Cardiology Chapter on Atherosclerosis

The general term for arterial wall thickening and loss of elasticity, leading to hardened arteries.

A type of arteriosclerosis affecting small arteries and arterioles, causing downstream ischemic injury.

A type of arteriosclerosis characterized by calcifications of the medial walls of muscular arteries, typically starting along the internal elastic membrane, often affecting adults over 50.

A type of arteriosclerosis where the inner layer of arteries thickens due to proliferation of smooth muscle cells.

A type of arteriosclerosis characterized by the formation of atheromas, which are plaques of fatty deposits, cholesterol, and other substances that accumulate within the arterial wall.

The buildup and progression of plaque inside blood vessels, leading to a narrowing of the vessel lumen and reduced blood flow.

A type of immune system complex that detects danger signals in cells and triggers an inflammatory response. It plays a key role in atherosclerosis development.

A protein that is part of the inflammasome, which is activated when certain danger signals are detected within cells.

A type of fat molecule that can become oxidized, triggering immune responses and contributing to the development of atherosclerosis.

A group of signaling molecules involved in cell communication, particularly in inflammation and immune responses.

The process by which cells migrate from one location to another, often in response to cues or signals in their environment.

An increase in the build-up of extracellular matrix, including collagen and proteoglycans, which can contribute to plaque formation in atherosclerosis.

A type of inflammatory cell that plays a significant role in the development of atherosclerosis. They engulf oxidized LDL and contribute to plaque buildup.

A type of atherosclerotic plaque that displays a smooth, plaque-free segment, indicating that the lesion is on one side of the artery.

A type of stain used to highlight collagen fibers in tissue samples, making them appear blue.

A thinning and weakening of the internal and external elastic membranes, along with a decrease in the thickness of the media of the artery, particularly noticeable under the most advanced atherosclerotic plaque.

The formation of new blood vessels, often associated with the development of atherosclerotic plaques.

A condition where blood flow to the heart is diminished, often due to a narrowing of the coronary arteries.

A type of pain in the calf, thigh, and buttock that is triggered by exercise and relieved by rest.

A narrowing of a blood vessel due to the buildup of atherosclerotic plaque.

The point at which a narrowing of a blood vessel becomes severe enough to cause tissue ischemia, usually when the lumen is reduced by 70% to 75%.

A thickening and narrowing of the inner layer of an artery, most often occurring in muscular arteries larger than arterioles. Often caused by inflammation (like in a healed arteritis) or mechanical injury (e.g., associated with stents or balloon angioplasty). Considered a healing response. Leads to stenosis of the vessel, which can cause issues like in-stent restenosis and major long-term limitations in organ transplants.

Raised lesions within the inner layer of an artery, composed of a soft core of lipid (cholesterol and cholesterol esters) covered by a fibrous cap.

The process of atheroma formation, involving complex interactions of cells and extracellular materials within the intimal layer of an artery. Can lead to a decrease in the number of underlying smooth muscle cells.

A critical event that triggers a cascade of events leading to potential heart attacks and strokes. It involves blockage of blood flow due to various causes, including: Mechanical obstruction caused by the plaque itself; Rupture of the plaque, leading to a blood clot that blocks the artery; Increased diffusion distance from the lumen to the media, causing ischemic injury and weakening of the vessel wall, leading to aneurysms.

A major risk factor for atherosclerosis. While rare, certain Mendelian disorders (e.g., familial hypercholesterolemia) are strongly associated. However, the more common predisposition is polygenic.

The risk of heart attack increases fivefold between ages 40 and 60. Death rates from ischemic heart disease also increase with age.

Statins, commonly prescribed to lower cholesterol levels, also have a beneficial effect on plaque stability.

Adrenergic stimulation, a response to stress, can raise blood pressure or constrict local blood vessels, putting pressure on plaque and potentially leading to disruption.

Circadian rhythms, especially the morning surge in adrenaline, can cause blood pressure spikes and platelet reactivity, increasing the risk of heart attacks.

Thrombosis, a blood clot forming on a plaque, is a central factor in acute coronary syndromes. It can partially or fully block the artery, impacting blood flow.

Vasoconstriction, narrowing of blood vessels, increases mechanical forces on plaques, potentially leading to disruption. Various factors can trigger it, including adrenaline, platelet activity and endothelial dysfunction.

Atherosclerosis is characterized by lesions within the blood vessel wall composed of a fibrous cap and a fatty core. The development of these lesions is influenced by injury and inflammation.

Atherothrombosis is a complex process that involves both atherosclerotic plaque development within the vessel wall and the formation of blood clots on top of the plaque.

Plaques in atherosclerosis are composed of various components, including smooth muscle cells, extracellular matrix, inflammatory cells, calcium deposits, lipids, and cellular debris.

A pro-inflammatory state linked to central obesity characterized by insulin resistance, hypertension, dyslipidemia (increased LDL and decreased HDL), and hypercoagulability.

A modified form of LDL containing apolipoprotein(a) linked to apolipoprotein B-100. Increased Lp(a) levels contribute to coronary and cerebrovascular disease risk.

The principal inhibitor of tissue-type plasminogen activator (tPA) and urokinase (uPA), which are responsible for breaking down blood clots.

Endothelial injury is a critical step in the development of atherosclerosis. It begins with seemingly normal endothelium exhibiting dysfunction, leading to increased permeability, enhanced leukocyte adhesion, and altered gene expression.

Hemodynamic disturbances, such as turbulent blood flow in areas like vessel branches, contribute to endothelial dysfunction and atherosclerosis.

Elevated levels of homocysteine in the blood are associated with increased risk of coronary atherosclerosis, peripheral vascular disease, stroke, and venous thrombosis.

An autosomal recessive disorder characterized by extremely high levels of homocysteine in the blood, often leading to early vascular disease.

Atherosclerosis is viewed as a chronic inflammatory response to injury of the arterial wall, involving modified lipoproteins, macrophages, T lymphocytes, and the interactions between endothelial cells and smooth muscle cells.

This sequence describes the progression of atherosclerosis, starting with endothelial injury, progressing to lipid accumulation, cell recruitment, and eventually the formation of atherosclerotic plaque.

Risk factors for Atherosclerosis can be categorized by factors that can be reduced (e.g., smoking cessation, weight loss, statin administration), genetic factors (e.g., hyperhomocysteinemia, lipoprotein(a)), and lifestyle factors (e.g., lack of exercise, stress, obesity).