Under the 2013 ACC/AHA guidelines, ASCVD risk assessment is directed at determining the patient’s absolute risk of develop- ing clinical coronary disease over the next 10 years. The mode of intervention is then determined by the individual’s degree of risk.
Factors in Risk Assessment
To assess the ASCVD risk for an individual, we need three kinds of information. Specifically, we need to (1) identify ASCVD risk factors, (2) calculate 10-year ASCVD risk, and (3) identify ASCVD risk equivalents.
Identifying ASCVD Risk Factors. Major risk factors that modify LDL treatment goals include positive risk factors (advancing age, African American race, hypertension, cigarette smoking, and low HDL cholesterol) and one negative risk factor (high HDL cholesterol). (LDL itself is not listed because the reason for counting these risk factors is to modify treatment of high LDL.)
We know that diabetes is a very strong predictor of develop- ing ASCVD. Accordingly, we no longer consider diabetes to be a risk factor. Instead, for the purpose of risk assessment, diabetes is now considered an ASCVD risk equivalent. That is, having diabetes is considered equivalent to having ASCVD as a predictor of a major coronary event.
Calculating 10-Year ASCVD Risk. The 2013 ACC/AHA cholesterol guideline defines high ASCVD risk as 7.5% or greater. Some people are automatically in this risk group—
specifically, those with existing ASCVD and those with diabetes. For all other people, 10-year risk must be calculated.
20–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–74 75–79
94 03 68 1011 1213
HDL (mg/dL) Points
50–5960 40–49 40
10 12
Point Total 10-Year Risk %
10-Year Risk ______%
00 12 34 56 78 109 1112 1314 1516 17
11 11 11 22 34 56 108 1216 2025 30
Systolic BP (mm Hg) If Untreated 120
120–129 130–139 140–159 160
0 01 12
If Treated 0 12 23 Total
Cholesterol Age 20–39
Points
160–199160 200–239 240–279 280
04 79 11
40–49Age
03 56 8
50–59Age
02 34 5
60–69Age
01 12 3
70–79Age
00 01 1
20–39Age
Points
Nonsmoker
Smoker 0
8
40–49Age 05
50–59Age 03
60–69Age 01
70–79Age 01
20–34 35–39 40–44 45–49 50–54 55–59 60–64 65–69 70–74 75–79
73 03 68 1012 1416
HDL (mg/dL) Points
50–5960 40–49 40
10 12
Point Total 10-Year Risk %
10-Year Risk ______%
99 1011 1213 1415 1617 1819 2021 2223 2524
11 11 12 23 45 68 1114 1722 3027
Systolic BP (mm Hg) If Untreated 120
120–129 130–139 140–159 160
0 12 34
If Treated 0 34 56 Total
Cholesterol Age 20–39
Points
160–199160 200–239 240–279 280
04 118 13
40–49Age
03 68 10
50–59Age
02 45 7
60–69Age
01 23 4
70–79Age
01 12 2
20–39Age
Points
Nonsmoker
Smoker 0
9
40–49Age 07
50–59Age 04
60–69Age 02
70–79Age 01
Fig. 50.3 ■ Tables for calculating Framingham Risk Prediction Scores.
To determine an individual’s 10-year risk of developing clinical coronary disease, simply circle the appropriate points for each of the five risk factors considered (age, total cholesterol, smoking status, HDL cholesterol, and systolic blood pressure) and then add up the points.
The point total indicates the 10-year risk. For example, a total of 13 points indicates a
Moderate Daily dose lowers LDL-C by approximately
30% to <50%
7.5% estimated 10-year ASCVD risk and age 40–75 years
Diabetes Type 1 or 2 age 40–75 years LDL-C 190 mg/dL
Clinical ASCVD
Age 75 years High-intensity statin (Moderate-intensity statin if not candidate for high-intensity statin)
ASCVD prevention benefit of statin therapy may be less clear in other groups In selected individuals, consider additional factors influencing ASCVD risk and potential ASCVD risk benefits and adverse effects, drug-drug interactions,
and patient preferences for statin treatment ASCVD Statin Benefit Groups
Heart healthy lifestyle habits are the foundation of ASCVD prevention.
