โรงพยาบาลสรรพสิทธิประสงค์
อุบลราชธานี
How to manage
ACS
Complications
นพ.วีระ มหาวนากูล
กลุม่ งานอายุรกรรม
โรงพยาบาลสรรพสิทธิประสงค์อบุ ลราชธานี
Complications of Acute Coronary
Syndrome
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Arrhythmic complications of ACS
Mechanical complications of ACS
Pump failure
Right ventricular infarction
Left ventricular aneurysm
Left ventricular pseudoaneurysm
Pericardial complications
Complications involving bleeding
Complications of percutaneous coronary
intervention
Complications of Myocardial
Infarction
• arrhythmic
• mechanical
• inflammatory (early pericarditis and post-MI
syndrome)
• right ventricular (RV) infarction and
cardiogenic shock
• left ventricular mural thrombus (LVMT)
Arrhythmic Complications
• 90% of patients  cardiac arrhythmia immediate or
during MI
• 25% of patients  first 24 hr
• The incidence of arrhythmia: STEMI > NSTEMI
• Most peri-infarct arrhythmias are benign  selflimited
• Hypotension  myocardial oxygen requirements 
malignant ventricular arrhythmias (aggressively
monitored and treated)
Arrhythmic Complications
Pathophysiology
• autonomic dysfunction  enhanced
automaticity of the myocardium and
conduction system
• Electrolyte imbalances (hypoK and hypoMg)
and hypoxia  cardiac arrhythmia
• damaged myocardium = substrate reentrant circuits (tissue refractoriness)
Peri-infarction arrhythmias
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Supraventricular tachyarrhythmias
Accelerated junctional rhythms
Bradyarrhythmias
Atrioventricular (AV) blocks
Intraventricular blocks
Ventricular arrhythmias
Reperfusion arrhythmias
Supraventricular tachyarrhythmias
Sinus Tachycardia
• enhanced sympathetic activity  transient
hypertension or hypotension Causes:
• Pain
• Anxiety
• Heart failure
• Hypovolemia
• Hypoxia
• Anemia
• Pericarditis
• Pulmonary embolism
Supraventricular tachyarrhythmias
Sinus Tachycardia
Treatment strategies:
• adequate pain medication,
• diuresis  heart failure
• Oxygenation
• volume repletion  hypovolemia
• anti-inflammatory agents  pericarditis
• Beta-blockers and/or nitroglycerin  relieve
ischemia
Supraventricular tachyarrhythmias
• Premature atrial contractions (PAC’s)
• PAC’s paroxysmal SVT, atrial flutter, or atrial
fibrillation
• ↑left ventricular (LV) diastolic pressure or
pericarditis (inflammation)  atrial distention
• No specific therapy: ?? occult heart failure ??
Supraventricular tachyarrhythmias
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Paroxysmal supraventricular tachycardia
(PSVT)
Incidence in AMI < 10%
No Hypotension  Adenosine (No data)
No significant LV failure  IV diltiazem or
beta-blocker
severe heart failure or hypotension 
synchronized electrical cardioversion
Supraventricular Tachycardia
Supraventricular Tachycardia
Supraventricular tachyarrhythmias
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Atrial flutter
< 5% of AMI. Transient
Sympathetic overstimulation of the atria
Treatment strategies: atrial fibrillation 
ventricular-rate control with drugs is less easily
• synchronized electrical cardioversion: with 50 J,
or the biphasic equivalent  relatively promptly
decrease coronary blood flow and/or
hemodynamic compromise
• refractory to medication  overdrive atrial
pacing
Atrial Flutter
Atrial Flutter
Atrial Flutter
Supraventricular tachyarrhythmias
• Atrial fibrillation
• 10-15% in AMI
• Onset < 1 hour  caused by LV failure,
ischemic injury to the atria, or RV infarction
• Pericarditis & conditions ↑left atrial pressure
 atrial fibrillation
• ↑mortality and stroke: Anterior wall MI.
