Acute Coronary Syndromes

Question 1

acute coronary syndromes are associated with…

Answer 1

acute plaque changes - either severe partial occlusion or complete occlusion

often due to plaque rupture - lipid core is highly thrombogenic, activates platelet adhesion and clotting cascade —> vessel occlusion —> dramatic decrease in blood supply

Question 2

what causes atherosclerotic plaques to rupture, leading to acute coronary syndromes?

Answer 2

thinning of cap due to inflammation within and metalloprotease activity

plaques with thin caps or large amounts of lipids are prone to rupture

this exposes the lipid core which is highly thrombogenic - platelets and clotting cascade are activated, and clot causes occlusion of vessel

Question 3

how long can severe ischemia generally last until irreversible necrosis occurs?

Answer 3

20-30 mins, after that irreversible necrosis occurs

preceded by cell/mitochondrial swelling, glycogen depletion, myofibril relaxation, ATP depletion (within minutes)

recall that necrotizing myocardium releases cardiac biomarkers - troponin I/T (specific, prolonged) and CK-MB (less specific, transient)

Question 4

describe the cause of NSTEMI/ how it presents

Answer 4

NSTEMI = NON-ST elevated MI = unstable angina

due to severe partial coronary occlusion —> sudden increase in frequency/duration/intensity of symptoms in patient with stable angina, occurring unexpectedly at rest, or new onset of severe anginal symptoms

associated with plaque disruption and thrombus formation with vasospasm

Question 5

which area of the heart is most affected by NSTEMI?

Answer 5

NSTEMI = NON-ST elevated MI = unstable angina

sub-endocardium (innermost) is most vulnerable to ischemia because it is farthest away from coronary blood supply

Question 6

how do the symptoms of NSTEMI/unstable angina differ from those of chronic stable angina?

Answer 6

chronic stable angina - predicable, brief, non-progressive symptoms

unstable angina - sudden increase in frequency/duration/intensity of symptoms in patient with stable angina, occurring unexpectedly at rest, or new onset of severe anginal symptoms

Question 7

what changes may be seen on ECG with unstable angina/NSTEMI? (2)

Answer 7

1. new ST segment depression*
2. new T wave inversion

*recall ST depression = incomplete occlusion/subendocardial ischemia, while ST elevation = total occlusion/ transmural ishcemia

Question 8

what can be used to distinguish between unstable angina and NSTEMI, which have the same clinical presentation and ECG?

Answer 8

ECG will show ST depression + T wave inversion

to determine if there is infarction, you need to measure cardiac biomarkers (esp. troponin I/T)

neg. for troponins = unstable angina
pos. for troponins = NSTEMI (non-ST elevation myocardial infarction)

Question 9

How are unstable angina and NSTEMI medically managed?

Answer 9

want to address symptoms, prevent thrombosis, and reduce remodeling

anti-anginal drugs:
1. nitrates - decrease EDV, wall tension
2. beta blockers - decrease O2 demand

anti-thrombotic drugs:
1. aspirin
2. anticoagulants

reduce remodeling:
1. ACE inhibitors - reduce mortality
2. high intensity statin - reduce mortality

Question 10

what are the contraindications for the following drugs used to manage unstable angina or NSTEMI?
a. nitrates
b. beta blockers
c. aspirin/anticoagulants

Answer 10

a. nitrates - patients with RV infarct (nitrates reduce preload, exacerbates condition)

b. beta blockers - patients with bradycardia, bronchospasm, heart failure, hypotension

c. aspirin/anticoagulants - patients with bleeding disorders

Question 11

when does STEMI occur?

Answer 11

STEMI = ST elevation myocardial infarction

symptoms occur due to abrupt cessation of coronary blood flow due to thrombosis (esp. vulnerable plaques) —> progressively (moves inward to outward) transmural injury

*recall ST elevation occurs with total occlusion (transmural), while ST depression occurs with partial occlusion

Question 12

what histological changes occur following STEMI?

give time frame for >24hours, 2-5days, 7-10days, 2 weeks, and up to 2 months

Answer 12

STEMI = ST elevation myocardial infarction

<24hours: edema creates spaces between cells, lactate dehydrogenase leakage, mitochondrial swelling, marginal contraction band necrosis

2-5days: neutrophils infiltrate and cause degradation

7-10days: macrophages infiltrate to phagocytose debris and necrotic myocytes

2weeks: granulation tissue forms

up to 2 months: collagen deposition and scar formation

Question 13

what causes marginal contraction band necrosis, a histological change observed in the first 24 hours following STEMI?

Answer 13

typically seen if there has been some re-perfusion to the necrotic area

increased calcium (from blood) causes contraction, and oxygen exposure causes ROS-mediated damage

Question 14

how do patients with STEMI present?