In individuals not receiving cholesterol-lowering drug therapy, recalculate estimated 10-year ASCVD risk every 4–6 years in individuals aged 40–75 years without clinical ASCVD or
diabetes and with LDL-C 70–189 mg/dL.
Age >75 years OR if not candidate for high-intensity statin Moderate-intensity statin
High-intensity statin (Moderate-intensity statin if not candidate for high-intensity statin)
Moderate-intensity statin
Moderate- to high-intensity statin Estimated 10-year ASCVD risk 7.5%
High-intensity statin
Estimate 10-year ASCVD Risk with pooled cohort equations Adults age >21 years and
a candidate for statin therapy
Daily dose lowersHigh LDL-C by approximately 50%
Yes
Yes
Yes
Yes
Yes Yes Yes
No
No
No
No Definitions of High- and
Moderate-Intensity Statin therapy
Fig. 50.4 ■ Recommendations for statin therapy for ASCVD prevention.
total time spent exercising than on the intensity of exercise or improvements in fitness.
Smoking Cessation. Smoking cigarettes raises LDL cholesterol and lowers HDL cholesterol, thereby increasing the risk of ASCVD. Smokers should be strongly encouraged to quit—and nonsmokers should be urged not to start. Drugs to aid smoking cessation are discussed in Chapter 39.
Weight Control. Weight loss can reduce both LDL cholesterol and ASCVD risk. This is especially important for people with metabolic syndrome (discussed in an upcoming section).
Drug Therapy
Drugs are not the first-line therapy for lowering LDL cholesterol.
Rather, drugs should be employed only if TLCs fail to reduce LDL cholesterol to an acceptable level—and then only if the combination of elevated LDL cholesterol and the patient’s ASCVD risk category justify drug use. When drugs are used, it is essential that lifestyle modification continues because the beneficial effects of diet and drugs are additive; drugs alone may be unable to achieve the LDL goal. It is important to note that the principal benefit of drug therapy is primary prevention:
Drugs are much better at preventing or slowing ASCVD than at promoting regression of established coronary atherosclerosis.
Furthermore, because LDL cholesterol levels will return to pretreatment values if drugs are withdrawn, treatment must continue lifelong. Patients should be made aware of this requirement.
Table 50.5 shows properties of the drug families used to lower LDL cholesterol. The most effective agents are the HMG-CoA reductase inhibitors (e.g., atorvastatin [Lipitor]), usually referred to simply as statins. Lesser used alternatives are bile-acid sequestrants (e.g., cholestyramine) and niacin (nicotinic acid). Although fibrates are listed in Table 50.5, these drugs are used primarily to reduce levels of TGs—not LDLs. Treatment is initiated with a single drug, almost always a statin. If the statin is ineffective, a bile-acid sequestrant can be added to the regimen.
In addition to lowering LDL cholesterol, drugs may be used to raise HDL cholesterol. The most effective agents are niacin and the fibrates. However, virtually all of the drugs that we use to lower LDL cholesterol have the added benefit of Therapeutic Lifestyle Changes
Therapeutic lifestyle changes are nondrug measures used to lower LDL cholesterol. TLCs focus on four main issues: diet, exercise, weight control, and smoking cessation. These measures are first-line treatment for LDL reduction and should be implemented before drug therapy. However, TLCs can be a challenge because some people do not eat healthier diets or exercise. Physical conditions such as arthritis can limit attempts at exercise, and economic and time limitations can be a barrier to healthier eating.
