Coronary Artery Disease - Essay Example

Coronary Artery Disease Introduction The coronary arteries supply the heart muscle (myocardium) with blood rich in oxygen and nutrients. Blockage of the coronary arteries is known as coronary artery disease or ischaemic heart disease. [1] Coronary artery disease is the most common cause of death in Europe, USA and Australia. In USA it affects 14 million men and women. [2] CAD related death has dramatically decreased during these 20 last years. All age ranges took benefit from the prognostic improvement of coronary artery disease.[3] Of 607 patients suffering from CAD in an Italian study 561 were men(92.4%) comparing with 46 women(7.6%).[4] Physiological view and pathogenesis The heart consists of 4 chambers: an atrium and a ventricle on the right, and an atrium and a ventricle on the left. Blood returning to the heart from veins all over the body flows into the right atrium, then blood flows into the right ventricle which pumps it out to the lungs for oxygenation of the blood. This oxygenated blood returns to the left atrium and then flows into the left ventricle, which pumps it at high pressure into the arteries, including the coronary arteries. The strength of the heart muscle (myocardium) depends on the oxygen and nutrient supply coming via the coronary arteries. The walls of these arteries are strong, elastic and flexible. The myocardium is supplied by 3 major coronary arteries. Two of them arise from a common stem, called left coronary artery which supplies the left side of the heart. Its left anterior descending (LAD) branch supplies the front part of the heart, while the left circumflex (LCX) branch supplies the left lateral and back side of the heart. The right coronary artery (RCA) is separate and supplies the right and the bottom parts of the heart. [2] The inner lining layer of the coronary arteries is quite smooth allowing blood to flow easily. With aging, cholesterol and calcium content in the walls of the coronary arteries increases, making them thickened and less elastic. The prolonged effect of risk factors with the consequence of aging, endothelial dysfunction becomes predominant, especially in the coronary arteries. Unhealthy habits, such as a diet rich in cholesterol and other fats, smoking and lack of physical activity accelerate the deposit of cholesterol, fatty compounds, calcium, and a blood clotting material called fibrin within the inner lining of coronary arteries. This process is known as atherosclerosis, or hardening of the arteries. The deposits, or plaques, may increase in size and block the arteries. If blockage is partial it causes chest pain (angina), if the blockage is complete it causes myocardial infarction(MI).[1] Since coronary artery disease often develops over decades, it can go virtually unnoticed until it produces a MI or heart attack. Causes of coronary artery disease Scientists think the disease starts when the very inner lining of the artery (endothelium) is damaged. [5] The damage may be caused by various factors including: . Smoking: Toxins in the blood from smoking cigarettes contribute to the development of atherosclerosis. . High blood pressure . High Cholesterol . Certain diseases, such as diabetes . Radiation therapy to the chest, as used for certain types of cancer Once the inner wall of an artery is damaged, fatty deposits (plaques) accumulate. If the surface of these fatty deposits breaks or ruptures, blood cells called platelets will clump at the site to try to repair the artery. This clump can block the artery, leading to heart attack. [1] Risk Factors . Heredity: Coronary heart disease runs in the family. . High cholesterol: Levels of cholesterol in the blood are above healthy levels. This is usually involves high levels of low-density lipoprotein(LDL), the bad cholesterol, and low levels of high-density lipoprotein(HDL) the good cholesterol. . Tobacco abuse: This includes not only smoking any form of tobacco (cigarettes, cigars, pipes) but also chewing tobacco. . High blood pressure (hypertension) . Diabetes . Obesity . Physical inactivity . High-fat diet . Emotional stress . Type A personality (impatient, aggressive, and competitive) [2] Risk factors often occur in clusters and may feed one another, such as obesity leading to diabetes and hypertension. When grouped together, certain risk factors put the patient at an ever greater risk of coronary artery disease. For example, metabolic syndrome,( a cluster of conditions that includes elevated blood pressure, high triglycerides, elevated insulin levels and excess body fat around the waist), greatly increases the risk of all types of heart disease.