthesis of the major vasodilators nitric oxide (NO), prostaglandins, and endothelium-derived hyperpolarizing factor (EDHF). NO, which is synthesized from L-arginine by the enzyme eNOS (endothelial NO synthase), is important not only for its vasodilator effects but also for its role in the inhibition of smooth muscle cell growth and proliferation, limiting of inflammation, and reduction of platelet aggregation. NO protects against ischemic stroke by increasing collateral flow to ischemic areas of the brain.5 Damage to the endothelium—whether gross denudation, disturbances in shear stresses, or the formation of atherosclerotic plaque—significantly impairs the dilatory and inhibitory functions. The increased activation of both endothelial and vascular cell nuclear factor and activator protein regulates the expression of genes that participate in atherogenic processes. Leukocyte-cell adhesion molecules form on the endothelium, and leukocyteattracting chemokines are produced.4 Ultimately, production of the potent vasoconstrictors ET-1 and angiotensin II, along with vasoconstrictor prostanoids, reduces the arterial lumen and leads to even greater complications in a lumen already constricted with arterial plaque.