Coronary Artery Disease

What is Coronary Artery Disease?

Coronary artery disease (CAD) (or atherosclerotic heart disease) is the end result of the accumulation of atheromatous plaques within the walls of the coronary arteries that supply the myocardium (the muscle of the heart) with oxygen and nutrients. It is sometimes also called coronary heart disease (CHD), but although CAD is the most common cause of CHD, it is not the only cause.

CAD is the leading cause of death worldwide. While the symptoms and signs of coronary artery disease are noted in the advanced state of disease, most individuals with coronary artery disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arises. 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 20 years of age.

According to present trends in the United States, half of healthy 40-year-old males will develop CAD in the future, and one in three healthy 40-year-old women. According to the Guinness Book of Records, Northern Ireland is the country with the most occurrences of CAD. By contrast, the Maasai of Africa have almost no heart disease.

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 artery 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 artery disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack).

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Coronary Artery Disease Pathophysiology

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. Myocardial cells may die from lack of oxygen and this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later myocardial scarring without heart muscle regrowth. Chronic high-grade stenosis of the coronary arteries can induce transient ischemia which leads to the induction of a ventricular arrhythmia, which may terminate into ventricular fibrillation leading to death.

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 narrowing of the lumen of the heart artery before sudden closure is often not severe, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. The events leading up to plaque rupture are not understood despite many theories. Myocardial infarction is almost never caused by temporary spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CAD.

CAD is associated with smoking, diabetes, and hypertension. A family history of early CAD is one of the less important predictors of CAD. Most of the familial association of coronary artery disease are related to common dietary habits. Screening for CAD includes evaluating high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels. Despite much press, most of the alternative risk factors including homocysteine, C-reactive protein (CRP), Lipoprotein (a), coronary calcium and more sophisticated lipid analysis have added little if any additional value to the conventional risk factors of smoking, diabetes and hypertension.

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Coronary Artery Disease Angina

Angina (chest pain) that occurs regularly with activity, after heavy meals, 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 betablocker therapy such as metoprolol or atenolol.

Nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms are also effective in relieving symptoms but are not known to reduce the chances of future heart attacks.

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 may be treated with oxygen, intravenous nitroglycerin, and aspirin. Interventional procedures such as angioplasty may be done.

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Coronary Artery Disease Risk Factors

The following are confirmed independent risk factors for the development of CAD:

  1. Hypercholesterolemia (specifically, serum LDL concentrations)
  2. Smoking
  3. Hypertension (high systolic pressure seems to be most significant in this regard)
  4. Hyperglycemia (due to diabetes mellitus or otherwise)
  5. Type A Behavioural Patterns, TABP. Added in 1981 as an independent risk factor after a majority of research into the field discovered that TABP's were twice as likely to exhibit CAD than any other personality type.
  6. Hemostatic Factors: High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD. Factor VII levels are higher in individuals with a high intake of dietary fat. Decreased fibrinolytic activity has been reported in patients with coronary atherosclerosis.
  7. Hereditary differences in such diverse aspects as lipoprotein structure and that of their associated receptors, homocysteine processing/metabolism, etc.
  8. High levels of Lp(a):

What is Lp(a)?

When LDL cholesterol combines with a substance known as Apoliprotein (a), the result is a compound known as Lp(a), or "ugly" cholesterol. Lp(a) is called ugly cholesterol because evidence from some research studies shows that in high levels, it can increase a person's risk of heart attack or stroke, even if cholesterol levels are otherwise "desirable." Lp(a) is measured through a blood sample and can be tested as part of a lipoprotein panel.

Genetics determines your levels of Lp(a) and even the size of the Lp(a) molecule itself. Lifestyle changes do not alter levels of Lp(a); instead, levels for most people tend to remain consistent over a lifetime except for women, who will experience a slight rise in levels with menopause. Some physicians request testing of Lp(a) for patients who have a strong family history of premature heart disease or hypercholesterolemia. It can be a valuable test, particularly when other types of cholesterol are at healthy levels, yet concern exists that heart disease is developing. Physicians will typically order this test if a patient has had a heart attack or stroke, yet cholesterol levels fall within a "healthy" category.

