Cardiovascular
diseases refers to the class of diseases that involve the heart and blood
vessels (arteries and vein). This diseases have similar causes, mechanisms and
treatment. Over 50millions Americans have cardiovascular problem and most other
western countries face high and increasing rates of cardiovascular disease. It
is the number one cause of death and disability in the United states and most
European countries (Mensah et al,
2003) There is therefore increased emphasis on preventing heart diseases by
modifying risk factors such as healthy eating, exercise and avoidance of
smoking (Mensah et al, 2003).
Atherosclerosis (build up of plaque deposits in arteries) is the most common type of heart disease. Atherosclerosis is a significant factor in many types of cardiovascular diseases like coronary heart disease (CHD), myocardial infarction (MI), angina pectoris, cerebral vascular diseases (CVD), peripheral artery disease (PAD), hypertension, thrombotic stroke, transient ischemic attack (TIAs), insufficient blood supply to lower limbs (Cludication), organ damage, thrombocytopenia, luekopenia and anemia (Bernard, 2010).
Stroke is the 3rd leading cause of death in the United states, but millions also suffer silent strokes (TIAs) each year that cause memory loss, neurologic disorders etc. Ischemic stroke is where a blood clot blocks the flow of oxygenated blood to a portion of the brain (occurs in 83% of all strokes). The majority of these cardiovascular diseases are related to atherosclerosis (Bernard, 2010).
Evidence
impacts high dietary fat as an important contributor to cardiovascular diseases
(Meijer et al, 1996). A diet high in
saturated fat and cholesterol has been associated with exaggerated
cardiovascular problem in healthy populations over relatively short periods of
time. For example strazincky et al (1993)
reported increased blood pressure and heart rate reactivity in healthy,
normotensive participants after consuming a high fat diet in a 2 week crossover
study. He observed simultaneous increase in cholesterol and triglyceride
concentration in blood which are risk factors to cardiovascular diseases
(Pearson et al, 2002).
Eating just one high saturated fat
meal can hinder the ability of high density lipoprotein (HDL) from protecting
against clogged arteries. 14 healthy Australian Volunteers between the ages of
18-40years were feed a high saturated fat diet comprised of a slice of carrot
cake and milkshake made with coconut oil. 3 hours after eating the saturated
fat cake and shake meal, the artery linning were unable to expand sufficiently
to increase blood flow to the body’s tissues and organs. After 6hours,
researchers noted that the anti-inflammatory qualities of the high density
lipoprotein cholesterol were reduced after the saturated fat-meal. (Fiona, 2006).
A high fat diets also contributes to obesity which increase peripheral resistance in the arterioles and can drive blood pressure up. It is a proven factor in atherosclerosis which narrows the pipes. Fat also interferes with insulin utilization and contributes to insulin resistance, which is a significant factor in many cases of hypertension. This was demonstrated in an experiment in which dog were fed a high fat diet for a period of 5 weeks. Not only did the dogs gain an average of 8pounds, their blood pressure and heart rate also rose considerably (Rumsey et al,1994).
All blood vessels are lined by endothelial cells (the layer being called endothelium). These endothelial cells play a crucial role in the initiation (pathogenesis) of arterial diseases. The commonest of these diseases is atherosclerosis (hardening of arteries). This may be due to a number of factors but the most common is the deposition of cholesterol in the sub-endothelial layer of arteries. Endothelial cells become injured either physically by abrasion or by toxic insult (such as from free radicals (McGreachie, 1998).
Unstable free radicals meeting with LDL-C on the endothelium of the arteries causes a reaction called lipid peroxidation which leads to lesions. The constant inflammatory assault that takes place at the site of these lesions can eventually take its toll on the fibrous cap that the immune system forms to keep it intact, large molecules which are normally confined to the blood are allowed to escape through the endothelium and become lodged in the smooth muscles cells in the arterial walls, macrophages also passes through and accumulates fat and cholesterol deposits (McGreachie, 1998, Bernard, 2010).
This process is very slow, but there is a gradual accumulation of this fatty and fibrous materials which not only makes the normally elastic artery hard (Sclerotic) but the deposits (known as plaques) may encroach on the arterial lumen and cause turbulent blood flow. This may lead to a narrowing of the artery (Thrombosis). Such serious consequences occurs in heart attacks and Myocardial infarction (McGreachie, 1998).