The CHD epidemic started in the 1950s affecting firstly western countries. Prior to the 1920s CHD was not common and caused only <10% of all deaths in the United States. However, by the 1950s this had escalated to >30% and it is now the leading cause of death. While its mortality has fallen by 50%, its incidence has decreased little or hardly at all. Mortality from CHD has also decreased among elderly persons, but information on changes in incidence in the elderly is limited. The main reasons for the decline in morbidity and mortality are due to changes in risk factors as well as improvement of treatment. Survival after myocardial infarction has improved and significant advances have also been made in the surgical and medical treatment of CHD.

Risk Factors and Prevention

Major risk factors for atherosclerosis have been well established. Epidemiological studies concluded that the causes for this epidemic are due to genetic factors in addition to other considerations such as age, smoking, hypertension, obesity, diabetes and cholesterol. Variations in disease occurrence in different nations still remain far from being fully explained. No single factor is responsible for CHD. It is a multifactorial disorder that is likely to be due to subclinical inflammation that many factors can contribute to, such as chronic infection, increased clotting tendencies and other irritants.

Genetics

It is believed that CVD results from many genes, each with a relatively small effect working alone or in combination with other modifier genes and/or environmental factors. Familial hypercholesterolaemia and hyperhomocystinuria are well-described examples. Insulin-like growth factor-1 (IGF-1) is believed to influence ageing and may be involved in the pathogenesis of CHD; however, a causative association is lacking. In the prospective (four-year) case-control study nested within the British Women’s Heart and Health Study, IGF-1 was inversely correlated with waist:hip ratio, fasting insulin, C-reactive protein, triglycerides and systolic blood pressure, and was positively correlated with HDL cholesterol but there was no evidence of CHD risk reduction in older women (60–79 years old).1 However, in another study high IGF-1 was independently associated with increased all-cause mortality and risk of development of heart failure in an elderly cohort of 642 individuals, aged 50–89 years, followed up for five years.2 Telomere length is another genetic factor associated with CV health and ageing. Telomere attrition is associated with elevated blood homocysteine and increased endothelial cell inflammatory markers and may underlie early fetal origins of CVD. The identification and characterization of genes that enhance prediction of disease risk and improve prevention and treatment of atherosclerosis need further genetic epidemiological studies.

Age and Sex

Prevalence of CHD increases with age from 2% for males and 0.5% for females at age 40–44 to peak at 18% and 12% respectively at age 85–89. Median age at onset is 67.5 years for males and 77.5 years for females. Lifetime risk is 35% for males and 28% for females. Prevalence of CHD decreased in individuals <65 and increased among those ≥75 years especially in women. CHD accounts for 22% of male deaths and 17% female deaths at all ages. Largely, epidemiology of CHD is changing from a fatal disease of middle-aged men to a more chronic condition of elderly women. CHD is intimately related to normal ageing in that its incidence continues to increase indefinitely with age. In a prospective study to investigate the influence of increasing age on incidence of CVD in 22 048 male physicians aged 40–84 who were free of major disease, incidence of CVD continued to increase to age 100 over 23 years of follow-up.3 Beginning at age 80, CVD was more likely to be diagnosed at death. The remaining lifetime risk of CVD at age 40 was 34.8%, 95% confidence interval (CI), 33.1–36.5% and at age 90 was 16.7% (95% CI, 12.9–20.6%). These findings suggest that people aged ≥80 may be living with a substantial amount of undiagnosed CVD. Additional research is needed to determine if continued screening and detection of CVD up to and beyond age 80 might help improve health in later life.

