References:
- Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 15th Edition, ISBN 978-197-51-6103-3, by Janice L. Hinkle, Kerry H. Cheever, and Kristen J. Overbaugh (Ch. 23)
The most prevalent type of cardiovascular disease in adults, most commonly caused by atherosclerosis, the abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls. These substances block and narrow the coronary vessel in a way that reduces blood flow to the myocardium. Atherosclerosis is a result of repetitious inflammatory response to injury of the artery wall and subsequent alteration in the structural and biochemical properties of the arterial walls.
Pathophysiology
- Vascular Endothelial Damage due to smoking, hypertension, hyperlipidemia, and other factors. Normal anti-thrombotic and vasodilating agents stop being produced.
- Inflammatory cells, such as macrophages, respond to inflammation. They ingest lipids and deposit them into the arterial wall, forming “fatty streaks”. Macrophages also oxidizes LDLs which is toxic to endothelial cells, contributing further to the problem.
- After deposition of lipids, the smooth muscle cells of the vessels forms a covering over the deposit of lipid and inflammatory infiltrate. This is what forms the resulting atheroma or “plaque” that protrudes into the lumen of the vessel, narrowing it and obstructing blood flow. Depending on the degree of inflammation and thickness of the formed cap, the plaque can remain stable or become unstable.
- Unstable atheroma are unable to withstand the stress of blood flow and vessel movement. These are known as vulnerable plaques, which can continue to grow and finally rupture.
- The rupture attracts platelets, causing thrombus formation. This is what can obstruct blood flow, leading to acute coronary syndrome that may eventually lead to an acute myocardial infarction.
There can be other causes of disease of the coronary arteries besides atherosclerosis such as vasospasm and profound hypotension.
Clinical Manifestations
Depending on the location and degree of narrowing of the arterial lumen, different symptoms and complications may arise. This makes for a large number of cases to be unattributed to coronary disease. In an epidemiologic study in Massachusetts, nearly 15% of men and women who had coronary events (unstable angina, MIs, sudden cardiac death) were asymptomatic prior to the coronary event. Patients may present with symptoms that do not include the classical angina pectoris attributed to myocardial ischemia. These include epigastric distress, pain that radiates to the jaw or left arm, shortness of breath (in patients with diabetes or heart failure), indigestion, nausea, palpitations, and numbness.
Nonetheless, patients with coronary artery insufficiency will likely develop angina pectoris, the chest pain brought about by myocardial ischemia. This often appears once there is significant coronary atherosclerosis. Over time, irreversible damaged myocardium undergoes degeneration (scarring) and produce myocardial dysfunction. Decreased cardiac output and heart failure fails to supply the heart with the oxygen that it requires, which can eventually reach its threshold and abruptly stop beating. This is known as sudden cardiac death.
Risk Factors
There are many circumstances that can increase the risk for coronary artery disease. There are two general categorizations of risk factors that can be applied in the healthcare setting: modifiable and nonmodifiable risk factors. Their names are self-explanatory; they denote whether a risk factor for an individual is something they are able to control, such as by changing their lifestyle, habits, or medications.
- Nonmodifiable Risk Factors:
- Family history, age, gender, race
- History of premature menopause (<40 y.o.) and history of pregnancy-associated disorders such as preeclampsia.
- Primary hypercholesterolemia (genetically-linked LDL elevation)
- Modifiable Risk Factors:
- Hyperlipidemia
- Tobacco use
- Hypertension
- Diabetes
- Metabolic Syndrome
- Obesity
- Physical Inactivity
- Chronic inflammatory conditions (e.g. rheumatoid arthritis, lupus, HIV/AIDS)
- Chronic kidney disease
Metabolic Syndrome
A diagnosis of this syndrome is based on the presence of three of the five following risk factors:
- Enlarged waist circumference: >35.4” in males, >31.4” in females
- Elevated triglycerides: at least 175 mg/dL, or currently receiving drug treatment for elevated triglycerides
- Reduced HDF: <40 mg/dL in males or <50 mg/dL in females , or currently receiving drug treatment for reduced HDL
- Hypertension: >130 mm Hg/>80 mm Hg on an average of two to three separate occasions, or currently on antihypertensive drug treatment for a history of hypertension.
- Elevated fasting glucose: >100 mg/dL on two separate occasions, or current drug treatment for elevated glucose.
Many people with type 2 diabetes fits this clinical picture. Theories suggest that in obesity excessive adipose tissue may secrete mediators (adipokines), free fatty acids, and other substances are known to modify insulin action and contribute to atherogenic changes in the cardiovascular changes.
C-reactive protein (CRP) is also known to be an inflammatory marker for cardiovascular risk, including acute coronary events and stroke. It is produced by the liver in response to stimulus such as tissue injury, and high levels of this protein may be found in people with diabetes and those who are likely to have an acute coronary event. To determine overall cardiovascular risk, clinicians may view high sensitivity C-reactive protein (hs-CRP) test results together with other screening tools such as measurements of lipid levels.
Gender
Heart disease has long been recognized as a cause of morbidity and mortality in men, but it has not always been readily recognized in women. Cardiovascular events occur an average of 10 years later in life in women than they do in men, while also having a higher incidence of complications from cardiovascular disease and a higher mortality rate. In addition, women tend to not recognize the symptoms of CAD as early as men, and they wait longer to report their symptoms and seek medical assistance.