Atrial fibrillation
Atrial fibrillation
Supraventricular tachyarrhythmias
Atrial fibrillation
unstable condition
• worsening ischemic pain and/or hypotension
 electrical cardioversion
• Synchronized electrical cardioversion 200 J or
the biphasic equivalent
• Conscious sedation (preferred) or general
anesthesia is advisable
Supraventricular tachyarrhythmias
Atrial fibrillation
stable condition
• immediate objective  controlling the
ventricular response
• Not respond to cardioversion  IV amiodarone
or IV digoxin (in patients with LV dysfunction or
heart failure)  achieve rate control.
• IV beta-blocker & IV diltiazem  alternative for
slowing the ventricular rate, with caution in
moderate-to-severe heart failure
Supraventricular tachyarrhythmias
Atrial fibrillation
• AF & atrial flutter  ↑risk of
thromboembolism
• Anticoagulation: unfractionated heparin or
low molecular weight heparin (LMWH) (If no
contraindications)
• Transient AF  ??? Anticoagulation
Accelerated Junctional Rhythm
• ↑ automaticity of the junctional tissue 
heart rate of 70-130 /min.
• most common in inferior MI
• Treatment  correcting the underlying
ischemia
Accelerated Junctional Rhythm
Arrhythmic Complications
Bradyarrhythmias
• Sinus bradycardia
• Junctional bradycardia
Arrhythmic Complications
Bradyarrhythmias
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Sinus bradycardia
common in acute inferior or posterior MI
first 1-2 hours after AMI
Mechanism: stimulation of cardiac vagal
afferent receptors  efferent cholinergic
stimulation of the heart (↓ myocardial oxygen
demand)  bradycardia and hypotension 
ventricular arrhythmias (treated aggressively)
Arrhythmic Complications
sinus bradycardia
• No adverse signs or symptoms  therapy is
typically unnecessary
• HR < 40 bpm with hypotension  atropine
sulfate 0.5-1 mg IV every 3-5 min. (maximum
of 0.03-0.04 mg/kg)
• inability to reverse hypotension with atropine
in inferior MI  volume depletion and/or RV
infarction
Arrhythmic Complications
sinus bradycardia
• atropine is ineffective  transcutaneous or
transvenous pacing
• Transplanted hearts do not respond to
atropine  require cardiac pacing
• Additional pharmacologic intervention 
dopamine 5-20 mcg/kg/min IV, epinephrine 210 mcg/min, and/or dobutamine.
Arrhythmic Complications
Junctional bradycardia
• Junctional bradycardia  a protective AV
junctional escape rhythm, rate of 35-60 bpm
in inferior MI
• Usually not associated with hemodynamic
compromise
• Treatment:not required
Arrhythmic Complications
AV and Intraventricular Blocks
• SA node ปกติรับเลือดจาก right coronary artery
(RCA) ประมาณ 60% และรับจาก left circumflex artery
(LCX) ประมาณ 40%
• AV node ปกติรับเลือดจาก RCA ประมาณ 90% และรับจาก
LCX ประมาณ 10%
• His bundle ส่วนใหญ่ได้ รับเลือดจาก RCA และส่วนน้ อยจาก
septal perforators จาก left anterior descending
artery (LAD)
Arrhythmic Complications
AV and Intraventricular Blocks
• Main bundle branch และ Right bundle branch
รับเลือดจาก septal perforators จาก LAD ส่วนน้ อยได้ รับ
collateral circulation จาก LCX และ RCA
• Posterior fascicle ได้ รับ dual blood supply จาก AV
nodal artery และ septal perforators จาก LAD
• Anterior fascicle ส่วนใหญ่ได้ รับเลือดจาก septal
perforators และส่วนน้ อยจาก AV nodal artery
Arrhythmic Complications
AV and Intraventricular Blocks
• First-degree AV block
• 15% of AMI, most common  inferior wall MI
• conduction disturbances above the His bundle
 CHB or asystole is rare
• CCB & ß-blockers  cause or exacerbate 1˚AV
block  stopped if hemodynamic impairment
/higher-degree block
• No specific therapy, atropine if BP ↓
• cardiac monitoring: possible  higher block.
