Atherosclerosis: Difference between revisions

== Complications of atherosclerosis ==

[[File:atherosclerosis_damage.svg|thumb|400px|right|Figure 11. Complications of atherosclerosis]]

The clinical complications of atherosclerosis are highly dependent on the location and size of affected vessels, the duration of the chronic process, and the type of plaque, since the severity of impairment of atherosclerosis differs throughout the vasculature. For example, ‘stable plaque’ can easily result into angina pectoris due to its thick fibrous cap that directly affects the diameter of the relatively small coronary vessels. On the other hand, ‘vulnerable plaque’ is non-stenotic, but can easily cause acute thrombosis and therefore myocardial infarction due to its fragility towards rupture when located at physically stressed areas such as bifurcations. Often with ‘vulnerable plaques’ there are relatively few symptoms, however they are more numerous and dispersed throughout the arteries compared to ‘stable plaque’. Thus, you can either have an occlusion due to the growing plaque or due to the embolization of the ruptured fragments of the original plaque. Due to the difficult detection of ‘vulnerable plaques’ while they are widely dispersed, it is highly important to tackle the risk factors prior to plaque rupture. Thus in the following paragraph, we will highlight the clinical risk factors associated with atherosclerosis. The four major clinical consequences of atherosclerosis are listed and explained below.<br />

== Risk factors of atherosclerosis ==

Recent studies have shown that atherosclerosis is not just the inevitable process of aging, but also a process with many modifiable components. A worldwide INTERHEART study has established the importance of nine potentially modifiable risk factors for atherosclerosis, which account for over 90% of the population-attributable risk of a first MI (figure 12). A variety of non-modifiable risk factors such as advanced age, gender and hereditary coronary heart disease are important to recognize in patients with atherosclerosis. Recently the role of several biological markers associated with the development of cardiovascular events are accentuated since one out of five cardiovascular events occur in patients lacking the earlier mentioned risk factors. <br />

=== Common risk factors ===

==== ''Dyslipidemia'' ====

One of the major modifiable risk factors for atherosclerosis is hypercholesterolemia. Study shows that dyslipidemia (defined as an elevated apo B to apo A-1 ratio) was responsible for 49% of the population-attributable risk of a first MI. In countries with high consumption of saturated fat and high cholesterol levels (e.g. the United States), observational studies have shown that the mortality rates from coronary disease are higher compared with those in countries with traditionally low consumption of saturated fat and cholesterol levels (e.g. Japan). Several trials have shown that the risk of ischemic heart disease positively correlates with higher total serum cholesterol levels. For example, the impact of hypercholesterolemia can be illustrated by an observational result from the Framingham Heart Study, which shows that a person with a total cholesterol level of 240 mg/dl has twice the coronary risk a person would have with a cholesterol level of 200 mg/dl. However, it is a mistake to think that all lipoproteins consisting of cholesterol are harmful since cholesterol can provide critical functions to all cells that need to form membranes and to synthesize products such as steroid hormones and bile salts. <br />

Incidence of atherosclerosis and coronary artery disease increases with higher levels of LDL particles. As mentioned earlier, LDL can accumulate in the intima of the artery in excess proportions and undergo chemical modifications that activate endothelial cells to proceed to atherosclerosis. When people generally refer to  ‘bad cholesterol’, they are referring to LDL particles. On the other hand, high level of high-density lipoprotein (HDL) is ‘good cholesterol’ since it protects against atherosclerosis by reversing the cholesterol transport from peripheral tissues to the liver for disposal and functions as an antioxidant. In order to give additional clearance to what is ‘bad cholesterol,’ all lipid and lipoprotein abnormalities that are associated with higher coronary risk will be named subsequently: increased total cholesterol, increased LDL-cholesterol, low HDL-cholesterol, elevated total-to-HDL-cholesterol ratio, hypertriglyceridemia, increased non-HDL-cholesterol, elevated lipoprotein A, elevated apolipoprotein B (apo B is primarily found in LDL), decreased apolipoprotein A-I (apo A-1 is found in HDL), small and dense LDL particles, and several genotypes of apolipoprotein E (apoE influences cholesterol and triglyceride levels as well as the risk of coronary heart disease).<br />

==== ''Lipid-Altering therapy'' ====

Controlling the serum lipid level is a key step to limit the consequences of atherosclerosis. Major clinical trials show that coronary events and mortality significantly decreased when total and LDL-cholesterol levels were reduced by primary and secondary prevention.<br />

==== ''Antihypertensive therapy'' ====

Antihypertensive therapy can either consist of lifestyle interventions or pharmacotherapy. Lifestyle modifications consist of diet, body weight reduction, increased activity, and cessation of smoking. As for diet, high consumption of fruits, vegetables, dairy products low in fat, fish oils, potassium and reduced consumption of sodium and alcohol are recommended.