Cardiovascular disease (CVD), the leading cause of morbidity and mortality, represents a major global health and economic burden worldwide [1, 2]. The World Health Organization report has projected that approximately half of all deaths in developed countries will be due to CVD by 2020. CVD is a multifactorial disorder, which encompasses a broad range of injuries of the vasculature and heart including atherosclerosis, coronary heart disease leading to myocardial infarction, peripheral vascular disease, stroke, aneurysms, and cardiomyopathy [3–6] (Fig. 10.1). There is no single cause for CVD, but there are a range of risk factors, which increase the likelihood for clinical manifestations of cardiovascular disease. These risk factors for CVD include obesity, dyslipidemia, diabetes, hypertension, smoking, and aging as well as a positive family history and environmental factors [5, 7–9]. A significant number of studies have shown a close association among these cardiovascular risk factors. Indeed, hypertension, dyslipidemia, obesity, insulin resistance, and chronic hyperglycemia often coexist and synergistically enhance the risk for CVD-related deaths [1, 5, 7, 8]. Reports suggest that diabetes increases the risk of stroke and myocardial infarction with diabetic patients demonstrating a 1.7 times higher risk of CVD death than nondiabetic individuals . In addition, the risk for CVD including coronary disease and stroke is elevated with a rise in blood pressure [8, 10]. Smoking is an avoidable risk factor of CVD, and a person’s risk of CVD mortality can be reduced by 36% over 2 years upon cessation of smoking . The burden of CVD risk increases with age and can be decreased partly by modifying and monitoring other coexisting CVD risk factors . CVD can also result from environmental and demographic factors. The high prevalence of CVD and its risk factors among the general population have motivated research investigating the pathological mechanisms of CVD and to develop novel approaches to prevent the progression of this disease. This has led to a better understanding of the underlying pathogenic mechanisms for the development and progression of CVD.
|Title of host publication||Modulation of Oxidative Stress in Cardiovascular diseases|
|Editors||Sajal Chakraborti, Naranjan S. Dhalla, Madhu Dikshit, Nirmal K. Ganguly|
|Place of Publication||Singapore, Singapore|
|Number of pages||17|
|Publication status||Published - 2019|
Jha, J. C., Bose, M., & Jandeleit-Dahm, K. A. M. (2019). Modulation of Oxidative Stress in Cardiovascular Diseases. In S. Chakraborti, N. S. Dhalla, M. Dikshit, & N. K. Ganguly (Eds.), Modulation of Oxidative Stress in Cardiovascular diseases (pp. 237-253). Springer. https://doi.org/10.1007/978-981-13-8946-7_10