[1] Sometimes coronary artery disease develops without any classic risk factors. Researchers are studying other possible factors, including: . C-reactive protein. The liver produces C-reactive protein (CRP) in response to injury or infection. CRP is also produced by muscle cells within the coronary arteries. CRP is a general sign of inflammation, which plays a central role in atherosclerosis. . Homocysteine. Homocysteine is an amino acid the body uses to make protein and to build and maintain tissue. Excessive levels of homocysteine may increase the risk of coronary artery disease and other cardiovascular conditions. . Fibrinogen. Fibrinogen is a protein in the body that plays an essential role in blood clotting, but too much fibrinogen may promote excessive clumping of platelets which are blood cells largely responsible for clotting. That can cause a clot to form in a coronary artery, leading to a heart attack or stroke. Fibrinogen may also be an indicator of inflammation that accompanies atherosclerosis. . Lipoprotein (a). This substance forms when a low-density lipoprotein (LDL) cholesterol particle attaches to a specific protein. The protein that carries lipoprotein (a) may disrupt the ability of the body to dissolve blood clots. High levels of lipoprotein (a) may be associated with an increased risk of cardiovascular disease, including coronary artery disease and heart attack. [1] Coronary heart disease signs and symptoms The most devastating sign of coronary heart disease is abrupt, unexpected cardiac arrest. Cardiac arrest commonly occurs in people who have had previous heart attacks, but it may occur as the first sign of heart disease. [2] Atherosclerosis may be present for years without causing symptoms. This slow disease process can begin in childhood. In some people, the condition can cause symptoms by the time they reach their 30s. In others, they do not have symptoms until they reach their 50s or 60s. But as the blockage gets worse, the slowed blood supply to the heart may start to cause something called angina pectoris, a Latin phrase that means, "strangling the chest." Patients often say that angina is like a squeezing, suffocating, or burning feeling in their chest. The pain usually happens when the heart has an extra demand for blood, like during exercise or times of emotional stress. [5] Angina tends to start in the center of the chest but may move or radiate the arm, neck, back, throat or jaw. [5]This atypical chest pain is more common in women. [1] Other causes of chest pain Pericarditis: Pain is felt in the center of the chest and is aggravated by movement, posture, respiration and coughing. It is sharp and severe. Aortic aneurysm: Central chest pain that radiate to the back is characteristic of a dissecting or enlarging aortic aneurysm and can mimic the pain of myocardial infarction. It is important to exclude a dissection since the administration of a thrombolytic agent in this condition would be catastrophic. Effort (Da Costas) syndrome: Left, submammary stabbing pain, is associated with anxiety. Oesophageal disease: It produces central chest pain similar to angina and can be difficult to differentiate. Other causes of chest pain are pulmonary embolism, pulmonary hypertension, costochondritis, pleurisy, pneumothorax and mediastinitis. [6] . Shortness of breath on exertion: If the heart can not pump enough blood to meet body needs, patient may develop shortness of breath which is a symptom of heart failure. . Palpitations: Usually heart beats are not felt by someone, rapid or strong heart beats means palpitation which is one of the symptoms, may be felt, in CAD or heart failure. . Dizziness or fainting: This may be occurring due to insufficient blood supply to the brain. . Weakness on exertion or rest . Irregular beats (Arrhythmia) Silent ischaemia is a condition in which no symptoms occur, these patient are diagnosed during screening electrocardiogram (ECG) or other tests showing evidence of ischaemia. Arteries may be blocked 50% or more without causing any symptoms. [2] Symptoms and signs of heart failure Symptoms include fatigue, short of breath, anorexia and nausea. They relate to distension and fluid accumulation in areas drained by the systemic veins. Physical signs are more marked than symptoms. These include jugular venous distension, tender smooth liver enlargement, dependent pitting oedema, development of free abdominal fluid (ascites), and pleural transudates which may appear in chest X-ray. Physical Examination: It may reveal evidence of weakened or irritable heart muscle, including sounds called gallops or murmurs. There may be evidence of lung congestion. [2] Screening and diagnosis . Electrocardiogram (ECG): An electrocardiogram records electrical signals as they travel through the heart. An ECG can often reveal evidence of a previous heart attack or one that is in progress. Certain abnormalities may indicate inadequate blood flow to the heart. [1] . Echocardiogram: This test uses sound waves to produce images of the heart. During echocardiogram the physician can determine whether all parts of the heart wall are contributing normally to hearts pumping activity. Parts that move weakly may have been damaged during a heart attack or be receiving too little oxygen. This may indicate coronary disease or various other conditions. [1] . Stress test: If signs and symptoms occur most often during exercise, patient may be asked to walk on a treadmill or ride a stationary bike during an ECG. This is known as stress test. In other cases patient ma is given some medicine, to stimulate the heart instead of exercise, during echocardiogram. Another stress test known as a nuclear stress test helps measure blood flow to heart muscle at rest and during stress to give image by special cameras in addition to ECG. When thallium is used as a radioactive substance it is called thallium test. [1] However stress echocardiogram test is more preferable because it does not use a radioactive agent [2] . Angiogram: To view blood flow through the heart, a special dye is injected into the arteries before a chest X-ray. This is known as angiogram. The dye outlines narrow spots and blockages on the X-ray images [1] . Electron beam computerized tomography(EBCT): This test, also known as ultrafast CT scan, can detect calcium within fatty deposits that narrow coronary arteries.