Sabtu, 04 September 2010

Heart Disease


What is Heart Disease ?

Heart disease is an umbrella term for a number of different diseases which affect the heart. The most common heart diseases are:

Coronary heart disease, a disease of the heart itself caused by the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium .

Ischaemic heart disease, another disease of the heart itself, characterized by reduced blood supply to the organ.

Cardiovascular disease, a sub-umbrella term for a number of diseases that affect the heart itself and/or the blood vessel system, especially the veins and arteries leading to and from the heart. Research on disease dimorphism suggests that women who suffer with cardiovascular disease usually suffer from forms that affect the blood vessels while men usually suffer from forms that affect the heart muscle itself. Known or associated causes of cardiovascular disease include diabetes mellitus, hypertension, hyperhomocysteinemia and hypercholesterolemia.

Pulmonary heart disease, a failure of the right side of the heart, not a good thing folks.

Hereditary heart disease, heart disease caused by unavoidable genetic factors since birth.

Hypertensive heart disease, heart disease caused by high blood pressure, especially localised high blood pressure .

Inflammatory heart disease, heart disease that involves inflammation of the heart muscle and/or the tissue surrounding it.

Valvular heart disease, heart disease that affects the valves of the heart.

Coronary Heart Disease

Coronary heart disease (CHD), also called coronary artery disease (CAD), ischaemic heart disease, and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death, and is also the most common reason for death of men and women over 65 years of age.

Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in calibre.

Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel, affecting the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material. This is a common misconception many have had.

Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.

As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.

A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.

An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary heart disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack).

Blood Flow to Heart

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth.

Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses as such exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks the rest being due to plaque rupture/ spasm. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD.

CHD is associated with smoking, obesity, hypertension and a chronic sub-clinical lack of vitamin C. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.

Angina that occurs regularly with activity, upon awakening, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms, and may be administered transdermally, sublingually or orally. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It is treated with morphine, oxygen, intravenous nitroglycerin, and aspirin. Interventional procedures such as angioplasty may be done.

Heart Disease Risk factors

The following are confirmed independent risk factors for the development of CAD, in order of decreasing importance:

*Hypercholesterolemia (specifically, serum LDL concentrations)
*Smoking
*Hypertension (high systolic pressure seems to be most significant in this regard)
* Hyperglycemia (due to diabetes mellitus or otherwise)

Hereditary differences in such diverse aspects as lipoprotein structure and that of their associated receptors, homocysteine processing/metabolism, etc.

Significant, but indirect risk factors include:

*Lack of exercise
*Stress
*Diet rich in saturated fats
*Diet low in antioxidants
*Obesity
*Men or Women over 65

Heart Disease Prevention

Coronary heart disease is the most common form of heart disease in the Western world. Prevention centers on the modifiable risk factors, which include decreasing cholesterol levels, addressing obesity and hypertension, avoiding a sedentary lifestyle, making healthy dietary choices, and stopping smoking. There is some evidence that lowering uric acid and homocysteine levels may contribute. In diabetes mellitus, there is little evidence that blood sugar control actually improves cardiac risk. Some recommend a diet rich in omega-3 fatty acids and vitamin C. The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary heart disease.

An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Among these markers are low density lipoprotein and asymmetric dimethylarginine. Patients with CHD and those trying to prevent CHD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats), limit carbohydrates and processed sugars to reduce production of Low density lipoproteins while increasing High density lipoproteins, keeping blood pressure normal, exercise and stop smoking. These measures limit the progression of the disease. Recent studies have shown that dramatic reduction in LDL levels can cause mild regression of coronary heart disease.

Diet and Heart Disease

It has been suggested that coronary heart disease is partially reversible using an intense dietary regime coupled with regular cardio exercise.

Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.

Cretan Mediterranean-style diet: The Seven Country Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and fat-rich animal products such as lamb, sausage and goat cheese. However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet in Corfu, another region of Greece, which had higher death rates.

The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause the development of endothelial dysfunction, a precursor to atherosclerosis.

Aspirin can reduce the incidence of cardiovascular events. The U.S. Preventive Services Task Force 'strongly recommends that clinicians discuss aspirin chemoprevention with adults who are at increased risk for coronary heart disease'. The Task Force defines increased risk as 'Men older than 40 years of age, postmenopausal women, and younger persons with risk factors for coronary heart disease (for example, hypertension, diabetes, or smoking) are at increased risk for heart disease and may wish to consider aspirin therapy'. More specifically, high-risk persons are 'those with a 5-year risk ≥ 3%'. A risk calculator is available.

Regarding healthy premenopausal women, the more recent Women's Health Study randomized controlled trial found no insignficant benefit from aspirin in the reduction of cardiac events; however there was a signficant reduction in stroke. Subgroup analysis showed that all benefit was confined to women over 65 years old. In spite of the insignficant benefit for women < 65 years old, recent practice guidelines by the American Heart Association recommend to 'consider' aspirin in 'healthy women' <65 years of age 'when benefit for ischemic stroke prevention is likely to outweigh adverse effects of therapy'.

Secondary prevention is preventing further sequelae of already established disease. Regarding coronary heart disease, this can mean risk factor management that is carried out during cardiac rehabilitation, a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardiac rehabilitation along with diet, smoking cessation, and blood pressure and cholesterol management .

Cardiovascular Disease

Cardiovascular disease refers to the class of diseases that involve the heart and/or blood vessels (arteries and veins). While the term technically refers to any disease that affects the cardiovascular system, it is usually used to refer to those related to atherosclerosis (arterial disease).

These conditions have similar causes, mechanisms, and treatments. In practice, cardiovascular disease is treated by cardiologists, thoracic surgeons, vascular surgeons, neurologists, and interventional radiologists, depending on the organ system that is being treated. There is considerable overlap in the specialities, and it is common for certain procedures to be performed by different types of specialists in the same hospital.

