ASE 2017 + Coronary Artery Disease

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Acute Coronary Syndrome (ACS)

A group of clinical conditions caused by a sudden reduction in blood flow to the myocardium (p. 1)

What causes ACS?

Rupture of an atherosclerotic plaque, followed by thrombus formation within a coronary artery (p. 1)

Why is ACS a medical emergency?

Prolonged ischemia can cause irreversible myocardial necrosis (cell death) (p. 1)

What are the three major ACS classifications?

1. Unstable angina (UA); 2. Non-ST elevation MI (NSTEMI); 3. ST-elevation MI (STEMI) (p. 1)

Role of the coronary arteries

Supply oxygen and nutrients to the myocardium (p. 1)

Three features of healthy coronary arteries

Wide open lumen, unobstructed blood flow, adequate oxygen delivery (p. 1)

Atherosclerosis: four changes that develop over time

Lipids accumulate within vessel walls → plaque develops → arterial lumen narrows → blood flow decreases (p. 1)

Four major components of atherosclerotic plaque

LDL cholesterol, inflammatory cells, fibrous tissue, calcium deposits (p. 1)

How ACS most commonly begins (4-step sequence)

Atherosclerotic plaque ruptures → vessel wall becomes exposed → platelets activate → clot formation begins (p. 1)

Two possible effects of the clot that forms after plaque rupture

Partial obstruction or complete obstruction of coronary blood flow (p. 1)

Ischemia (consequence of coronary occlusion)

Reduced oxygen supply causing reversible myocardial dysfunction (p. 2)

Injury (consequence of coronary occlusion)

More severe oxygen deprivation producing cellular damage (p. 2)

Infarction (consequence of coronary occlusion)

Prolonged ischemia leading to irreversible myocardial necrosis (p. 2)

Ischemia vs infarction: which is reversible?

Ischemia = reversible myocardial dysfunction; infarction = irreversible myocardial necrosis (p. 2)

Unstable angina (UA): definition

Myocardial ischemia without myocardial cell death (p. 2)

Four characteristics of unstable angina

Symptoms occur at rest; increasing frequency of chest pain; increasing severity of symptoms; elevated risk of infarction (p. 2)

Which ACS has negative biomarkers?

Unstable angina: troponin negative, CK-MB negative (p. 2)

EKG findings in unstable angina

May show ST depression, T-wave inversion, or a normal EKG (pp. 2, 9)

Unstable angina: key point

No myocardial necrosis has occurred (p. 2)

Two cardiac biomarkers used to classify ACS

Troponin and CK-MB (pp. 2-3)

NSTEMI: definition

Myocardial infarction resulting from partial coronary artery occlusion (p. 2)

NSTEMI: pathophysiology

Blood flow is reduced enough to cause myocardial necrosis, but not full-thickness infarction (p. 2)

Which ACS has elevated biomarkers without ST elevation?

NSTEMI: troponin elevated, CK-MB elevated, no ST elevation (pp. 2, 9)

Common EKG findings in NSTEMI

ST depression, T-wave inversion, nonspecific ST-T abnormalities (pp. 2, 9)

NSTEMI: key point

Myocardial damage is present despite the absence of ST elevation (p. 2)

Which ACS typically involves complete coronary occlusion?

STEMI: myocardial infarction caused by complete coronary artery occlusion (p. 3)

STEMI: pathophysiology

Prolonged complete obstruction produces full-thickness myocardial injury (p. 3)

STEMI biomarkers

Troponin elevated, CK-MB elevated (p. 3)

EKG findings in STEMI

ST elevation, reciprocal ST depression, hyperacute T waves, development of Q waves (pp. 3, 9)

STEMI: key point

Requires immediate reperfusion therapy (p. 3)

Biomarkers across the ACS spectrum

UA: troponin and CK-MB negative. NSTEMI and STEMI: both elevated (pp. 2-3)

Partial vs complete coronary occlusion: which ACS type?

Partial = NSTEMI (necrosis, not full-thickness). Complete = STEMI (full-thickness injury) (pp. 2-3)

Four nonmodifiable ACS risk factors

Age, gender, family history, genetics (p. 3)

Age as an ACS risk factor

Risk increases with advancing age (p. 3)

Gender as an ACS risk factor

Men are generally affected earlier than women (p. 3)

Family history that increases ACS risk

A male first-degree relative <55 years or a female first-degree relative <65 years (p. 3)

Genetics as an ACS risk factor

Inherited predisposition contributes to disease development (p. 3)

Seven modifiable ACS risk factors

Hypertension, hyperlipidemia, diabetes mellitus, smoking, obesity, sedentary lifestyle, stress (pp. 3-4)

How hypertension contributes to ACS

Damages vessel endothelium and accelerates plaque development (p. 3)

How hyperlipidemia contributes to ACS

Elevated LDL cholesterol promotes atherosclerosis (p. 3)

Diabetes mellitus as an ACS risk factor

Significantly increases coronary artery disease risk (p. 3)

Three effects of smoking that promote ACS

Vasoconstriction, platelet aggregation, endothelial injury (p. 3)

Obesity is associated with which three conditions?