[1] This test is used more to screen young people.[2] . Magnetic resonance angiography (MRA): This technique uses magnetic waves to produce a 3-D image of the coronary arteries, where areas of narrowing or blockage can be checked. However details may be not as clear as those produced by angiogram. [1] Complications When coronary arteries narrow, the heart muscle may not receive enough blood when demand increases especially during physical activity. This can cause chest pain or shortness of breath. If a cholesterol plaque ruptures, complete blockage of the coronary artery may provoke a heart attack. The lack of blood flow to the heart during a heart attack leads to irreversible damage to heart muscle. The amount of damage depends in part on how early patient receives treatment. If the heart has been damaged and can not pump enough blood to meet body needs, heart failure may occur. [1] A Swiss study concluded that CAD is a strong and independent predictor of mortality among patients with acute heart failure. [7] Medical Treatment Treatment aims to balance blood supply to the heart with heart oxygen demand, and prevent worsening of coronary heart disease. Aspirin: A small dose of aspirin (75 mg to 100mg) daily, reduces the risk of developing angina or heart attack (myocardial infarction) by reducing the tendency of the heart to clot. Side effects of aspirin include ulcers or bleeding problems. [2] Cholesterol medications: Aggressively lowering low-density lipoprotein (LDL) cholesterol can stop or even reverse the buildup of fatty deposits in the arteries. Boosting high-density lipoprotein (HDL) cholesterol may help too. Examples of drugs lowering LDL cholesterol are statins. These statin drugs work by reducing the amounts of lipids in the blood. This changes the inner linning of the blood vessels so plaques are less likely to form or become large. They slow or stop the progression of coronary heart disease and also reduce risk of heat attacks. Recently clinical trials have shown beneficial effects immediately after a heart attack or threatened heart attack, even before the fat lowering effect is maximal, meaning they stabilize the plaque. [2] Large randomised clinical trials of cholesterol-lowering therapy have conclusively demonstrated decreased morbidity and mortality in patients with established coronary artery disease.[8][9] Brands of statins include Lipitor, Pravachol, Zocor, Mevacor and Crestor.[2] Beta blockers: These drugs slow heart rate and decrease blood pressure, so it decreases the hearts demand for oxygen. If the patient had a heart attack, beta blockers reduce the risk of future attacks [1] Nitroglycerin: This drug is a vasodilator presents in different forms; tablets, spray and patches. It can control chest pain by opening the coronary arteries and reducing the hearts demand for blood. [1] ACE inhibitors: Angiotensin-converting enzymes (ACE) inhibitors work by dilating blood vessels and increasing blood flow. They recently have been shown to reduce the numbers of heart attacks and deaths in patients with coronary heart disease, unrelated to their blood pressure lowering effect. They are useful in patients with diabetes and those with weakened heart muscles. [2] Calcium channel blockers: These medications relax the smooth muscle layer that surrounds a coronary artery and cause the vessels to open, increasing blood flow to the heart they also control high blood pressure. [1] Invasive Procedures Percutaneous coronary interventions Angioplasty: This technique opens narrowed arteries. It is performed by interventional cardiologists. They use a long, thin tube called a catheter that has a small balloon on its tip. They inflate the balloon at the blockage site in the artery to flatten the plaque against the artery wall. Angioplasty is also called percutaneous transluminal coronary angioplasty (PTCA) [6] The procedure: A guide wire is inserted into an artery in the leg (femoral artery) and is guided to the site of narrowing in the coronary artery. The catheter is slipped over this guide wire and positioned at the blockage, where the balloon is inflated. After treatment, the guide wire and catheter with its balloon are removed. The hospital stay and recovery time for angioplasty is shorter than that of by pass. However, about 35% of patients are at risk for more blockage in the treated area. This is called restenosis. Restenosis usually happens within 6 months after angioplasty. [6] Stent: A