Lipid

How does coronary heart disease (CHD) differ from coronary artery disease (CAD)?

CHD includes CAD and other coronary artery conditions, such as spasm and inflammation.

What defines coronary artery disease?

Narrowing or blockage of coronary arteries caused by plaque buildup.

What are the nonmodifiable CAD risk factors?

Age, family history, gender, and race.

At what age does CAD risk increase in men, according to the lecture?

After age 45.

At what age does CAD risk increase in women, according to the lecture?

After age 55.

What paternal or sibling history qualifies as premature CAD in a male relative?

CAD before age 45 in a father or brother.

What maternal or sibling history qualifies as premature CAD in a female relative?

CAD before age 55 in a mother or sister.

Which sex has greater CAD risk?

Men.

Which racial or ethnic groups have higher CAD risk in the lecture?

African American, Hispanic American, and South Asian Indian.

What are the modifiable CAD risk factors listed in the lecture?

Hypertension, smoking, hyperlipidemia, diabetes, alcohol use, physical inactivity, diet, abdominal obesity, and psychosocial factors.

Is a family history of premature CAD modifiable or nonmodifiable?

Nonmodifiable.

Is abdominal obesity a modifiable or nonmodifiable CAD risk factor?

Modifiable.

What is the number-one preventable cause of death and illness in the United States?

Smoking.

How much does CAD risk decrease one year after smoking cessation?

50%.

What should be a primary target for CAD risk reduction in a smoker?

Smoking cessation.

How does elevated LDL affect CAD risk?

Increases risk.

How does higher HDL affect CAD risk?

Decreases risk.

What can clinical risk scores guide in patients with hypercholesterolemia?

Prevention strategies.

What drug class is used for primary prevention in the lecture’s hypercholesterolemia discussion?

Statins.

How many listed abnormalities are required for metabolic syndrome?

Three or more.

What are the five components of metabolic syndrome in the lecture?

Abdominal obesity, elevated triglycerides, low HDL, elevated fasting glucose, and hypertension.

What triglyceride level meets the lecture’s metabolic syndrome criterion?

≥150 mg/dL.

What HDL level meets the metabolic syndrome criterion in men?

What HDL level meets the metabolic syndrome criterion in women?

What fasting glucose level meets the lecture’s metabolic syndrome criterion?

≥110 mg/dL.

What body-fat distribution is a component of metabolic syndrome?

Abdominal obesity.

What blood pressure disorder is a component of metabolic syndrome?

Hypertension.

A man has triglycerides of 160 mg/dL, HDL of 35 mg/dL, and fasting glucose of 115 mg/dL. Does he meet the lecture’s metabolic syndrome criteria?

Yes; he has three qualifying abnormalities.

What sustained percentage of weight loss is likely to improve metabolic risk factors?

3–5%.

What lipid abnormality improves with sustained weight loss of 3–5%?

Elevated triglycerides.

What glycemic measures improve with sustained weight loss of 3–5%?

Blood glucose and HbA1c.

How does sustained weight loss of 3–5% affect diabetes development?

Reduces development of diabetes.

What additional benefit occurs with greater weight loss?

Further blood pressure reduction.

What activity change is an important component of weight loss?

Increasing physical activity.

Which dietary pattern has proven benefit in the lecture?

Mediterranean diet.

What is the best-known inflammatory marker for chronic, low-grade inflammation?

High-sensitivity C-reactive protein (hsCRP).

Where is hsCRP produced?

The liver.

What stimulates production of hsCRP?

Systemic inflammation.

What type of protein is hsCRP?

An acute-phase protein.

How does hsCRP’s prognostic value relate to lipid levels?

It is independent of and additive to lipid levels.

What hsCRP level indicates low cardiovascular risk?

What hsCRP level indicates intermediate cardiovascular risk?

1–3 mg/L.

What hsCRP level indicates high cardiovascular risk?

3 mg/L.

According to the lecture, what usually explains hsCRP >100 mg/L?

Infection or injury causing a false-positive cardiovascular risk signal.

What prevention decisions may hsCRP help guide?

Primary and secondary prevention strategies.

What three processes contribute to CHD development?

Endothelial cell dysfunction, dyslipidemia, and inflammation.

What dietary factors contribute to early atherosclerosis?

Excessive cholesterol and saturated fat intake.

What early arterial lesion forms following endothelial dysfunction?

A fatty streak.

What accumulates beneath the endothelium in an early atherosclerotic lesion?

Lipids and lipid-laden macrophages.

What is the major atherogenic lipid?

LDL.

