Coronary Atherosclerosis Overview

Coronary Atherosclerosis

• Characterized by lipid and fibrous tissue accumulation within the vessel wall, narrowing coronary vessels and reducing blood flow to the myocardium.
• Lipids accumulate in the intima of the artery, triggering an inflammatory response with T lymphocytes and monocytes infiltrating the area.
• Lipid accumulation develops into a fatty-fibrous lesion, often containing a lipid core covered by a fibrous cap, known as an atheroma or plaque, protruding into the artery's lumen.
• Thin fibrous caps can rupture, releasing lipids into the bloodstream, promoting clot formation and potentially leading to sudden death or acute myocardial infarction.

Clinical Manifestations

• Symptoms and complications depend on location and severity of narrowing, thrombus formation, and obstruction of blood flow to the myocardium.
• Myocardial ischemia can manifest with acute chest pain, shortness of breath, and nausea.

Risk Factors

• Non-modifiable:
  • Family history of Coronary Artery Disease (CAD)
  • Increasing age
  • Gender
  • Lack of estrogen in women
• Modifiable:
  • High blood cholesterol level
  • Hypertension
  • Cigarette smoking, tobacco use
  • Diabetes mellitus
  • Obesity
  • Physical inactivity

Prevention

• Controlling Cholesterol Abnormalities:
  • Dietary Measures: Limit saturated and trans fats, increase soluble fiber intake
  • Physical Activity: At least 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous-intensity aerobic activity per week.
  • Medications:
    • Statins: Examples include atorvastatin (Lipitor)
• Promoting Cessation of Tobacco Use
• Managing Hypertension
• Controlling Diabetes

Myocardial Ischemia

• Occurs due to an imbalance between the myocardium's metabolic needs and oxygenated blood flow.
• Increased Myocardial O2 Demand: Exercise, smoking, heavy meals, fever, heart failure, dysrhythmias, stress, hypertension, cold weather, aortic stenosis
• Reduced Myocardial O2 Supply: Coronary artery narrowing caused by a thrombus, vasospasm, or rapid progression of atherosclerosis

Angina Pectoris

• Clinical syndrome characterized by episodes of chest pain or pressure caused by insufficient coronary blood flow, leading to decreased oxygen supply to the myocardium.
• Pain can occur in the chest, neck, arms, or back.
• Often described as pain or pressure behind the sternum, radiating to the left arm.

Pathophysiology of Angina

• Usually caused by atherosclerosis with a significant obstruction of a major coronary artery.
• Associated factors include physical exertion, exposure to cold, eating heavy meals, and stress.

Types of Angina

• Stable angina: Predictable, consistent pain during exertion, relieved by rest and/or nitroglycerin.
• Unstable angina: More intense than stable angina, may not be relieved by rest or nitroglycerin. It can wake the person from sleep, requiring more than nitrates for pain relief. Changes in frequency or severity require immediate medical evaluation.
• Variant angina (Prinzmetal's angina): Occurs at rest, often cyclic, occurring at the same time each day. Associated with smoking, alcohol use, and stimulant drug use. May involve coronary artery spasm, leading to ST-segment elevation and chest pain.
• Silent ischemia: Objective evidence of ischemia (ECG changes on stress test) without reported symptoms.

Clinical Manifestations of Angina

• Chest pain, discomfort, tightness, or a heavy sensation.
• Pain may radiate to the neck, jaw, shoulders, and upper arm (often the left arm).
• Apprehension and a feeling of impending death.
• Weakness or numbness in the arms, wrists, and hands.
• Shortness of breath.
• Pallor.
• Diaphoresis.
• Dizziness.
• Nausea and vomiting.

Assessment & Diagnostic Findings for Angina

• Patient history and pain assessment.
• Lead ECG: May show ischemic changes like T-wave inversions.
• Laboratory studies: Cardiac biomarker analysis.
• Exercise or pharmacologic stress test.
• Invasive procedures, like cardiac catheterization and coronary angiography, to assess coronary artery patency.

Medical Management of Angina

• Nitrates: Nitroglycerin (Nitrostat, Nitro-Bid) to reduce myocardial oxygen consumption through selective vasodilation.
• Beta-blockers: Metoprolol, Atenolol, to reduce myocardial oxygen consumption by blocking beta-adrenergic stimulation of the heart, slowing heart rate and conduction.
• Calcium channel blockers: Amlodipine, Diltiazem, Felodipine, used for patients unresponsive to beta-blockers. Helps with vasospasm by relaxing blood vessels, reducing blood pressure, and increasing coronary perfusion.
• Antiplatelet Medications: Aspirin, Clopidogrel (Plavix) to prevent platelet aggregation

Acute Coronary Syndrome (ACS)

• An emergent situation marked by an acute onset of myocardial ischemia leading to myocardial death, if not treated promptly.
• Includes unstable angina, non-ST segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI).

