Atherosclerotic cardiovascular disease (ASCVD) refers to conditions caused by the buildup of plaque in the artery walls, a process known as atherosclerosis. The term “clinical ASCVD” defines a patient who has already experienced a major cardiovascular event due to this underlying disease. This distinction moves the patient from being “at risk” (primary prevention) to having “established disease” (secondary prevention), requiring more aggressive treatment to prevent future occurrences. ASCVD-related conditions represent a leading cause of illness and death worldwide, making the understanding of its established form a high priority for public health.
Specific Events That Define Clinical ASCVD
A diagnosis of clinical ASCVD is confirmed when a patient has a history of specific events that result from the underlying process of atherosclerosis. These events are grouped into three main categories based on the location of the affected arteries. The occurrence of any one condition is sufficient to classify a patient as having established ASCVD.
Coronary Heart Disease
Coronary heart disease involves the arteries supplying the heart muscle itself. This category includes a history of myocardial infarction, commonly known as a heart attack, which is the death of heart tissue due to a lack of blood flow. It also covers acute coronary syndrome (ACS), stable or unstable angina (chest pain caused by reduced blood flow), and any procedure for coronary revascularization, such as bypass surgery or angioplasty.
Cerebrovascular Disease
Cerebrovascular disease affects the arteries leading to or within the brain. The primary events here are ischemic stroke, caused by a clot blocking blood flow to the brain, and a transient ischemic attack (TIA), often called a “mini-stroke,” which involves temporary symptoms of stroke. Both conditions are typically caused by plaque buildup in the carotid arteries of the neck or other brain arteries.
Peripheral Artery Disease (PAD)
Peripheral artery disease (PAD) is defined by the narrowing of arteries outside the heart and brain, most commonly in the legs. Symptomatic PAD, often presenting as pain or cramping in the legs during exercise (claudication), or a history of related procedures like revascularization or amputation, qualifies as clinical ASCVD. This category also includes atherosclerotic aortic aneurysm, which is a ballooning of the body’s main artery caused by plaque damage.
The Underlying Mechanism: Atherosclerosis
The foundation of clinical ASCVD is atherosclerosis, a slow, progressive inflammatory disease of the arterial wall that can begin early in life. The process starts when the inner lining of the artery, called the endothelium, becomes damaged or dysfunctional, often due to factors like high blood pressure, elevated low-density lipoprotein cholesterol (LDL-C), or smoking. This damage allows LDL-C particles to penetrate the arterial wall, where they become modified and trigger an inflammatory response.
Immune cells called monocytes move into the wall and transform into macrophages, which then engulf the trapped lipids, becoming foam cells. The accumulation of these foam cells creates a fatty streak, which is the earliest visible lesion of atherosclerosis. Over time, smooth muscle cells migrate to the area and secrete collagen, forming a fibrous cap over the fatty core, resulting in a mature atherosclerotic plaque.
This growing plaque narrows the artery, restricting blood flow and causing symptoms like angina or claudication when oxygen demand increases, a condition called ischemia. A more immediate and life-threatening event occurs if the fibrous cap ruptures or erodes. When this unstable plaque breaks open, it exposes the fatty, thrombogenic material inside to the bloodstream, which triggers the rapid formation of a blood clot (thrombus).
This sudden blood clot can completely block the artery, leading to an acute event. In the coronary arteries, this blockage causes a myocardial infarction (heart attack), and in the cerebral arteries, it results in an ischemic stroke. The size of the lipid core and the thickness of the fibrous cap are factors that determine how vulnerable a plaque is to rupture, highlighting the chronic inflammatory nature of the disease.
Diagnosing Established ASCVD
The diagnosis of established clinical ASCVD is based on confirming a patient’s history of one of the defining events and then assessing the extent of the underlying disease. The process typically begins with a detailed patient history, focusing on symptoms like chest pain, shortness of breath, or leg pain, and a physical examination to check for signs such as reduced pulses in the extremities.
Laboratory Tests
Laboratory tests analyze biomarkers associated with the disease. A lipid panel measures cholesterol levels, including LDL-C, which is a primary target for treatment. High-sensitivity C-reactive protein (hsCRP), a marker of systemic inflammation, can also be measured; levels at or above 2.0 mg/L indicate increased risk.
Imaging and Functional Tests
Imaging and functional tests locate and quantify the severity of arterial blockage:
- An electrocardiogram (ECG) records the heart’s electrical activity, showing evidence of past or current heart damage.
- Stress testing determines how the heart responds to physical exertion, often using exercise or medication.
- Angiography involves injecting a dye to visualize arteries under X-ray, measuring the degree of narrowing.
- The Ankle-Brachial Index (ABI) compares blood pressure in the ankle to the arm; an ABI below 0.9 is diagnostic for PAD.
- Brain imaging, such as CT or MRI, confirms an ischemic stroke or TIA and assesses tissue damage.