What happens to LDL after it enters the arterial intima?

It becomes oxidized.

How do foam cells form?

Macrophages ingest LDL.

What cap develops as an atherosclerotic plaque matures?

A fibrous cap.

What happens to the vessel lumen as a plaque calcifies and the vessel wall remodels?

It narrows.

What degree of coronary stenosis is required to reduce myocardial oxygen supply at rest?

90%.

What acute process can follow atherosclerotic plaque rupture?

Intravascular thrombosis.

What vascular response may accompany thrombosis after plaque rupture?

Coronary vasospasm.

What determines the outcome of plaque rupture in the lecture?

Whether the vessel becomes fully occluded.

What acute coronary syndromes can result from plaque rupture?

Unstable angina or myocardial infarction.

What occurs if plaque rupture results in complete coronary occlusion?

Acute myocardial necrosis.

What may happen if a ruptured plaque restabilizes?

It may leave more severe stenosis.

How does plaque lipid content affect vulnerability to rupture?

Higher lipid content increases vulnerability.

How does plaque macrophage concentration affect vulnerability to rupture?

Higher macrophage concentration increases vulnerability.

What fibrous cap feature increases plaque vulnerability to rupture?

A very thin fibrous cap.

What can be the first manifestation of CAD from an early vulnerable plaque?

Acute MI or sudden death.

Do most infarctions occur at sites of preexisting critical stenosis?

No.

What is the goal of primary CAD prevention?

Prevent CAD from developing in patients with no history of CAD.

What is the goal of secondary CAD prevention?

Prevent progression, complications, or recurrent events in patients with existing CAD.

Which lifestyle interventions support both primary and secondary CAD prevention?

Diet, exercise, weight management, and smoking cessation.

What blood pressure intervention helps prevent CAD and delay progression?

Lowering elevated blood pressure.

Which patients should receive a statin according to the lecture?

All patients at significant risk for cardiovascular events, regardless of cholesterol levels.

How does lowering LDL affect atherosclerosis progression?

Delays progression and may produce regression.

How does LDL-lowering therapy affect new atherosclerotic lesions?

Reduces new lesion formation.

How does LDL-lowering therapy affect endothelial function?

Restores endothelial function.

How does LDL-lowering therapy affect cardiovascular event rates?

Markedly reduces event rates.

Which major outcomes do statins prevent according to the lecture?

Deaths, coronary events, and stroke.

Which patient characteristics do not eliminate the lecture’s stated statin benefits?

Age, race, baseline cholesterol level, or presence of hypertension.

Which patients should receive ACE inhibitors for CAD prevention according to the lecture?

High-risk patients, including those with diabetes plus additional risk factors or clinical atherosclerotic disease.

What benefit does the lecture report for fish oil supplements in CAD prevention?

No benefit.

What benefit does the lecture report for treatments aimed at raising HDL?

No benefit.

What benefit does the lecture report for vitamin E therapy in CAD prevention?

No benefit.

What benefit does the lecture report for lowering homocysteine levels?

No benefit.

What benefit does the lecture report for hormone replacement therapy in CAD prevention?

No benefit.

How does the lecture characterize aspirin’s benefit for primary prevention?

Little benefit.

How effective is antiplatelet therapy for secondary prevention?

Very effective.

Which oral diabetes drug class has proven cardiovascular benefit in patients with type 2 diabetes?

SGLT-2 inhibitors.

Which injectable diabetes drug class has proven cardiovascular benefit in patients with type 2 diabetes?

GLP-1 receptor agonists.

Can CAD be asymptomatic?

Yes.

What symptomatic presentations of CAD are listed in the lecture?

Angina, myocardial infarction, or arrhythmia.

What proportion of MI patients do not have chest pain?

One third.

How is myocardial ischemic chest discomfort typically described?

Dull, aching, pressure, heaviness, tightness, or squeezing.

Where is myocardial ischemic chest discomfort typically located?

Retrosternal or left precordial.

Where can myocardial ischemic pain be referred?

Jaw, shoulders, arms, upper abdomen, or back.

What may progressive ischemic symptoms or symptoms at rest indicate?

Unstable angina due to plaque rupture and thrombosis.

What activity typically first provokes ischemic symptoms?

Exercise.

What nonexercise stressors can provoke ischemic symptoms?

Cold exposure, meals, or emotions.

How quickly do ischemic symptoms often resolve?

Quickly.

Is myocardial ischemic pain related to position?

No.

Is myocardial ischemic pain reproduced by palpation?

No.

What respiratory symptom may accompany myocardial ischemia?

Shortness of breath.