Ethnicity and Race

Prevalence of CHD and related risk factors vary among different ethnic groups. The pattern of this variation is complex, and could be related to genetic or socioeconomic differences. For example, populations of African descent living in Europe and the United States have a higher incidence of stroke and lower incidence of CHD than in their white counterparts. They have higher rates of hypertension, which may explain their high rate of stroke. Similarly, in China mortality from CHD is still lower than in western countries while mortality due to stroke is several times higher largely due to the high prevalence of hypertension. The lower rate of CHD may be explained by low rates of other risk factors including smoking.4 In the Indian subcontinent CVD is expected to increase rapidly and it will be the host of >50% of cases of heart disease in the world within the next 15 years. Risk factors for this epidemic are similar to those elsewhere in the world; however, ∼50% of CHD-related deaths occur in people <70 years compared with only 22% in the west. Also Asians living in western countries have a 50% greater premature mortality risk from CHD than the general population.

Diet

Dietary factors are related to the risk of CHD through several biological mechanisms. For example: (i) Fish consumption provides cardio-protective benefits through favourable effects on lipid profile, threshold for arrhythmias, platelet activity, inflammation, endothelial function, atherosclerosis and hypertension. Consumption of fish 1–2 times per week or at least 5–10% of energy from polyunsaturated fatty acids reduces the risk of CHD in older people relative to lower intakes.5 (ii) Antioxidants present in fruit and vegetables improve endothelial function, inhibit platelet activation and lower blood pressure. (iii) High salt consumption is directly related to hypertension, myocardial infarctions and strokes. Modest reductions in salt lower systolic blood pressure by at least 2 mmHg reducing the prevalence of hypertension by 17%, cardiac events by 30% and overall mortality by 20%. Older people will gain the greatest advantage from lowering their salt intake, most likely because they are more salt sensitive. (iv) Alcohol intake has a U-shaped relationship with the risk of CHD. ‘Moderate drinking’ defined as one drink for women and two drinks for men per day reduces the risk of CHD by 25%. Data relating to multivitamin use and the risk of CVD are inconsistent. Broader adherence to recommendations for daily intake of fruit, vegetables, low salt, alcohol in moderation and fish may take away 20–30% of the burden of CVD and result in one extra life-year if started early by the age of 40 years.6

Cholesterol

Cholesterol is a risk factor for CVD in the middle aged but appears to be less potent at older ages. However, dietary cholesterol is more detrimental in people with diabetes, regardless of age, because of dyslipidaemia and increased insulin resistance. In the Health, Ageing and Body Composition Study of 1941 community-dwelling elderly people aged 70–79, there were no significant associations between dietary fats and CVD risk, hazard ratio (HR) 1.47, 95% CI, 0.93–2.32 for the upper versus lower tertile, p for trend 0.10 after nine years of follow-up. However, dietary cholesterol was associated with increased CVD risk among older people with diabetes (3.66, 1.09–12.29).7 Possible reasons for these results are attenuated association between lipids and CV risk among older people, differences in baseline CV risk between old and young, or selective survivorship of older people leading to a population sample less vulnerable to environmental factors such as dietary fat.

Exercise

Although few studies have been conducted in the elderly, most have reported physical activity to be beneficial in preventing premature mortality but with some concerns about adverse effects especially in frail elderly with comorbidities. Physical activity may trigger sudden death and may have a higher risk of injury. However, in a Japanese study of 10 385 elderly (aged 65–84), most of whom were under treatment for pre-existing disease, every physical activity was associated with a reduced risk of all causes and CVD mortality after seven years of follow-up. Hazard ratios (95% CI) for CVD mortality among participants with ≥5 days of physical activity per week for the total sample and those with pre-existing diseases were 0.38 (0.22–0.55) and 0.35 (0.24–0.52) respectively, compared with no physical activity. In spite of possible adverse effects, this study indicated that elderly people with a pre-existing disease benefit from any level of physical activity in a dose-response relationship to mortality.8

