Wilu's paper: chapter 3, coronary heart disease

CHAPTER 3 CORONARY HEART DISEASE 3.1 Definition Coronary Heart Disease (CHD), also known as Coronary Artery Disease, develops when fat, calcium, and plaque (or scar tissue) build up in the arteries that lead to the heart. Coronary arteries allow the heart to receive oxygen and other nutrients that are required for pumping blood to the rest of the body. CHD, however, causes the arteries to harden and constrict, impeding both blood flow and delivery of these vital nutrients. Coronary 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) with oxygen and nutrients. 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. 3.2 Etiology Coronary heart disease (CHD) is the leading cause of death in the United States for men and women. According to the American Heart Association, more than 15 million people have some form of the condition. In West Jakarta, more than 100 case of coronary heart disease caused death in 2006. Men in their 40s have a higher risk of CHD than women. But, as women get older, their risk increases so that it is almost equal to a man's risk. 3.3 Epidemiology Coronary heart disease is the most common cause of morbidity and mortality in the developed world. More than 50,000 deaths a year are attributed to coronary heart disease in Indonesia. At least a third of the individuals that die of coronary heart disease are younger than 55 years of age. This disease costs much per year in medical treatment and lost income. 3.4 Signs and symptoms The classic symptom of Coronary Heart Disease is angina, the direct result of inadequate flow of oxygen to the myocardium. It’s usually described as a burning, squeezing, or tight feeling in the substernal or precordial chest that may radiate to the left arm, neck, jaw, or shoulder blade. Approximately 50% of women don’t present with the typical symptoms of angina. These women experience vague symptoms such as fatigue, shortness of breath, abdominal pain, nausea, or vomiting. Symptoms are less visible in females, the elderly, and people with diabetes. Other symptoms include: pressure,fullness or a squeezing pain in chest for more than a few minutes,pain going from chest to shoulders and arms,more chest pain,pain in upper abdomen,shortness of breath,sweating,impending sense of doom, lightheadedness, fainting, nausea and vomiting, choking feeling, lightheadedness, dizziness, weakness 3.5 Causes and Risk Factors Heart disease is caused by narrowing of the coronary arteries that feed the heart. Like any muscle, the heart needs a constant supply of oxygen and nutrients, which are carried to it by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, the result is coronary heart disease. If not enough oxygen-carrying blood reaches the heart, you may experience chest pain called angina. If the blood supply to a portion of the heart is completely cut off by total blockage of a coronary artery, the result is a heart attack. This is usually due to a sudden closure from a blood clot forming on top of a previous narrowing. The following are confirmed independent risk factors for the development of Coronary Heart Disease, 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) Type A behavioural Patterns, TAPB. Added in 1981 as an independent risk factor after a majority or research into the field discovered that TAPB’s were twice as likely to cause CHD than any other personality type. Hereditary differences in such diverse aspects as lipoprotein structure and that of their associated receptors, homocysteine processing/metabolism. The significant but indirect risk factors, include : Lack of exercise, Stress, Diet rich in saturated fats, Diet low in antioxidants, Obesity and Men over 50. 3.6 Complications When your coronary arteries narrow, your heart may not receive enough blood when demand is greatest - particularly during physical activity. This can cause chest pain or shortness of breath. If a cholesterol plaque ruptures, complete blockage of your heart artery may trigger a heart attack. The lack of blood flow to your heart during a heart attack leads to irreversible damage to your heart muscle. The amount of damage depends in part on how quickly you receive treatment. If your heart has been damaged and can't pump enough blood to meet your body's needs, you may experience heart failure 3.7 Screening and diagnosis Many tests help diagnose CHD. Usually, your doctor will order more than one test before making a definite diagnosis.Tests may include: Electrocardiogram (ECG), Exercise stress test, Echocardiogram, Nuclear scan, Coronary angiography/arteriography, Electron-beam computed tomography (EBCT) to look for calcium in the lining of the arteries -- the more calcium, the higher your chance for CHD, Coronary CT angiography, and Magnetic resonance angiography 3.8 Treatments Coronary Heart Disease can be treated with a variety of drugs that help reduce the effects that the disease has on its host body. One of the most commonly used drugs to treat Coronary Heart Disease is aspirin, which reduces the tendency of blood to form clots over a rupturing artery (a common cause of heart attacks). Another type of medication, beta-blockers, decreases the heart rate and blood pressure so that the heart's demand for oxygen lowers. Statins drugs, also a popular means of treating Coronary Heart Disease, reduce the amount of fats and cholesterol in your blood so that plaques are less likely to form or increase in size in the blood vessels.For extreme cases of Coronary Heart Disease the only option is often bypass surgery. 3.9 Preventions Coronary heart disease is the most common form of heart disease. Prevention centers on the modifieable risk factors, which include decreasing cholesterol levels, addressing obesity and hypertension, avoiding a sedentary lifestyle, making healthy dietary choices, and stopping smoking. It has been suggested that coronary heart disease is partially reversible using an intense dietary regime coupled with regular cardio exercise. 3.10 Prognosis Everyone recovers differently. Some people can maintain a healthy life by changing their diet, stopping smoking, and taking medications exactly as the doctor prescribes. Others may need medical procedures such as angioplasty or surgery. Although everyone is different, early detection of Coronary Heart Disease generally results in a better outcome.

