Coronary Atherosclerosis: Plaque Formation

Coronary Atherosclerosis

• Coronary atherosclerosis is the most prevalent cardiovascular disease.
• It involves an abnormal accumulation of lipids, fatty substances, and fibrous tissue in artery walls.
• This causes blocked and narrowed vessels, reducing blood flow to the heart muscle (myocardium).
• Starts with injury to the endothelium triggering inflammation that progresses to atherosclerosis.
• Injury is initiated by factors like smoking, hypertension, and hyperlipidemia.
• Endothelial changes stop antithrombotic and vasodilating agent production.

Plaque Formation and Clinical Manifestations

• Inflammation attracts monocytes/macrophages that ingest lipids, creating "foam cells."
• Foam cells transport lipids into the arterial wall.
• Lipid deposits form fatty streaks on the arterial wall, followed by smooth muscle cell proliferation.
• These deposits called atheromas or plaques protrude into the vessel, causing narrowing and obstruction.
• Activated macrophages release biochemical substances, further damaging the endothelium.
• Oxidized LDL becomes toxic to endothelial cells, fueling atherosclerosis progression.
• Plaque stability depends on inflammation and thickness.
  • Stable plaques have a thick fibrous cap and can handle blood flow stress.
  • Unstable plaques have a thin cap and may rupture.
• Ruptured plaques attract platelets, leading to thrombus formation and obstructed blood flow.
• This can lead to an acute coronary syndrome (ACS) and myocardial infarction (MI), resulting in necrosis.
• Location and degree of narrowing determine clinical manifestations.
• Inadequate blood supply deprives heart muscle cells of oxygen, leading to myocardial ischemia.
• Angina pectoris presents as chest pain resulting from myocardial ischemia.
• Prolonged or severe blood supply reduction causes irreversible damage/death of myocardial cells.
• Damaged myocardium degenerates to scar tissue, causing dysfunction and inability to pump well.
• Scar tissue and dysfunction result in low cardiac output and heart failure.
• Decreased blood supply from CAD can cause sudden cardiac death.
• Symptoms can range from asymptomatic to epigastric distress radiating to the jaw or left arm.
• Shortness of breath is common in older patients with diabetes or heart failure.
• Atypical symptoms in women include indigestion, nausea, and fatigue.

Risk Factors and Prevention

• Nonmodifiable risk factors include family history, age, gender, and race.
• Modifiable risk factors include hyperlipidemia, tobacco use, hypertension, diabetes, metabolic syndrome, obesity, physical inactivity, chronic inflammation, chronic kidney disease, and PVD.
• Metabolic Syndrome is diagnosed with at least 3 of the following: central obesity, dyslipidemia, hypertension, insulin resistance, or a proinflammatory state.
• Obesity leads to metabolic changes.
• Prevention involves controlling cholesterol abnormalities.

Diagnostic Tests and Management

• Key elements for heart health: total cholesterol, LDL, HDL, and triglycerides.
• Adults should have a fasting lipid profile every 5 years, or more if abnormal.
• Goal levels: LDL <100 mg/dL (or <70 for high-risk), total cholesterol <200 mg/DI, HDL >40 mg/dL for males and >50 mg/dL for females, and triglycerides <150 mg/DI.
• Use diet, physical activity, and lipoprotein medications.
• Smoking cessation contributes to severity via catecholamine release, LDL oxidation, and increased carbon monoxide levels.

Managing Hypertension and Diabetes

• An elevated BP over >130/80 indicates hypertension and results in increased stiffness of vessel walls, leading to vessel injury.
• Hypertension increases the heart's workload, causing hypertrophy and heart failure.
• Hyperglycemia fosters dyslipidemia, increases platelet aggregation, and alters RBC function (thrombus formation).
• Treatment includes insulin and metformin.