Answer 14

STEMI = ST elevation myocardial infarction

pain described as heavy, squeezing, crushing which is severe and longer-lasting (>30mins) - centralized to central portion of chest, inner aspect of arms/shoulders/neck/jaw

associated with weakness, sweating, nausea, diaphoresis, “sense of impending doom”

high SNS tone —> pallor with cool skin, high HR/BP

Question 15

for each location of myocardial infarction, give the artery that was most likely occluded and the ECG leads that would indicate damage here:
a. left anterior surface of heart
b. left lateral surface of heart
c. posterior and inferior surface of heart

Answer 15

a. left anterior surface of heart: LAD - V1-4 (anterior leads)

b. left lateral surface of heart: L circumflex - V5-6 (anterior/lateral leads), I, aVL

c. posterior and inferior surface of heart: right coronary/PDA - II, III, aVF

Question 16

for each set of leads showing activity indicative of myocardial infarction, name the coronary artery most likely occluded:
a. V1-4
b. V5-6, I, aVL
c. II, III, aVF

Answer 16

a. V1-4: anterior leads, most likely LAD

b. V5-6, I, aVL: left lateral heart, most likely left circumflex

c. II, III, aVF: posterior/inferior heart, most likely right coronary/PDA

Question 17

what is reperfusion therapy in the context of STEMI

Answer 17

STEMI = ST elevation myocardial infarction = transmural occlusion

repurfusion therapy means opening up the artery and placing a stent

Question 18

describe the initial pharmacological management of STEMI

Answer 18

1. anti-anginal drugs: nitrates (except for RV infarction!), beta blockers (lower O2 demand)
2. reduce remodeling: ACE inhibitors (within 24 hours), high intensity statins (reduce mortality)
3. anti-thrombotic drugs: aspirin, anticoagulants

*note STEMI should be managed with stent automatically, but if facilities are not capable of this procedure, fibrinolytic therapy can be given also to dissolve the clot

Question 19

what causes stunned myocardium?

Answer 19

following an acute ischemic event and reperfusion, a portion of myocardium does not respond right away (the muscle is “stunned” by the ischemic event)

can return to normal over time

Question 20

hibernating vs stunned myocardium

Answer 20

hibernating: heart has reduced its level of activity due to chronic inadequate blood supply

stunned: following acute ischemic event and reperfusion, a portion of myocardium doesn’t respond right away (it’s “stunned”)

in both situations, gradually can return to normal following reperfusion

Question 21

what is usually the earliest complication of acute MI?

Answer 21

ventricular arrhythmia (fibrillation or tachycardia) - most common cause of sudden cardiac death following acute MI

can be primary (due to ischemia) - onset within 4 hours
or secondary (due to remodeling or scar) - onset within 48 hours

Question 22

when are bradyarrhythmias or heart block most commonly seen following acute MI?

Answer 22

common, especially with inferior MI (right coronary artery occlusion)

often resolve spontaneously if onset is within 24 hours

inferior MI (RCA) —> sinus bradycardia (SA nodal artery), Mobitz Type I and complete heart block (AV nodal artery)

anterior MI (LAD) —> Mobitz Type II block, bundle branch block

Question 23

what factor is the development of cardiogenic shock following acute MI most dependent on?

Answer 23

cardiogenic shock following acute MI is strongly dependent on infarct size, occurs 5-7 hours post-MI

leading cause of death for patients with acute MI, half within 48 hours (not sudden cardiac death as with V-tach/fib)

heart cannot recover systolic function —> low CO, BP, pulmonary edema, cool/clammy/cyanotic extremities, agitation/confusion, soft heart sounds + S3, etc, etc, etc

Question 24

when is peri-infarction pericarditis most common following acute MI?

Answer 24

peri-infarction pericarditis is most common with transmural infarcts

occur within first week, associated with epicardial hemorrhage

resolve spontaneously

Question 25

how does cardiogenic shock progress following acute MI? (what are the clinical findings)

Answer 25

heart cannot recover systolic function —> low CO, BP, pulmonary edema, cool/clammy/cyanotic extremities, agitation/confusion, soft heart sounds + S3, etc, etc, etc

Question 26

how does pericardial inflammation present as a post-MI complication? (symptomatically)

Answer 26

chest pain (sharp, centrally located) that is improved by sitting up/leaning forward and pericardial friction rub

Question 27

contrast peri-infarction pericarditis with Dressler syndrome

Answer 27

both can occur following acute MI

peri-infarction pericarditis: early (within 1 week), inflammation causes blood to pool in pericardium, resolves with NSAIDS, does not affect prognosis

Dressler syndrome: within 2 weeks, autoimmune response to heart antigens released from necrotic cells, ECG shows diffuse ST elevation

Question 28

ischemic mitral regurgitation and papillary muscle rupture following acute MI most often affects which papillary muscle? what can this lead to?

Answer 28

most often affects posterior papillary muscle (supplied by dominant artery - usually PDA of RCA), occurs 3-5 days post MI

recall posterior papillary muscle has single blood supply, while anterolateral papillary muscle has dual blood supply from LAD and circumflex

can lead to pulmonary edema, followed by cardiogenic shock

can be accompanied by acute mitral regurgitation (early systolic murmur)

Question 29

when is ventricular septal rupture most common following acute MI? what signs are indicative of this?

Answer 29

ventricular septal return most common with anterior MI (LAD supplies anterior 2/3 of septum), occurs 3-5 days post-MI

accompanied by holosystolic murmur at lower left sternal border (ventricular shunt), pain, dyspnea, signs of pulmonary congestion

Question 30

when does ventricular free wall rupture typically occur following acute MI, and what is the clinical outcome of this?

Answer 30

ventricular free wall rupture occurs within 1 week

complete rupture causes rapid/sudden death from cardiac tamponade —> hypotension, JVD, muffled heart sounds

Question 31

what are the signs of ventricular septal rupture following acute MI?

Answer 31

ventricular septal return most common with anterior MI (LAD supplies anterior 2/3 of septum), occurs 3-5 days post-MI

accompanied by holosystolic murmur at lower left sternal border (ventricular shunt), pain, dyspnea, signs of pulmonary congestion

Question 32

explain how LV aneurysm can be a complication of acute MI

Answer 32

LV aneurysm can be delayed complication, via mural (read: wall) thrombus formation and worsening heart failure or ventricular tachyarrhythmia