Cardiovascular disease (CVD) covers all disease processes of the heart and blood vessels. In 2007, 46 623 Australians died from CVD, accounting for just over a third of all deaths in that year.1 CVD is the second largest contributor to the burden of disease in Australia after cancer—estimated at 18% and 19% respectively in 2003.2
Premature CVD is highly preventable. Tobacco smoking, raised blood pressure, elevated blood cholesterol, insufficient physical activity, overweight and obesity, poor nutrition, drinking at harmful levels and diabetes are major preventable risk factors for CVD. There is also recognition that socio-economic and psychosocial factors, such as low income, unemployment, depression and social isolation influence the development of CVD. Disease trends in Australia show that CVD impacts most heavily on population groups that suffer socio-economic disadvantage, including Australia's Aboriginal people and Torres Strait Islanders.1,2
Cigarette smoking contributes to CVD in a number of ways. Toxic products from cigarette smoke, in particular nicotine and carbon monoxide (CO), circulate in the bloodstream, interfering with the efficient working of the endothelium (the inner cellular layer of the arterial wall), eliciting blood fat abnormalities and impairing glucose regulation. Each effect is implicated in the development of atherosclerotic lesions (collections of cholesterol, fat and other matter) in the arterial walls. These collections narrow the arteries, gradually impairing blood flow, and making the arteries harder, less elastic, and more liable to rupture. The process leading to atherosclerosis—plaque (fatty streaks) deposited within the inner layers of the arteries—is slow and complex, often starting in childhood and progressing with age. Smoking also has a direct effect on platelets (blood cells involved in the clotting process), leading to increased activation and stickiness. This in turn causes an increased risk of thrombosis, or development of blood clots.3
Smoking a cigarette also temporarily increases heart rate and blood pressure and also affects the ability of the heart to contract. These circulatory changes result in increased work for the heart muscles, which in turn raises the body's demand for oxygen. At the same time, the body is deprived of oxygen through the effects of CO on reducing transport oxygen. The resulting imbalance in oxygen supply and demand promotes the complications of atherosclerosis. These include ischaemia (lack of oxygen due to poor blood supply), with resultant angina pectoris (chest pain or tightness) or myocardial dysfunction (poor heart muscle function).3,4
While nicotine and CO in tobacco smoke are strongly implicated in the processes leading to development of CVD, other chemicals may also be involved.3 There is now strong evidence that exposure to secondhand cigarette smoke is also a cause of coronary heart disease in non-smokers (see Chapter 4).
Coronary heart disease (CHD), also known as ischaemic heart disease, is the most common form of CVD, and the most common cause of sudden death in Australia.5 It occurs when the arteries supplying the heart become progressively narrowed by a fatty fibrous plaque or atheroma. This reduces the blood flow, forcing the heart to work harder to compensate, and can lead to symptoms of angina. If the plaque breaks up, a blood clot may form, blocking the artery completely. If not promptly treated, this can lead to death of vital heart muscle due to oxygen starvation (termed acute myocardial infarction or heart attack), or, in the worst case, sudden death.3
Smoking is a cause of CHD,3,6 increasing the risk of disease incidence by between two- and four-fold, the risk increasing with heaviness of smoking.7 Even light smoking significantly increases the risk of dying from CHD, the steepest increase in risk occurring in smokers of up to four cigarettes a day.8
Smokers who have CHD are more likely to die of the disease than non-smokers with the disease. The mortality rate for CHD among heavy smokers is up to three times higher than that of non-smokers.7 The heaviest burden of excess death due to tobacco-caused CHD is felt in early middle age. In Australia in 2004–05, 40% of all deaths due to CHD occurring in males between the ages of 35 and 39 were due to smoking. Among women aged 40–44, smoking caused about 34% of all deaths due to CHD. The effects of active smoking compared with no exposure are likely to be underestimated because most CVD studies have not excluded persons who had secondhand smoke exposure from the comparison group.