Most Western countries face high and increasing rates of cardiovascular disease. Each year, heart disease kills more Americans than cancer. Diseases of the heart alone caused 30% of all deaths, with other diseases of the cardiovascular system causing substantial further death and disability. It is the number 1 cause of death and disability in the United States and most European countries. A large histological study (PDAY) showed vascular injury accumulates from adolescence, making primary prevention efforts necessary from childhood. By the time that heart problems are detected, the underlying cause (atherosclerosis) is usually quite advanced, having progressed for decades. There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise and avoidance of smoking.

There are many risk factors which associate with (but are not all causes of) various forms of cardiovascular disease. These include the following:

*Age Gender, men under age 64 are much more likely to die of coronary heart disease than women, although the gender difference declines with age. (The gender difference is less pronounced in blacks than in whites, but it is still significant )
*Absence of key nutritional elements, such as omega-3 fats and polyphenol antioxidants
*Diabetes mellitus
*Hypercholesterolemia (elevated cholesterol levels) and abnormal lipoprotein particle profile (cholesterol subtypes)
*Elevated Heart Rate
*Tobacco smoking
*Higher fibrinogen and PAI-1 blood concentrations
*Elevated homocysteine, or even upper half of normal
*Elevated blood levels of asymmetric dimethylarginine
*High blood pressure
*Exposure to high levels of environmental noise
*Obesity, especially central or male-type obesity; apart from being linked to diabetes, this form of obesity independently increases cardiovascular risk, presumedly by inducing an inflammatory and procoagulant state
*Insulin resistance, especially when excess food calories are ingested
*Genetic factors/Family history of cardiovascular disease
*Physical inactivity/ Sedentary lifestyle
*Depression
*Stress

Although men have a higher rate of cardiovascular disease than women, it is also the number one health problem for women in industrialized countries. After menopause, the risk for women approaches that of men. Hormone replacement therapy alleviates a number of post-menopausal problems, but appears to increase the risk of cardiovascular disease.

Attempts to prevent cardiovascular disease are more effective when they remove and prevent causes, and they often take the form of modifying risk factors. Some factors, such as sex (male or female), age, and family history, cannot be modified. Smoking cessation (or abstinence) is one of the most effective and easily modifiable changes. Regular cardiovascular exercise (aerobic exercise) complements the healthful eating habits.

According to the American Heart Association, build up of plaque on the arteries (atherosclerosis), partly as a result of high cholesterol and fat diet, is a leading cause for cardiovascular diseases. The combination of healthy diet and exercise is a means to improve serum cholesterol levels and reduce risks of cardiovascular diseases; if not, a physician may prescribe "cholesterol-lowering" drugs, such as the statins. These medications have additional protective benefits aside from their lipoprotein profile improvement. Aspirin may also be prescribed, as it has been shown to decrease the clot formation that may lead to myocardial infarctions and strokes; it is routinely prescribed for patients with one or more cardiovascular risk factors.

One possible way to decrease risk of cardiovascular disease is keep your total cholesterol below 150. In the Framingham Heart Study, those with total cholesterol below 150 only very rarely got coronary heart disease.

Eating oily fish at least twice a week may help reduce the risk of sudden death and arrhythmias. A 2005 review of 97 clinical trials by Studer et al. noted that omega-3 fats gave lower risk ratios than did statins. Olive oil is said to have benefits. Studies of individual heart cells showed that fatty acids blocked excessive sodium and calcium currents in the heart, which could otherwise cause dangerous, unpredictable changes in its rhythm.

Interestingly, although cardiovascular is the number one cause of death for individuals in modern society, a majority of young people are unconcerned about their risk for development of this disease. Atherosclerosis is a process that develops over decades and is often silent until an acute event (heart attack) develops in later life. Population based studies in the youth show that the precursors of heart disease start in adolescence. The process of atherosclerosis evolves over decades, and begins as early as childhood. The Pathobiological Determinants of Atherosclerosis in Youth Study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 15–19 years. However, most adolescents are more concerned about other risks such as HIV, accidents, and cancer than cardiovascular disease. This is extremely important considering that 1 in 3 people will die from complications attributable to atherosclerosis. In order to stem the tide of cardiovascular disease, primary prevention is needed. Primary prevention starts with education and awareness that cardiovascular disease poses the greatest threat and measures to prevent or reverse this disease must be taken.

Treatment of cardiovascular disease depends on the specific form of the disease in each patient, but effective treatment always includes preventive lifestyle changes discussed above. Medications, such as blood pressure reducing medications, aspirin and the statin cholesterol-lowering drugs may be helpful. In some circumstances, surgery or angioplasty may be warranted to reopen, repair, or replace damaged blood vessels.

The causes, prevention, and/or treatment of all forms of cardiovascular disease are active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis. A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is an inflammatory marker that may be present in increased levels in the blood in patients at risk for cardiovascular disease. Its exact role in predicting disease is the subject of debate.

Some areas currently being researched include possible links between infection with Chlamydia pneumoniae and coronary artery disease. The Chlamydia link has become less plausible with the absence of improvement after antibiotic use .

Pulmonary heart disease - Cor pulmonale is a medical term used to describe a change in structure and function of the right ventricle of the heart as a result of a respiratory disorder. RVH (right ventricular hypertrophy) is the predominant change in chronic cor pulmonale, however in acute cases dilation dominates. Both hypertrophy and dilation are the result of increased right ventricular pressure. Dilation is essentially a stretching of the ventricle, the immediate result of increasing the pressure in an elastic container. Ventricular hypertrophy is an adaptive response to a long-term increase in pressure. Additional muscle grows to allow for the increased force in contraction required to move the blood against greater resistance. To be classified as cor pulmonale, the cause must originate in the pulmonary circulation. Vascular remodelling of the pulmonary circulation as a result of tissue damage (causes including disease, hypoxic injury, chemical agents, etc.) or chronic hypoxic vasoconstriction are two major causes. RVH due to a systemic defect is not classified as cor pulmonale. Left untreated, cor pulmonale can lead to right-heart failure and death.

