Chapter 37
Coronary Artery Disease and Acute Coronary Syndrome
KEY POINTS
CORONARY ARTERY DISEASE
• Coronary artery disease (CAD) is a type of blood vessel disorder included in the general
category of atherosclerosis. Atherosclerosis is characterized by lipid deposits within the intimal
wall of an artery.
• CAD is a progressive disease that develops in stages over many years. When it becomes
symptomatic, the disease process is usually well advanced.
• Normally, some arterial collateral circulation exists within the coronary circulation. The growth
and extent depends on the inherited predisposition to develop new blood vessels and the
presence of chronic ischemia.
• Many risk factors have been associated with CAD.
• Nonmodifiable risk factors include age, gender, ethnicity, and genetics.
• Modifiable risk factors include high serum lipids, high BP, tobacco use, physical inactivity,
obesity, diabetes, metabolic syndrome, psychologic states (e.g., anger, depression), high
homocysteine level and substance use.
• High serum lipid levels are one of the most firmly established risk factors for CAD.
• High-density lipoproteins (HDLs) carry lipids away from arteries to the liver for metabolism.
High serum HDL levels are desirable.
• Physical activity, eating more healthy fats, losing weight, moderate alcohol intake and quitting
smoking help increase HDL levels.
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• High low-density lipoprotein (LDL) levels correlate most closely with an increased incidence
of atherosclerosis and CAD. Therefore, low serum LDL levels are desirable.
• Hypertension increases the risk of CAD, stroke, peripheral vascular disease, heart failure, and
death.
• The risk of developing CAD is much higher in those who smoke tobacco or use smokeless
tobacco than in those who do not.
• The incidence of CAD is 2 to 4 times greater among people who have diabetes, even those with
well-controlled blood glucose levels.
INTERPROFESSIONAL AND NURSING CARE: CORONARY ARTERY
DISEASE
• Prevention and early treatment of CAD involve a multifaceted approach and must be
ongoing throughout the lifespan.
• Management risk starts with controlling or changing the additive effects of modifiable
risk factors.
• A regular physical activity program should be implemented.
• Diet should limit saturated fats and cholesterol and emphasize complex carbohydrates
(e.g., whole grains, fruits, vegetables) and fiber.
• A complete lipid profile is recommended every 5 years beginning at age 20.
• Guidelines recommend the following groups of people receive statin therapy:
• Patients with known CVD
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• Patients with primary elevations of LDL cholesterol levels greater than or equal to 190
mg/dL
(e.g., familial hypercholesterolemia)
• Patients between 40 and 75 years old with diabetes and LDL cholesterol levels between 70
and 189 mg/dL
• Patients between 40 and 75 years old with LDL cholesterol levels between 70 and 189
mg/dL and a 10-year risk for CVD of at least 7.5%
• The statins are the most widely used drugs. Niacin, fibric acid derivatives, bile-acid
sequestrants, PCSK9 inhibitors, and other agents are options.
• Antiplatelet therapy with low-dose aspirin is recommended for people at risk for CAD. For
people who are aspirin intolerant, alternatives (e.g., clopidogrel [Plavix]) are considered.
GERONTOLOGIC CONSIDERATIONS: CORONARY ARTERY DISEASE
• The incidence of heart disease is greatly increased as one ages and is the leading cause of
death in older adults. Strategies to reduce CAD risk are effective in this age group.
Aggressive treatment of hypertension and hyperlipidemia helps stabilize plaques in the
coronary arteries of older adults, and quitting smoking helps decrease the risk for CAD
at any age. Encourage the older patient to consider a planned program of physical
activity.
CHRONIC STABLE ANGINA
• Chronic stable angina refers to chest pain that occurs intermittently over a long period
with the same pattern of onset, duration, and intensity of symptoms.
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• Some patients may deny feeling pain, but describe a pressure, heaviness, discomfort,
or ache in the chest. Some describe only shortness of breath.
• Although most angina pain occurs substernally, it may radiate to the jaw, neck,
shoulders and/or arms.
• Anginal pain usually lasts for only a few minutes and often subsides when the
precipitating factor is relieved. Pain at rest is unusual.
