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These studies suggest that cardiovascular diseases are influenced by inflammation, oxidative stress, genetic factors, environmental exposures, and specific population risks, with animal models and advanced genetic research being essential for developing new treatments.
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Cardiovascular diseases (CVDs) are the leading cause of global mortality, encompassing conditions such as ischemic heart disease, stroke, heart failure, and peripheral arterial disease. The World Health Organization (WHO) reported that nearly one-third of all deaths in 2019 were due to myocardial or vascular diseases, with myocardial infarction and stroke accounting for 85% of these deaths. The prevalence of CVDs continues to rise, driven by various risk factors and lifestyle changes.
Chronic inflammation and oxidative stress are major contributors to the development and progression of CVDs. Inflammatory cells contribute to vascular oxidative stress, which is closely linked to atherosclerosis. Established therapies for inflammatory disorders have shown protective cardiovascular effects by normalizing oxidative stress. Recent clinical trials have demonstrated that specific anti-inflammatory therapies, such as monoclonal antibodies against cytokines, can reduce cardiovascular mortality in patients with atherosclerotic disease.
South Asian (SA) migrants to high-income nations exhibit a significantly higher burden of coronary artery disease (CAD) compared to Europids, with a prevalence 1.5-2 times greater. Factors such as increased abdominal obesity, type 2 diabetes mellitus, and dyslipidemia are primary drivers of this excess burden. Lifestyle changes post-immigration, including sedentary behavior and dietary modifications, further exacerbate the risk. Novel biomarkers like leptin and adipokines may provide additional insights into the cardiometabolic risks in this population.
Environmental exposures, including ambient air pollution and heavy metals like arsenic, cadmium, and lead, significantly contribute to the development and severity of CVDs. These exposures can initiate or exacerbate pathophysiological processes such as blood pressure control, carbohydrate and lipid metabolism, and vascular function. Reducing environmental exposures through evidence-based clinical and public health strategies could substantially lower the global burden of CVD-related death and disability.
Type 2 diabetes is a major risk factor for CVD, significantly increasing the risk of cardiovascular events and mortality. Studies have shown that diabetic individuals have a higher prevalence of CVD, with diabetic men and women having twice and three times the risk, respectively, compared to non-diabetics. Key risk factors include elevated LDL cholesterol, low HDL cholesterol, and albuminuria. Preventive strategies targeting these factors, along with exploring new areas such as cytokines and growth factors, are crucial for reducing CVD risk in diabetic populations.
Genetic predisposition plays a significant role in the development of various cardiovascular conditions, from myocardial infarction to congenital heart disease. Advances in next-generation sequencing and the use of pluripotent human cells have enhanced our understanding of how genetic variations contribute to CVD. However, challenges remain in translating genomic localization into mechanistic insights that can inform targeted therapies.
Patients with end-stage renal disease (ESRD) on hemodialysis (HD) face a significantly higher risk of CVD, with mortality rates 20 times higher than the general population. Non-traditional risk factors such as chronic volume overload, anemia, inflammation, and oxidative stress contribute to this increased risk. Understanding these factors is essential for developing effective prevention and treatment strategies for CVD in HD patients.
The immune system plays a crucial role in the pathogenesis of many cardiovascular diseases. Atherosclerosis, the primary cause of coronary artery disease, stroke, and peripheral vascular disease, is widely recognized as a chronic inflammatory condition. Inflammation also contributes to atrial fibrillation and cardiac remodeling post-myocardial infarction. Advances in imaging and therapeutic strategies targeting the immune response offer new opportunities for managing CVDs.
Cardiovascular diseases remain a leading cause of global morbidity and mortality, driven by a complex interplay of genetic, environmental, and lifestyle factors. Advances in understanding the roles of inflammation, oxidative stress, and genetic predisposition are paving the way for more effective prevention and treatment strategies. Continued research and multidisciplinary collaboration are essential to address the growing burden of CVDs worldwide.
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