Pulmonary heart diseaseTreatment - Elimination of the cause is the most important intervention. In pulmonary embolism, thrombolysis (enzymatic dissolution of the blood clot) is advocated if there is dysfunction of the right ventricle. In COPD, long-term oxygen therapy may improve cor pulmonale.

Cor pulmonale may lead to congestive heart failure (CHF), with worsening of respiration due to pulmonary edema, swelling of the legs due to peripheral edema and painful congestive hepatomegaly. This situation requires diuretics (to decrease strain on the heart), sometimes nitrates (to improve blood flow) and occasionally inotropes (to improve heart contractility). CHF is a negative prognostic indicator in cor pulmonale.

What is the Heart ?

The heart is a pear shaped, muscular organ in vertebrates, responsible for pumping blood through the blood vessels by repeated, rhythmic contractions, or a similar structure in annelids, mollusks, and arthropods. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδία, kardia, for "heart." The heart is composed of cardiac muscle, an involuntary muscle tissue which is found only within this muscle.

The human embryonic heart begins beating approximately 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (bpm). The embryonic heart rate (EHR) then accelerates linearly for the first month of beating, peaking at 165-185 bpm during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 bpm per day, or about 10 bpm every three days, an increase of 100 bpm in the first month. There is no difference in male and female heart rates before birth

In the human body, the heart is normally situated to the left of the middle of the thorax, underneath the breastbone (see diagrams). The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is enclosed by a sac known as the pericardium and is surrounded by the lungs. The pericardium is a double membrane structure containing a serous fluid to reduce friction during heart contractions. The mediastinum, a subdivision of the thoracic cavity, is the name of the heart cavity.

The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. This physical location is between the sixth and seventh rib, just to the left of the sternum . In normal adults, the mass of the heart is 250-350 g (9-12 oz), or about three fourths the size of a clenched fist, but extremely diseased hearts can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria (singular: atrium ) and the two lower ventricles. On the left is a picture of a fresh human heart which was removed from a 64-year-old British male.

The function of the right side of the heart (see right heart) is to collect deoxygenated blood, in the right atrium, from the body and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through a passive process called diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body. On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.

If a person is encountered in cardiac arrest (no heartbeat), cardiopulmonary resuscitation (CPR) should be started, and help called. If an automated external defibrillator is available, this device may automatically administer defibrillation if this is indicated.

Heart cancer is an extremely rare form of cancer of the heart. Heart cancer is divided into primary tumors of the heart and secondary tumors of the heart. Most heart cancers are benign myxomas, fibromas, rhabdomyomas and hamartomas, although malignant sarcomas (such as angiosarcoma or cardiac sarcoma) have been known to occur. In a study of 12,487 autopsies performed in Hong Kong seven cardiac tumors were found, most of which were benign. However, cancer can also spread to heart from other parts of the body. In addition the heart can be affected by treatment for cancer in other parts of the body

A congenital heart defect (CHD) is a defect in the structure of the heart and great vessels of the newborn. Most heart defects either obstruct blood flow in the heart or vessels near it or cause blood to flow through the heart in an abnormal pattern, although other defects affecting heart rhythm (such as long QT syndrome) can also occur. Heart defects are among the most common birth defects, and are the leading cause of birth defect-related deaths.

Slightly less than 1% of all newborn infants have congenital heart disease. Eight defects are more common than all others and make up 80% of all congenital heart diseases, whereas the remaining 20% consist of many independently infrequent conditions or combinations of several defects. Ventricular septal defect (VSD) is generally considered to be the most common type of malformation, accounting for about 1/3 of all congenital heart defects.

The incidence is higher when a parent or a sibling has a heart defect (4-5%), in stillborns (3-4%), abortuses (10-25%), and premature infants (2%).

The number of adults with problems connected to a congenital heart defect is rising and is passing the number of children with congenital heart defects in most western countries. This group is called GUCH patients.

The cause of most congenital heart defects is unknown. Where a cause is known, it may be of a multifactorial origin and/or a result of genetic predisposition and environmental factors. Known genetic causes of heart disease includes chromosomal abnormalities such as trisomies 21, 13, and 18, as well as a range of newly recognised genetic point mutations, point deletions and other genetic abnormalities as seen in syndromes such as CATCH 22, familial ASD with heart block, Alagille syndrome, Noonan syndrome, and many more.

Known antenatal environmental factors include maternal infections (Rubella), drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus).

Symptoms and signs are related to the type and severity of the heart defects. Some children have no signs while others may exhibit shortness of breath, cyanosis, chest pain, syncope, sweating, heart murmur, respiratory infections, underdeveloping of limbs and muscles, poor feeding, or poor growth. Most defects cause a whispering sound, or murmur, as blood moves through the heart causing some of these symptoms. All of these symptoms occur at a young age of a child or infant which is typically found during a physical examination.

Heart rate is a term used to describe the frequency of the cardiac cycle. It is considered one of the four vital signs. Usually it is calculated as the number of contractions (heart beats) of the heart in one minute and expressed as "beats per minute" (bpm). See "Heart" for information on embryofetal heart rates. The heart beats up to 120 times per minute in childhood. When resting, the adult human heart beats at about 70 bpm (males) and 75 bpm (females), but this rate varies among people. However, the resting heart rate can be significantly lower in athletes. The infant/neonatal rate of heartbeat is around 130-150 bpm, the toddler's about 100–130 bpm, the older child's about 90–110 bpm, and the adolescent's about 80–100 bpm.

The pulse is the most straightforward way of measuring the heart rate, but it can be deceptive when some heart beats do not have much cardiac output. In these cases (as happens in some arrhythmias), the heart rate may be considerably higher than the pulse rate. Auscultation is also a method of heart rate measurement.