Menopause has also been implicated in CAD. Hormone therapy is not an effective method for primary or secondary prevention of CAD; contrarily, the use of estrogen in hormone therapy during menopause is linked to increased incidence of CAD, breast cancer, deep vein thrombosis, stroke, and pulmonary embolism.
Prevention
A large focus is placed on four modifiable risk factors—cholesterol abnormalities, tobacco use, hypertension, and diabetes.
Controlling Cholesterol Abnormalities
High blood cholesterol and heart disease are established to be linked, and the metabolism of fats is known to be an important contributor to the development of heart disease. Ingested cholesterol is processed into lipoproteins (chylomicrons) which are important for lipoprotein-based cell membranes and other processes. However, when an excess of LDL is produced, LDL particles adhere to receptors in the arterial endothelium where they are ingested by macrophages and a plaque is formed.
- Monitoring is important. All adults over 20 years old should have a fasting lipid profile done at least every five years, and more often if abnormal findings are found.
- Normal findings: LDL <100 mg/dL (<70 mg/dL if very high risk), Total <200 mg/dL, HDL >40 mg/dL (M) and >50 mg/dL (F), and Triglycerides <150 mg/dL.
- Of the four readings, total cholesterol is a clear predictor of coronary events and LDL is the target of therapy due to its strong association with advancing CAD.
- HDLs are considered “good cholesterol” due to their mechanism of transporting LDLs and other lipoproteins to the liver to be degraded and excreted. A higher HDL level is a strong negative risk factor for heart disease.
Dietary measures are a first-line method for reducing LDLs. The American Heart Association’s diet recommendations or the Mediterranean diet have been reported to reduce mortality from cardiovascular disease. There are commonalities between both eating plans: more plant foods, minimally processed foods, seasonally fresh foods, inclusion of fish, and minimal intake of red meat.
- Sweets and sugar-sweetened beverages should also be limited.
- A strict vegetarian diet can significantly reduce blood lipids, glucose, body mass index, and blood pressure; however, it may not be acceptable to all patients who need to modify risk factors.
- Referral to a dietitian can help patients in following an acceptable and appropriate diet.
Physical activity and weight reduction can help manage elevated triglyceride levels. The goal is moderate-intensity aerobic activity of at least 150 minutes per week or vigorous-intensity aerobic activity of at least 75 minutes per week, or an equivalent combination.
- Muscle-strengthening activities on two or more days each week that work all muscle groups is also good.
- Patient interest is important for maintaining motivation; patients should also wean into the lifestyle at an appropriate pace.
- A good marker for appropriate exercise intensity is the individual’s ability to talk; exercise should not preclude their ability to talk— if the individual is unable to hold a conversation while engaging in exercise, consider stopping or switching to a lower-intensity exercise.
- Stop any activity if the occurrence of chest pain, unexpected shortness of breath, lightheadedness, or nausea occurs.
Medications are supplementary to dietary measures and physical activity; these are only used if diet alone has been ineffective in normalizing serum cholesterol levels. Lipid-lowering agents include 3-hydroxyl-3-methylglutaryl (HMG-CoA; -statins), fibric acids (or fibrates), bile acid sequestrants (or resins), cholesterol absorption inhibitors, and proprotein convertase subtilisin-kexin type 9 (PCSK9; expensive, used in high cardiovascular risk) agents.
Promoting Cessation of Tobacco Use
Tobacco contributes to the development and severity of CAD in at least three ways: (a) Nicotinic acid releases catecholamines which increase heart rate and blood pressure, and produces vasoconstriction; (b) Tobacco increases LDL oxidation, damaging vascular epithelium; and (c) an increased carbon monoxide level in the blood decreases oxygen supply to the myocardium.
In individuals at risk, smoking must be ceased with any means possible; educational programs, counseling, consistent motivation and reinforcement messages, support groups, and medications. Complementary therapies have also helped some individuals (acupuncture, guided imagery, hypnosis). Risk will decrease within the first year of cessation and will continue to decrease as long as they refrain from smoking.
- Medications such as nicotine patches, nicotine lozenges, nicotine gum, varenicline, or bupropion may assist with stopping the use of tobacco. However, these still retain the negative effects of nicotine: increased catecholamines and increased platelet adhesion. The lowest effective doses and shortest time possible is used for therapy.
Second-hand smoke also increases the risk for CAD by 25% to 30% and for stroke by 20% to 30%.
Managing Hypertension
A blood pressure >130 mm Hg systolic and/or >80 mm Hg diastolic is considered as hypertension. A single reading is not adequate to make a diagnosis. Averaging two or three measurements obtained on two to three different occasions will provide a more accurate measurement.
Long-standing hypertension may result in increased vessel wall stiffness, leading to vessel injury and resulting inflammatory response. This leads to the release of growth-promoting factors that cause vessel hypertrophy and hyper-responsiveness, accelerating and aggravating atherosclerosis. These changes also increase the work required from the left ventricle, which causes the heart to hypertrophy and potentially lead to heart failure.
Controlling Diabetes
Heart disease is accelerated by diabetes. Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function, which can lead to thrombus formation. These alterations may impair endothelial cell-dependent vasodilation and smooth muscle function, promoting the development of atherosclerosis.
Treatment with insulin, metformin, and other therapeutic interventions that lower plasma glucose levels can lead to improved endothelial function and patient outcomes.