Gender Considerations

• Cardiovascular events in women occur 10 years later than in men.
• Women have a higher incidence of complications related to CVD and don't recognize symptoms early on.
• Menopause accumulates risk factors.
• Hormone therapy is not an effective prevention for CAD
• Men commonly report heavy chest pain radiating to the left arm while women may present with fatigue/indigestion

Medications

• HMG-CoA Reductase Inhibitors (Statins): Decrease total cholesterol and LDL, and increase HDL. Frequently initial therapy. Adverse effects include myalgia and liver damage. Administer in the evening.
• Fibrates: Increase HDL and decrease triglycerides. Adverse effects include diarrhea and myalgia
• Bile Acid Sequestrants: Decrease LDL and slightly increase HDL. Side effects: constipation & GI bleeding. Take before meals.
• Cholesterol Absorption Inhibitor: Decreases LDL. Used with statins. Side effects include abdominal pain, arthralgia, and myalgia.
• Proprotein Convertase Subtilisin–Kexin Type 9 Agents: Lowers LDL. Given via subcutaneous injection. Side effects include rhinitis, sore throat, and muscle pain.

Angina Pectoris

• Angina pectoris is a clinical syndrome characterized by pain or pressure in the chest when oxygen demand exceeds supply.
• Atherosclerosis leads to insufficient coronary blood flow and decreased oxygen supply.
• Obstruction of at least one major coronary artery causes ischemia.
• Angina is a result of decreased blood flow and oxygen. Causes:
• Physical extertion increases the heart's demand.
• Cold exposure causes vasoconstriction and increased blood pressure, increasing demand.
• Eating heavy meals diverts blood flow to the digestive system.
• Stress releases catecholamines, increasing workload.
• Stable angina is predictable pain on exertion relieved by rest and nitroglycerin.
• Unstable angina: symptoms increase in frequency and severity, may not be relieved by rest or nitroglycerin, and requires medical intervention.
• Intractable/refractory angina is severe incapacitating chest pain.
• Variant angina is pain at rest with ST-segment elevation.
• Silent ischemia is objective evidence of ischemia, but patient reports no symptoms
• Clinical Manifestations chest: pain / heavy sensation, poorly localized in jaw, neck, shoulders & arms
• Cardiac ischemia is suggested by sob, pallor, cold sweat, n/v, lightheadedness/diziness, numbness/weakness and indigestion
• Diagnosis begins with patient history
• A 12-lead ECG shows T-wave inversion or ST-segment elevation.
• Conduct lab studies for cardiac biomarkers.
• Perform exercise or pharmacologic stress tests with ECG and/or echocardiogram monitoring.
• Perform nuclear scans or invasive procedures of cardiac catherization

Treatment

Medical

• Decrease oxygen demand and increase oxygen supply. Pharmacologic
• Nitrates (standard): Light sensitive drugs! They dilate veins, causing venous pooling and decreasing preload. Side Effect: headache! Caution in hypovolemic patients.
• Beta-adrenergic blocking agents reduction of myocardial oxygen consumption by blocking beta adrenergic stimulation of the heart. Target resting HR 50-60 bpm
• Calcium channel blockers (indicated for vasospam) decrease AS node function that decreases strength and workload of the heart

Medications and Procedures

• Nitroglycerin dilates veins and decreases preload and afterload
• Beta-adrenergic blocking agents reduce HR, BP, and contractility.
• Calcium channel blockers decrease HR and strength of heart
• Cardiac side effects & contraindications include hypotension, bradycardia, advanced atrioventricular block, and acute heart failure
• Reperfusion procedures restore blood supply, like percutaneous transluminal coronary angioplasty (PTCA) with stents, and CABG

Antiplatelet and Anticoagulant Medications

• Aspirin prevents platelet aggregation
• Administer is 162-325 mg initially, then 81-325mg daily.
• May cause GI upset and bleeding. Chewing enables quicker action.
• Adenosine Diphosphate Receptor Antagonists: block platelet activation via different pathways that aspirin
• Clopidogrel is often prescribed with aspirin.
• Heparin: IV heparin prevents new clot formation. Dose depends on aPTT.
• Patients should be put on bleed precautions that can increase HR & decrease BP
• Enoxaparin and Dalteparin is indicated for for unstable angina-potential risk of rebound ischemic events- does not require monitoring

Nursing Management

• Determine location of pain. Prodromal symptoms should be noted.
• Ask: Can you feel pain anywhere else? What does it feel like? Rate it. When did it begin? What brings it on? What helps it go away?
• Focus management to promote pain relief and reducing anxiety