Myocardial Infarction (MI)

• Irreversible myocardial necrosis or cell death due to decreased or absent coronary blood flow to a specific area of the myocardium.
• Often called acute MI, meaning a sudden onset and life-threatening condition.
• Usually linked to ST-segment elevation on a 12-lead ECG.

### Pathophysiology of MI

• Prolonged ischemia results from an imbalance between oxygen supply and demand.
• Irreversible cell damage and muscle death occur.
• Coronary artery thrombosis is the most common cause of infarction, often triggered by plaque rupture.

### Clinical Manifestations of MI

• Acute onset of chest pain, often poorly localized, radiating to the neck, jaw, shoulders, and inner aspects of the upper arms.
• Tightness, choking, strangling sensations, and a feeling of impending death.
• Shortness of breath.
• Indigestion, nausea.
• Unusual fatigue, weakness.

### Assessment & Diagnostic Findings for MI

• Patient history and pain assessment.
• 12-lead ECG is critical to make a diagnosis.
• Blood laboratory values: Increased cardiac biomarkers.
• Exercise or pharmacologic stress test: Monitor heart function with ECG and echocardiogram.

### Differentiation of ACS subtypes

• Unstable angina: Clinical manifestations of ischemia, but ECG and cardiac biomarkers do not show evidence of acute MI.
• STEMI: ECG evidence of acute MI with characteristic ST-segment elevation in 2 leads on a 12-lead ECG.
• NSTEMI: Elevated cardiac biomarkers (e.g., troponin), but no definitive ECG evidence of acute MI.

### Laboratory Studies for MI

• Cardiac Enzymes:
  • Creatine kinase (CK): Elevated levels indicate heart cell damage, especially the CK-MB isoenzyme.
  • Myoglobin: Rises 2-3 hours after MI, not cardiac-specific.
  • Troponin T and I: Most sensitive and specific marker of cardiac damage, with levels rising 3-12 hours after MI.

### Medical Management of MI

• Goals are to rapidly restore blood flow and limit myocardial damage.
• Initial Management: Prompt transport to the emergency department (ED)
• Inpatient Management:
  • Oxygen therapy: To reduce myocardial oxygen demand and prevent tissue hypoxia.
  • Pain management: Nitrates (e.g., nitroglycerin) to reduce chest pain and improve blood flow.
  • Antiplatelet therapy: Aspirin to prevent further platelet aggregation and thrombus formation.
  • Anticoagulation: Heparin to prevent new clot formation.
  • Beta-blockers: To reduce myocardial oxygen demand and heart rate.
  • ACE inhibitors: To inhibit vasoconstriction and reduce blood pressure.
  • Cardiac monitoring: Continuous electrocardiographic monitoring to track heart rhythm and detect any abnormalities.

### Reperfusion Therapy for MI

• Percutaneous coronary intervention (PCI): Opening the occluded coronary artery. The goal is to perform PCI within 90 minutes of arrival to the ED, or within 90 minutes of symptom onset.
• Thrombolytic therapy: Dissolves blood clots in the coronary arteries, given within 30 minutes of presentation to the hospital. Must be administered within 6 hours of symptom onset. Example medications: Alteplase (Activase), Reteplase (Retavase), Tenecteplase (TNKase).

### Cardiac Rehabilitation

• Goal is to extend life and improve quality of life for patients who have had a MI.
• Three phases:
  • Phase I: Begins upon diagnosis of atherosclerosis, focusing on education, risk factor modification, and supervised exercise.
  • Phase II: Occurs after discharge, involving supervised exercise programs and continued education.
  • Phase III: Long-term outpatient program to maintain cardiovascular stability and conditioning.

### Nursing Process for Patients with Angina and ACS

• Nursing Diagnosis:
  • Ineffective cardiac tissue perfusion secondary to CAD.
  • Death anxiety related to cardiac symptoms.
  • Deficient knowledge about the underlying disease and complications.
  • Noncompliance with therapeutic regimens.
  • Acute pain related to increased myocardial oxygen demand and decreased oxygen supply.
  • Risk for decreased cardiac tissue perfusion related to reduced coronary blood flow.
  • Risk for imbalanced fluid volume.
  • Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction.
  • Anxiety related to cardiac event and possible death.
  • Deficient knowledge about post-ACS self-care.

### Nursing Management

• Monitor vital signs, ECG, and symptoms to detect complications.
• Administer medications as prescribed.
• Educate patients about the disease, risk factors, medications, lifestyle modifications, and self-care after discharge.
• Implement pain management strategies and provide psychological support.
• Promote physical activity and encourage smoking cessation.