Obesity

Obesity is a risk factor for CHD, poor health and excess mortality. Thresholds for normal weight or obesity defined as body mass index (BMI) were primarily based on evidence from studies in younger adults. In older people the relationship between weight and CV risk is more complex. It remains unclear whether overweight and obese cut points are overly restrictive measures for predicting mortality in older people. In a study to examine all cause and cause-specific mortality associated with underweight (BMI <18.5), normal weight (BMI 18.5–24.9), overweight (BMI 25.0–29.9), and obesity (BMI > or = 30.0) in an elderly cohort of 4677 men and 4563 women aged 70–75, mortality risk was lowest for overweight participants after 10 years of follow-up. Risk of death for overweight participants was 13% less than for normal weight participants (HR 0.87, 95% CI, 0.78–0.94). Minimum mortality risk was found at a BMI of 26.6 (95% CI, 25.7–27.5) in men and 26.26 (95% CI, 25.5–26.9) in women. Risk of death was similar for obese and normal weight participants (HR 0.98, 95% CI, 0.85–1.11).9 It appears that extreme obesity is harmful but overweight older people are not at greater mortality risk, and there is little evidence that dieting in this age group confers any benefit.

Smoking

Smoking is a major modifiable risk factor for CVD and causes 11% of all CVD-related mortality. Smoking contributes to the pathogenesis of CHD through promotion of atherosclerosis, triggering of coronary thrombosis, coronary artery spasm, cardiac arrhythmias and the reduced capacity of blood to deliver oxygen. The magnitude of the burden produced by smoking increases rather than decreases with ageing. While relative risk for smoking on CHD is similar in the elderly and middle aged, there is a twofold increase in excess absolute risk in the elderly. Benefits of cessation for older smokers are similar in magnitude to those of younger smokers who quit. The risk of CHD drops by 50% one year after smoking cessation and approaches that of a person who has never smoked within 3–4 years, even in individuals older than 60 years. Smoking cessation is highly cost-effective and should be viewed as a therapeutic rather than just a preventive intervention regardless of age.10

Socioeconomic Factors

There is an inverse relationship between socioeconomic status (SES) and prevalence of CV risk factors. People with lower SES tend to adopt unhealthier behaviours, such as smoking and unhealthy dietary habits, and seem to have an increased prevalence of CV risk factors resulting in socioeconomic inequalities in CV health. Although there is a strong social class gradient in CHD risk in middle age, the evidence in old age is limited. In a population-based study of 3761 British men aged 60–79 years there was a graded relationship between social class and CHD incidence after 6.5 years of follow-up. The HR for CHD incidence comparing social class V (unskilled workers) with social class I (professionals) was 2.14 (95% CI, 1.06–4.33; p for trend = 0.11) after adjustment for behavioural factors. Absolute difference in CHD risk between highest and lowest social classes was 4%. Socioeconomic inequalities in CHD persist in the elderly and are at least partly explained by behavioural factors. Improving behavioural factors (especially smoking) could reduce these inequalities by one third.11

Hypertension

Hypertension is a major risk factor for CVD in elderly. It reduces life expectancy by seven years. Prevalence of hypertension is 20% in developed countries. However, prevalence is significantly higher in older people affecting 70% of those >80 years. Black Americans develop hypertension earlier in life and it tends to be more severe than in the white population. There is a strong but complex association between blood pressure (BP) and age. Up to 50 years of age, systolic and diastolic BP rise in tandem. After age 50, systolic BP continues to rise, whereas diastolic BP tends to fall. Below age 50, diastolic BP is the major predictor of CHD risk, whereas above age 60, systolic BP is more important. There is also an enhanced risk for CHD associated with increased pulse pressure. The risk of a fatal CHD event doubles for every 20/10 mmHg increment above 115/75 mmHg. Absolute risk of adverse outcomes increases with age reaching 16-fold higher for persons 80–89 years than for those 40–49 years. A 10 mmHg reduction of systolic BP would predict a 50–60% lower risk of stroke death and a 40–50% lower risk of CHD death. In very old individuals (≥85 years old) the association between hypertension and mortality is weaker and treating hypertension reduces risk of death by 21%, risk of stroke by 30% and risk of cardiac failure by 64%. The target for BP is <140/90 mmHg in general and <130/80 mmHg in individuals with diabetes or chronic kidney disease. Evidence that excessive lowering of diastolic BP in older hypertensive individuals with wide pulse pressures may compromise cardiac outcomes (J curve) is inconsistent and no consensus exists regarding the minimum safe level of diastolic BP in these individuals.12

