Cardiac stimulants, early development

Body iron level and iron depletion play an important role in the gender differences seen in death from cardiac disease. There is a better correlation with heart disease mortality in iron levels compared with levels of cholesterol (5). It was found that risk of coronary heart disease (6) and carotid atherosclerosis (7) is associated with increased iron stores. However, impaired endothelium-derived nitric oxide activity may be without overt atherosclerosis in patients with risk factors and may be associated with the presence of atherosclerosis (4). Thus, endothelial dysfunction related to iron activity not only may be an early marker for cardiovascular risk but also may contribute to the pathogenesis of atherosclerosis (2) by the stimulation of low-density lipoproteins (LDL) and membrane lipid peroxidation (I) and may be a key to the understanding of early mechanism in the development of atheroma (7,8). Nakayama et al. (9) showed the role of heme oxygenase induction in the modulation of macrophage activation in atherosclerosis. However, Howes et al. (10) concludes that at the moment, the available evidence on iron hypothesis remains circumstantial. Moreover, Kiechl et al. (7) showed that the adverse effect of iron is hypercholesterolemia, In patients... 

Numerous neuroendocrine biomarkers correlate with severity of cardiac dysfunction. Heart failure is associated with increase in peripheral vascular resistance due to increases in sympathetic tone, norepinephrine, renin, angiotensin II, arginine vasopressin, and endothelin-1. The increased venous pressure causes atrial distension that stimulates production and release of atrial and brain natriuretic peptides (ANP, BNP) from the atria and ventricles, respectively. ANP inhibits the renin-angiotensin-aldosterone system. In humans and mammals, BNP has been found to be an early biomarker of left ventricular hypertrophy developing with doxorubicin cardiotoxicity, congestive heart failure, or occult dilated cardiomyopathy (Erkus et al. 2006 Walker 2006 Oyama, Sisson, and Solter 2007). 

A more frequent complication is restenosis of the angioplasty site which occurs in 25-30% of patients over 6-9 months " . Pathological studies in patients with recurrence of symptoms are infrequent but demonstrate proliferation of fibroblasts and vascular smooth muscle cells overlying and distinct from the traumatized atherosclerotic plaque . Similar lesions have been described in early atherosclerosis and there is evidence to suggest a role for platelets in the development of such lesions , possibly through release of platelet-derived growth factors which stimulate fibroblast and vascular smooth muscle proliferation . Thus, depletion or inhibition of platelets prevents the development of atherosclerosis in animal models and aspirin inhibits the accelerated coronary atherosclerosis which occurs in cardiac transplant recipients. Furthermore, restenosis is more frequent when there is evidence of a thrombus at the angioplasty site consistent with previous... 

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