Ischemic Heart Disease: Coronary Artery Disease

Introduction to Ischemic Heart Disease

• Ischemic Heart Disease is caused by a reduction of blood flow to the heart muscle, depriving it of oxygen

Learning Objectives

• Differentiate a differential diagnosis of chest pain and angina "mimickers."
• Describe the pathophysiology of atherosclerosis, stable and unstable coronary artery disease.
• Describe the treatment of stable coronary artery disease.
• Differentiate the clinical and ECG differences between STEMI and UA/NSTEMI and differences between Anterior and Inferior MI.
• Review the management of acute coronary syndrome

Coronary Anatomy

• Left Coronary Artery (LCA), Left Anterior Descending (LAD), also known as the interventricular artery, (Left) Circumflex Artery (Cx), M1 Left marginal, M2 arteries, D1 Diagonal, D2 branches
• Right Coronary Artery (RCA), Posterior Descending Artery (PDA), Right Marginal Artery (RMA)

The Normal Artery

• Composed to the Tunica Intima, Tunica Media and Tunica Adventitia

Atherosclerosis

• A chronic inflammatory process triggered by the accumulation of cholesterol-containing particles in the arterial wall
• Major risk factors include age, dyslipidemia, increased BMI, smoking, diabetes, hypertension, diet low in fruits and vegetables, sedentary lifestyle, and family history of premature coronary disease
• Men under age 55 and women under age 65 face an increased risk

Framingham Heart Study

• A cohort study of residents of Framingham, Massachusetts that began in 1948 and is still ongoing

• The term "cardiovascular risk factor" originated from this study

• Risk of MI or death at 10 years can be calculated

• A family history of premature CAD doubles the risk from 20% to 40%

• Male first-degree relatives under 55 and female first-degree relatives under 65, increase the risk

• CLEM (Cardiovascular life expectancy model) and Pooled cohort models also exist

Stages of Atherosclerosis

• Initiation begins with fatty streaks and intimal thickening with pools of lipid
• Inflammation and smooth muscle cell proliferation can cause endothelial dysfunction due to oxidation of accumulated LDL, where activated macrophages take up LDL particles and form "foam cells"
• Activate and potentiate inflammatory responses cause tissue damage
• Fibroatheroma is when Foam cell necrosis releases free cholesterol creating a "necrotic core"
• Encapsulation occurs by surrounding fibrous tissue (the "fibrous cap")
• Plaque angiogenesis can lead to hemorrhage and plaque enlargement
• Plaque can be "stable" (thick cap, fibrous, calcified) or "vulnerable" (thin cap, prone to rupture)

Plaque Rupture

• A thin fibrous cap can lead to a thrombous and stenosis

Balance of Myocardial Demand

• Supply relies on factors like heart rate, oxygen content of blood, and coronary perfusion
• Demand is impacted by heart rate, contractility, afterload, and preload

Angina Pectoris

• Chest pain is caused by a mismatch between oxygen supply and myocardial demand
• Typical angina is defined as having substernal chest pain, brought on by exertion or emotional distress, and relieved by rest or nitroglycerin
• Atypical chest pain features two out of three of these
• Non-cardiac chest pain has zero or one of these
• Only 10-15% of people with ischemia have typical angina

Anginal Equivalents

• Many people experience coronary disease without experiencing "typical angina"
• People with diabetes could experience anginal equivalents
• People describe "chest pain" in different ways
• Can be culture or language dependent and can be described as discomfort, ache, sharp, burning, squeezing, tightness, or “all in”
• Dyspnea, jaw pain, arm pain, or "heartburn" can present as anginal equivalents
• Ischemia can also be completely silent

Cardiac Causes of Chest Pain

• Obstructive coronary disease is a primary cause
• Ischemia with no obstructive coronary artery disease (INOCA)
• Coronary vasospasm, also known as Prinzmetal Angina, can lead to cardiac related chest pain
• Coronary microvascular dysfunction
• Anomalous coronary artery anatomy
• Cardiomyopathy, Congenital heart disease, Valvular heart disease, Arrhythmia and Severe anemia or hypoxia

