Fig. 10.8 • Genetics. Family history is the most important independent risk factor for atherosclerosis. Certain mendelian disorders are strongly associated with atherosclerosis (e.g., familial hypercholesterolemia) (Chapter 7), but these account for only a small percentage of cases. Most
Men 8.7 5.5 13.7 9.2 16.5 11.3 23.4 17 28.827.7 3836.8 57.556.4 Women
Fig. 10.8 Estimated10-yearriskforcoronaryarterydiseasein55-year-oldmenandwomenasafunctionofestablishedriskfactors—hyperlipidemia,hypertension,smoking,anddiabetes.BP,bloodpressure;ECG,electrocardiogram;HDL-C,high-densitylipoproteincholesterol;LVH,leftventricularhypertrophy.(Data from O’Donnell CJ, Kannel WB: Cardiovascular risks of hypertension: lessons from observational studies, JHypertension16[Suppl 6]:3, 1998.) http://ebooksmedicine.net
Table 10.3 Major Risk Factors for Atherosclerosis familial risk is related to multifactorial traits that go hand-in-hand with atherosclerosis, including hypertension, and, diabetes.
Age. Atherosclerosis usually remains clinically silent until lesions reach a critical threshold in middle age or later. Thus, the incidence of myocardial infarction increases 5-fold between 40 and 60 years of age. Death rates from IHD continue to rise with each successive decade.
Gender. All other factors being equal, premenopausal women are relatively protected against atherosclerosis (and its consequences) compared with age-matched men. Thus, myocardial infarction and other complications of atherosclerosis are uncommon in premenopausal women in the absence of other predisposing factors such as diabetes, hyperlipidemia, or severe hypertension. After menopause, however, the incidence of atherosclerosis-related disease increases and can even exceed that in men. Although a salutary effect of estrogen has long been proposed to explain this gender difference, clinical trials have shown no benefit of hormonal therapy for prevention of vascular disease. Indeed, estrogen replacement after 65 years of age appears to actually increase cardiovascular risk. In addition to atherosclerosis, gender also influences other factors that can affect outcome in patients with IHD, such as hemostasis, infarct healing, and myocardial remodeling.
Hyperlipidemia—and, more specifically, hypercholesterolemia—is a major risk factor for development of atherosclerosis and is sufficient to induce lesions in the absence of other risk factors. The main cholesterol component associated with increased risk is low-density lipoprotein (LDL) cholesterol (“bad cholesterol”); LDL distributes cholesterol to peripheral tissues. By contrast, high-density lipoprotein (HDL) cholesterol (“good cholesterol”) mobilizes cholesterol from developing and existing vascular plaques and transports it to the liver for biliary excretion. Consequently, higher levels of HDL correlate with reduced risk. Recognition of these relationships has spurred the development of dietary and pharmacologic interventions that lower total serum cholesterol or LDL and/or raise serum HDL, as follows:
High dietary intake of cholesterol and saturated fats (e.g., present in egg yolks, animal fats, and butter) raises plasma cholesterol levels. Conversely, diets low in cholesterol and/or containing higher ratios of polyunsaturated fats, lower plasma cholesterol levels.