%0 Journal Article
%T The Influence of Arsenic, Lead, and Mercury on the Development of Cardiovascular Diseases
%A Peter Jennrich
%J ISRN Hypertension
%D 2013
%R 10.5402/2013/234034
%X As a group, cardiovascular disease (CVD) is the leading cause of death worldwide. It killed twice as many people as infectious and parasitic disease and three times as many people as all forms of cancer. There are other crucial risk factors next to the major risk factors identified by the Framingham Heart Study. In the last few years, detailed studies showed the correlation between environmental pollution and the development of CVD. The question, which environmental toxin is particularly harmful, is answered by CERCLA Priority List of Hazardous Substances with the following toxins: arsenic, lead, and mercury. The effect of these potential toxic metals on the development of cardiovascular diseases includes pathomechanisms as the accumulation of free radicals, damage of endothelial nitric oxide synthase, lipid peroxidation, and endocrine influences. This leads to the damage of vascular endothelium, atherosclerosis, high blood pressure, and an increased mortality from cardiovascular diseases. The cardiovascular effects of arsenic, lead, and mercury exposure and its impact on cardiovascular mortality need to be included in the diagnosis and the treatment of CVD. 1. Introduction Cardiovascular disease is the genus for pathological change of heart, blood vessels, and blood flow. The fibrous change of arterial vascular walls is the mutual pathological correlate. Usually, it is caused by the damage of endothelium, which is the boundary layer between blood stream and vascular wall and has important functions in vasodilatation, modulation of inflammatory processes, and haemostasis. The interaction of nitric oxide (NO) via oxygen radicals, the reduction of nitric oxide synthase (NOS) cofactors as well as the inhibition of endothelial NOS itself through phosphorylation are regarded as central mechanisms of pathophysiology of endothelial dysfunction [1]. In the pathophysiology of atherosclerosis, the endothelial dysfunction fosters the adhesiveness of vascular wall for leukocytes, monocytes recruitment and transformation into foam cells, and finally the formation of vascular plaques. The endothelial dysfunction is considered as a great influence on the development of atherosclerosis and correlates with cardiovascular morbidity and mortality [2, 3]. In 2009, barely 42% of all cases of death were caused by cardiovascular diseases. Those diseases particularly result in death among elderly people: most of the deceased people (91%) were 65 years old and elder. All together, 150 334 men and 206 128 women died by the influence of vascular diseases. 60 153 people died of a
%U http://www.hindawi.com/journals/isrn.hypertension/2013/234034/