The heart contains two cardiac pacemakers that spontaneously cause the heart to beat. These can be controlled by the autonomic nervous system and circulating adrenaline. The vagus nerve (which is pneumogastric nerve or cranial nerve X) which governs heart rate can be controlled through breathing.

Measuring heart rate - The pulse rate (which in most people is identical to the heart rate) can be measured at any point on the body where an artery is close to the surface. Such places are wrist (radial artery), neck (carotid artery), elbow (brachial artery), and groin (femoral artery). The pulse can also be felt directly over the heart. NOTE: The thumb should never be used for measuring heart rate. Producing an electrocardiogram, or ECG (also abbreviated EKG), is one of the most precise methods of heart rate measurement. Continuous electrocardiographic monitoring of the heart is routinely done in many clinical settings, especially in critical care medicine. Commercial heart rate monitors are also available, consisting of a chest strap with electrodes. The signal is transmitted to a wrist receiver for display. Heart rate monitors allow accurate measurements to be taken continuously and can be used during exercise when manual measurement would be difficult or impossible (such as when the hands are being used). It is also common to find heart rate by listening, via a stethoscope, to the movement created by the heart as it contracts within the chest

Heart rate variability (HRV) is the variation of beat-to-beat intervals. A healthy heart has a large HRV, while decreased or absent variability may indicate cardiac disease. HRV also decreases with exercise-induced tachycardia. HRV has been the focus of increased research to use it as a physiological marker to classify different pathological disorders.

One aspect of heart rate variability can be used as a measurement of fitness, specifically the speed at which one's heart rate drops upon termination of vigorous exercise. The speed at which a person's heart rate returns to resting is considerably faster for a fit person than an unfit person. A drop of 20 beats in a minute is typical for a healthy person. A drop of less than 12 beats per minute after maximal exercise has been correlated with a significant increase in mortality

Maximum heart rate (also called MHR, or HRmax) is the maximum heart rate that a person should achieve during maximal physical exertion. Research indicates it is most closely linked to a person's age; a person's HRmax will decline as they age. Some research indicates the speed at which it declines over time is related to fitness—the more fit a person is, the more slowly it declines as they age.

HRmax is utilized frequently in the fitness industry, specifically during the calculation of target heart rate when prescribing a fitness regimen. A quick way to estimate MHR is to subtract your age from 220, but HRmax can vary significantly between same-aged individuals so direct measurement using a heart rate monitor (and with medical supervision or at least permission and advice) should be used by those seeking maximum safety and effectiveness in their training. People who have participated in sports and athletic activities in early years will have a higher MR than those less active as children.

Training Heart rates - (Warm up) — 50–60% of maximum heart rate: The easiest zone and probably the best zone for people just starting a fitness program. It can also be used as a warm up for more serious walkers. This zone has been shown to help decrease body fat, blood pressure and cholesterol. It also decreases the risk of degenerative diseases and has a low risk of injury. Fats are 85% of food energy burned in this zone.

Fitness Zone (Fat Burning) — 60–70% of maximum heart rate: This zone provides the same benefits as the healthy heart zone, but is more intense and burns more total food energy. The percent of food energy from fat is still 85%.

Aerobic Zone (Endurance Training) — 70–80% of maximum heart rate: The aerobic zone will improve your cardiovascular and respiratory system and increase the size and strength of your heart. This is the preferred zone if you are training for an endurance event. More food energy is burned with 50% from fat.

Anaerobic Zone (Performance Training) — 80–90% of maximum heart rate: Benefits of this zone include an improved FPRIVATE "TYPE=PICT;ALT=V_{\mathrm{O}_2 }" maximum (the highest amount of oxygen one can consume during exercise) and thus an improved cardio-respiratory system, and a higher lactate tolerance ability which means your endurance will improve and you'll be able to fight fatigue better. This is a high intensity zone burning more food energy, 15% from fat.

Red Line (Maximum Effort) — 90–100% of maximum heart rate: Although this zone burns the highest amount of food energy, it is very intense. Most people can only stay in this zone for short periods. You should only train in this zone if you have a very high fitness level and have been cleared by a physician to do so.

Recovery heart rate - The recovery heart rate is one that is taken several minutes after exercise. It is taken anywhere between 2–10 minutes after exercise. It is taken for 15 seconds, and is multiplied by four in order to calculate beats per minute (bpm). The goal is not to exceed 120 bpm.

Target heart rate (THR), or training heart rate, is a desired range of heart rate reached during aerobic exercise which enables one's heart and lungs to receive the most benefit from a workout. This theoretical range varies based on one's physical condition, age, and previous training. Below are two ways to calculate one's Target Heart Rate. In each of these methods, there is an element called "intensity" which is expressed as a percentage. THR can be calculated by using a range of 50%–85% intensity.

Heart rate reserve (HRR) is a term used to describe the difference between a person's maximum heart rate and predicted heart rate (or actual heart rate). Some methods of measurement of exercise intensity measure percentage of heart rate reserve. Additionally, as a person increases their cardiovascular fitness, their HRrest will drop, thus the heart rate reserve will increase. Percentage of HRR is equivalent to percentage of VO2reserve.

Heart rate abnormalities :

Tachycardia is a resting heart rate more than 100 beats per minute. This number can vary as smaller people and children have faster heart rates than adults.

Bradycardia is defined as a heart rate less than 60 beats per minute although it is seldom symptomatic until below 50 bpm. Trained athletes tend to have slow resting heart rates, and resting bradycardia in athletes should not be considered abnormal if the individual has no symptoms associated with it. Again, this number can vary as smaller people and children have faster heart rates than adults

In medicine, a person's pulse is the throbbing of their arteries as an effect of the heart beat. It can be felt at the neck, at the wrist and other places.

Pressure waves move through the blood vessels, which are pliable; these waves are not caused by the forward movement of the blood. When the heart contracts, blood is ejected into the aorta and the aorta stretches. At this point the wave of distention (pulse wave) is pronounced but relatively slow-moving (3 to 6 m/s). As it travels towards the peripheral blood vessels, it gradually diminishes and becomes faster. In the large arterial branches, its velocity is 7 to 10 m/s; in the small arteries, it is 15 to 35 m/s. The pressure pulse is transmitted 15 or more times more rapidly than the blood flow.