Arrhythmic Complications
AV and Intraventricular Blocks
• Second-degree AV block
• Mobitz type I (Wenckebach) AV block  10%
of AMI (most common  inferior MI), 90% of
2˚ AV block in AMI
• Not affect overall prognosis
• Not require treatment. If HR is inadequate for
perfusion  atropine 0.5-1 mg IV
• Transcutaneous/temporary transvenous
pacing  Rare
AV Block
1st AV block
2nd AV block Mobitz I (Wenckebach)
Arrhythmic Complications
AV and Intraventricular Blocks
• Mobitz type II AV block accounts: < 1% in AMI
(10% of all second-degree AV blocks)
• associated with anterior infarction
• poor prognosis (ถ้ าร่วมกับมี complete heart block
 mortality rate ประมาณ 80%)
• immediately  transcutaneous
pacing/atropine
• Atropine helps in 50% of cases, but
occasionally worsens the block
Mobitz I & II AV Block
Arrhythmic Complications
AV and Intraventricular Blocks
• Third-degree AV block
• 5-15% in AMI (anterior or inferior MI)
• inferior MI: gradually progress from 1˚AV
block / Mobitz I AV block
• most patients  supranodal or intranodal 
escape rhythm  stable, narrow QRS & rates
> 40 bpm
• 30%  below the His bundle  escape
rhythm < 40 bpm & wide QRS complex
Third degree heart block
Arrhythmic Complications
AV and Intraventricular Blocks
• CHB in inferior MI usually responds to
atropine
• resolves within a few days without the need
for a temporary or permanent pacemaker
• Mortality rate for inferior MI + CHB  15%
(Higher in RV infarction)
• Atropine  may not help & worsen the block
 Temporary transcutaneous / transvenous
pacing
Complete Heart Block
Arrhythmic Complications
AV and Intraventricular Blocks
• persistent symptomatic bradycardia
/unresolved with lysis or percutaneous
coronary intervention  Permanent pacing
• anterior MI: intraventricular block / Mobitz
type II AV block  third-degree AV block 
high mortality rate
• Immediate treatment: atropine and/or
transcutaneous / temporary transvenous
pacing
• If survive  often permanent pacemaker
Arrhythmic Complications
AV and Intraventricular Blocks
• Intraventricular blocks
• 1 or more fascicular block  15% of AMI
• Isolated left anterior fascicular block (LAFB) 
3-5% of AMI (complete AV block uncommon)
• Isolated left posterior fascicular block (LPFB)
1-2% of AMI (blood supply of the posterior
fascicle is larger than that of the anterior
fascicle  relatively large infarct and high
mortality rate)
Arrhythmic Complications
AV and Intraventricular Blocks
• The right bundle branch: dominant blood
supply from the left anterior descending (LAD)
artery.
• new RBBB  2% of AMI, suggests a large
infarct territory  cardiogenic shock & Death
• RBBB with LAFB (bifascicular block) เกิดจาก
occlusion of the proximal LAD coronary artery
(Mortality related to the amount of muscle
loss, CHB-uncommon)
Arrhythmic Complications
RBBB
Arrhythmic Complications
AV and Intraventricular Blocks
• Bifascicular block + first-degree AV block 
trifascicular block (40%  complete heart
block)
Trifascicular Block
Arrhythmic Complications:
Ventricular Arrhythmias
• Acute phase arrhythmia เกิดใน 48 ชัว่ โมงแรก สาเหตุ
ส่วนใหญ่จะเป็ น reversible cause เช่น ภาวะ ischemia,
left ventricular wall stress ถ้ าได้ รับการแก้ ไขก็จะไม่มีผล
ต่อการพยากรณ์โรคในระยะยาว
• Chronic phase arrhythmia มักจะเป็ น
monomorphic VT กลไกการเกิดเป็ น reentry ซึง่ เกิดจาก
การที่มีแผลเป็ นในผนังกล้ ามเนื ้อหัวใจ ผู้ป่วยกลุม่ นี ้มีการพยากรณ์โรค
ระยะยาวไม่ดี มีโอกาสเกิด sudden cardiac death สูงใน
อนาคต
Arrhythmic Complications:
Ventricular Arrhythmias
• Premature ventricular contractions (PVC’s)
• prophylactic suppression of PVCs with
antiarrhythmic drugs (lidocaine, etc)  not
recommended.
• Prophylaxis  ↑ risk of fatal bradycardia
/asystole  suppression of escape pacemakers
(lidocaine เพื่อรักษา PVCs กลับทาให้ อตั ราตายเพิ่มสูงขึ ้นจาก
bradyarrhythmia และ asystole ปั จจุบนั จึงมีที่ใช้ น้อยมาก)
• attention  correct electrolytic or metabolic
abnormalities, identify & treat recurrent
ischemia.