PRINZMETAL’S ANGINA
• Prinzmetal’s angina is a rare form of angina that often occurs at rest, usually in response
to spasm of a major coronary artery. When spasms occur, the patient has angina and
transient ST segment elevation.
• Prinzmetal’s angina may be seen in patients with a history of migraine headaches and
Raynaud’s phenomenon.
• Tobacco, alcohol, amphetamines, and cocaine use may precipitate coronary artery spasm.
• The pain may be relieved by moderate exercise or it may disappear spontaneously.
• Calcium channel blockers and/or nitrates are used to treat angina associated with
coronary artery spasm.
MICROVASCULAR ANGINA
• In microvascular angina, chest pain occurs in the absence of significant CAD or coronary
spasm of a major coronary artery. The pain is related to myocardial ischemia associated
with atherosclerosis or spasm of the small distal coronary vessels.
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INTERPROFESSIONAL AND NURSING CARE: CHRONIC STABLE
ANGINA
• Chronic stable angina can progress or develop into unstable angina or an acute
coronary syndrome. Therefore, any change in the usual pattern of angina should be
evaluated.
• The treatment of chronic stable angina is aimed at decreasing oxygen demand and/or
increasing oxygen supply and reducing CAD risk factors.
• In addition to antiplatelet and lipid-lowering drug therapy, the most common drugs
used to manage chronic stable angina are nitrates, ACE inhibitors, -blockers, and
calcium channel blockers.
• Short-acting nitrates are first-line therapy for the treatment of an acute episode of
angina. Nitrates dilate peripheral blood vessels, coronary arteries, and collateral
vessels.
• Angiotensin-converting enzyme (ACE) inhibitors and -blockers are used to manage
chronic stable angina.
• ACE inhibitors result in vasodilation and decreased blood volume as well as reduction
in the risk of MI, stroke, and death. They have a role in limiting ventricular
remodeling in patients who have had a myocardial infarction (MI).
• -blockers decrease myocardial contractility, heart rate, systemic vascular resistance,
and BP, which reduce myocardial oxygen demand and relieve anginal symptoms.
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• β1 receptors are found in the heart.
• β2 receptors are found in blood vessels, lungs, and liver.
• Some β-blockers are referred to as cardioselective β-blockers because they only block
β1 receptors.
• Calcium channel blockers can be used if patients are intolerant of -blockers
• Common diagnostic tests for a patient who describes chest pain or when a patient with
chronic stable angina has a change in the anginal pattern include:
• 12-lead ECG to look for any changes that may show ACS
• Laboratory tests (e.g., cardiac biomarkers) to identify if the patient is experiencing an
ACS
• Echocardiogram to look for resting left ventricular wall motion abnormalities
• Exercise or pharmacologic stress test if the ECG and cardiac biomarkers are negative
• Cardiac catheterization with possible balloon angioplasty and stent (percutaneous
coronary intervention [PCI])
• PCI may be done at the same time as the catheterization or later.
• There are 2 types of stents: bare metal stents and drug-eluting stents. Drug-eluting
stents reduce the risk of in-stent re-stenosis (overgrowth of the intimal lining) but need
a minimum of 12 months of dual antiplatelet therapy.
• After catheterization with or without PCI, your major responsibilities involve (1)
monitoring for signs of recurrent angina; (2) frequent assessment of vital signs,
including HR and rhythm; (3) evaluation of the insertion site for signs of bleeding; (4)
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neurovascular assessment of the extremity used; and (5) maintenance of bed rest per
agency policy.
• Coronary revascularization with coronary artery bypass graft (CABG) surgery is
recommended for patients who do not respond to medical management, have left main
coronary artery or 3vessel (3 different coronary arteries) disease, are not candidates
for PCI, or have failed PCI with ongoing chest pain. CABG may be the
revascularization option for patient with diabetes, LV dysfunction, and/or CKD.
• For patients having CABG surgery, care is provided in the ICU for the first 24 to 36
hours, where ongoing monitoring of the patient’s ECG and hemodynamic status is
critical.
• After transfer from the ICU, postoperative care focuses on monitoring for
dysrhythmias, providing wound care, managing pain, preventing complications (e.g.,
venous thromboembolism, bleeding, atelectasis, pneumonia), and patient teaching.
