Obesity

Overweight and obesity, although recognized independent risk factors for CHD, are typically not included in coronary risk charts ( Jones et al. 2001). One rationale for this is that obesity has significant comorbidity with hypertension, hyperlipidemia, and glucose intolerance, and in that sense it becomes a surrogate marker for these disorders with well-defined risk parameters. Nevertheless, the plateau in CHD prevalence in the United States is attributed in large measure to the epidemic of obesity, with nearly 27% of the population registering a body mass index greater than 30 kg/m2, the established cutoff for defining obesity (Flegal and Troiano 2000). This figure is 80% greater than that noted two decades prior. Longitudinal data, such as the 18-year Nijmegen Cohort Study, which examined changes in serum total cholesterol levels in a cohort of men and women, clearly demonstrate that weight gain correlates over time with increased cholesterol, and weight gain itself exerts a significantly greater influence on the rise in serum cholesterol than does initial body weight (Bakx et al. 2000). The distribution of weight gain is also increasingly recognized as an important independent risk factor for significant metabolic and atherosclerotic disease because of

Table 4-2. Ten-year Framingham cardiovascular risk estimation charts

Males

Table 4-2. Ten-year Framingham cardiovascular risk estimation charts

Males

Age

Points

20-34

-9

3S-39

-4

40-44

0

4S-49

3

S0-S4

6

SS-S9

8

60-64

10

6S-69

11

70-74

12

7S-79

13

Points

Total cholesterol

Age

Age

Age

Age

Age

(mg/dL)

20-39

40-49

50-59

60-69

70-79

<160

0

0

0

0

0

160-199

4

3

2

1

1

200-239

7

S

3

1

0

240-279

9

6

4

2

1

>280

11

8

S

3

1

Points

Age

Age

Age

Age

Age

20-39

40-49

50-59

60-69

70-79

Nonsmoker

0

0

0

0

0

Smoker

8

S

3

1

1

HDL (mg/dL)

Points

>60

-1

S0-S9

0

40-49

1

<40

2

Systolic BP (mm Hg)

If untreated

If treated

<120

0

0

120-129

0

1

130-139

1

2

140-1S9

1

2

>160

2

3

Point

10-year

total

cardiovascular risk (%)

<0

<1

0-4

1

S

2

6

2

7

3

8

4

9

S

10

6

11

8

12

10

13

12

14

16

1S

20

16

2S

>17

>30

Source. Expert Panel. JAMA 28S:2486-2489, 2001.

Source. Expert Panel. JAMA 28S:2486-2489, 2001.

Table 4-2. Ten-year Framingham cardiovascular risk estimation charts (continued)

Females

Age

Points

2G-34

-7

35-39

-3

4G-44

G

45-49

3

5G-54

6

55-59

8

6G-64

1G

65-69

12

7G-74

14

75-79

16

Points

Total cholesterol

Age

Age

Age

Age

Age

(mg/dL)

20-39

40-49

50-59

60-69

70-79

<16G

G

G

G

G

G

16G-199

4

3

2

1

1

2GG-239

8

6

4

2

1

24G-279

11

8

5

3

2

>28G

13

1G

7

4

Age Age Age Age Age

Nonsmoker 0 0 0 0 0

HDL (mg/dL) Points

5G-59 G

4G-49 1

Systolic BP (mm Hg) If untreated If treated

120-129 1 3

130-139 2 4

140-159 3 5

Point 10-year total cardiovascular risk (%)

13 2

14 2

15 3

16 4

17 5

21 14

22 17

23 22

Note. HDL=high-density lipoprotein; BP=blood pressure.

the association between truncal obesity and the metabolic syndrome, or syndrome X, which comprises a cluster of abnormalities including abdominal obesity, dyslipidemia with elevated triglycerides and low HDL cholesterol, hypertension, hypercoagulability, and evidence of insulin resistance (with or without overt glucose intolerance) (Bard et al. 2001; Grundy 1999). An estimated 22% of adults in the United States meet criteria for the metabolic syndrome, making this an intense focus of research among epidemiologists and clinicians (Ford et al. 2002).

Although obesity is not included in coronary risk charts for the aforementioned reasons, the association between obesity and cardiovascular disease is indeed strong, with compelling data demonstrating that even modest amounts of weight loss (e.g., 8.5% of body mass) may achieve significant benefits in cardiovascular risk, in part due to favorable effects on serum lipids and glucose homeostasis (Melanson et al. 2001; Rossner et al.

2000). A return to ideal body weight may reduce overall cardiovascular risk as much as 35%-55% (Wood and Joint European Societies Task

2001). Of particular relevance is the fact that recent estimates of obesity prevalence among patients with schizophrenia are 1.5 to 2 times that for the general population (Allison and Casey 2001; Allison et al. 1999a). The trend toward overweight and obesity was present among patients with schizophrenia, particularly females, prior to the advent of atypical antip-sychotics, but the concern has increased dramatically over the past 5 years due to evidence of profound weight gain with certain atypical antipsychotics, particularly olanzapine and clozapine, to an extent much greater than that achieved even with low-potency typical agents such as chlorprom-azine (Allison et al. 1999b; Blackburn 2000; Meyer 2001a). Moreover, the weight gain from atypical antipsychotics is primarily in the form of greater adiposity, not increases in lean muscle mass (Eder et al. 2001).