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Wilu's paper: chapter 2, cholesterol

CHAPTER 2 CHOLESTEROL 2.1 Definition Cholesterol is a sterol (a combination steroid and steroid), a lipid found in the cell membranes of all body tissues, and is transported in the blood plasma of all animals. Trace amounts of cholesterol are also found in plant membranes.The name originates from the Greek chole- (bile) and stereos (solid), and the chemical suffix -ol for an alcohol, as researchers first identified cholesterol in solid form in gallstones in 1784. Cholesterol is a soft, fat-like, waxy substance found in the bloodstream and in all your body's cells. It's normal to have cholesterol. Cholesterol is an important part of a healthy body because it's used for producing cell membranes and some hormones, and serves other needed bodily functions. But too much cholesterol in the blood is a major risk for coronary heart disease (which leads to heart attack) and for stroke. Cholesterol also aids in the manufacture of bile (which is stored in the gallbladder and helps digest fats), and is also important for the metabolism of fat soluble vitamins, including vitamins A,D,E and K. It is the major precursor for the synthesis of vitamin D and of the various steroid hormones (which include cortisol and aldosterone in the adrenal glands, and the sex hormones progesterone, the various estrogens, testosterones, and derivates). There are different kinds of cholesterol. The liver converts unburned food metabolites into very low density lipoproteins (VLDL) and secretes them into plasma where they are converted to low-density lipoprotein (LDL) particles and non-esterified fatty acids, which can affect other body cells. In healthy individuals, the relatively few LDL particles are large. In contrast, large numbers of small dense LDL (sdLDL) particles are strongly associated with the presence of atheromatous disease within the arteries. For this reason, LDL is referred to as "bad cholesterol". High-density lipoprotein (HDL) particles transport cholesterol back to the liver for excretion, but vary considerably in their effectiveness for doing this. Having large numbers of large HDL particles correlates with better health outcomes, and hence it is commonly called "good cholesterol". In contrast, having small amounts of large HDL particles is independently associated with atheromatous disease progression within the arteries. 2.2 Synthesize of cholesterol Most of the cholesterol is synthesized by the body and some has dietary origin. Although formerly believed, the cholesterol level in blood is not raised by increasing the amount of cholesterol in the diet. Cholesterol is more abundant in tissues which either synthesize more or have more abundant densely-packed membranes, for example, the liver, spinal cord, brain, and atheromata (arterial plaques). Cholesterol plays a central role in many biochemical processes, but is best known for the association of cardiovascular disease with various lipoprotein cholesterol transport patterns and high levels of cholesterol in the blood. Cholesterol is insoluble in blood, but is transported in the circulatory system bound to one of the varieties of lipoprotein, spherical particles which have an exterior composed mainly of water-soluble proteins. Cholesterol is required in the membrane of mammalian cells for normal cellular function, and is either synthesized in the endoplasmic reticulum, or derived from the diet, in which case it is delivered by the bloodstream in low-density lipoproteins. These are taken into the cell by receptor-mediated endocytosis in clathrin-coated pits, and then hydrolysed in lysosomes. Cholesterol is primarily synthesized from acetyl coA through the HMG-CoA reductase pathway in many cells and tissues. About 20-25% of total daily production (~1 g/day) occurs in the liver; other sites of higher synthesis rates include the intestines, adrenal glands and reproductive organs. For a person fo about 150 pounds (68kg), typical daily dietary intake is 200 to 300 mg. Of the cholesterol input to the intestines via bile production, 92-97% is reabsorbed in the intestines and recycled via enterohepatic circulation. Biosynthesis of cholesterol is directly regulated by the cholesterol levels present, though the homeostatic mechanisms involved are only partly understood. A higher intake from food leads to a net decrease in endogenous production, while lower intake from food has the opposite effect. The main regulatory mechanism is the sensing of intracellular cholesterol in the endoplasmic reticulum by the protein SREBP (Sterol Regulatory Element Binding Protein 1 and 2). In the presence of cholesterol, SREBP is bound to two other proteins: SCAP (SREBP-cleavage activating protein) and Insig1. When cholesterol levels fall, Insig-1 dissociates from the SREBP-SCAP complex, allowing the complex to migrate to the Golgi apparatus, where SREBP is cleaved by S1P and S2P (site 1/2 protease), two enzymes that are activated by SCAP when cholesterol levels are low. The cleaved SREBP then migrates to the nucleus and acts as a transcription factor to bind to the SRE (sterol regulatory element) of a number of genes to stimulate their transcription. Among the genes transcribed are the LDL receptor and HMG-CoA reductase. The former scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol. 2.3 The Risk Factors You're more likely to have high cholesterol if you're inactive, obese or eat unhealthy foods. Although high cholesterol can lead to heart disease on its own, other factors compound the risk: · Smoking. Cigarette smoking damages the walls of your blood vessels, making them likely to accumulate fatty deposits. Smoking may also lower your level of HDL cholesterol. · High blood pressure. Increased pressure on your artery walls damages your arteries, which can speed the accumulation of fatty deposits. · Diabetes. High blood sugar contributes to high LDL cholesterol and low HDL cholesterol. High blood sugar also damages the lining of your arteries. · Family history of heart disease. If a parent or sibling developed heart disease before age 55, high cholesterol levels place you at a greater than average risk of developing heart disease. 2.4 Screening and Diagnosis Cholesterol screening and diagnosis maybe done either by testing the entire adult population or by making use of routine contacts in primary health care (opportunistic screening). The main screening test for blood cholesterol is the measurement of total blood cholesterol in blood samples obtained by either venepuncture or finger prick. Measurements in cholesterol screening may not accurately reflect the true cholesterol level due to measurement error (bias and imprecision) and natural biological variation in cholesterol levels within an individual. These sources of error can result in misclassification and lead to incorrect diagnosis and the possibility of unnecessary treatment. However, bias can be reduced in laboratory equipment by regular calibration againts a standard, and precision increased by using good equipment and repeat analyses. 2.5 Preventions To keep our cholesterol under control, we must do the following : - Schedule a screening - Eat foods low in cholesterol and saturated fat - Maintain a healthy weight - Exercise regularly - Follow the healthcare professional's advice

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