Acute Coronary Syndrome and Myocardial Infarction

• Develops from an acute onset of myocardial ischemia that results in myocardial death if interventions do not occur promptly.
• Includes unstable angina, NSTEMI & STEMI
• Begins with reduced coronary artery blood flow, often due to plaque rupture. A clot begins to form, but the artery is only partially occluded.
• Acute situations are known as preinfarction angina which are likely to result in a MI
• In MI plaque ruptures that results in subsequent thrombus resulting in artery complete occlusion- leads to myocardial necrosis death
• Various descriptions: The type {NSTEMI,STEMI}, the location to ventricular wall, time within process
• Patient should be administered O2 (2-4L/min) with a caution administered to patients with hypovolemia
• Morphine is administered for pain/anxiety. If dysrhythmias develop, administer beta blocker with the first 24hr

Manifestations & Diagnosis

• Chest pain that occurs suddenly and continuously continues despite rest & medications w/ prodromal symptoms or CAD dx
• Patients may experience : Chest pain,SOb, indigestion, nausea, anxiety / cool, pale, moist skin & increased HR & RR with patient history
• Diagnosis begin with patient history and should take ~10 min that recognizes present & previous illnesses related
• If no other medical facilities are viable, use thrombolytics. Ensure patient is not in active stage of bleeding
• Patients with STEMI get transferred to cardiac cath lab

Electrocardiogram

• 12 lead ECG should be obtained within 10 minutes of onset of pain!
• Expected ECG change→ T-wave inversion, ST-segment elevation and development of abnormal Q wave

Echocardiogram

• Used to evaluate ventricular function & detect hypo/akinetic wall motion/determine ejection fraction

Lab Tests

• Cardiac enzymes & biomarkers are used to diagnose acute MI.
• Based on cellular contents- tests can be accelerated quickly- the speed of result is based on circulation of myocardial cells when dead

Troponin

• Protein in myocardial cells regulation contractile process- 3 isomers
• Increased troponin →Reliable marker of myocardial injury/increase within few hrs & elevated >2 wks can detect recent damage

Creatine Kinase

• Found in cardiac cells & increases with damage- increase within hrs & peak is 24hrs

Goals of Medical Management

• Minimize myocardial damage/ preserve function & prevent complications
• Supplemental O2 (2-4L/min) via nasal-chew aspirin
• Resolution of the pain + ECG changes indicate balance of equilibrium & reperfusion

Interventions

• Reperfusion procedures may be used to restore blood supply to myocardium *
  └ PCI procedures→ percutaneous transluminal coronary angioplasty {PTCA}; intracoronary stents} and CABG

Nursing Management

• Monitor vital signs, pulse oximetry, and ECG continuously.
• Assess heart and breath sounds as well as skin color.
• Monitor lab results, especially cardiac enzymes and electrolytes.
• Observe for signs of bleeding and dysrhythmias.
• Report significant changes promptly.
• Provide ongoing education to the patient and family.

Thoracic Aortic Aneurysm

• Pain is a significant risk for patients with aneurysms. Constant, boring, and may only occur when laying down.
• Hoarseness, stridor, vocal weakness result from pressure on the laryngeal nerve, can cause dysphagia
• Assess compressions in the chest for any dilations in the neck that affects the heart
• CTA should be performed

Therapeutic Management

• Treatment based on if pt is symptomatic & is expanding.
• Beta blockers may be ordered
• Medications such as sodium nitroprusside are emergent at use.
• The goal of surgery is to repair aneurysm and restore it with vascular graft that will require pt's to ICU post-sx

Abdominal Aortic Aneurysm

• Most common cause is atherosclerosis
• Occurs for men 2-6 timers more often than women; and white verus black ~2-3 times
• Most prevelant in older patients >65
• Most aneurisms will occur below renal arteries- untreated leads to eventual rupture & death

Assessing Pt

• If pt is lying down , complain of HR beating- some cases are severe back pain w/ blood pressure dropping
• May result in hematomas

Goal

• If aneurysm is stable, monitor BP
• Medical sx is the mainstay of therapy
• Pt's head needs to be elevated 45 degrees past >2hrs and needs bedside assess and vital 15 mins intervals