To be able to answer this question we have to know the main difference between arteries and veins. Arteries are vessels that transport blood from the heart to the farthest spots in the body. Arterial blood has bright red color because of oxyhemoglobin (oxygenated hemoglobin). When a lot of calcium and cholesterol accumulates in the arterial walls, the plaque is created. The most worrisome consequence of arterial plaque is a list of cardiovascular diseases it could cause: a heart attack, a stroke, and a peripheral arterial disease. The condition of hardening and narrowing of arteries caused by plaque is also called atherosclerosis. Depending on the artery that is struck, atherosclerosis results in dysfunction of vital organs such as heart and brain and even leads to death. Veins are the ‘‘afferent’’ wing of our circulatory system, meaning that they send blood low in oxygen back to the heart. The color of the blood they carry is dark because of the lack of oxygen. Common venous disorders include venous insufficiency and deep venous thrombosis. The former one is an inability of veins to send blood up to the heart. The latter one can pose much greater harm, even to our lives. Deep venous thrombosis presents a blood clot that resides in a vein until it breaks off, ends up in our lungs and causes the deadly pulmonary embolism.
THE DIFFERENCE IN THE STRUCTURE OF THE WALLS AND CLOTS OF ARTERIES AND VEINS
Atherosclerosis is an asymptomatic and long process. When oxidized, lipoprotein binds white blood cells to the arteries endothelium and damages it. That’s when the inflammation takes place, and it is additionally promoted by LDL’s that sneak cholesterol and triglycerides into your arteries. This could cause stiffening of your arteries if you don’t have enough good cholesterol to get the bad one to the kidneys to flush them out. The arteries’ hardening, atherosclerosis, is caused by the plaque which is separated into 2 categories: stable and unstable. The stable plaque has an extracellular matrix and smooth muscle cells, while the unstable one contains macrophages and foam cells (extracellular matrix separating the lesion from the arterial lumen). The former, also known as the fibrous cap, is susceptible to detaching and consequently exposing a thrombus-forming element to the bloodstream-collagen. Arteries are multi-layered vessels. The innermost layer is called tunica intima, made of squamous epithelium immersed in connective tissue membrane with elastic fibers. The middle and the thickest layer is tunica media that provides support to our arteries and is greatly in charge of blood pressure control. Tunica Externa is the outermost layer that connects arteries to the neighboring tissues thanks to its collagen and elastin. Its density varies from really thick to soft depending on the closeness to the tunica media. The veins have less smooth muscle and elastic tissue, so they have to rely on valves and contractions of your skeletal biggest muscles to push the blood through. Taking into account that the same blood goes through all the vessels, how come that only the arteries get blocked by the plaque? How do veins not get clogged by plaque despite the fact that their structure is more or less the same to the arteries? The answer is simple – the abundance of muscles in arteries is the key for this puzzle. When smooth muscles die off, lactic acid is produced. For people who are in an alkaline state, it won’t be hard to clean the acid off with all the oxygen in their blood. However, if your diet is high in acids, the plaque is sure to stay in your arteries. In order to avoid confusion, what has to be highlighted is that veins can be clogged too. Red clots made of platelets and red blood cells can form due to the set of reasons that are altogether called Virschow’s triad: venous stasis, hypercoagulability, and changes to the blood vessel walls. The clot is usually formed in the leg can wander off all the way to the lungs causing pulmonary embolism. However, the structure of the red clot is much different than the plaque and it doesn’t cause the hardening and narrowing of vessels. Oswald Colleb, a very eminent pharmacology professor at the University of Gottingen at the beginning of the 20th century, made some discoveries that shook the world of medicine. In the experiment on dogs and rabbits that he carried out, the animals showed some atherosclerotic lesions after being fed on a lactic acid diet. The amount of lactic acid in 100gr of the animals’ blood was 150 after the endeavor, which was 3 times as big as it had been before the start. Other than producing lactic acid, the endo lethal lining of muscles provides nitric oxide. This substance triggers another useful molecule- cyclic GMP- which relaxes the arterial muscles while preparing them for the next contraction. Studies also showed that nitric oxide burns away fat and sugar which is certainly what we want in order to avoid plaque in arteries.
THE DIFFERENCE IN PRESSURE IN VEINS AND ARTERIES
The discrepancy between the pressures under which both types of vessels work also makes a great difference in the clot formation in veins and arteries. Blood pressure is generally connected to the arterial pressure but measuring the venous pressure is also essential in intensive care medicine in order to monitor the proper return of blood to the heart. Ordinary values of venous pressure are 5mm/Hg in the right atrium and 8mm/Hg in the left atrium. There are 3 kinds of venous pressure: central venous pressure which determines right ventricular and diastolic volume; jugular venous pressure which can help differentiate between a heart and lung disease; portal venous pressure which is the blood pressure in the portal vein (5-10 mm/Hg). Venous pressure is one of the primary elements of mean arterial pressure (the overall pressure of the circulatory system) along with total cardiac output (all the blood pumped from the heart). It actually presents the resistance to blood flow which is an essential contrast to the high flexibility of arteries. They respond to the heart rhythm and transfer the pace to the veins which can stretch in accordance with the amount of blood they get. This is how the overall blood pressure is balanced: the high pressure in arteries is nullified by the low pressure in veins. Arteries, on the other hand, are trained by 10 times higher pressure than veins. There are systolic (the highest pressure), diastolic (the lowest pressure), and pulse arterial pressure. The way high pressure in arteries causes plaque is still to be explored, but considering that, generally, high blood pressure inflicts injury to the vessels’ walls, many claim high pressure in arteries makes them prone to the damage that initiates plaque.
The reason why plaque occurs exclusively in veins is still very vague. The explanation involving lactic acids and nitric oxide does seem more credible than the statement that cholesterol is the sole reason for plaque, but it still leaves much to be desired for, especially in terms of experimental trials that involve humans.