NUR 521 Exam 2 Study Guide Part 2
Module 5: Chapters 44-47
ASCVD- Atherosclerotic Cardiovascular Disease:
Cholesterol plays a role in atherosclerotic cardiovascular disease (ASCVD). ASCVD includes the
vessels of the heart as well as the brain. Damage to these vessels can result in myocardial
infarction (MI) or stroke. Moderate cardiac ASCVD usually manifests first as anginal pain. Severe
cardiac ASCVD sets the stage for acute coronary syndrome (ACS) and MI.
In the United States, cardiac ASCVD is the leading killer of men and women, causing 801,000
deaths in 2013. According to the American Heart Association (AHA), about 92 million Americans
have a history of coronary events (angina, MI, or both). More than half of these people are
women.
Atherosclerotic cardiovascular disease (ASCVD) begins as a fatty streak in the arterial wall. This
is followed by deposition of fibrous plaque. As atherosclerotic plaque grows, it impedes
coronary blood flow, causing anginal pain. Worse yet, atherosclerosis encourages formation of
thrombi, which can block flow to the brain and heart entirely, thereby causing MI and stroke.
Atherosclerosis can develop in any artery and therefore compromise circulation to any tissue.
The risk for developing ASCVD is directly related to increased levels of blood cholesterol, in
the form of low-density lipoproteins (LDLs). By reducing levels of LDL cholesterol, we can slow
progression of atherosclerosis, reduce the risk for serious ASCVD and its potential
consequences, and prolong life. The preferred method for lowering LDL cholesterol is
modification of diet combined with exercise. Drugs are employed only when diet modification
and exercise are insufficient.
, Lipoproteins are tiny, spherical
structures that consist of a
hydrophobic core, composed of
cholesterol and TGs, surrounded by a
hydrophilic shell, composed primarily
of phospholipids.
All lipoproteins have one or more
apolipoprotein molecules embedded
in their shell. Lipoproteins, have three
functions:
• They serve as recognition sites for
cell-surface receptors and thereby
allow cells to bind with and ingest
lipoproteins.
• They activate enzymes that
metabolize lipoproteins.
• They increase the structural stability
of lipoproteins
There are six major classes of plasma lipoproteins.
Distinctions among classes are based on size, density, apolipoprotein content, transport
function, and primary core lipids (cholesterol or TG). From a pharmacologic perspective, the
features of greatest interest are lipid content, apolipoprotein content, and transport function.
Of the six major classes of lipoproteins, three are especially important in coronary
atherosclerosis. These classes are named (1) very-low-density lipoproteins (VLDLs), (2) low-
density lipoproteins (LDLs), and (3) high-density lipoproteins (HDLs).
Very-Low Density Lipoproteins: VLDLs contain mainly triglycerides (and some cholesterol), and
they account for nearly all of the TGs in blood. The main physiologic role of VLDLs is to deliver
triglycerides from the liver to adipose tissue and muscle, which can use the TGs as fuel. The role
of VLDLs in atherosclerosis is unclear. Although several studies suggest a link between elevated
levels of VLDLs and development of atherosclerosis, this link has not been firmly established.
However, we do know that elevation of TG levels (above 500 mg/dL) increases the risk for
pancreatitis.
,Low-Density Lipoproteins: LDLs contain cholesterol as their primary core lipid, and they
account for the majority (60% to 70%) of all cholesterol in blood. The physiologic role of LDLs is
delivery of cholesterol to non hepatic tissues. LDLs can be viewed as byproducts of VLDL
metabolism, in that the lipids and apolipoproteins that compose LDLs are remnants of VLDL
degradation.
Of all lipoproteins, LDLs make the greatest contribution to coronary atherosclerosis. The
probability of developing ASCVD is directly related to the level of LDLs in blood. Conversely, by
reducing LDL levels, we decrease the risk for ASCVD. Accordingly, when cholesterol-lowering
drugs are used, the main goal is to reduce elevated LDL levels. Multiple studies have shown
that, by reducing LDL levels, we can arrest or perhaps even reverse atherosclerosis and can
thereby reduce mortality from ASCVD. In fact, for each 1% reduction in the LDL level, there is
about a 1% reduction in the risk for a major cardiovascular (CV) event.
High-Density Lipoproteins: Like LDLs, HDLs contain cholesterol as their primary core lipid, and
they account for 20% to 30% of all cholesterol in the blood. In contrast to LDLs, whose function
is delivery of cholesterol to peripheral tissues, HDLs carry cholesterol from peripheral tissues
back to the liver. That is, HDLs promote cholesterol removal.
The influence of HDLs on ASCVD is dramatically different from that of LDLs. Whereas elevation
of LDLs increases the risk for ASCVD, elevation of HDLs reduces the risk for ASCVD. That is, high
HDL levels actively protect against ASCVD.