Hypertension, diabetes, dyslipidemia (p. 4)

Sedentary lifestyle as an ACS risk factor

Reduces cardiovascular fitness and increases risk factors (p. 4)

Stress as an ACS risk factor

Contributes to hypertension and inflammatory responses (p. 4)

Most common symptom of ACS

Chest pain (p. 4)

Five ways patients describe ACS chest pain

Pressure, tightness, squeezing, heaviness, crushing pain (p. 4)

Six places ACS chest pain may radiate

Left arm, both arms, jaw, neck, shoulder, back (p. 4)

Seven associated symptoms of ACS

Dyspnea, diaphoresis, nausea, vomiting, palpitations, dizziness, syncope (p. 4)

Three groups in whom atypical ACS presentations are common

Women, elderly patients, diabetics (p. 4)

Five atypical ACS symptoms

Fatigue, shortness of breath, weakness, indigestion, nausea (p. 4)

Progression of ischemic EKG changes (Section VI order)

1. Hyperacute T waves → 2. ST-segment elevation → 3. Q-wave formation → 4. T-wave inversion (p. 5)

Earliest STEMI finding on EKG

Hyperacute T waves (p. 5)

Three characteristics of hyperacute T waves

Broad, tall, symmetric (p. 5)

What does ST-segment elevation indicate?

Acute transmural injury (p. 5)

Criterion for ST-segment elevation

Elevation in contiguous leads (p. 5)

What does Q-wave formation indicate?

Myocardial necrosis (p. 5)

Characteristics of Q waves in MI

Deep and wide; may become permanent (p. 5)

What does T-wave inversion represent? (Section VI)

Ischemia or evolving infarction (p. 5)

Which leads indicate an inferior MI?

II, III, aVF (p. 5)

Which vessel is most commonly involved in an inferior STEMI?

RCA (usually) (p. 5)

Echo findings in inferior MI

Inferior wall hypokinesis or akinesis (p. 5)

Septal MI: leads and vessel

Leads V1-V2; LAD (p. 5)

Echo finding in septal MI

Septal wall motion abnormalities (p. 5)

Anterior MI: leads and vessel

Leads V3-V4; LAD (p. 5)

Echo finding in anterior MI

Anterior wall dysfunction (p. 5)

Which vessel supplies both the septal and anterior MI territories?

LAD (p. 5)

Lateral MI: leads

I, aVL, V5, V6 (p. 6)

Lateral MI: vessels

LCX and diagonal branches (p. 6)

Echo finding in lateral MI

Lateral wall motion abnormalities (p. 6)

Posterior MI: reciprocal EKG findings

ST depression in V1-V3 and tall R waves in V1-V3 (p. 6)

Posterior MI: vessels

RCA or LCX (p. 6)

Leads II, III, aVF → which MI location?

Inferior (p. 5)

Leads V1-V2 → which MI location?

Septal (p. 5)

Leads V3-V4 → which MI location?

Anterior (p. 5)

Leads I, aVL, V5, V6 → which MI location?

Lateral (p. 6)

ST depression + tall R waves in V1-V3 → which MI location?

Posterior (seen as reciprocal findings) (p. 6)

Which two MI locations can involve the RCA?

Inferior (usually RCA) and posterior (RCA or LCX) (pp. 5-6)

Which two MI locations can involve the LCX?

Lateral (LCX or diagonal branches) and posterior (RCA or LCX) (p. 6)

Reciprocal changes: definition

ST-segment changes occurring opposite the region of infarction (p. 6)

Reciprocal changes in inferior STEMI

ST elevation in II, III, aVF with reciprocal ST depression in I and aVL (pp. 6, 8)

Clinical significance of reciprocal changes

Strongly supports the diagnosis of acute MI (p. 6)

MONA-BASH

Mnemonic for initial medical therapy in the emergency treatment of ACS (p. 6)

MONA (first half of MONA-BASH)

Morphine (selected patients), Oxygen (if hypoxic), Nitroglycerin, Aspirin (p. 6)

BASH (second half of MONA-BASH)

Beta blockers, ACE inhibitors/ARBs, Statins, Heparin/anticoagulation (p. 6)

Which two MONA-BASH therapies are conditional?

Morphine (selected patients only) and oxygen (only if hypoxic) (p. 6)

PCI

Percutaneous Coronary Intervention (p. 6)

Three components of PCI

Coronary angiography, balloon angioplasty, coronary stenting (p. 6)

Goal of PCI

Restore blood flow as quickly as possible (p. 6)

CABG

Coronary Artery Bypass Grafting (p. 7)

Three indications for CABG

Multivessel disease, left main coronary disease, failed PCI (p. 7)

Goal of CABG

Create alternate routes around blocked vessels (p. 7)

What is the preferred reperfusion therapy for STEMI?

PCI: STEMI needs immediate reperfusion, and PCI's goal is restoring blood flow as quickly as possible (pp. 3, 6)

Why echo matters early in ACS (sonographer correlation)

ACS often produces echocardiographic findings before laboratory data are available (p. 7)

Seven common echocardiographic findings in ACS

Regional wall motion abnormalities, hypokinesis, akinesis, dyskinesis, reduced ejection fraction, ventricular remodeling, mechanical complications of MI (p. 7)

What echocardiographic finding commonly accompanies ACS?

Regional wall motion abnormalities (pp. 7, 9)

ACS Memory Pyramid sequence

Plaque rupture → thrombus → ischemia → injury → infarction (pp. 7-8)

Purpose of the ACS Memory Pyramid

Shows how myocardial ischemia progresses and which EKG changes appear as coronary blood flow worsens; used for EKG interpretation, case studies, and test prep (p. 7)

Pyramid stage: Ischemia

Reduced oxygen supply; EKG = T-wave inversion (pp. 7-8)

Pyramid stage: Injury

Active myocardial damage; EKG = ST-segment elevation (pp. 7-8)