The TLC Diet. This diet has two objectives: (1) reducing LDL cholesterol and (2) establishing and maintaining a healthy weight. The central feature of the diet is reduced intake of cholesterol and saturated fats: Individuals should limit intake of cholesterol to 200 mg/day or less and intake of saturated fat to 7% or less of total calories. Intake of trans fats—found primarily in snack crackers, commercial baked goods, and fried foods—should be minimized. (Many food manufacturers are adding “no trans fat” labels to their product labels, making shopping somewhat easier.)
If the basic TLC diet fails to lower LDL cholesterol ade- quately, ATP III recommends two additional measures: increased intake of soluble fiber (10 to 25 gm/day; oatmeal is a good source) and increased intake of plant stanols and sterols (2 gm/day). Plant stanols and sterols are cholesterol-lowering chemicals found (albeit in very small amounts) in certain vegetable oils (e.g., canola), nuts (walnuts are a good source), certain fruits, and most beans and many other vegetables. They are also found in some of the cholesterol-lowering margarines, commonly advertised as “buttery spreads” (see later in this chapter under Plant Stanol and Sterol Esters).
Exercise. An inactive lifestyle carries an increased risk of ASCVD. Conversely, participating in regular exercise lowers ASCVD risk. Running and swimming, for example, can decrease LDL cholesterol and elevate HDL cholesterol, thereby reducing risk. In addition, exercise can reduce blood pressure, improve overall CV performance, and decrease insulin resistance (important because many people with high cholesterol also have diabetes). Accordingly, ATP III encourages regular physical activity (defined as 30 to 60 minutes of activity on most days).
Improvements in the plasma lipid profile depend more on the
Adapted from 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Available at http://circ.ahajournals .org/content/early/2013/11/11/01.cir.0000437738.63853.7a.
High-Intensity Therapy Moderate-Intensity Therapy Low-Intensity Therapy
Daily dose lowers LCL-C on average
by ≥ 50% Daily dose lowers LDL-C on average
by ~30% to <50% Daily dose lowers LDL-C on average
by <30%
Atorvastatin: 40–80 mg
Rosuvastatin: 20 mg Atorvastatin: 10 mg
Rosuvastatin: 10 mg Simvastatin: 20–40 mg Pravastatin: 40 mg Lovastatin: 40 mg
Simvastatin: 10 mg Pravastatin: 10–20 mg Lovastatin: 20 mg TABLE 50.4 ■ High-, Moderate-, and Low-Intensity Statin Therapy
• Waist circumference 40 inches or more for most men or 35 inches or more for most women (these limits can vary depending on ethnicity, country, or geographic region within a country)
Treatment has two primary goals: reducing the risk of athero- sclerotic disease and reducing the risk of type 2 diabetes.
According to ATP III, basic therapy consists of weight control and increased physical activity, which, together, can reduce all symptoms of the metabolic syndrome. In addition, specific treatment should be directed at lowering blood pressure and TG levels. Patients should take low-dose aspirin to reduce the risk of thrombosis, unless they are at high risk of intracranial bleeds (hemorrhagic stroke).
Although the term metabolic syndrome is widely used, there is debate about its clinical relevance. In the CV community, most clinicians believe the term has great utility. By contrast, in the diabetes community, many clinicians feel the term is misleading, in that it implies the existence of a specific disease entity, even though it is defined only by a cluster of risk factors that may or may not have a common underlying cause. Fur- thermore, they point out that the risk associated with a diagnosis of metabolic syndrome is no greater than the sum of the risks of its components. Accordingly, until there is more proof that the metabolic syndrome actually exists, they believe the term serves no clinical purpose and hence should be avoided. This position was voiced in a joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. The American Heart Association and the National Heart, Lung, and Blood Institute countered with a joint statement of their own, reasserting their belief that the metabolic syndrome is an important clinical entity. Although the two camps disagree about whether the metabolic syndrome increasing HDL cholesterol, at least to some degree. This rise
of HDL, therefore, can be considered a beneficial “side effect.”