PVC’s
PVC’s
Arrhythmic Complications:
Ventricular Arrhythmias
• Accelerated idioventricular rhythm (AIVR)
• 20% of AMI
• wide QRS complex /regular escape rate faster
than the atrial rate, but < 100 bpm
• AV dissociation is frequent
• Slow, nonconducted P waves
• unrelated to the fast, wide QRS rhythm
• short & terminate spontaneously
Arrhythmic Complications:
Ventricular Arrhythmias
Arrhythmic Complications:
Ventricular Arrhythmias
• Accelerated idioventricular rhythm
• SA node or AV node  sustain structural damage
& depress nodal automaticity
and/or
• an abnormal ectopic focus in the ventricle 
dominant pacemaker
• Do not affect prognosis
• No definitive evidence  untreated occurrence
increases the incidence of ventricular fibrillation
or death
Arrhythmic Complications:
Ventricular Arrhythmias
• Accelerated idioventricular rhythm
• พบบ่อยใน early reperfusion  neither sensitive
nor specific marker for reperfusion
• Suppression  bradycardia or asystole  left
untreated
Arrhythmic Complications
Nonsustained ventricular tachycardia
• 3 or more consecutive ventricular ectopic beats ,
> 100 bpm and lasting < 30 sec
• multiple runs of nonsustained VT  sudden
hemodynamic collapse
• antiarrhythmic  No morbidity/mortality benefit
• > 48 hr after infarction in LV systolic dysfunction
(LVEF < 0.40)  ↑ risk for sudden cardiac death
 electrophysiologic testing & appropriate
therapy
Arrhythmic Complications
Nonsustained ventricular tachycardia
• Multiple episodes of nonsustained VT 
intensified monitoring & attention to
electrolyte imbalances
• Keep Serum K > 4.5 mEq/L, and Mg > 2.0
mEq/L
• Ongoing ischemia  aggressively be sought
and corrected
Arrhythmic Complications
Sustained ventricular tachycardia
• 3 or more consecutive ventricular ectopic
beats ,rate > 100 bpm and lasting > 30 sec or
causing hemodynamic compromise that
requires intervention
• 20% hospital mortality rate
• Rapid polymorphic VT ( >150 bpm) associated
with hemodynamic instability  immediate
unsynchronized cardioversion of 200 J (or
biphasic energy equivalent)
Arrhythmic Complications
Sustained ventricular tachycardia
• Monomorphic VT  synchronized 100 J (or
biphasic energy equivalent)
• Antiarrhythmic therapy: amiodarone (drug of
choice) or procainamide may be attempted
before electrical cardioversion
• Correct electrolyte abnormalities, acid-base
disturbances, hypoxia, or medication
• Persistent/recurrent VT  overdrive pacing
Arrhythmic Complications
Sustained ventricular tachycardia
• lidocaine 1-1.5 mg/kg bolus และให้ ทาง iv drip ต่อ
2-4 mg/min ให้ ลดขนาดยาในผู้สงู อายุ, มีภาวะ CHF หรื อ
hepatic dysfunction
• amiodarone 150 mg iv ใน 10 นาทีและให้ iv drip ต่อ
1 mg/min ใน 6 ชัว่ โมง ต่อไปให้ 0.5 mg/min
Arrhythmic Complications
ventricular fibrillation
• Primary VF  greatest in the first hour, 60% of
episodes occur within 4 hours, and 80% occur
within 12 hours
• Secondary or late VF  48 hr after an MI 
usually associated with pump failure and
cardiogenic shock, large infarct, an
intraventricular conduction delay, and an
anteroseptal MI (In-hospital mortality rate of
40-60%)
Arrhythmic Complications
ventricular fibrillation
• Treatment: unsynchronized electrical
countershock 200-300 J (or biphasic energy
equivalent)
• electromechanical dissociation (EMD) or
pulseless electrical activity (PEA)  extensive
myocardial ischemia/necrosis or cardiac rupture
• IV amiodarone/lidocaine  facilitate successful
electrical defibrillation & prevent recurrent/
refractory episodes, continued IV infusion for 1224 hr
• early use of ß-blockers in MI  ↓ ventricular
fibrillation/death
Arrhythmic Complications
Reperfusion Arrhythmias
• believed to be a marker of successful coronary
reperfusion
• high incidence in patients with AMI in whom
coronary reperfusion is unsuccessful
• neither sensitive nor specific for reperfusion
 treated Accelerated Idioventricular Rhythm
(AIVR)
• อาจจะเป็ น PVCs, AIVR, VT หรื อ VF
Mechanical Complications of MI
• Ventricular free wall rupture (VFWR)
• ventricular septal rupture(VSR)
• papillary muscle rupture with severe mitral
regurgitation (MR)
Ventricular free wall rupture (VFWR)
• most serious complication of AMI
• VFWR leads to acute hemopericardium and death
from cardiac tamponade
• incidence 0.8-6.2 % declined with better 24
hour systolic blood pressure control; ↑use of
reperfusion therapy, beta blockers, and ACE
inhibitors; and ↓use of heparin
• Percutaneous transluminal coronary angioplasty
(PTCA) had an incidence of free wall rupture <
receiving thrombolytic therapy.
