International Task Force for Prevention of
Coronary Heart Disease
CORONARY HEART DISEASE: REDUCING THE RISK
The powerful role of overweight (body mass index (BMI) 8 ³ 25 kg/m2) and of obesity (BMI ³ 30 kg/m2, Table 1) may have been underemphasized in earlier guidelines on CHD prevention. Overweight is not only a cause of many other CHD risk factors (Figure 3) but is itself a risk factor for CHD. Reduction and prevention of overweight are critically important and cannot be too strongly urged. Obesity is a major cause of disease and is diagnosed when the BMI exceeds 30 kg/m2 (Table 1).
Figure 3: Higher age-standardized LDL-cholesterol and triglyceride, and lower HDL-cholesterol are associated with greater body mass index in men (left, n = 12 367) and women (right, n = 5 722) in the Münster Heart Study (PROCAM)., The geometric mean of triglyceride concentration is shown.
Table 1:
Cut-off points for body mass index
8
proposed by a World Health
Organization Committee for the classification of overweight
(WHO Expert Committee. Physical Status: the use and interpretation
of anthropometry. WHO Technical Report Series no. 854. Geneva:
WHO, 1995)
Cut-off points for body mass index
8
proposed by a World Health Organisation Committee for the classification
of overweight(WHO Expert Committee. Physical Status: the use and
interpretation of anthropometry. WHO Technical Report Series no. 854. Geneva: WHO, 1995)
|
body mass index |
WHO classification |
popular description |
|---|---|---|
|
<18.5 kg/m2 |
underweight |
thin |
|
18.5-24.9 kg/m2 |
- |
"healthy", "normal", or "acceptable" weight |
|
25.0-29.9 kg/m2 |
grade 1 overweight |
overweight |
|
30.0-39.9 kg/m2 |
grade 2 overweight |
obesity |
|
>40.0 kg/m2 |
grade 3 overweight |
morbid obesity |
The distribution of excess adipose tissue profoundly affects its role as a risk factor for CHD, a point which may not have received sufficient emphasis in the past. Specifically, excess of truncal and intra-abdominal fat (central obesity), has an important adverse influence on lipid levels, blood pressure and glucose tolerance and is in fact a risk factor for coronary disease. Thus, central obesity should be sought and treated with particular care. Central obesity is assessed by measuring the waist:hip ratio. The girth of the waist is measured in a horizontal plane at the level of the umbilicus and hip girth is measured in a horizontal plane at the widest part of the hips and buttocks. A waist:hip ratio of > 1 in men and > 0.85 in women is taken to indicate a so-called android fat distribution and central obesity. Abdominal skinfold thickness should also be checked and recorded. It has also been suggested that waist circumference (Table 2) may predict intra-abdominal fat as accurately as the waist:hip ratio.
Table 2: Upper limits for waist circumference in men and women. Level 1 is based on the WHO classification of overweight (BMI > 25 kg/m2) in combination with high waist:hip ratio (WHR ³ 0.95 in men and ³ 0.80 in women). Level 2 is based on the WHO classification of obesity (BMI ³ 30 kg/m2) in combination with high waist:hip ratio.
|
level 1 ("alerting zone") |
level 2 ("action level") |
|
|---|---|---|
|
men |
³ 94 cm (~37 inches) |
³ 102 cm (~40 inches) |
|
women |
³ 80 cm (~32 inches) |
³ 88 cm (~35 inches) |
Hypertension is an independent risk factor for stroke, coronary heart
disease and other cardiovascular diseases. Treatment decreases deaths
from stroke, coronary disease and heart failure and is of benefit in
both mild and severe hypertension, at all ages up to 75 years. A meta-analysis
of 14 randomised controlled trials of blood pressure reduction concluded
that treatment significantly reduced stroke incidence by 42% and CHD
incidence by 14% within 5 years. Hypertension tends to coexist with
metabolic and thrombogenic risk factors; this clustering is partly
related to truncal obesity and inheritance. Hypertension is defined
as a systolic blood pressure of 140 mmHg or greater and/or a diastolic
blood pressure of 90 mmHg or greater. This definition is widely
acknowledged. However, cardiovascular risk is related to blood
pressure over a wide range encompassing pressures below this cut-point.
An isolated increase in systolic pressure also confers increased risk
of coronary heart disease and requires treatment. The prevalence of
hypertension in the adult population of most countries is about 20%;
however prevalence increases steadily with advancing age, so that by
age 65 years 40% to 50% of the population is hypertensive. The NHANES
studies in the United States showed that between 1976 and 1988 the
detection of hypertension improved from 51% to 73%, while the proportion
of hypertensives receiving treatment increased from 31% to 55%. During
this period, the proportion achieving good blood pressure control improved,
but remained low, increasing from 10% to 29%. Since then, there has been
no further improvement in these figures. Moreover, in the last few years
the age-adjusted stroke rates has risen slightly and the rate of decline
in CHD has slowed down. The data from Europe are similar. Thus, a great
deal needs to be done to achieve better diagnosis and treatment.
It is important in diagnosis and management of hypertension that blood
pressure readings be taken in a reproducible fashion. In general,
readings should be taken from the left arm with the subject sitting
and the arm at heart level. One reading should be taken at the start
of the interview and a second at the end of the interview, the second
reading should be recorded. The importance of genetic factors is well
recognised in hypertension, and is evidenced by twin studies and by
the correlation of blood pressures among siblings. Nevertheless the
causal role of several life style and dietary habits on blood pressure
are increasingly well documented and are relevant to both prevention
and treatment.
2.2.3 Clinical evidence of cardiovascular disease
One recent advance in risk assessment is based on the recognition
that asymptomatic atherosclerosis can be strongly predictive of
increased risk. Using ultrasound imaging of both carotid arteries,
the presence of stenoses predicts a 6-fold increase in risk of
myocardial infarction compared with per-sons with normal arteries;
the presence of plaque(s) predicts a 4-fold increase, and thickening
of the intima and media without plaque or stenosis indicates a 2-fold
increase in risk. In patients without symptomatic cardiovascular
disease and without ischaemic ECG abnormalities, a quantitative Doppler
ultrasound study of the carotid arteries is of value when risk status,
and consequently choice of treatment, remain uncertain. Increased risk
is also conferred by the presence of atherosclerosis of the peripheral
arteries, as evidenced by a history of intermittent claudication, absent
foot pulses, doppler sonographic studies or a subnormal ratio of ankle
to brachial blood pressure. In one study, only 10% of patients with
peripheral vascular disease were found to have normal coronary arteries,
while 30% had advanced coronary atherosclerosis. Up to 50% of patients
with intermittent claudication have atherosclerosis of the carotid arteries
9.
and many of them have concomitant renovascular disease with or without
hypertension. In patients with peripheral vascular disease, the mortality
rate is two to three times greater than in the general age- and sex-matched
population; 10-20% of deaths in such patients are due to stroke and 40-60%
to coronary artery disease
10
10a
10b.
Evidence of peripheral arterial disease or stenosis confer the
same level of risk as historical or other evidence of cardiovascular
disease, and place the patient's management in the category of
secondary prevention.