Coronary Artery Disease & Atherosclerosis

Objectives - Understand plaque development, understand normal artery structure, and identify risk factors for atherothrombotic diseases.

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Coronary Artery Disease

The source states that when heart disease or coronary artery disease is discussed, it commonly identifies atherosclerosis of the arteries as a common cause.

Key terms:

Atherogenesis is mainly caused by sedentary lifestyle with increased consumption of a high-fat diet. The process can take a long time and often occurs naturally as a person ages.

Normal Artery Structure

Endothelial cells within the artery are naturally resistant to plaque buildup. They have protective methods that keep thrombin and blood cells from binding to the wall, including a heparin-like substance that helps prevent clots and thrombosis.

The smooth muscle of larger arteries contracts and relaxes in a normal arterial wall, helping regulate blood flow through arterial beds.

Three structures are affected by plaque buildup:

Atherosclerosis Development

The first steps toward lipid accumulation begin with a diet rich in cholesterol and saturated fat, allowing small lipoproteins to accumulate in the intima.

As lipoproteins attach and enter the tunica intima, an immune response occurs. Cytokines and other materials attract more cells to the local area, causing buildup of tissue and low-density lipids.

More cells then attach and bind to endothelial cells that are normally resistant to these adhesions. The source links most lipoprotein binding to the body's immune response with leukocytes, cytokines, and chemokines.

As plaque grows, complications include turbulent flow, increased clot formation, and further blockage. Cell death in the inner arterial portions plus hardening of the tunica media and adventitia reduce normal arterial function.

Mineralization may occur as plaque ages. The source compares mineralization to normal bone calcification and notes it is often seen in plaque deposits that have been present for an extended time.

Complications of Atherosclerosis

Atherosclerotic plaque progression varies based on genetics, lifestyle, socioeconomic and lifestyle choices, and age. In most cases, atherosclerosis is discussed for its effect on the heart.

Stenosis is abnormal narrowing of a blood vessel or other organ or structure. In coronary disease, stenosis from plaque can impair heart function. A stenosis greater than 60% can cause flow limitation during increased demand.

This can produce chronic stable angina pectoris or intermittent claudication during increased demand.

Plaque disruption causes most coronary events. Plaque may fracture away and block a coronary artery, or erode the intima until thrombosis blocks the artery. This can lead to an immediate cardiac event and increased risk of death.

Ischemia, Infarction, and CAD Identification

The source identifies the heart as the main focus for a cardiopulmonary technician, even though atherosclerosis can occur anywhere in the body.

Definitions:

• Ischemia: insufficient blood supply to an organ, usually due to a blocked artery
• Infarction: tissue necrosis caused by impaired arterial or venous blood supply due to mechanical factors such as emboli, thrombi, or plaque
• Acute myocardial infarction: occurs while circulation to a heart region is obstructed and necrosis is occurring

Identification of CAD is typically done through EKG, biomarkers, or cardiac catheterization. The source notes that EKG is discussed in Cardiac Diagnostics I and cardiac catheterization in Cardiac Diagnostics II.

Cardiac Biomarkers

Troponin is the primary indicator of an acute coronary event or acute myocardial infarction. It is typically elevated 4 to 6 hours after AMI onset and remains elevated for 8 to 12 days.

Troponin should not be the only indicator because other muscular damage or insults can cause false positives. It is done in conjunction with an EKG.

CK2, or creatine kinase, is another molecular indicator. It is typically elevated within 6 to 12 hours after infarction onset, peaks at 18 to 24 hours, and returns to baseline after 48 hours. Insults, injuries, and high levels of endurance training can cause false positives. The source states CK2 is a better molecular indicator for acute MIs because its half-life is shorter than troponin.

Risk Factors for Atherothrombotic Diseases

The source lists:

• Smoking
• Hypertension
• Low-density lipoproteins and cholesterol
• Diabetes, insulin resistance, and metabolic syndromes

Other than advanced age, smoking remains the single most important risk factor for coronary artery disease. Ischemic heart disease underlies 35% to 40% of smoking-related deaths. Smoking affects the heart through unfavorable effects on blood pressure and sympathetic tone, reduced myocardial oxygen supply, spontaneous platelet aggregation, and increased adhesion of foreign particles to endothelial cells.

Hypertension is chronic elevated pressure of blood against arterial walls. It is determined by the volume of blood the heart pumps and the resistance to blood flow in systemic arteries. The more cardiac output and systemic vascular resistance increase, the higher the blood pressure.

Hypertension is a major risk factor for coronary heart disease, heart failure, cerebrovascular disease, peripheral arterial disease, renal failure, atrial fibrillation, total mortality, loss of cognitive function, and increased dementia incidence.

Hypertension risk factors include age, ethnicity, family history, genetic factors, lower education and socioeconomic status, greater weight, lower physical activity, tobacco use, psychosocial stressors, sleep apnea, and diet.

LDL cholesterol is the best-established plasma-based atherothrombotic risk factor causally linked to incident MI and cardiovascular death. High LDL cholesterol levels predict future cardiovascular events. Increased LDL exposure increases clinical event risk in older patients.

HDL can carry LDL away from the tunica interna to the liver, where LDL can be broken down. This prevents LDL from depositing on vascular walls.

Insulin resistance and diabetes are major cardiovascular risk factors. Diabetes increases metabolic age. Cardiovascular disease risk starts to increase before clinical diabetes. Insulin resistance promotes atherosclerosis even before frank diabetes. Metabolic syndromes and diabetic disease can increase inflammatory markers and plaque development.