Ventricular free wall rupture (VFWR)
• ส่วนใหญ่ 1st week after AMI
• Involve: anterior or lateral wall
• Acute  severe chest pain, abrupt
electromechanical dissociation, asystole,
hemodynamic collapse, and death
• Subacute  pseudoaneurysms (vary in size
,high risk to rupture) syncope, hypotension,
shock, arrhythmia, prolonged & recurrent
chest pain
Ventricular free wall rupture (VFWR)
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Risk factors
Age > 70 years
Female
no previous MI
Q waves on ECG
Hypertension during the initial phase of STEMI
Corticosteroid/NSAID use
Fibrinolytic therapy > 14 hr after STEMI onset
Ventricular free wall rupture (VFWR)
• Echocardiography  moderate-to-large
pericardial effusion with signs of impending
tamponade
• Most important prevention strategy: early
reperfusion therapy
• IABP, IV fluids, inotropic agents, emergency
pericardiocentesis.
• Stable  emergency surgical repair
• mortality rate: high & depend on preoperative
hemodynamic status
ventricular septal rupture(VSR)
• high mortality rate
• Bimodal: high incidence in the first 24 hr,
another peak on days 3-5 (rarely > 2 weeks)
• median time (onset of AMI to septal rupture):
1 Day in GUSTO-I, 16 hr in SHOCK-Trial
• most common in large anterior MI (occlusion
of the LAD artery causing extensive septal
infarcts)  ST-segment elevations and Q
waves in inferior leads (II, III, aVF)
ventricular septal rupture(VSR)
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Risk factors
Age >65 y
Female
Single-vessel disease
Extensive MI
Poor septal collateral circulation
RV involvement
ventricular septal rupture(VSR)
• Clinical presentation
• chest pain, shortness of breath, hypotension,
biventricular failure & shock with (hours to
days)
• new, loud & harsh holosystolic murmur 
LLSB & palpable parasternal systolic thrill, S3
gallops (เทียบกับ acute MR  soft systolic
murmur at the apex, without thrill)
• กรณี cardiogenic shock  identify murmur ยาก
ventricular septal rupture(VSR)
• Echocardiography (color Flow) Tool of
choice
• Cardiac catheterization  confirm Dx, ประเมิน
degree of left-to-right shunt, ตาแหน่งของ VSR, แยก
โรค VSR จากภาวะ MR , ดู coronary artery lesion
ventricular septal rupture(VSR)
• Key management: prompt diagnosis & an
aggressive approach to hemodynamic
stabilization, angiography, and surgery
• Oxygen, IABP
• use of vasodilators (↓ afterload & LV pressure
& left-to-right shunt)
• diuretics, and inotropic agents
• Medical therapy  temporary stabilization
before surgery
ventricular septal rupture(VSR)
• GUSTO-I  30-day mortality rate ของผู้ป่วยที่รักษา
โดย surgical repair = 47% VS medical = 94% และ
1-year mortality rate = 53% vs 97%
• Current guidelines of the ACC/AHA  patients
with septal rupture complicating AMI 
urgent surgical intervention, regardless of
their clinical status
• Percutaneous closure of septal rupture 
relatively new approach
acute mitral regurgitation
• MR is a common complication, results from local
and global LV remodeling  predictor of heart
failure & death
• เกิด 7-10 days หลัง MI, onset may vary according to
the mechanism of MR. MR จาก Papillary muscle
rupture เกิดในช่วง 1-14 วัน (median 1 วัน)
• Mild-to-moderate MR  silent, พบจากการทา
Doppler echocardiography
• Severe acute MR (rupture of papillary muscles or
chordae tendineae)  abrupt hemodynamic
deterioration with cardiogenic shock  อัตราตายสูง
