Prevention and Assessment



Prevention and Assessment





17.1 Prevention of CAD

See also ASHD.

Circ 1999;100:988


Risk Assessment

See Table 17.1 and Figures 17.1 and 17.2 for assessment.


Smoking

Compared with other preventive interventions, smoking cessation is extremely cost-effective. The more intensive the intervention, the lower the cost. Intensive counseling and the nicotine patch are particularly useful (Jama 1997;278:1759).

AHCPR recommendations: Every person who smokes should be offered smoking cessation treatment at every office visit. Cessation treatments even as brief as 3 min per visit are effective. More intense treatment is more effective in producing long-term abstinence. Three treatment elements, in particular, are effective, and one or more of these elements should be included in smoking cessation treatment: (1) nicotine replacement therapy (nicotine patches or gum), (2) social support (clinician-provided encouragement and assistance), and (3) skills training/problem solving (techniques on achieving and maintaining abstinence).









Table 17.1 Categories of Risk Factors for CAD































































Causative Risk Factors


Cigarette smoking


Elevated blood pressure


Elevated serum cholesterol (or LDL cholesterol)


Alternative: elevated apolipoprotein B


Low HDL cholesterol


Diabetes mellitus


Coronary plaque burden as a risk factor


Age


Nonspecific ST-segment changes on resting EKG


Conditional Risk Factors


Triglycerides1


Small LDL particles1


Lp(a)1


Homocysteine1


Coagulation factors1


Plasminogen activating factor inhibitor-1


Fibrinogen


C-reactive protein


Predisposing Risk Factors


Overweight and obesity (especially abdominal obesity)2


Physical inactivity2


Male sex


Family h/o premature CHD


Socioeconomic factors


Behavioral factors (eg, mental depression)


Insulin resistance


Susceptibility risk factor


Left ventricular hypertrophy


1 These factors are considered conditional risk factors when serum levels are abnormally high.

2 Obesity and physical inactivity are counted as major risk factors by the AHA. (Circ 2000;101:111)








Figure 17.1 Calculation of CAD risk in men (ATP-III). (NIH)







Figure 17.1 continued

Substantial evidence exists for risk factor clustering in smokers. Smokers are more likely than nonsmokers to have elevated lipids and HT (Circ 1997;96:3243).

Post-CABG, smokers 1 yr after surgery had more than twice the risk for MI and reoperation compared withpts who stopped smoking. Pts who were still smoking at 5 yr after surgery had even more elevated risks for MI, reoperation, and increased risk for angina. Pts who started to smoke again within 5 yr after surgery had increased risks for reoperation and angina. No differences in outcome were found betweenpts who stopped smoking since surgery and nonsmokers (Circ 1996;93:42).







Figure 17.2 Calculation of CAD risk in women (ATP-III). (NIH)







Figure 17.2 continued

Data on exposure to passive smoking as assessed by self-report suggest that regular exposure increases risk of CAD among nonsmoking women (Circ 1997;95:237).

Data on smokeless tobacco are inconclusive: Adverse CV effects are less than those caused by smoking but are greater than those found in non-tobacco users (Arch IM 2004;164:1845).


BP

HCTZ, atenolol, captopril, clonidine, diltiazem, and prazosin have no long-term adverse effects on plasma lipids. Previously reported short-term adverse effects from using HCTZ are limited to nonresponders (Arch IM 1999;159:551).

MRFIT (7-yr multifactor intervention program for lowering BP and serum cholesterol and for smoking cessation among high-risk
men): At 16 yr, the intervention group had an 11.4% lower CAD mortality rate and a 20.4% lower rate for acute MI (Circ 1996; 94:946).


Lipids

The risk/benefit ratio supports use of statins in CAD. Elevated hepatic enzyme or CK levels < 10× nl require close monitoring but do not automatially mandate cessation of rx (Circ 2002;40:567).

In a study of 1017 young men followed 27-42 yr, the risk of developing CV disease in midlife correlated with earliest serum cholesterol levels (J Am Coll Cardiol 2002;40:2122; Nejm 1993;328:313). Statin therapy appears to be safe and effective in children with homozygous familial hyperlipidemia (Circ 2002;106:2231).