ACUTE CORONARY SYNDROME
• Acute coronary syndrome (ACS) develops when ischemia is prolonged and not
immediately reversible. ACS includes the spectrum of non-ST elevation acute coronary
syndrome (unstable angina and non–ST-segment-elevation myocardial infarction
[NSTEMI]) and ST-segment-elevation myocardial infarction (STEMI).
• Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a
worsening pattern from the patient’s chronic stable angina pattern. UA is unpredictable
and must be treated immediately.
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MYOCARDIAL INFARCTION
• Myocardial infarction (MI) occurs because of an abrupt stoppage of blood flow through a
coronary artery, causing irreversible myocardial cell death. Serum cardiac biomarkers are
released into the blood.
• STEMI, caused by an occlusive thrombus, results in ST elevation in the ECG leads facing the
area of infarction. It requires immediate treatment with PCI (first line) or thrombolytic
(fibrinolytic) therapy (in hospitals not capable of performing PCI) to limit the infarct size.
• NSTEMI, caused by a nonocclusive thrombus, often causes ST depression and/or T wave
inversion in the ECG leads facing the area of infarction. Patients usually undergo cardiac
catheterization with possible PCI within 12 to 72 hours if there are no contraindications.
• The acute MI evolves over hours to days.
• MIs mostly affect the left ventricle and are described based on the location of damage.
• Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
may mean the patient is having an MI. The pain is usually described as a heavy, pressure, tight,
burning, constriction, or crushing feeling, often associated with shortness of breath.
• Complications after MI can occur.
• Dysrhythmias are the most common complication. Ventricular tachycardia and ventricular
fibrillation the most common cause of death for patients in the prehospital period.
• Other complications include heart failure, cardiogenic shock, papillary muscle dysfunction or
rupture, ventricular aneurysm, ventricular septal or free wall rupture, and pericarditis.
• Primary diagnostic studies used to determine whether a person has a STEMI, an NSTEMI or
UA include an ECG and serum cardiac biomarkers.
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• ST elevation in the leads facing the infarcted area is seen with STEMI.
• ST depression and/or T wave inversion in the leads facing the infarcted area is seen with
NSTEMI or UA.
• The definitive answer to distinguish between UA and NSTEMI comes from the cardiac
biomarkers. They are high with an NSTEMI and normal with UA.
If the patient is experiencing a STEMI, the patient must get to the cardiac catheterization
laboratory within 90 minutes of presentation in a PCI capable hospital or receive thrombolytic
therapy within 30 minutes in agencies without PCI capability.
INTERPROFESSIONAL AND NURSING CARE: ACUTE CORONARY
SYNDROME
• Rapid diagnosis and treatment for a patient with ACS is necessary to preserve cardiac function.
• For patients with UA/NSTEMI, cardiac catheterization with possible percutaneous coronary
intervention (PCI) (i.e., balloon angioplasty/stent) is considered once angina is controlled or if
angina returns or increases in severity.
• For patients with STEMI, reperfusion therapy is the recommended treatment of choice.
• Cardiac catheterization is used to find and assess the severity of the blockage(s). A PCI is then
performed to open the artery to limit the infarction size.
• Thrombolytic therapy aims to limit the infarction size by dissolving the thrombus in the
coronary artery to reperfuse the heart muscle.
Drug Therapy
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• Initial management of the patient with ACS includes antiplatelet therapy (e.g., chewable aspirin
for UA patients plus clopidogrel or ticagrelor [for STEMI and NSTEMI patients]), IV NTG,
and atorvastatin (Lipitor).
• Systemic anticoagulation with either subcutaneous LMWH or IV UH is only started on patients
with UA or NSTEMI since STEMI patients go quickly to the cardiac catheterization
laboratory.
• Glycoprotein IIb/IIIa inhibitors may be used if PCI is anticipated.
Oral -blockers are started within 24 hours if there are no contraindications and should be
continued indefinitely.
• Calcium channel blockers may be used if the patient is intolerant of β-blockers but must be
used cautiously because they can decrease contractility.
• ACE inhibitors are added after an MI if there are no contraindications. ACE inhibitors may
help prevent ventricular remodeling after an MI. For patients intolerant of ACE inhibitors,
angiotensin receptor blockers should be used.
