Arterial Blockage - Heart Disease

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In spite of abundant knowledge, space-age technology, arterial disease also called atherosclerosis remains the top killer in the Western World. In fact, it is escalating so that young adults in their 20's are now having heart attacks. Why is this? We explore this later. Medical science is treating coronary thrombosis (heart attack) far more efficiently in the Emergency Rooms where lives are saved and if quick enough, damage to the heart avoided or reduced. But prevention is still way behind as Western society's nutritional status health worsens.

Anatomy of a Blocked Artery - Atherosclerosis

The heart, brain and lower limbs are the most vulnerable to serious effects of arterial clogging. In other parts of the body, if one artery is blocked others can supply blood into the starved area. This is less likely in the heart. When the blood vessel blocks, the muscle of the heart dies. This is a 'heart attack' or coronary thrombosis' or 'myocardial infarction' (MI). If the blockage is severe but not total, the insufficient blood supply is called 'ischaemia'. This can cause pain in the chest, arms, throat or jaw; even the upper back. This is termed 'angina'. It is usually reversible with drugs and oxygen.

When the same occurs in blood vessels supplying the brain, if completely blocked, the result is a full stroke; a part of the brain dies. If there is ischaemia only, then recovery may be full. This is termed a Transient Ischemia Attack, or 'TIA'. Atheroma plaque builds up in many vessels but critical areas are the main carotid arteries in the neck, which are accessible to treatment as well as Ultrasound and CT screening.

If arterial supply to the lower limbs is reduced, then the victim may experience aching in the calves during walking. It is termed 'Intermittent Claudication'.
Typically, the large arteries in the groin and thigh are narrowed by plaque, but also the smaller lower leg vessels can be narrowed especially in smokers and diabetics. Smaller vessels are not as straightforward to surgically treat.

Why does plaque form

It used to be thought that cholesterol (fat) in the blood was the prime cause. This led to the hasty doctrine of reduced fat diets which changed the whole food industry. Results? No change in dire statistics. This incomplete science also spawned the 'Food Pyramid' which damned fats and encouraged carbohydrate. For the last 30 years, diets have become very high in refined carbohydrates and sugars in the panic to get rid of fat. Atheroma disease has escalated. It didnt work.
Science has had to look elsewhere for causation of heart (and general) arterial disease. Lets look at the artery itself and what happens.

There are three layers: an outer fibrous, a middle muscular and an inner cell lining (called the intima or endothelium).
The 'smooth muscle' middle layer is responsible for opening and closing the artery according to blood flow needs. Also the muscle cells themselves can migrate to the inner lining in response to signals of local injury; so they have additional roles.
The Endothelium (inner lining) is in direct contact with the circulating blood, toxins, waste products, bacteria as well as subjected to blood pressure fluctuations and injury. Endothelium cells have many roles; in response they secrete substances that can attract smooth muscle cells, blood platelets etc. This initiates local areas of inflammation just like anywhere in the body when damage occurs or infection threatens. It is an immune or repairing response. Of course as the artery ages, it also becomes more vulnerable to damage. Diminishing nutrients, lowered protective hormones as well as increasing toxic burdens accelerates the plaque process. As the endothelium becomes damaged and inflammed, certain fats enter into the arterial wall, are taken up by smooth muscle cells and blood cells called phagocytes resulting in 'foam cells'. This process causes a swelling into the lumen (vessel inner tube space) hence reducing blood flow. Calcification (hardening) occurs over time and the body attempts to heal over the plaque. Many atheroma plaques are 'stable' and even if they reduce the 'lumen' diametre by 60% few symptoms result. Problems occur when plaque continues to grow and block (occlude) the artery or when it ruptures, causing a huge local response of released chemical substances, sticky platelets meshing with fibrin in a desperate attempt to contain the damage. Its called a thrombus.

Here its touch and go as to whether safe containment happens or the clot blocks the artery completely causing a heart attack or stroke, or the clot may break off and get swept along the artery until it finally jams and completely blocks off vital blood supply. Result: a full heart attack or 'myocardial infarction'.

Factors affecting endothelial injury and atheroma

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main risk factors	additional important risk factors usually not done as routine testing
age smoking blood pressure diabetes - high glucose high cholesterol elevated LDL low HDL high triglycerides overweight family history lack of exercise	insulin resistance hs-CRP homocysteine elevated fibrinogen high Lp(a) abnormal subclasses of LDL, HDL low testosterone in men low growth hormone low DHEA low or too high thyroid hormone heavy metal burden high iron low Vit D level micronutritional status certain bacterial infections poor dental/oral health

Detection of Heart Disease and other Vascular Atheroma risk

In addition to the current Risk Profile Matrix, other tests can be vital in preparing a protocol for atheroma prevention or treatment.

Lipid Studies Total cholesterol Triglycerides HDL LDL Total/HDL ratio LDL/HDL ratio Lipoprotein (a)	Lipids are fats. There are many subclasses: Total of all fat. Some 'good' , some 'bad' Tryglycerides: OK unless high, then a risk Large HDL can be protective. A 'good' fat carrying protein. Small LDL fat is very destructive A low Total/HDL ratio is beneficial A low LDL/HDL ratio is beneficial Lp(a) Powerfully destructive Refer to the special page on Lipids for more indepth reading and treatment of 'Lipids'. See right side-bar.
hs-CRP	High-sensitivity C-Reactive Protein is claimed to be indicative of arterial inflammation. Problem is it can also be elevated by a host other inflammatory problems like arthritis, cancer etc. Its more risky when LDL is high.
Fasting glucose	If above normal it may indicate a tendency to diabetes or insulin resistance. It accelerates glycation, a deadly protein-glucose product.
Fasting Insulin	Detection of insulin resistance and its role in many diseases. Also termed the Metabolic Syndrome (Syndrome X).
Fibrinogen	A principle blood clotting protein that turns into fibrin. Several factors increase fibrinogen and blood clotting risk.
Homocysteine	Causes inflammation of the endothelium, accelerating plaque. Is OK unless very high
Free Testosterone	Men with low testosterone have higher risks of heart attack.
Thyroid hormones	A key metabolic hormone.