Lower tar and nicotine cigarettes have not been shown to reduce the incidence of CHD due to smokers increasing the number of cigarettes smoked per day or by taking deeper, faster, more or longer puffs. Thus, such cigarettes do not provide a lower risk alternative for smokers who cannot or do not wish to quit.3
The risks of myocardial infarction and death from CHD are lower among former smokers than among continuing smokers. The latest report of the US Surgeon General states that the risk halves within the first year and takes between 10–14 years before it approaches that of a lifetime non-smoker.3 The International Agency for Research on Cancer9 describes the benefits of quitting more conservatively:
'... there is a substantial reduction in risk of CHD compared with that of continuing smokers with the first two to four years of smoking abstinence, followed by a slower decline of risk, with risk approaching that of never smokers in fifteen to twenty years. For methodological reasons, the assessment of risk reduction is problematic within the first two years of cessation.'(p 342)
The International Agency for Research on Cancer also cites a reduced risk of 35% within two to four years for persons already suffering from CHD, and says studies on subjects without diagnosed CHD are 'compatible with this conclusion and point toward similar relative risk reduction.' 9(p 336).
A stroke occurs when blood flow to the brain is interrupted, leading to injury or death of brain tissue. This occurs most commonly because of arterial blockage caused by atherosclerosis or a blood clot, an event known as an ischaemic stroke. Happening less often, but more likely to be fatal when it does arise, is a haemorrhagic stroke, in which bleeding occurs from a leaking or ruptured arterial wall at a point weakened by atherosclerosis. Sometimes the artery stretches at the site of weakness, causing it to balloon out, forming an aneurysm. The bigger the aneurysm, the more likely it is to rupture, causing haemorrhage and a resultant stroke.
One in five people experiencing their first stroke episode will die within four weeks, and one in three will die within 12 months. Among the people who survive the first month after their first-ever stroke, about half will survive five years.10 Stroke is a major cause of disability in Australia. By the end of the first year following a stroke, about half of stroke survivors still require assistance with daily activities.10
Smoking is an important cause of stroke, with the risk of having a stroke rising with the amount of tobacco smoked.3,11 Smokers are one and a half times more likely to have a stroke than non-smokers.6,3
As with CVD, the impact of stroke caused by tobacco is greatest among the middle aged. In Australia in 2004–05, 40% of all deaths due to stroke in men aged between 35 and 39 were caused by smoking. The greatest impact occurred in women aged 40–44, among whom 35% of all stroke deaths were due to tobacco.12 Research has shown that the risk of having a stroke decreases steadily after quitting smoking, ex-smokers having the same risk as never-smokers after 5–15 years, depending on the study.6,3
Atherosclerotic peripheral arterial disease (PAD) occurs when blockages within the blood vessels prevent proper blood circulation. PAD most commonly occurs in the legs and feet, but it can also develop in the arms and hands. This may result in severe pain (claudication), especially when physically active. PAD can lead to death of part of the limb. Amputation may be necessary for relief of pain, and to prevent the development of gangrene. Given that it's the same atherosclerotic disease process, it is not uncommon for individuals with PAD to die from heart attack or stroke.13
Smoking is a cause of PAD. There is a strong dose–response relationship between the number of cigarettes smoked and the likelihood of developing PAD even after adjustment for other CVD risk factors.3 In Australia in 2004–05, about 37% of all deaths due to PAD in males aged over 35 were attributable to smoking, as were 30% of all PAD deaths in women aged over 35.12
Patients who suffer vascular-related leg pain are less likely to suffer serious obstruction of the arteries in their legs if they quit. Quitting smoking also reduces the risk of re-occlusion after peripheral vascular surgery.