Non-Cardiac Causes of Chest Pain

• Aortic dissection that causes tearing, severe, mid-scapular back pain
• Pneumothorax and Pulmonary embolism cause sharp pain that worsens with inspiration
• Esophageal Rupture, known as Boerhaave's, produces chest pain, dysphagia, and vomiting
• Pericarditis causes sharp pain, worsens with inspiration, is worse when supine, and gets relieved by sitting up and leaning forward
• Additional causes include Costochondritis, Esophageal spasm and GERD, Malignancy, Pneumonia, Inflammatory illness like systemic lupus, Pulmonary hypertension, Herpes Zoster, Anxiety, and Chronic pain syndromes

Types of Ischemic Heart Disease

• Ischemic Heart Disease is broken down into Stable Coronary Disease and Acute Coronary Syndrome
• Acute coronary syndrome (ACS): further broken down into: unstable angina/NSTEMI, STEMI, and MINOCA
• MINOCA is myocardial infarction with normal coronary arteries
• NSTEMI is non-ST elevation myocardial infarction
• STEMI is ST elevation myocardial infarction

Stable Coronary Syndrome

• Includes chest pain that does not occur at rest and is not of recent onset, meaning more than 2 months
• Chest pain that is recent onset, less than 2 months, only occurs with heavy exertion, and has not changed substantially in severity or frequency

Probability of Coronary Disease

• Chest Pain Criteria includes substernal chest discomfort with characteristic quality and duration
• Provoked by exertion or emotional stress and is relieved promptly by rest or nitroglycerin
• Low Risk is less than 10%, Intermediate Risk: 10-90% and High Risk is greater than 90%

Stable Coronary Syndrome Diagnosis

• Diagnostic clues include clinical history suggesting ischemic heart disease
• Methods of investigation include exercise stress test, nuclear coronary perfusion imaging using PET or SPECT, exercise, vasodilator or dobutamine and the stress echocardiogram
• A CT coronary angiogram or a Coronary angiography (gold standard) can be used

Coronary Angiography

• A catheter is inserted into the leg and guided up the aorta
• The catheter tip then stops at the left coronary artery
• Contrast agent is injected into arteries and X-ray imaging shows stenosis in left coronary artery

Stable Coronary Disease - Treatment

• The three main facets of management are Secondary Prevention
• Medical management of symptoms and Revascularization

Stable Coronary Disease - Secondary Prevention Includes

• Following a Healthy diet consisting of DASH or Mediterranean diet
• Undergoing Lipid-lowering Statin therapy regardless of LDL cholesterol
• Target LDL is to be less than 1.8 mmol/L
• Practicing Blood pressure management, Office <140/90, Home <135/85, diabetes <130/80 and prioritize ACE or ARB therapy
• Regular exercise involving at least 30 minutes of aerobic exercise, at least 5 days per week
• Smoking cessation, Diabetes control: target hemoglobin A1C less than 7%, weight loss: target BMI 19.5 – 25, and take Baby aspirin daily

Stable Coronary Disease: Anti-Anginal Medications

• Beta blockers: Side effects can include fatigue, depression, and erectile dysfunction
• Nitrates taken orally, via spray or patch
• Calcium channel blockers and Funny channel blockers (Ivabradine)
• Other pharmacologic or non-pharmacologic therapies are less established

Stable Coronary Disease – Revascularization

• The two main approaches are Coronary artery bypass surgery, called CABG and Percutaneous coronary intervention, called PCI
• Typically reserved for patients with severe left main or multivessel disease (ie. Prognostic disease) and left ventricular dysfunction
• Patients with Symptoms do not improve despite optimal medical therapy or are intolerant of medical therapy
• Controversy exists about best method: CABG or PCI
• CABG is typically reserved for complex disease, especially for diabetics
• No study has ever shown that PCI improves mortality in stable coronary disease, but it does improve symptoms and quality of life

Ischemia Causing Heart Failure

• Can lead to heart failure with new left ventricular dysfunction
• Ischemia is the top cause
• The next steps would be to Typically undergo invasive or non-invasive assessment, then Medical optimization and revascularization

Unstable Angina

• Also known as Acute Coronary Syndrome

Unstable Angina-Specifics

• Chest pain occurs at rest, is of recent onset (ie less than 2 months) and occurs with mild-moderate exertion
• Chest pain is worsening in severity or frequency (“crescendo pattern")
• There is an absence of myocardial injury, with No elevation in cardiac enzymes (e.g. troponin, creatine kinase)
• This is because plaque rupture results in narrowing but not occlusion of the artery

