The terms arteriosclerosis and atherosclerosis are often used as if they mean the same thing, causing confusion about two distinct arterial conditions. Both terms describe issues that affect the arteries, the blood vessels responsible for carrying oxygen-rich blood through the body. While they are related, they refer to different underlying problems within the arterial walls. This article will clarify the specific differences in how they develop, the risks they pose, and how they are managed.
Arteriosclerosis Explained: The General Hardening of Arteries
Arteriosclerosis is a broad term for any condition causing the walls of arteries to become thick and stiff. Healthy arteries are flexible and elastic, allowing them to expand and contract with each heartbeat to manage blood flow efficiently. Arteriosclerosis describes the loss of this elasticity, a process often called “hardening of the arteries,” which can interfere with circulation.
This condition is a general category of arterial disease with several types. One type involves age-related scarring, while another, known as Mönckeberg’s arteriosclerosis, is characterized by calcium deposits in the middle layer of the arterial walls. Another form, arteriolosclerosis, affects the body’s smallest arteries, called arterioles, causing their walls to thicken and narrow.
The process of arteriosclerosis develops gradually over many years and often progresses without any noticeable symptoms. As the arteries lose their flexibility, the heart must work harder to pump blood through the rigid vessels, which can lead to an increase in blood pressure. The stiffening is a result of complex processes that can involve inflammation and the deposition of various substances in the artery wall.
Atherosclerosis Explained: The Specific Buildup of Plaque
Atherosclerosis is a specific type of arteriosclerosis defined by a distinct mechanism: the buildup of a waxy substance known as plaque on the inner lining of the arteries. Plaque is composed of a mixture of cholesterol, fatty substances, cellular waste products, calcium, and fibrin. As this plaque accumulates, it causes the artery walls to thicken and harden.
The formation of plaque begins with injury to the artery’s inner lining, called the endothelium. This damage can be caused by physical stress from turbulent blood flow or inflammatory stress from factors like smoking. The injured artery wall sends chemical signals that attract white blood cells, which then move into the artery wall and begin to collect cholesterol and other fats.
Over time, these cells, along with smooth muscle cells and other materials, accumulate to form plaques. These deposits can grow large enough to narrow the channel of the artery, restricting the amount of blood that can pass through. This process can develop slowly and may begin as early as childhood, though it often progresses more rapidly in adulthood.
Comparing Core Differences in Progression and Risk
The primary relationship is that atherosclerosis is the most common form of arteriosclerosis. The plaque buildup characteristic of atherosclerosis is a main driver of the artery hardening seen in the broader condition. While both result in stiffened arteries, their underlying mechanisms and associated risks differ.
Arteriosclerosis, in its broader sense, can be a consequence of the aging process, where artery walls naturally lose some flexibility over time. In contrast, atherosclerosis is an inflammatory disease driven by the accumulation of plaque. This process is closely linked to risk factors that promote plaque formation, such as high levels of low-density lipoprotein (LDL) cholesterol, smoking, and diabetes.
General arteriosclerosis leads to a gradual stiffening of the arteries, which steadily increases blood pressure and puts a long-term strain on the heart. Atherosclerosis, while also a gradual process, carries the additional risk of sudden events. The plaques formed in atherosclerosis can be unstable, with a thin cap covering a soft core, and are prone to rupturing. This can trigger the formation of a blood clot that completely blocks an artery, leading to a heart attack or stroke.
Distinct Diagnostic and Treatment Pathways
Identifying risk factors is a part of diagnosis for both conditions. Blood pressure measurement is a straightforward way to assess the strain on arteries, a central issue in general arteriosclerosis. For atherosclerosis, blood tests that measure cholesterol and triglyceride levels are important, as these are the core components of plaque.
Imaging tests can provide a more direct view of the arteries. A Doppler ultrasound can measure the speed of blood flow, which can reveal blockages caused by plaque. An ankle-brachial index test, which compares blood pressure at the ankle to that in the arm, is used to check for atherosclerosis in the arteries of the legs and feet. For more detailed imaging, a cardiac catheterization with an angiogram can visualize the coronary arteries to see if they are narrowed or blocked by plaque.
Treatment for both conditions starts with lifestyle changes, including a heart-healthy diet, regular exercise, and smoking cessation. Medication strategies are targeted at the specific underlying problem. Drugs that lower blood pressure are used to manage the effects of general arteriosclerosis. For atherosclerosis, medications like statins are prescribed to lower LDL cholesterol and reduce plaque buildup. In cases of severe blockage, procedures such as angioplasty with stenting or bypass surgery may be necessary to restore blood flow.