**5. References**

76 Dyslipidemia - From Prevention to Treatment

A study examined the associations of PM2.5 with heart rate variability, a marker of autonomic function, and whether metabolic syndrome modified these associations. It found significant correlations; which were stronger among individuals with metabolic syndrome than among those without it. This study proposed that autonomic dysfunction may be a mechanism through which PM exposure affects cardiovascular risk, especially among

Exposure to high and low air temperatures are associated with cardiovascular mortality, the underlying mechanisms are still under investigation. In a cohort in the US, 478 men with a mean age of 74.2 years were followed up from 1995 to 2008. Associations of three temperature variables, i.e. ambient, apparent, and dew point temperature with serum lipid profile were studied with linear mixed models by including possible confounders such as air pollution and a random intercept for each individual. HDL decreased -1.76%, and -5.58% for each 5°C increase in mean ambient temperature. For the same increase in mean ambient temperature, LDL increased by 1.74% and 1.87%. Similar results were also found for apparent and dew point temperatures. No changes were found in total cholesterol or triglycerides in relation to temperature increase. This study suggested that changes in HDL and LDL levels, which are associated with an increase in ambient temperature, may be among the underlying mechanisms of temperature-related cardiovascular mortality

A study in Taiwan found that increased 1-year average ozone, PM and nitrogen dioxide were associated with elevated blood pressure, total cholesterol, fasting glucose, and HbA1c. PM2.5 was more significantly associated with end-point variables than other gaseous pollutants (Chuang et al., 2011). A study on the association of blood markers of cardiovascular risk and air pollution in a national sample of the U.S. population found that PM10, but not gaseous air pollutants, is associated with blood markers of cardiovascular risk (Schwartz, 2001). In a study in Italy, the carboxyhaemoglobin concentration had an inverse correlation with HDL-C (Biava et al., 1992). In addition to the outdoor environment, the

In recent years, global climate change has affected many biological and environmental factors. Of its most important effects are the increasing levels of atmospheric carbon dioxide, ultraviolet radiation, and ocean temperatures. In turn, they have resulted in decreased marine phytoplankton growth and reduced synthesis of omega-3 polyunsaturated fatty acids. It is suggested that the detrimental effects of climate change on the oceans may reduce the availability of dietary omega-3, which may have detrimental effects on serum lipid

Climate change may alter concentrations of air pollutants or alterations in mechanisms of pollutant transport and thus influence individual and public health. The potential impacts of climate change and air pollution on lipid disorders is considered as an important area of investigation. This is of special concern for low- and middle-income countries, where the burden of air pollution and climate-related health disorders, and the burden of noncommunicable diseases are emerging. Effects of environmental factors on dyslipidemia should be considered in primordial and primary prevention of chronic diseases from early

health hazards of indoor pollution should be considered (Kaplan, 2010).

persons with metabolic syndrome (Park et al., 2010).

(Halonen et al., 2011).

profile (Kang, 2011).

**4. Conclusion** 

life.


**5** 

**Dyslipidemia and Type 2 Diabetes Mellitus:** 

Dyslipidemia is the major risk factors for macrovascular complications leading to cardiovascular disease (CVD) in type 2 diabetes mellitus (T2DM). In addition to this, endothelial dysfunction, platelet hyperactivity, impaired fibrinolytic balance and abnormal blood flow may accelerate atherosclerosis and increased risk of thrombotic vascular events (Colwell & Nesto, 2003). Macrovascular disease is the most common cause of morbidity and mortality in T2DM (Koskinen, 1998). Macrovascular disease is defined as illnesses affecting the larger arteries supplying the heart, brain, and the legs, thereby causing ischemic heart disease, cerebrovascular disease, and peripheral vascular disease (Thompson, 1999). In patients with diabetes, alteration in distribution of lipid increased risk of atherosclerosis. Specifically, insulin resistance and insulin deficiency was identified as phenotype of dyslipidemia in diabetes mellitus (Taskinen, 2003; Krauss & Siri, 2004; Chahil & Ginsberg, 2006). This was characterized with high plasma triglyceride level, low HDL cholesterol level and increased level of small dense LDL-cholesterol (Mooradian, 2008). In these patient also, the increment of free fatty-acid release is due to insulin resistance. With the presence of adequate glycogen stores in the liver, this will promote triglyceride production, which stimulates the secretion of apolipoprotein B (Apo B) and VLDL cholesterol (Mooradian, 2008). Hepatic production of VLDL cholesterol is enhanced due to disability of insulin to inhibit the release of free fatty-acid. Low HDL cholesterol levels were also associated with hyperinsulinemia. There are several associations between dyslipidemia and the increased risk of cardiovascular disease in patients with type 2 diabetes mellitus. Low HDL cholesterol and increased triglyceride levels may contribute to the increased risk of cardiovascular disease. In conjunction with increased small dense LDL cholesterol and low HDL cholesterol levels, further evidence suggests that acceleration of atherosclerosis in diabetes mellitus and insulin-resistant conditions is regulated by hypertriglyceridemia. Nevertheless, the association between LDL cholesterol and CHD risk is stronger compared to the association between hypertriglyceridemia and CHD risk. Type 2 diabetes is also associated with insulin resistance and hyperinsulinemia or syndrome X comprises hypertension, dyslipidemia,

**1. Introduction** 

**Implications and Role of Antiplatelet** 

**Agents in Primary Prevention of** 

**Cardiovascular Disease** 

*Department of Pharmacy, Faculty of Medicine,* 

*University of Malaya, Kuala Lumpur,* 

Hasniza Zaman Huri

*Malaysia* 