The term pulse is also used, although incorrectly, to denote the frequency of the heart beat, usually measured in beats per minute. In most people, the pulse is an accurate measure of heart rate. Under certain circumstances, including arrhythmias, some of the heart beats are ineffective and the aorta is not stretched enough to create a palpable pressure wave. The pulse is irregular and the heart rate can be (much) higher than the pulse rate. In this case, the heart rate should be determined by auscultation of the heart apex, in which case it is not the pulse. The pulse deficit (difference between heart beats and pulsations at the periphery) should be determined by simultaneous palpation at the radial artery and auscultation at the heart apex.

A normal pulse rate for a healthy adult, while resting, can range from 60 to 100 beats per minute (BPM). During sleep, this can drop to as low as 40 BPM; during strenuous exercise, it can rise as high as 200–220 BPM. Generally, pulse rates are higher in younger persons. A resting heart rate for an infant is as high as or higher than an adult's pulse rate during strenuous exercise.

Besides its rate, the pulse has other qualities which reflect the state of the cardiovascular system, such as its rhythm, fullness and the shape of the pulse wave. Certain diseases cause characteristic changes in these qualities. The absence of a pulse at the temple of the skull can be a sign of giant cell arteritis; absent or decreased pulses in the limbs may indicate peripheral artery occlusive disease.

Pulses are manually palpated with fingers or thumb. When palpating the carotid artery, the femoral artery or the brachial artery, the thumb may be used. However, the thumb has its own pulse which can interfere with detecting the patient's pulse at other points, where two or three fingers should be used. Fingers or thumb must be placed near an artery and pressed gently against a firm structure, usually a bone, in order to feel the pulse.

An alternative way of finding the pulse rate is by palpating or listening to the heartbeat. This is most commonly done with the examiner's palm or a through a stethoscope. Before the invention of the stethoscope examiners would press their ear directly to the chest.

Common pulse points :

radial pulse - located on the thumb side of the wrist (radial artery)

ulnar pulse - located on the little finger side of the wrist (ulnar artery)

carotid pulse - located in the neck (carotid artery). The carotid artery should be palpated gently. Stimulating its baroreceptors with vigorous palpitation can provoke severe bradycardia or even stop the heart in some sensitive persons. Also, a person's two carotid arteries should not be palpated at the same time, to avoid a risk of fainting or brain ischemia.

brachial pulse - located between the biceps and triceps, on the medial side of the elbow cavity; frequently used in place of carotid pulse in infants (brachial artery)

femoral pulse - located in the thigh (femoral artery)

popliteal pulse - located behind the knee in the popliteal fossa, found by holding the bent knee. The patient bends the knee at approximately 120°, and the physician holds it in both hands to find the popliteal artery in the pit behind the knee.

dorsalis pedis pulse - located on top of the foot (dorsalis pedis artery)

tibialis posterior pulse - located in the back of the ankle behind the medial malleolus (posterior tibial artery).

temporal pulse - located on the temple directly in front of the ear (temporal artery)

The ease of palpability of a pulse is dictated by the patient's blood pressure. If his or her systolic blood pressure is below 90 mmHg, the radial pulse will not be palpable. Below 80 mmHg, the brachial pulse will not be palpable. Below 60 mmHg, the carotid pulse will not be palpable. Since systolic blood pressure rarely drops that low, the lack of a carotid pulse usually indicates death. It is not unheard of, however, for patients with certain injuries, illnesses or other medical problems to be conscious and aware with no palpable pulse.

Lung Cancer


What is Lung Cancer ?

Lung Cancer is the malignant transformation and expansion of lung tissue, and is the most lethal of all cancers worldwide, responsible for up to 3 million deaths annually. Although Lung Cancer was previously an illness that predominantly affected males, the incidence in women has been increasing in the last few decades, which has been attributed to the rising ratio of female to male smokers. Currently, Lung Cancer is the leading cause of cancer death in women, overshadowing breast cancer, ovarian cancer and uterine cancers combined.

However, it is of note that there are certain types of lung cancers that appear in otherwise healthy patients who have never smoked.

Current research indicates that the factor with the greatest impact on risk of Lung Cancer is long-term exposure to inhaled carcinogens. The most common means of such exposure is tobacco smoke.

Treatment and prognosis depend upon the histological type of cancer, the stage (degree of spread), and the patient's performance status. Treatments include surgery, chemotherapy, and radiotherapy.

Signs and Symptoms of Lung Cancer

*Dyspnea (shortness of breath)
*Hemoptysis (coughing up blood)
*Chronic coughing or change in regular coughing pattern
*Wheezing
*Chest pain or pain in the abdomen
*Cachexia (weight loss), fatigue and loss of appetite
*Dysphonia (hoarse voice)
*Clubbing of the fingernails (uncommon)
*Difficulty swallowing

If the cancer grows into the lumen it may obstruct the airway, causing breathing difficulties. This can lead to accumulation of secretions behind the blockage, predisposing the patient to pneumonia.

Many lung cancers have a rich blood supply. The surface of the cancer may be fragile, leading to bleeding from the cancer into the airway. This blood may subsequently be coughed up.

Depending on the type of tumor, so-called paraneoplastic phenomena may initially attract attention to the disease. In Lung Cancer, this may be Lambert-Eaton myasthenic syndrome (muscle weakness due to auto-antibodies), hypercalcemia and SIADH. Tumors in the top (apex) of the lung, known as Pancoast tumors, may invade the local part of the sympathetic nervous system, leading to changed sweating patterns and eye muscle problems (a combination known as Horner's syndrome), as well as muscle weakness in the hands due to invasion of the brachial plexus.

