Arteriosclerosis is a broad term for the thickening and stiffening of artery walls. It’s not a single disease but a category that includes several conditions affecting how flexible your arteries are. The most common type, atherosclerosis, involves fatty plaque building up inside artery walls. But arteriosclerosis also covers other forms of arterial hardening that have nothing to do with plaque. The distinction matters because the causes, affected arteries, and treatments can differ significantly.
Arterial stiffening is remarkably common with age. Data from the Framingham Heart Study found that only about 30% of people in their 50s still had healthy, flexible arteries. By age 70, that number dropped to just 1%. In other words, some degree of arteriosclerosis affects nearly everyone who lives long enough, though its severity and consequences vary widely.
How Arteriosclerosis Differs From Atherosclerosis
People often use these two terms interchangeably, but they describe different things. Arteriosclerosis is the umbrella term for any process that makes arteries harder and less elastic. Atherosclerosis is one specific type, caused by plaque (a mix of fat, cholesterol, calcium, and other substances) accumulating inside artery walls. Most of the time when doctors talk about arteriosclerosis, they’re referring to atherosclerosis, simply because it’s the most widespread form.
Another type, called Monckeberg medial calcific sclerosis, involves calcium deposits forming in the middle layer of small and medium-sized arteries, particularly in the arms and legs. It doesn’t involve plaque. This form is usually discovered by accident on an X-ray or ultrasound, showing up as bright white lines along the artery walls. It’s especially common in people with diabetes or advanced kidney disease: roughly 17% of newly diagnosed diabetics and 27% of people with end-stage kidney disease show signs of it.
What Happens Inside Stiffening Arteries
Healthy arteries are elastic. They stretch slightly with each heartbeat and spring back between beats, which helps smooth out blood flow and keep pressure steady. Arteriosclerosis disrupts this process through several overlapping mechanisms. The elastic fibers in artery walls break down over time and get replaced by stiffer collagen. Chemical cross-links form between these fibers, making the wall even more rigid. Calcium deposits accumulate. Inflammation driven by oxidative stress damages the inner lining of the artery, and the smooth muscle cells within the wall itself become stiffer.
The result is an artery that can’t absorb the force of each heartbeat the way it once did. Blood pressure rises, the heart works harder to push blood through less flexible tubes, and organs downstream receive blood in sharper, more forceful pulses rather than a steady flow. This puts extra strain on the heart, brain, and kidneys over years and decades.
Why It Often Has No Symptoms
Arteriosclerosis typically develops silently over many years. Most people have no symptoms in the early stages. When symptoms do appear, they usually show up during physical or emotional stress, when the body needs more oxygen than the compromised arteries can deliver.
The specific symptoms depend on which arteries are affected. Narrowed heart arteries cause chest pain or shortness of breath during exertion. Stiffened arteries in the legs may cause cramping or pain while walking. Reduced blood flow to the brain can cause dizziness, confusion, or sudden weakness on one side of the body. Narrowed kidney arteries can quietly worsen blood pressure and kidney function without any obvious warning signs. In some cases, a doctor may detect early changes simply by listening with a stethoscope for a whooshing sound (called a bruit) over the neck or abdomen, indicating turbulent blood flow through a narrowed artery.
Erectile dysfunction can be one of the earliest noticeable signs in men, since the small arteries supplying the penis are among the first affected by reduced blood flow.
Major Risk Factors
High blood pressure is the single biggest driver of arterial stiffening. The 2025 guidelines from the American Heart Association and American College of Cardiology note that once blood pressure rises above 120/80, there may already be irreversible vascular damage, even if treatment starts later. Stage 1 hypertension begins at 130/80, and stage 2 at 140/90. Higher blood pressure is linked to elevated risk for heart disease, stroke, heart failure, peripheral artery disease, kidney disease, and dementia.
Other major risk factors include high cholesterol, smoking, diabetes, obesity, and a sedentary lifestyle. These overlap and amplify each other. A person with both diabetes and high blood pressure, for instance, faces arterial changes far more rapidly than someone with just one of those conditions. Family history also plays a role, particularly if a close relative developed heart disease before age 55 (for men) or 65 (for women).
Excess sodium in the diet contributes through multiple pathways. It raises blood pressure by increasing blood volume and the resistance in blood vessels, which accelerates arterial wall remodeling. But sodium also directly damages the delicate inner lining of arteries by triggering oxidative stress and inflammation, independent of its effect on blood pressure.
Potential Complications
When arteriosclerosis progresses far enough, it can trigger serious events. Plaque can rupture and form a blood clot that blocks an artery entirely, causing a heart attack (if in the heart’s arteries) or a stroke (if in arteries feeding the brain). A weakened, stiffened artery wall can bulge outward, forming an aneurysm that may eventually rupture. Chronically reduced blood flow to the kidneys leads to progressive kidney disease. In severe cases, blocked arteries in the legs can cause tissue death, known as gangrene, though this is rare.
How Arterial Stiffness Is Measured
The gold standard for assessing arterial stiffness is a test called pulse wave velocity, or PWV. It measures how fast the pressure wave from each heartbeat travels along your arteries. Stiffer arteries transmit the wave faster, so a higher number means more stiffness. The most commonly used version measures the wave speed between the carotid artery in the neck and the femoral artery in the groin, reflecting the stiffness of the aorta, your body’s largest artery.
The test itself is straightforward: sensors placed on the skin detect the pulse at two points, and a computer calculates the speed. It’s considered the most accurate method available. Other approaches include Doppler ultrasound, MRI, and oscillometric devices that estimate stiffness during a standard blood pressure reading. The ankle-brachial index, which compares blood pressure in the ankle to the arm, is another common screening tool. A value above 1.1 can indicate calcification in the leg arteries.
Exercise and Arterial Flexibility
Regular aerobic exercise is one of the most effective ways to slow or partially reverse arterial stiffening. A controlled trial testing different exercise routines found that all groups showed significantly lower arterial stiffness after just eight weeks. Participants who exercised at low intensity for as little as 15 minutes a day saw meaningful improvements, and there was no significant difference between low and moderate intensity groups. The researchers concluded that exercising for at least 15 minutes daily is enough to produce measurable reductions in arterial stiffness.
The likely mechanism is that regular physical activity improves the function of the artery’s inner lining, reduces inflammation, and helps maintain the balance between elastic and stiff fibers in the artery wall. These benefits appear to be partly independent of weight loss or blood pressure changes, though exercise helps with those too.
Medical Treatment
Treatment focuses on controlling the conditions that drive arterial stiffening. Blood pressure medications are central, and certain types appear to have benefits beyond just lowering pressure. Blood pressure drugs that block the renin-angiotensin system have been shown to reduce arterial stiffness partly through mechanisms independent of blood pressure lowering itself. They appear to directly influence the structural remodeling happening in artery walls. Clinical guidelines now recommend this class of medication as a preferred option for reducing arterial stiffness in people with advanced kidney disease.
Managing cholesterol, blood sugar, and body weight all play important roles. For people with significant plaque buildup, cholesterol-lowering medications can stabilize existing plaques and reduce the risk of rupture. Quitting smoking produces rapid improvements in artery function. Reducing sodium intake helps both by lowering blood pressure and by reducing the direct inflammatory damage that excess salt causes to artery walls.
Arteriosclerosis can’t be fully reversed once it’s advanced, but the combination of lifestyle changes and appropriate medication can slow progression substantially, reduce complications, and in some cases restore a degree of arterial flexibility that meaningfully lowers cardiovascular risk.