stent is a small, sieved, coil-like metallic tube or scaffold mounted over a balloon. The balloon is inflated at the site of blockage, which expand the stent. The balloon is the withdrawn after being deflated, and the stent stays in place. [2] The opened stent keeps the vessel open and stops the artery from collapsing. Restenosis rates with this procedure are around 15% to 20%. Because restenosis is a problem with stent procedure, newer stents covered with medicines are manufactured. These covering medicines keep the artery from closing up again. These stents are called coated stents or drug-eluting stents. [6] Van Domburg R T, et al, concluded that long term survival and infarct free survival was good, particularly in non-diabetic men with single vessel disease and good ventricular function, who had a single stent implanted in a native coronary artery. A dramatic improvement was observed in event free survival, both early and late with the replacement of anticoagulation by ticlopidine. This, of course, cannot be separated from improved stent implantation techniques between 1986 and 1995. Ultimately, almost 40% of the patients experienced an adverse cardiac event (manly repeat intervention) in the long term. New advances in restenosis treatment and in the secondary prevention must be directed at this aspect of patient management after stenting. [10] Atherectomy: If the plaques are too rigid, bulky or calcified to be treated with angioplasty or a stent the plaques must be removed by cutting with a drill-like device. This works only if the narrowed area or blockage is limited to a small potion of an artery. Devices commonly used for atherectomy include directional atherectomy(DCA) catheter, rotational atherectomy or rotablator(PTRA) transluminal extraction catheter (TEC) or AngioJet.[2] Laser ablation: This technique uses a catheter that has a metal or fiberoptic probe on the tip. The laser uses light to burn away plaque and open the vessel enough so that a balloon can further widen the opening. [5] Brachytherapy: Radiation is applied to the blockage to clear it. The radiation comes from a very tiny source placed inside or near the artery. This technique is used for treating arteries that have undergone angioplasty or stenting but have restenosis. Percutaneous transmyocardial revascularization (PTMR) PTMR is performed by cardiologist in the cardiac catheterization laboratory. After the area is numbed with anaesthesia, the cardiologist inserts a catheter in an artery in the leg that lead to the heart. A laser is then fed through the catheter and used to create tiny holes in the heart muscle. These holes become channels for blood to flow to oxygen-starved areas of the heart. Researchers believe that the procedure may cause new vessels to form, reducing the pain of angina. IT is used in patients not responding to medicines, angioplasty or coronary artery bypass surgery. [5] Coronary artery bypass surgery This surgical intervention involves "bypassing" blood flow around one or more narrowed vessels. This approach is reserved for patients whose disease is either severe or is not improved or stabilized by medication and less invasive procedures. [2] Coronary artery bypass grafting (CABG): This is the standard operation for blockages of coronary arteries. If multiple arteries are blocked or if the left main artery shows marked blockage, bypass surgery is the best treatment of choice. The blocked arteries are bypassed with blood vessels taken from the chest (internal mammary), arm (radial artery) or a leg (saphenous vein). [2] During operation, the heart is stopped temporarily and the patient is connected to a bypass pump which works as a heart. These operations are very successful with low rate of complications. [2] Minimally invasive coronary artery bypass: It is less invasive bypass surgery procedure. The incision is smaller, and the operation may be done while the heart is still beating. This reduces risk of complications. The technique may reduce patient recovery time, so costs decrease. However this procedure is only used for patients whose blockages can be bypassed through this small incision and whose risk complications are low. [5] Future therapy: Researchers are exploring new technique for treating coronary artery disease, such as gene therapy. In this experimental technique, gene and growth factor protein may be injected through a catheter or directly into the heart to stimulate growth of new vessels and restore blood flow to the heart. Gene-coated stents that could encourage the repair of coronary arteries are being studied as well. [1] Follow up Follow up of the patients are essential because coronary artery disease is a chronic, restlessly progressive disease. Reducing risk factors may only slow its pace. Even angioplasty or bypass surgery only reduces the severity of the disease. It does not cure the condition. It often comes back and gets worse, requiring further treatment for patients with previous heart attacks or bypass, especially if the patient has not corrected the abnormal risk factors. [2] For better follow up the following conditions should be assessed: [2] . New symptoms or