In many patients, the cancer has already spread beyond the original site by the time they have symptoms and seek medical attention. Common sites of metastasis include the bone, such as the spine (causing back pain and occasionally spinal cord compression), the liver and the brain.

Diagnosis of Lung Cancer

Performing a chest X-ray is the first step if a patient reports symptoms that may be suggestive of Lung Cancer. This may reveal an obvious mass, widening of the mediastinum (suggestive of spread to lymph nodes there), atelectasis (collapse), consolidation (infection) and pleural effusion. If there are no X-ray findings but the suspicion is high (e.g. a heavy smoker with blood-stained sputum), bronchoscopy and/or a CT scan may provide the necessary information. In any case, bronchoscopy or CT-guided biopsy is often necessary to identify the tumor type.

If investigations have confirmed Lung Cancer, scan results and often positron emission tomography (PET) are used to determine whether the disease is localised and amenable to surgery or whether it has spread to the point it cannot be cured surgically. PET is not useful as screening, as not all malignancies are positive on PET scan (such as bronchoalveolar carcinoma), and lung infections may be positive on PET Scan.

Blood tests and spirometry (lung function testing) are also necessary to assess whether the patient is well enough to be operated on. If spirometry reveals a very poor respiratory reserve, as may occur in chronic smokers, surgery may be contraindicated.

Types of Lung Cancer

There are two main types of Lung Cancer categorized by the size and appearance of the malignant cells seen by a histopathologist under a microscope: non-small cell (80%) and small-cell (roughly 20%) Lung Cancer. This classification although based on simple pathomorphological criteria has very important implications for clinical management and prognosis of the disease.

Non-small cell Lung Cancer

The non-small cell lung cancers (NSCLC) are grouped together because their prognosis and management is roughly identical. When it cannot be subtyped, it is frequently coded to 8046/3. The subtypes are: (M8070/3 ) Squamous cell carcinoma, accounting for 20% to 25% of NSCLC, also starts in the larger breathing tubes but grows slower meaning that the size of these tumours varies on diagnosis. (M8140/3 )

Adenocarcinoma is the most common subtype of NSCLC, accounting for 50% to 60% of NSCLC. It is a form which starts near the gas-exchanging surface of the lung. Most cases of the adenocarcinoma are associated with smoking. However, among non-smokers and in particular female non-smokers, adenocarcinoma is the most common form of Lung Cancer. A subtype of adenocarcinoma, the bronchioalveolar carcinoma, is more common in female non-smokers and may have different responses to treatment.

Large cell carcinoma is a fast-growing form that grows near the surface of the lung. It is primarily a diagnosis of exclusion, and when more investigation is done, it is usually reclassified to squamous cell carcinoma or adenocarcinoma.
Small cell Lung Cancer

Small cell carcinoma (SCLC, also called "oat cell carcinoma") is the less common form of Lung Cancer. It tends to start in the larger breathing tubes and grows rapidly becoming quite large. The oncogene most commonly involved is L-myc. The "oat" cell contains dense neurosecretory granules which give this an endocrine / paraneoplastic syndrome association. It is initially more sensitive to chemotherapy, but ultimately carries a worse prognosis and is often metastatic at presentation. This type of Lung Cancer is strongly associated with smoking.

Other types :

*Carcinoid
*Adenoid cystic carcinoma
*Cylindroma
*Mucoepidermoid carcinoma

Metastatic

The lung is a common place for metastasis from tumors in other parts of the body. These cancers, however, are identified by the site of origin, i.e., a breast cancer metastasis to the lung is still known as breast cancer. The adrenal glands, liver, brain, and bone are the most common sites of metastasis from primary Lung Cancer itself.

Causes

Exposure to carcinogens, such as those present in tobacco smoke, immediately causes cumulative changes to the tissue lining the bronchi of the lungs (the bronchial mucous membrane) and more tissue gets damaged until a tumour develops.

There are four major causes of Lung Cancer (and cancer in general):

*Carcinogens such as those in cigarette smoke
*Radiation exposure
*Genetic susceptibility
*Viral infection

Contributor to Lung Cancer

Smoking, particularly of cigarettes, is by far the main contributor to Lung Cancer, which at least in theory makes it one of the easiest diseases to prevent. In the United States, smoking is estimated to account for 87% of Lung Cancer cases (90% in men and 79% in women), and in the UK for 90%. Cigarette smoke contains 19 known carcinogens including radioisotopes from the radon decay sequence, nitrosamine, and benzopyrene.

Additionally, nicotine appears to depress the immune response to malignant growths in exposed tissue. The length of time a person continues to smoke as well as the amount smoked increases the person's chances of contracting Lung Cancer. If a person stops smoking, these chances steadily decrease as damage to the lungs is repaired and contaminant particles are gradually vacated. More recent work has shown that, across the developed world, almost 90% of Lung Cancer deaths are caused by smoking.

Passive smoking—the inhalation of smoke from another's smoking— is claimed to be a cause of Lung Cancer in non-smokers. Studies from the USA (1986,1992, 1997,2001, 2003), Europe (1998), the UK (1998), and Australia (1997) have consistently shown a significant increase in relative risk among those exposed to passive smoke.

The EPA in 1993 claimed that about 3,000 Lung Cancer-related deaths a year were caused by passive smoking. However, since this report was based on a study that was alleged to be heavily biased and was ruled by a federal judge to be "unscientific", the EPA report was declared null and void by a federal judge in 1998.

Asbestos

Asbestos can cause a variety of lung diseases. It increases the risk of developing Lung Cancer. There is a synergistic effect between tobacco smoking and asbestos in the formation of Lung Cancer. Asbestos can also cause cancer of the pleura, called mesothelioma (which is distinct from Lung Cancer).