Smoking

Smoking cessation continues to be a primary focus of lifestyle modification aimed at reduction of cardiovascular risk because of the powerful association between smoking and CHD. A meta-analysis of prospective epidemiological studies spanning four decades of research established the relative risk for cardiovascular disease among smokers of 20 cigarettes per day at 1.78 (Law et al. 1997). The range of relative risk varies with age and is 4.46 at age 45, 3.07 at age 55, 1.78 at age 65, and 1.34 at age 75. Even among those who smoke only 1 cigarette per day, the relative risk of CHD compared with those who never smoke ranges from 1.93 at age 45 to 1.39 at age 65. Utilizing an epidemiological risk estimation method known as rate advancement period, one can calculate that, on average, smokers are expected to advance their risk of MI by approximately 11 years compared with never or former smokers (Liese et al. 2000). Discontinuing smoking may thereby reduce the risk of CHD by as much as 50%, with the overall risk returning to that of the general population after 20 years of abstinence (Eliasson et al. 2001; Villablanca et al. 2000). The relationship between smoking and CHD derives from numerous chemicals in cigarette smoke that act via multiple mechanisms to cause atherosclerosis, vascular injury, and increased coagulability (Villablanca et al. 2000). Limited exposure to such chemicals in the form of passive environmental smoke can increase the risk of cardiovascular disease as much as 30% (Smith et al. 2000).

Patients with schizophrenia have a prevalence rate of smoking nearly twice that of the general population, with estimates of 58%-88% in outpatient groups, and 79% or more in chronic inpatient settings (de Leon et al. 1995; Kelly and McCreadie 1999; Hughes et al. 1986). The connections between nicotine, smoking behavior, and schizophrenia are covered extensively in Chapter 5 of this volume, but it is worthwhile to note that those with schizophrenia not only have a higher prevalence of smoking, but also smoke more cigarettes on average, and more deeply, thereby increasing their exposure to mutagens and other noxious elements in cigarette smoke (Olincy et al. 1997). As a contributing risk factor for CHD, smoking remains the single most important lifestyle variable, and the greatest contributor to excess mortality from cardiovascular causes.

Hypertension

Hypertension does not appear to be more prevalent in patients with schizophrenia, although data are conflicting in this regard. One recent cross-sectional study of cardiovascular risk factors among 234 outpatients with schizophrenia in Melbourne, Australia, found no significant difference in the prevalence of hypertension compared with the general population (Davidson et al. 2001). Curkendall and colleagues' study of 3,022 Canadian patients with schizophrenia (mean age 49.6 years) found a 13.7% prevalence of hypertension, compared with a 16.7% prevalence noted in age- and gender-matched control subjects (Curkendall et al. 2001). The latter is comparable to the 15% prevalence obtained by a chart review of 179 state hospital patients in upstate New York (Bellnier et al. 2001). However, Cohn's naturalistic study of 133 long-term Canadian inpatients found a prevalence of hypertension in males and females of 28% and 24%, respectively, which was significantly greater than the values of 16% and 13% for male and female age- and gender-matched control subjects (Cohn and Remington 2001).

Similarly, the Patient Outcomes Research Team (PORT) study of 719 persons with schizophrenia found that 34.1% reported having been given a diagnosis of hypertension at some time by a physician, although only 19.7% stated that they currently had hypertension at the time of the survey (Dixon et al. 1999). Although patients with schizophrenia are prone to undertreat-ment of medical illnesses, 80.6% of those with active hypertension at time of survey were receiving antihypertensive therapy.

As with the other established risk factors, the association between hypertension and CHD has been elucidated through results of large, prospective clinical trials. The Nijmegen Cohort Study, a prospective cohort study of 7,092 Caucasian men and women with an 18-year follow-up, revealed that both systolic and diastolic blood pressure were independently associated with the likelihood of developing CHD. The significant risk ratios for systolic hypertension were 1.6 for men and 2.1 for women, and for diastolic hypertension 1.4 for men and 2.0 for women (Bakx et al. 2001). Data from a 32-year prospective follow-up study of 3,267 initially healthy male business executives showed that total mortality curves of the whole cohort increased significantly beyond 140 mm Hg systolic or 85 mm Hg diastolic (Strandberg et al. 2001). The impact of hypertension on CHD mortality is such that in patients with untreated hypertension and hyper-lipidemia, starting antihypertensive therapy in those ages 35-74 results in a greater net reduction in deaths from coronary artery disease than lipid-lowering treatment alone (Perreault et al. 1999).

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