Primary disorders of lipid metabolism such as familial hypercholesterolemia (FH),
chylomicronemia, familial combined hyperlipidemia, familial dysbetalipoproteinemia classify
according to Fredrickson phenotype.
Secondary dyslipidemia can result from diabetes mellitus, hypothyroidism, obstructive liver
diseases, chronic renal failure, drugs that increase LDL-C including retinoids, cyclosporine A, and
phenothiazines and drugs that decrease HDL-C including progestins, androgens, beta-blockers,
and anabolic steroids.
Based on the types of lipid abnormalities, dyslipidemias can be categorized as the following:
, • high total cholesterol (TC)
• high low-density lipoprotein cholesterol (LDL-C)
• high non-high-density lipoprotein cholesterol (non-HDL-C)
• high triglycerides (TG)
• Low high-density lipoprotein cholesterol (HDL-C)
Non-HDL is your HDL subtracted from your total cholesterol.
Basically, this tells you the total amount of all the “bad” cholesterol.
LDLs initiate and fuel development of atherosclerosis. The process begins with transport of LDLs
from the arterial lumen into endothelial cells that line the lumens of blood vessels. From there,
they move into the space that underlies the arterial epithelium. When in the subendothelial
space, components of LDLs undergo oxidation. This step is critical in that oxidized LDLs do the
following:
• Attract monocytes from the circulation into the subendothelial space, after which the
monocytes are converted to macrophages (which are critical to atherogenesis)
• Inhibit macrophage mobility, thereby keeping macrophages at the site of atherogenesis
• Undergo uptake by macrophages (macrophages do not take up LDLs that have not been
oxidized)
• Damage the vascular endothelium, as they are cytotoxic
How do you calculate a patient’s risk for ASCVD???
Calculating a patient's risk for atherosclerotic cardiovascular disease (ASCVD) typically involves
using established risk assessment tools. One commonly used tool is the ASCVD Risk Estimator,
which incorporates factors such as age, gender, race, total cholesterol, HDL cholesterol, systolic
blood pressure, diabetes status, and smoking status.
The equation used for the ASCVD Risk Estimator is:
ASCVD Risk=1−(1−10-year risk of ASCVD)
This equation estimates the 10-year risk of developing a first ASCVD event. The American
College of Cardiology (ACC) and American Heart Association (AHA) provide online calculators
and guidelines to assist healthcare professionals in determining a patient's risk.
Module 5: Chapters 44-47
ASCVD- Atherosclerotic Cardiovascular Disease:
Cholesterol plays a role in atherosclerotic cardiovascular disease (ASCVD). ASCVD includes the
vessels of the heart as well as the brain. Damage to these vessels can result in myocardial
infarction (MI) or stroke. Moderate cardiac ASCVD usually manifests first as anginal pain. Severe
cardiac ASCVD sets the stage for acute coronary syndrome (ACS) and MI.
In the United States, cardiac ASCVD is the leading killer of men and women, causing 801,000
deaths in 2013. According to the American Heart Association (AHA), about 92 million Americans
have a history of coronary events (angina, MI, or both). More than half of these people are
women.
Atherosclerotic cardiovascular disease (ASCVD) begins as a fatty streak in the arterial wall. This
is followed by deposition of fibrous plaque. As atherosclerotic plaque grows, it impedes
coronary blood flow, causing anginal pain. Worse yet, atherosclerosis encourages formation of
thrombi, which can block flow to the brain and heart entirely, thereby causing MI and stroke.
Atherosclerosis can develop in any artery and therefore compromise circulation to any tissue.
The risk for developing ASCVD is directly related to increased levels of blood cholesterol, in
the form of low-density lipoproteins (LDLs). By reducing levels of LDL cholesterol, we can slow
progression of atherosclerosis, reduce the risk for serious ASCVD and its potential
consequences, and prolong life. The preferred method for lowering LDL cholesterol is
modification of diet combined with exercise. Drugs are employed only when diet modification
and exercise are insufficient.
, Lipoproteins are tiny, spherical
structures that consist of a
hydrophobic core, composed of
cholesterol and TGs, surrounded by a
hydrophilic shell, composed primarily
of phospholipids.
All lipoproteins have one or more
apolipoprotein molecules embedded
in their shell. Lipoproteins, have three
functions:
• They serve as recognition sites for
cell-surface receptors and thereby
allow cells to bind with and ingest
lipoproteins.
• They activate enzymes that
metabolize lipoproteins.
• They increase the structural stability
of lipoproteins
There are six major classes of plasma lipoproteins.
Distinctions among classes are based on size, density, apolipoprotein content, transport
function, and primary core lipids (cholesterol or TG). From a pharmacologic perspective, the
features of greatest interest are lipid content, apolipoprotein content, and transport function.