Radon gas

Radon is a colorless and odourless gas generated by the breakdown of radioactive radium, which in turn is the decay product of uranium, found in the earth's crust. Radon exposure is the second major cause of Lung Cancer after smoking. The radiation decay products ionize genetic material, causing mutations that sometimes turn cancerous. Radon gas levels vary by locality and the composition of the underlying soil and rocks. For example, in areas such as Cornwall in the UK (which has granite as substrata), radon gas is a major problem, and buildings have to be force-ventilated with fans to lower radon gas concentrations. In the US, the EPA estimates that one in 15 homes has radon levels above the recommended guideline of 4 pCi/L (150 Bq/m3). Iowa has the highest average radon concentrations in the United States. Radon causes Lung Cancer because it causes arbitrary damage to the chromosomes and DNA molecules contained in the nucleus of the cell.

Genetics and viruses

Oncogenes are genes that are believed make people more susceptible to cancer. Proto-oncogenes are believed to turn into oncogenes when exposed to particular carcinogens. Viruses are also suspected of causing cancer in humans, as this link has already been proven in animals. Genetic susceptibility and viral infection are not of major importance in Lung Cancer, but they may influence pathogenesis.

Lung Cancer staging

Lung Cancer staging is an important part of the assessment of prognosis and potential treatment for Lung Cancer.

Treatment for Lung Cancer

Treatment for Lung Cancer depends on the cancer's specific cell type, how far it has spread, and the patient's performance status. Common treatments include surgery, chemotherapy, and radiation therapy. The 5-year overall survival rate is 14%.

Surgery for Lung Cancer

Surgery is usually only an option in non-small cell Lung Cancer and if the disease is limited to one lung and has not spread beyond its confines. This is assessed with medical imaging (computed tomography, positron emission tomography). Furthermore, as stated, a sufficient respiratory reserve needs to be present to allow for the removal of lung tissue. Procedures performed include lobectomy (removal of one lobe), bilobectomy (two lobes) or pneumonectomy (removal of a whole lung). Smaller resections include wedge excision or segmentectomy (part of a lobe).

The role of sub lobar resection (extended wedge resection) continues to be debated for the primary management of NSCLC. Although overall survival appears to be equivalent to that of lobectomy resection, the local recurrence rate has been documented to be over three times more common (19% compared to 5%).

Accordingly, sub lobar resection has historically been used as a "compromise resection" approach for the management of small (less than 3 centimeters diameter) stage I peripheral NSCLC identified in patients with impaired cardiopulmonary reserve. Recent reports of the use of intraoperative radioactive iodine brachytherapy implants at the margins of sublobar resection suggest that local recurrence can be reduced to that of lobectomy when this is used as a surgical adjunct to sublobar resection.

The role of anatomic segmentectomy (a larger sublobar resection) with complete lymph node staging has also been found to have potential survival benefits similar to lobectomy. Such resections should be limited to peripheral small (less than 2 cm diameter) stage I NSCLC where a margin of resection equivalent to the diameter of the tumor can be achieved.

Five-year prognosis is often as good as 70% following complete resection of limited (lesions limited to the lung tissue without lymph node spread - stage I) disease.

After surgery, adjuvant chemotherapy may be recommended if lymph nodes within the lung tissues resected (stage II) or the mediastinum (lymph nodes in the peri-tracheal region, stage III) are found to be positive for cancer spread. Survival may be improved by up to 15% above patients receiving only surgical resection in these circumstances. The role of adjuvant chemotherapy for patients with large stage I NSCLC (tumor diameter greater than 3 cm without lymph node involvement, stage IB) remains controversial.

Trials of preoperative chemotherapy in resectable NSCLC have been inconclusive.The NCI Canada study JBR.10 treated patients with stage IB to IIB NSCLC with vinorelbine and cisplatin chemotherapy and showed a significant survival benefit of 15% over 5 years. However subgroup analysis of patients in stage IB showed that chemotherapy did not result in any survival gain in them. Similarly, while the Italian ANITA study showed a survival benefit of 8% over 5 years with vinorelbine and cisplatin chemotherapy in stages 1B to 3A patients, subgroup analysis also showed no benefit in the IB stage.

The Cancer and Leukemia Group B (CALGB) study was a randomized study which examined the use of carboplatin and paclitaxel chemotherapy in patients with stage 1B disease. Unfortunately, although initial results in 2004 were encouraging, an update reported that the findings are now negative with no survival advantage with the use of adjuvant chemotherapy in patients with this stage of disease. However, exploratory analysis of patients in the CALGB study suggested that perhaps those with tumors equal or greater than 4 cm in size may still benefit.

At present, it is standard practice to offer patients with resected stage II-IIIA NSCLC adjuvant third generation platinum-based chemotherapy (e.g. cisplatin and vinorelbine). Adjuvant chemotherapy for patients with stage 1B remains controversial as clinical trials have not clearly demonstrated a survival benefit.
Chemotherapy

Small-cell Lung Cancer is treated primarily with chemotherapy, as surgery has no demonstrable influence on survival. Primary chemotherapy is also given in metastatic NSCLC.

The combination regimen depends on the tumour type:

NSCLC: cisplatin or carboplatin, in combination with gemcitabine, paclitaxel, docetaxel, etoposide or vinorelbine. In metastatic Lung Cancer, the addition of bevacizumab when added to carboplatin and paclitaxel was found to improve survival (though in this study, patients with squamous cell Lung Cancer were excluded because of problems with pulmonary hemorrhage in this group in the past).

SCLC: cisplatin or carboplatin, in combination etoposide or ifosfamide; combinations with gemcitabine, paclitaxel, vinorelbine, topotecan and irinotecan are being studied.

Targeted therapy

In recent years, various molecular targeted therapies have been developed for the treatment of advanced Lung Cancer. However despite an exciting start it was not shown to increase survival, although females, Asians, non-smokers and those with the adenocarcinoma cell type appear to be deriving most benefit from gefitinib.

A number of targeted agents are at the early stages of clinical research, such as cyclo-oxygenase-2 (COX-2) inhibitors, the pre-apoptic inhibitor exisulind, proteasome inhibitors, bexarotene (Targretin) and vaccines

Treatment of non-small cell Lung Cancer is evolving.