Abdominal aortic aneurysm is a weakening of the wall of the aorta (the major artery carrying oxygenated blood from the heart to the body) in the region below the diaphragm. The weakening occurs as a result of atherosclerotic lesions developing in the aortic wall. The wall may eventually stretch and then leak or burst. Abdominal aortic aneurysm is frequently fatal.3
Smoking is a cause of abdominal aortic aneurysm, the risk rising with increased exposure to tobacco smoke. Smoking is one of the few currently modifiable risk factors for this disease. With increasing time after stopping smoking, the risk of developing an abdominal aneurysm appears to slowly decline.3
Sudden cardiac death describes death occurring due to sudden, unexpected loss of heart function. Most sudden death is due to CVD, in particular CHD accompanied by smoking. Cardiac dysrhythmias (irregular muscular contractions of the heart, also referred to as cardiac arrhythmias) also cause sudden cardiac death. Smokers have a three-fold greater risk of suffering sudden cardiac death than non-smokers.3,6, 7 Importantly, cigarette smoking may be the only modifiable risk factor for sudden cardiac death in the presence or absence or CHD.3
In Australia it is estimated that smoking causes 30–40% of all deaths due to cardiac dysrhythmias in men aged 35–59, and about one-third of all deaths due to cardiac dysrhythmias in women aged 35–44.12
Congestive heart failure (CHF) occurs when the heart becomes less able to pump blood through the body effectively. The heart may become enlarged or thicken, and fluid may collect in lungs (causing shortness of breath) or in other parts of the body (causing swelling or weight gain). CHF usually occurs in individuals with a history of heart problems such as high blood pressure or coronary heart disease.14 As well as contributing to the disease processes that primarily lead to CHF, smoking is an independent risk factor for CHF.6
CHF sufferers experience high levels of disability and have a reduced life expectancy.6 In Australia, it is estimated that smoking causes 30–40% of all deaths due to CHF in men aged 35–59, and about one-third of all deaths due to CHF in women aged 35–44.12
In conclusion, cigarette smoking and exposure to secondhand cigarette smoke are major causes of CVD. The risk arises from atheroma narrowing the affected blood vessels and with a higher risk of acute thrombosis. The cardiovascular risks attributable to cigarette smoking escalate with smoking just a few cigarettes per day, low level exposure to secondhand cigarette smoke and the duration of smoking. Stopping cigarette smoking and eliminating exposure to secondhand cigarette smoke rapidly and substantially reduces the risks of various CVDs.
1. Australian Institute of Health and Welfare. Australia's health 2010. Australia's health series no. 12, cat. no. AUS 122. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468376
2. Begg S, Vos T, Barker B, Stevenson C, Stanley L and Lopez A. The burden of disease and injury in Australia 2003. cat. no. PHE 82. Canberra: Australian Institute of Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317
3. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
4. Benowitz N. Drug therapy: pharmacologic aspects of cigarette smoking and nicotine addiction. New England Journal of Medicine 1988;319(20):1318–30. Available from: http://content.nejm.org/cgi/content/brief/319/20/1318
5. Australian Institute of Health and Welfare. Cardiovascular disease mortality: trends at different ages. Cardiovascular disease series no. 31, cat. no. 47. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468344
6. US Department of Health and Human Services. The health consequences of smoking. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office of the Surgeon General, 2004. Available from: http://www.surgeongeneral.gov/library/smokingconsequences/
7. US Department of Health and Human Services. The health consequences of smoking: cardiovascular disease. Rockville, Maryland: Public Health Service, Office on Smoking and Health, 1983. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/pre_1994/index.htm
8. Bjartveit K and Tverdal A. Health consequences of smoking 1-4 cigarettes per day: response to G F Cope (E-letter). Tobacco Control 2006;15(1):71-2. Available from: http://tc.bmjjournals.com
9. International Agency for Research on Cancer. Reversal of risk after quitting smoking. IARC handbooks of cancer prevention, tobacco control, Vol. 11. Lyon, France: IARC, 2007. Available from: http://apps.who.int/bookorders/anglais/detart1.jsp?sesslan=1&codlan=1&codcol=76&codcch=22
10. Senes S. How we manage stroke in Australia. Cardiovascular disease series no.24, cat. no. CVD 31. Canberra: Australian Institute of Health and Welfare, 2006. Available from: http://www.aihw.gov.au/publication-detail/?id=6442467815
11. Doll R, Peto R, Boreham J and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. British Medical Journal (Clinical Research Ed.) 2004;328(7455):1519. Available from: http://www.bmj.com/cgi/content/abstract/328/7455/1519
12. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004–05. P3 2625. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File/mono64.pdf
13. Australian Institute of Health and Welfare and National Heart Foundation of Australia. Heart, stroke and vascular diseases—Australian facts 2004. Cardiovascular disease series no. 22, cat. no. CVD 27. Canberra: AIHW and NHFA, 2004. Available from: http://www.aihw.gov.au/publications/cvd/hsvd04/hsvd04.pdf
14. National Heart Foundation of Australia. Let's talk about heart failure. Canberra: NHFA, February 2003. Available from: http://www.heartfoundation.org.au/document/NHF/heartfailureinfosheet.pdf