Inpts at high risk for development of CAD, LDL goal of < 70 mg/dL is a therapeutic option (J Am Coll Cardiol 2004;44:720).

In elderlypts (4736pts with mean age 72), baseline total, non-HDL, and LDL cholesterol levels and ratios of total, non-HDL, and LDL to HDL cholesterol are significantly related to CAD incidence. HDL cholesterol and triglycerides were not significant (SHEP program) (Circ 1996;94:2381).

In a small controlled study, cholesterol lowering with lovastatin produced a significant reduction in the number of episodes of ST-segment depression on AECG inpts with known ASHD (Circ 1997;95:324).

In middle-aged/elderly white men, a high level of fasting triglycerides is an independent risk factor for ASHD (Circ 1998;97:1029).

In a 5-yr prospective follow-up study of 2156 French Canadian men, Lp(a) was not an independent risk factor for ASHD but increased risk when associated with other lipid risk factors (J Am Coll Cardiol 1998;31:519).

Although current guidelines target reduction of LDL as the primary goal, rx ofpts with low HDL has been shown to reduce future event risk (Circ 2003;109:1809).


In all populations studied,pts who were prescribed lipid-lowering drugs remained without filled prescriptions for over 1/3 of the study year. After 5 yr, ˜50% of the surviving cohort had stopped using lipid-lowering rx altogether (Jama 1998;279:1458).


Activity

In a study of 25,714 adult men age 44 ± 10 yrs, low cardiorespiratory fitness was an independent predictor of CVD and all-cause mortality (Jama 1999;282:1547). In previously sedentary healthy adults, lifestyle and physical activity intervention was as effective as a structured exercise program in improving cardiorespiratory fitness and BP (Jama 1999;281:327). In the Physicians’ Health Study, habitual vigorous exercise reduced the risk of sudden death during exercise (Nejm 2000;343:1355).

In older (mean age 68 ± 5 yr)pts s/p MI, CABG, peak aerobic capacity improves with aerobic conditioning. The mechanism appears to be associated with peripheral skeletal muscle adaptations with no discernible improvements in CO (Circ 1996;94:323).

Regular weekly exercise can improve lipid profile independent of weight loss (Nejm 2002;347:1483). Walking and vigorous exercise are associated with a reduction in the incidence of CV events in postmenopausal women (Nejm 2002;347:716).

In a study of men with known ASHD who were enrolled in a program of physical exercise and low-fat diet, coronary stenoses progressed at a significantly slower rate than in the control group. Angiographic changes appeared to be largely due to chronic physical exercise (Circ 1997;96:2534).

Women with heart disease participating in a cardiac rehab program showed a 38% decrease in total cholesterol/HDL cholesterol over 5 yr (14% decrease in men). Total cholesterol decreased 20% in women and 8% in men, and LDL cholesterol decreased 34% in women and 15% in men (Circ 1995;92:773).


In a Finnish twin cohort study, leisure-time physical activity was associated with reduced mortality even after genetic and other familial factors were taken into account (Jama 1998;279:440).

Ornish: Intensive lifestyle changes may lead to regression of coronary atherosclerosis after 1 yr. More regression occurred after 5 yr than after 1 yr in an experimental group, while coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred in controls (Jama 1998;280:2001).


Exercise Prescription

If an individual is < 40 yr old and asymptomatic, no further workup is needed. If an individual is > 40 yr old, an exercise test is recommended if vigorous exercise is planned. If test is normal, no further restrictions are needed. If test is abnormal, the individual should be treated as if he/she has CAD. If the pt has no known CVD but major risk factors or sx that suggest CAD, an exercise test is needed.

In the absence of ischemia/significant arrhythmias, exercise intensity should approximate 50-80% of VO2max, as ascertained by exercise test (use target of 20 beat/min above resting HR until test performed); target HR is 50-75% of heart rate reserve:

Resting HR + (0.5 or 0.75) × (max HR − resting HR)

Target work intensity: Achieve training HR after 5-10 min of steady-state workload, expressed in METs. For walking on a level surface, activity can be prescribed as the step rate found on a treadmill to generate the desired HR.

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Jul 21, 2016 | Posted by in CARDIOLOGY | Comments Off on Prevention and Assessment

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