• Nitrates may be used if the patient has persistent chest pain.
• Lipid lowering drugs are continued indefinitely if the patient can tolerate the drug.
• Stool softeners are given to aid bowel movement and prevent straining and the resultant vagal
stimulation from the Valsalva maneuver.
• Dual antiplatelet therapy should continue for 1 year after an MI whether the patient receives a
stent or not.
• Aspirin should be continued for life.
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NURSING RESPONSIBLITIES: ACUTE CORONARY SYNDROME
• Initial treatment of a patient with ACS includes pain assessment and relief, physiologic
monitoring, promotion of rest and comfort, alleviation of stress and anxiety, and assessment of
the patient’s emotional and behavioral reactions.
• Nitroglycerin, morphine, and supplemental oxygen should be given as needed to eliminate or
reduce chest pain.
• Continuous ECG monitoring, frequent vital signs, intake and output, and physical assessment
should be done. Included is an assessment of heart and breath sounds and inspection for
evidence of complications (e.g., early heart failure, dysrhythmias).
• Bed rest may be ordered for the first few days after an MI involving a large portion of the
ventricle. A patient with an uncomplicated MI may rest in a chair within 8 to 12 hours after the
event.
• Anxiety is common after ACS. Your role is to identify the source of anxiety, assist the patient
in reducing it, and provide appropriate patient teaching.
• It is important to ensure adequate rest periods free from interruption. Comfort measures that
can promote rest include a quiet environment, use of relaxation techniques (e.g., music therapy,
guided imagery), and assurance that staff is nearby and responsive to the patient's needs.
• Patient teaching must occur at every stage of the hospitalization and recovery.
• In the hospital, the activity level is gradually increased.
• Depression is common among patients with CAD, and more so in women. Screen for
depression in patients with CAD and recommend appropriate referrals.
Ambulatory Care
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• Cardiac rehabilitation restores a person to an optimal state of function in 6 areas: (1)
physiological; (2) psychological; (3) mental; (4) spiritual; (5) economic; and (6) vocational.
• Patients should be referred to an outpatient or home-based cardiac rehabilitation program, but
cardiac rehabilitation is significantly used.
• Provide sexual counseling for cardiac patients and their partners. The patient’s concern about
resumption of sexual activity often produces more stress than the physiologic act itself.
• The inability to perform sexually after MI is common and sexual dysfunction usually decreases
after several attempts.
• Patients should know that drugs used for erectile dysfunction should not be used with nitrates
as severe hypotension may occur.
• Typically, it is safe to resume sexual activity 7 to 10 days after an uncomplicated MI.
SUDDEN CARDIAC DEATH
• Sudden cardiac death (SCD) is a sudden unexpected death occurring within 1 hour of symptom
onset.
• The majority of SCD is caused by acute ventricular dysrhythmias (e.g., ventricular tachycardia,
ventricular fibrillation). They may be associated with an acute MI or a prior (old) MI.
• Risk factors for SCD include ventricular dysrhythmias after a prior (old) MI, left ventricular
dysfunction (EF less than 30%), LV hypertrophy, hypertrophic cardiomyopathy, myocarditis,
and changes in the conduction system (e.g., prolonged QT syndrome).
• Patients who had a prior (old) MI and survive SCD are at risk for another SCD event because
of the continued electrical instability of the scarred heart muscle that caused the first event to
occur.
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• Patients who have SCD associated with an acute MI undergo at least 40 days of maximal
medical therapy to see if there is recovery in the EF before an ICD can be implanted.
• People who survive a SCD event need a diagnostic work-up to determine whether they had an
acute MI. This includes cardiac biomarkers, ECG, and cardiac catheterization. Significant CAD
may be a reversible cause, so patients may be referred for PCI or CABG surgery.
• If no reversible cause of SCD is identified, an electrophysiology study (EPS) may be done.
• The most common approach to preventing a recurrence and improving survival is the use of an
implantable cardioverter-defibrillator (ICD).
• Survivors of SCD may develop a “time bomb” mentality, fearing the recurrence of cardiac
arrest. They and their caregivers often become anxious, angry, hopeless, and depressed. They
may need to deal with other issues, such as driving restrictions, role reversal, and change in
occupation.
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