signs of disease progression should be evaluated by periodic physical examination and ECG or stress tests. . Silent ischaemia could be assessed by periodic treadmill or radionuclide stress tests or stress echocardiography. Assessment of patient progress in risk reduction and how well treatment is working by: [2] . Checking weight and activity levels . Checking blood lipid levels, including LDL, HDL, and triglycerides, especially if the patient is diabetic (LDL should be less than 100) . If patient is diabetic blood sugar should be checked regularly and frequently. . Checking blood pressure, it should be less than 130/80 . Checking progress with quitting smoking . Evaluating any side effects of medications and treating them if necessary. Treatment of heart failure Treatment of chronic heart failure is aimed at relieving symptoms, retarding progression and improving survival. The management of heart failure needs that any factor aggravating the failure should be identified and treated. In other hand the cause of heart failure should be discovered and where possible corrected. The prevention of heart failure is of great importance. Specific measures include cessation of smoking, effective treatment of high blood pressure (hypertension) and elevated cholesterol blood level, and pharmacological therapy following myocardial infarction. [6] Drugs: Diuretics: These act by promoting the renal excretion of salt and water by blocking tubular reabsorption of sodium chloride. The resulting loss of fluids reduces ventricular filling pressures of the heart (preload) and produces consistent haemodynamic and symptomatic benefits in patient with heart failure and rapidly relieve dyspnoea (shortness of breath) and peripheral oedema (swelling around the ankle and both legs). The intravenous administration of loop diuretics such as frusemide relieves pulmonary oedema rapidly by means of arteriolar vasodilatation reducing afterload, an action that is independent of its diuretic effect. [6] Although heart failure symptoms are improved by diuretic treatment alone, they do not provide any survival benefits. More over, their use may be complicated by over-diuresis and electrolyte depletion (potassium and magnesium), which may predispose to the development of lethal ventricular arrhythmia, hyper-kalaemia (potassium sparing diuretics) and other metabolic disturbances (hyperuricaemia and dyslipidaemia) and gynaecomastia. [6] Vasodilator therapy: Diuretics and sodium restriction serve to activate the rennin-angiotensin system, enhancing formation of angiotensin (a potent vasoconstrictor) and an increase in afterload. A variety of other neural and hormaonal reactions also serve to increase preload and afterload pressure of the heart. These compensatory mechanisms are initially beneficial in maintaining blood pressure and redistributing blood flow, but in later stages of heart failure they reduce cardiac output. The high venous pressures in heart failure are also related to the activation of the sympathetic nervous system and the presence of circulating vasoconstrictors. [6] Several controlled studies have established the benefits of vasodilator therapy in heart failure. The trials have shown that in addition to producing considerable symptomatic improvement in patients with symptomatic heart failure, vasodilators improve prognosis and limit the development of progressive heart failure. These vasodilators include: Arteriolar vasodilators: Alpha adrenergic blockers (e.g. prazocin) and direct smooth muscle relaxants (e.g. hydralazine) are potent arteriolar vasodilators. Calcium-channel blockers also reduce afterload, but first generation calcium antagonists (diltiazem, nifedipine) may have a detrimental effect on left ventricular function in patient with heart failure. It is suggested that the second generation calcium antagonist amlodipine is safe in heart failure and of possible prognostic benefit in patients with non-ischaemic aetiology. The reduction in afterload causes an increase in cardiac output [7]. Venodilators Short-acting and long-acting nitrates (e.g. glyceryl trinitrate and isosorbide mononitrate) act by reducing preload and lowering venous pressure with resulting reduction in pulmonary and peripheral oedema. Reduction of filling pressure does not significantly enhance cardiac output because the heart is operating on the flat portion of the ventricular filling curve. With chronic use, tolerance develops with loss of efficacy and consequent worsening of heart failure. Combined therapy with hydralazine and oral nitrates has been shown to improve mortality and exercise performance, and may be used when ACE inhibitors are contraindicated. [6] Angiotensin-converting enzyme inhibitors Ace inhibitors lower systemic vascular resistance and venous pressure and reduce levels of circulating catecholamines, thus improving myocardial performance. The beneficial haemodynamic effect of these drugs appears to be independent of their inhibition of ACE as they are equally effective when plasma rennin activity is normal. [6] Angiotensin 11 receptor antagonists (e.g. Losartan) They have similar haemodynamic actions to ACE inhibitors