Of the six major classes of lipoproteins, three are especially important in coronary
atherosclerosis. These classes are named (1) very-low-density lipoproteins (VLDLs), (2) low-
density lipoproteins (LDLs), and (3) high-density lipoproteins (HDLs).
Very-Low Density Lipoproteins: VLDLs contain mainly triglycerides (and some cholesterol), and
they account for nearly all of the TGs in blood. The main physiologic role of VLDLs is to deliver
triglycerides from the liver to adipose tissue and muscle, which can use the TGs as fuel. The role
of VLDLs in atherosclerosis is unclear. Although several studies suggest a link between elevated
levels of VLDLs and development of atherosclerosis, this link has not been firmly established.
However, we do know that elevation of TG levels (above 500 mg/dL) increases the risk for
pancreatitis.
,Low-Density Lipoproteins: LDLs contain cholesterol as their primary core lipid, and they
account for the majority (60% to 70%) of all cholesterol in blood. The physiologic role of LDLs is
delivery of cholesterol to non hepatic tissues. LDLs can be viewed as byproducts of VLDL
metabolism, in that the lipids and apolipoproteins that compose LDLs are remnants of VLDL
degradation.
Of all lipoproteins, LDLs make the greatest contribution to coronary atherosclerosis. The
probability of developing ASCVD is directly related to the level of LDLs in blood. Conversely, by
reducing LDL levels, we decrease the risk for ASCVD. Accordingly, when cholesterol-lowering
drugs are used, the main goal is to reduce elevated LDL levels. Multiple studies have shown
that, by reducing LDL levels, we can arrest or perhaps even reverse atherosclerosis and can
thereby reduce mortality from ASCVD. In fact, for each 1% reduction in the LDL level, there is
about a 1% reduction in the risk for a major cardiovascular (CV) event.
High-Density Lipoproteins: Like LDLs, HDLs contain cholesterol as their primary core lipid, and
they account for 20% to 30% of all cholesterol in the blood. In contrast to LDLs, whose function
is delivery of cholesterol to peripheral tissues, HDLs carry cholesterol from peripheral tissues
back to the liver. That is, HDLs promote cholesterol removal.
The influence of HDLs on ASCVD is dramatically different from that of LDLs. Whereas elevation
of LDLs increases the risk for ASCVD, elevation of HDLs reduces the risk for ASCVD. That is, high
HDL levels actively protect against ASCVD.
Primary disorders of lipid metabolism such as familial hypercholesterolemia (FH),
chylomicronemia, familial combined hyperlipidemia, familial dysbetalipoproteinemia classify
according to Fredrickson phenotype.
Secondary dyslipidemia can result from diabetes mellitus, hypothyroidism, obstructive liver
diseases, chronic renal failure, drugs that increase LDL-C including retinoids, cyclosporine A, and
phenothiazines and drugs that decrease HDL-C including progestins, androgens, beta-blockers,
and anabolic steroids.
Based on the types of lipid abnormalities, dyslipidemias can be categorized as the following:
, • high total cholesterol (TC)
• high low-density lipoprotein cholesterol (LDL-C)
• high non-high-density lipoprotein cholesterol (non-HDL-C)
• high triglycerides (TG)
• Low high-density lipoprotein cholesterol (HDL-C)
Non-HDL is your HDL subtracted from your total cholesterol.
Basically, this tells you the total amount of all the “bad” cholesterol.
LDLs initiate and fuel development of atherosclerosis. The process begins with transport of LDLs
from the arterial lumen into endothelial cells that line the lumens of blood vessels. From there,
they move into the space that underlies the arterial epithelium. When in the subendothelial
space, components of LDLs undergo oxidation. This step is critical in that oxidized LDLs do the
following:
• Attract monocytes from the circulation into the subendothelial space, after which the
monocytes are converted to macrophages (which are critical to atherogenesis)
• Inhibit macrophage mobility, thereby keeping macrophages at the site of atherogenesis
• Undergo uptake by macrophages (macrophages do not take up LDLs that have not been
oxidized)
• Damage the vascular endothelium, as they are cytotoxic
How do you calculate a patient’s risk for ASCVD???
Calculating a patient's risk for atherosclerotic cardiovascular disease (ASCVD) typically involves
using established risk assessment tools. One commonly used tool is the ASCVD Risk Estimator,
which incorporates factors such as age, gender, race, total cholesterol, HDL cholesterol, systolic
blood pressure, diabetes status, and smoking status.
The equation used for the ASCVD Risk Estimator is:
ASCVD Risk=1−(1−10-year risk of ASCVD)
This equation estimates the 10-year risk of developing a first ASCVD event. The American
College of Cardiology (ACC) and American Heart Association (AHA) provide online calculators
and guidelines to assist healthcare professionals in determining a patient's risk.