Berkeley Heart Lab, Inc., based in Burlingame, California, offers a number of advanced lipid tests-including a test for levels of Lp(a)-that provide quantitative determinations of lipoprotein subclasses. According to Jeffrey Aroy of Berkeley HeartLab, Inc., "the value of the quantitative measurements is that they go beyond simply noting whether levels are 'good' or 'bad.' Instead, these measurements not only provide guidance for therapeutic treatment, but also provide valuable insight into the success of therapy and the need for adjusting treatment approaches on an ongoing basis."

Approximately 50 percent of people who have heart attacks do not have elevated cholesterol levels. These individuals, however, typically have higher levels of CRP, Lp(a), Apo S, or homocysteine. As researchers continue to learn about the exact mechanisms of heart disease, more tests are developed to identify and measure these other risk factors and markers.

Treatment for elevated Lp(a) includes niacin therapy. Some experts believe that antioxidant

therapy is also useful. People with high levels of Lp(a) benefit by concentrating their efforts OR lowering LDL levels since at lower levels, it is harder for LDL particles to attach to plaque buildup. Lowering LDL levels ultimately lowers the level of risk.

According to a study published in the New England Journal of Medicine in November 2003, researchers found that elevated levels of Lp(a) among healthy men age sixty-five years and older are predictive of the risk of stroke and death. Study participants with the highest levels of Lp(a) were more likely to experience a stroke and were 76 percent more likely to die than men with the lowest levels. These researchers support the use of Lp(a) testing as a screening tool to measure the risk of stroke and heart disease in older men.

Significant, but indirect risk factors include:

  • Lack of exercise
  • Stress
  • Diet rich in saturated fats
  • Diet low in antioxidants
  • Obesity
  • Men over 60; Women over 65

Risk factors can be classified as

  1. Fixed: age, sex, family history
  2. Modifiable: smoking, hypertension, diabetes mellitus, obesity, etc.

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Coronary Artery Disease Prevention

Coronary artery 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 homocysteine levels may contribute to more heart attacks (NORVIT trial). In diabetes mellitus, there is little evidence that very tight blood sugar control actually improves cardiac risk although improved sugar control appears to decrease other undesirable problems like kidney failure and blindness. 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 artery disease although this remains without scientific cause and effect proof.

An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Patients with CAD and those trying to prevent CAD 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, triacylglycerol and apolipoprotein-B.

It is also important to keep blood pressure normal, exercise and stop smoking. These measures reduces the development of heart attacks. Recent studies have shown that dramatic reduction in LDL levels can cause regression of coronary artery disease in as many as 2/3 of patients after just one year of sustained treatment.

Menaquinone (Vitamin K2), but not phylloquinone (Vitamin K1), intake is associated with reduced risk of CAD mortality, all-cause mortality and severe aortic calcification.

CAD has always been a tough disease to diagnose without the use of invasive or stressful activities. The development of the Multifunction Cardiogram (MCG) has changed the way CAD is diagnosed. The MCG consists of a 2 lead resting EKG signal is transformed into a mathematical model and compared against tens of thousands of clinical trials to diagnose a patient with an objective severity score, as well as secondary and tertiary results about the patients condition. The results from MCG tests have been validated in 8 clinical trials which resulted in a database of over 50,000 patients where the system has demonstrated accuracy comparable to coronary angiography (90% overall sensitivity, 85% specificity).

This level of accuracy comes from the application of advanced techniques in signal processing and systems analysis combined with a large scale clinical database which allows MCG to provide quantitative, evidence-based results to assist physicians in reaching a diagnosis. The MCG has also been awarded a Category III CPT code by the American Medical Association in the July 2009 CPT update.

Secondary prevention is preventing further sequelae of already established disease. Regarding coronary artery 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. Beta blockers may also be used for this purpose.

Anti-platelet therapy

A meta-analysis of randomized controlled trials by the international Cochrane Collaboration found "that the use of clopidogrel plus aspirin is associated with a reduction in the risk of cardiovascular events compared with aspirin alone in patients with acute non-ST coronary syndrome. In patients at high risk of cardiovascular disease but not presenting acutely, there is only weak evidence of benefit and hazards of treatment almost match any benefit obtained.".

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