Diabetes Mellitus

Diabetes has been recognized as an independent major CV risk factor. In spite of various known metabolic and microvascular complications of diabetes, cardiovascular disease remains the most common cause of death in diabetic persons of all age groups affecting around 65–80%. Diabetes itself, in the absence of associated CHD constitutes a risk similar to those of non-diabetic individuals with a previous history of myocardial infarction. Increased risk of CVD in diabetes is not fully explained by traditional risk factors and could be related to increased insulin resistance. Risk of CHD and myocardial infarction rises by 30% and 14% respectively for every 1% increase in HbA1c. Whether hyperglycaemia itself is a risk for CHD is not very clear. Hyperglycaemia leads to an increase in oxidative stress which, in combination with other risk factors, may cause an accelerated progression of atherosclerosis.

Metabolic Syndrome

Metabolic syndrome is a constellation of central obesity, impaired fasting glucose, hypertension, high triglycerides and low HDL cholesterol. Pathophysiology of metabolic syndrome includes decreased physical activity and increased inflammation. In older people vitamin D deficiency,13 leading to increased parathyroid hormone and insulin resistance, in combination with low testosterone, leading to increased waist:hip ratio, are other contributing factors. Metabolic syndrome affects >40% of persons >60 years old and is more common in men. Comparative utility of metabolic syndrome versus its individual components for predicting adverse outcomes in older populations is not well established. In an Italian study of 2910 subjects aged ≥65 years, metabolic syndrome was associated with increased all-cause mortality in all subjects (HR 1.41, 95% CI, 1.16–1.72, p < 0.001), in men (1.42, 1.06–1.89, p < 0.017), and in women (1.47, 1.13–1.91, p < 0.004). It was also associated with increased CV mortality in all subjects (1.60, 1.17–2.19, p < 0.003), in men (1.66, 1.00–2.76, p < 0.051), and in women (1.60, 1.06–2.33, p < 0.025). Among metabolic syndrome components, all-cause mortality is better predicted by high glucose in all subjects (1.27, 1.02–1.59, p < 0.037) and in women (1.61, 1.16–2.24, p < 0.005) and by low HDL cholesterol in women (1.48, 1.08–2.02, p < 0.014), whereas CV mortality is better predicted by high glucose (2.17, 1.28–3.68, p < 0.004) and low HDL cholesterol (1.78, 1.07–2.95, p > 0.026) in women.14 In a similar US study of 4258 older people ≥65 years free of CVD, those with metabolic syndrome had a 22% higher mortality, relative risk (RR) 1.22, 95% CI, 1.11–1.34 compared with persons without metabolic syndrome after multivariable adjustment. Higher risk with metabolic syndrome was confined to persons having an elevated fasting glucose level >6.1 mmol l−1 (RR 1.41, 95% CI, 1.27–1.57) or hypertension (RR 1.26, 95% CI, 1.15–1.39) as one of the diagnostic criteria of metabolic syndrome. Persons having metabolic syndrome without high fasting glucose or metabolic syndrome without hypertension did not have higher risk (RR 0.97, 95% CI, 0.85–1.11 and 0.92, 0.71–1.19 respectively). Persons having both hypertension and high fasting glucose had 82% higher mortality (RR 1.82, 95% CI, 1.58–10.9).

In older people individual components of metabolic syndrome predict CVD mortality with equal or higher HR when compared with metabolic syndrome. Therefore, these findings suggest that the metabolic syndrome concept is a marker of CVD risk, but may not have any more advantage in predicting cardiac risk than its individual components.15

Frailty and Disability