Types of Myocardial Infarction

• Acute myocardial injury is due to ischemia resulting in a rise and/or fall in troponin, with at least one value above the 99th percentile upper limit of normal is
• Type 1: due to plaque rupture or erosion resulting in coronary thrombosis
• Type 2: due to imbalance between oxygen supply and demand, in the absence of coronary thrombosis
• Type 3: death due to myocardial ischemia before blood samples can be obtained
• Type 4: due to percutaneous coronary intervention
• Type 5: due to coronary artery bypass grafting

Myocardial Infarction Indicators

• Non-ST elevation myocardial infarction, called NSTEMI occurs when troponin is elevated in the absence of ST elevation
• Typically plaque rupture results in coronary narrowing and distal embolization of thrombus, but not complete occlusion
• ST elevation myocardial infarction is a STEMI, and plaque rupture results in complete occlusion of the artery
• ST elevation in 2 or more contiguous leads is the indicator
• 1 mm of ST elevation is visible in all leads except V2 and V3
• V2/V3 has 2.5 mm in males under 40, 2 mm in males over 40 and 1.5 mm in females
• ST elevation can localize the affected artery

ECG

• A normal ST-segment is present

Inferolateral STEMI

• ACUTE MI is suspected

Unstable Angina & NSTEMI - Acute Treatment

• This includes Airway, breathing, and circulation
• Supplemental oxygen is used if needed
• Nitrates and morphine for pain relief
• Chewable ASA 160 mg
• Second antiplatelet: clopidogrel or ticagrelor
• The use of Anticoagulant: heparin, enoxaparin or fondaparinux is required
• Admit to hospital, usually for coronary angiogram and revascularization
• If pain-free and stable, OK to wait for an angiogram

STEMI - Acute Treatment

• Airway, breathing and circulation
• Oxygen if oxygen saturation is low
• Nitrates and morphine for pain relief, however, nitrates can cause severe hypotension in inferior STEMI with RV involvement
• Opioids only if necessary, as they can slow absorption of medication
• Chewable ASA 160 mg and a Second antiplatelet: clopidogrel or ticagrelor
• An Anticoagulant: heparin, enoxaparin or fondaparinux is required
• Immediate revascularization and Do not wait for bloodwork, serial ECGs

STEMI - Revascularization

• Time is muscle
• If can achieve first medical contact to device time within 90-120 minutes, activate the STEMI team for primary PCI (ie restore flow with a stent or balloon)
• If cannot achieve PCI in a timely matter, administer thrombolytics like Tenecteplase (TNK); formerly TPA or streptokinase
• Success can be deemed from resolution of pain and 50-75% decrease in ST elevation
• Transport immediately to PCI capable hospital in case TNK may not work
• Even if they do work, patients should undergo urgent angiography, typically within 24 hours of thrombolytics
• Limited benefit to undergoing this after 12 - 24 hours since onset of pain

UA/NSTEMI/STEMI – Medical Management

• This includes lifelong ASA 81 mg indefinitely as well as Second antiplatelet where clopidogrel or ticagrelor is administered
• This is typically continued for 1 year, regardless of undergoing any additional stenting
• Extended use may occur if the disease is deemed complex and extensive stenting is required
• High dose statin therapy should be used despite "pleiotropic" effects in addition to lipid lowering
• ACE-I/ARB therapy should be administered, especially if hypertension, or if ejection fraction is less than 40%
• Beta blocker therapy use depends on the availability for "revascularization era"
• Stronger indication if LV ejection fraction is less than 40% and is contraindicated in cardiogenic shock
• Assess the use of mineralocortocoid receptor agonists, like spironolactone or eplerenone dependent on heart failure
• Assess if patient is diabetic or if LVEF is less than 40% with heart failure

UA/NSTEMI/STEMI – Medical Management Second Prevention

• Follow a healthy diet
• Include a DASH or mediterranean diet
• Lipid lowering therapy
• Statin therapy regardless of LDL cholesterol
• Target LDL less than 1.8 mmol/L
• Blood pressure management: Office <140/90, Home <135/85, diabetes <130/80; prioritize ACE or ARB therapy
• A regular exercise Routine should be used
• At least 30 minutes of aerobic exercise, at least 5 days per week
• Resistance activities may prove useful
• Emphasize Smoking cessation, and maintain Diabetes control by targeting hemoglobin A1C less than 7%
• Incorporate Stress management, encourage weight loss by targeting BMI 19.5 – 25 and take advantage of a Cardiac rehabilitation program