Beta blockers Studies using a variety of beta blockers (metoprolol, bisoprolol) have shown that these drugs improve symptomatic class, exercise tolerance and left ventricular function in patients with heart failure. Following the administration of beta blockers, ejection fraction may decline, but it usually returns to baseline within a month and then increases after 3 moths. So, initial doses should be low. They should be used in patients who remain symptomatic despite treatment with diuretics, vasodilators and digoxin. [6] Digitalis glycosides (Digoxin) While several small placebo-controlled trials have shown that digoxin improves exercise tolerance, increase left ventricular ejection fraction and relieves the symptoms And signs of congestive cardiac failure, other studies have indicated that digoxin may increase mortality in patients with myocardial infarction. [6] With improvement of formulation, digoxin toxicity has become less problematic but it is prone to occur in the elderly patients with renal dysfunction. The most common features of digoxin toxicity are: . Anorexia, nausea, altered vision . Arrhythmia . Digoxin levels >2.5nmol/L Other drugs include: Beta adrenergic agonists Phosphodiesterase inhibitors Ibopamine Anticoagulants Antiarrhythmic agents Non-pharmacological treatment of heart failure Revascularisation: While coronary artery disease is the most common cause of heart failure, the role of revasculaisation in patient with heart failure is unclear. Patients with angina and left ventricular dysfunction have a higher mortality from surgery (10-20%) Pacemaker or implantable cardioverter-defibrillator In patients with a history of sustained ventricular tachycardia or ventricular fibrillation, implantation of a pace maker is effective in terminating further episodes of ventricular arrhythmia. Its effect on survival in relation to established drug therapies require further studies. [6] Cardiac transplantation Cardiac transplantation has become the treatment of choice for younger patient with severe intractable heart failure, whose life expectancy is less than six months. With careful recipient selection, the expected one-year survival for patients following transplantation is over 80%, and is 70% at five years. Irrespective of survival, quality of life is dramatically improved for the majority of patients. [6] Prevention of Heart Disease Monitoring and modifying certain risk factors is the best way to prevent CAD and heart disease in general: . Adoption of healthy life style early in life . Early assessment of the heart condition if there is a family history of CAD . Diet: A balanced, low fat diet is good not only for people with high cholesterol but for every one. . Quitting smoking . Physical activity: exercise helps to lower blood pressure, increase levels of good cholesterol (HDL) and control of weight. . Obesity is frequently associated with high blood pressure, diabetes, high cholesterol LDL levels and triglycerides, and low HDL. A high-fiber, low-fat diet and regular exercise can help in reduction of weight. . Medical counseling before use of Viagra, Cialis and Levitra for impotence. Zobair Kabir, et al, found that primary prevention achieved a two-fold larger reduction in CAD deaths comparing with secondary prevention. [11] Complementary therapy Garlic can be used to reduce the risk of heart disease by lowering blood fats and cholesterol levels. Gincko biloba is commonly used to improve blood circulation and can be used to improve body physical condition Ginseng is generally used for debility and weakness, for example during recovery from illness. It can be used to reduce blood cholesterol levels, but overuse of ginseng has been associated with raised blood pressure. References 1. Mayo Clinic Staff. Coronary artery disease. Jul 7, 2006. www.mayoclinic.com 2. Coronary heart disease. www.emedicinehealth.com/coronary_heart_disease 3. Ferrieres J. The epidemiology of coronary artery disease in older than 75 years. Arch Mal Coer Vais. 2006; 99 spec No 4; 7-12 4. Luis Gruberg. Sirolimus-Eluting Stent in patients with bifurcation lesions in multivessel coronary artery disease: a substudy of the ARTS 11. www.medscape.com/viewarticle/523052 5. Texas Heart Institute Heart Information Center. Coronary artery disease. www.texasheartinstitute.org 6. Kumar P and Clark M. Clinical Medicine. Fourth edition, 1998. Page678-683 7. Purek L, Laule-Kilian K, Christ A and et al. Coronary artery disease and outcome in acute congestive heart failure. http://www.heart.bmj.com/cgi/content/full/92/5/598 8. Coronary Prevention Study Group. N Engl J Med 1995; 333: 1301-7 9. The Long-Term Intervention With Pravastin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Eng J Med 1998; 339: 1349-7 10. Van Domburg R T, Foley D P, Jaegere P P T and et al. Long term outcome after coronary stent implantation, a 10 year single center experience of 1000 patients. Heart 1999, 82: 1127-1134 11. Zubair K, Bennett K, Emer S and et al. Comparing primary prevention with secondary prevention to explain decreasing coronary heart disease death rates in Ireland, 1985-2000. www.medscape.com/viewarticle/560306 Read More