Radiotherapy

Radiotherapy is often given together with chemotherapy, and may be used with curative intent in patients who are not eligible for surgery. A radiation dose of 40 or more Gy in many fractions is commonly used with curative intent in non-small cell Lung Cancer; typically in North America, the dose prescribed is 60 or 66 Gy in 30 to 33 fractions given once daily, 5 days a week, for 6 to 6½ weeks. For small cell Lung Cancer cases that are potentially curable, in addition to chemotherapy, chest radiation is often recommended. For these small cell Lung Cancer cases, chest radiation doses of 40 Gy or more in many fractions are commonly given; typically in North America, the dose prescribed is 45 to 50 Gy and can be given in either once daily treatments for 5 weeks or twice daily treatments for 3 weeks.

For both non-small cell Lung Cancer and small cell Lung Cancer patients, radiation of disease in the chest to smaller doses (typically 20 Gy in 5 fractions) may be used for symptom control.

Interventional radiology

Radiofrequency ablation is increasing in popularity for this condition as it is nontoxic and causes very little pain. It seems especially effective when combined with chemotherapy as it catches the cells inside a tumor—the ones difficult to get with chemotherapy due to reduced blood supply to the inside of the tumor. It is done by inserting a small heat probe into the tumor to cook the tumor cells. The body then disposes of the cooked cells through its normal eliminative processes.

The population segment most likely to develop Lung Cancer is the over-fifties who also have a history of smoking. Lung Cancer is the second most commonly occurring form of cancer in most western countries, and it is the leading cancer-related cause of death for men and women. In the US, 175,000 new cases are expected in 2006: 90,700 in men and 80,000 in women. Although the rate of men dying from Lung Cancer is declining in western countries, it is actually increasing for women due to the increased takeup of smoking by this group.

Among lifetime non-smokers, men who have never smoked have higher age-standardized Lung Cancer death rates than women. Of the 80,000 women who are diagnosed with Lung Cancer in 2006, approximately 70,000 are expected to die from it.

Lung Cancer was extremely rare prior to the advent of cigarette smoking. In 1878, malignant lung tumors made up only 1% of all cancers seen at autopsy; this had risen to 10-15% by the early 1900s. Case reports in the medical literature numbered only 374 worldwide in 1912. The British Doctors Study, published in the 1950s, first offered solid epidemiological evidence on the link between Lung Cancer and smoking.

Not all cases of Lung Cancer are due to smoking, but the role of passive smoking is increasingly being recognised as a risk factor for Lung Cancer, leading to policy interventions to decrease undesired exposure of non-smokers to others' tobacco smoke.

In the Second World and Third World, smoking-related Lung Cancer is rising rapidly in incidence. Countries such as China are expected to see a marked increase in Lung Cancer cases as smoking is exceedingly common and other causes of death (such as infections) are becoming less common, revealing an "iceberg" of pulmonary neoplasms. Cheap tobacco products and heavy advertising are seen by health campaigners as a major problem in these countries.

Prevention of Lung Cancer

Prevention is the most cost-effective means of fighting Lung Cancer on the national and global scales. While in most countries industrial and domestic carcinogens have been identified and banned, tobacco smoking is still widespread. Eliminating tobacco smoking is a primary goal in the fight to prevent Lung Cancer, and smoking cessation is the most important preventative tool in this process.

Policy interventions to decrease passive smoking (e.g. in restaurants and workplaces) have become more common in various Western countries, with California taking a lead in banning smoking in public establishments in 1998, Ireland playing a similar role in Europe in 2004, followed by Italy and Norway in 2005 and Scotland as well as several others in 2006. New Zealand has also recently banned smoking in public places.

Only the Asian state of Bhutan has a complete smoking ban (since 2005). In many countries pressure groups are campaigning for similar bans. Arguments cited against such bans is criminalisation of smoking, increased risk of smuggling and the risk that such a ban cannot be enforced.

Screening and secondary prevention

Regular chest radiography and sputum examination programs were not effective in reducing mortality from Lung Cancer. Earlier studies showed earlier detection of Lung Cancer was possible but mortality was not improved.

Simply detecting a tumor at an earlier stage may not necessarily yield improved mortality. For example, plain radiography resulted in increased time from diagnosis of cancer until death and those cancers being detected by screening tended to be earlier stages. However, these patients continued to die at the same rate as those who are not screened. At present, no professional or specialty organization advocates screening for Lung Cancer outside of clinical trials.

A computed tomography (CT) scan can uncover tumors not yet visible on an X-ray. CT scanning is now being actively evaluated as a screening tool for Lung Cancer in high risk patients, and it is showing promising results. The Cancer Institute is currently completing a randomized trial comparing CT scans with chest radiographs. Several single-institution trials are ongoing around the world.

Early Lung Cancer Action Project published the results of CT screening on over 31,000 high-risk patients in late 2006 . In this study 85% of the 484 detected lung cancers were stage I and thus highly treatable. Mathematically these stage I patients would have an expected 10-year survival of 88%. However, there was no randomization of patients (all received CT scans and there was no comparison group receiving only x-rays) and the patients were not actually followed out to 10 years post detection (the median followup was 40 months).

In contrast, a March 2008 study found no benefit. 3,200 current or former smokers were screened for 4 years and offered 3 or 4 CT scans. Lung Cancer diagnoses were 3 times as high, and surgeries were 10 times as high, as predicted by a model, but there were no significant differences between observed and expected numbers of advanced cancers or deaths.

Randomized controlled studies are underway in this area to see if decreased long-term mortality can be directly observed from CT screening.

It should be noted that screening studies have only been done in high risk populations, such as smokers and workers with occupational exposure to certain substances. This is important when one considers that repeated radiation exposure from screening could actually induce carcinogenesis in a small percentage of screened subjects, so this risk should be mitigated by a (relatively) high prevalence of Lung Cancer in the population being screened.