acute mitral regurgitation
• Risk factors: advanced age, female, large
infarct, previous AMI, recurrent ischemia,
multivessel coronary artery disease & heart
failure
• Posteromedial papillary muscle >
anterolateral papillary muscle (PM มี single
blood supply ขณะที่ AL มี dual supply)
• Papillary muscle rupture  flailing or prolapse
of the leaflets  severe MR
acute mitral regurgitation
• Papillary muscle dysfunction due to scarring or
recurrent ischemia  MR in the subacute and
chronic phases, resolve spontaneously
• Large posterior infarctions  acute MR จาก
asymmetric annular dilation and altered function
and geometry ของ papillary muscle
• Dx: Echocardiography with color flow Doppler
imaging
• CXR  pulmonary edema without cardiac
enlargement
acute mitral regurgitation
• Presentation:
• mild or moderate MR  asymptomatic
• acute severe MR  shortness of breath,
fatigue, a new apical holosystolic murmur
(may be early-to-mid systolic , no thrill), flash
pulmonary edema & shock
acute mitral regurgitation
• Cardiac catheterization should be performed
to determine the extent and severity of
coronary artery disease
• Treatment: Determination of hemodynamic
stability & exact mechanism of MR
• Medication: afterload reduction diuretics,
sodium nitroprusside & nitrates in no
hypotension
• Intra-aortic balloon counterpulsation (IABP) in
hemodynamic compromise
acute mitral regurgitation
• Emergency surgical intervention is the
treatment of choice for papillary muscle
rupture
• MV repair ดีกว่า Replacement ในกรณีไม่มี papillary
necrosis
• emergency surgery avoided กรณี intermittent
MR due to recurrent ischemia  angioplasty
or coronary artery bypass grafting (CABG)
Etiologies, Prevalence, and Mortality*
Causes
Incidence
78%
Mortality
59%
Severe mitral
regurgitation
6.9%
55%
Ventricular septal
rupture
3.9%
87%
Isolated right
ventricular shock
2.8%
55%
Predominant left
ventricular failure
1.4%
55%
Free wall rupture and
tamponade
Average
60%
*Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, et al. Cardiogenic shock complicating acute myocardial infarction-etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries
for cardiogenic shocK. J Am Coll Cardiol 2000;36(3 Suppl A):1063-70.
Left Ventricular Aneurysm
• a localized area of myocardium with abnormal
outward bulging and deformation during both
systole and diastole
• approximately 3-15%
• Risk factors: female, total occlusion of the LAD
artery, single-vessel disease & absence of
previous angina
• 80%  anterolateral wall (asso. CTO of LAD)
Left Ventricular Aneurysm
• ECG  ST elevation persists several weeks
after AMI & same leads showing the acute
infarct
• Echocardiography  93% sensitivity & 94%
specificity
• cardiac catheterization  standard for Dx
Left Ventricular Aneurysm
Inferior wall
aneurysm
Left Ventricular Aneurysm
• small or clinically insignificant aneurysms 
conservative, close follow-up
• Medical therapy: angiotensin-converting enzyme
(ACE) inhibitors  reduce afterload, infarct
extension & LV remodeling
• Anticoagulation  severe LV dysfunction and/or
thrombus in the LV or aneurysm
• Surgical resection: if severe heart failure,
ventricular tachyarrhythmias refractory to
medical treatment, recurrent thromboembolism
Left ventricular mural thrombus
• anterior wall infarcts
• 20-40% (60% in large anterior-wall AMIs, not
treated with anticoagulant therapy)
• high risk of systemic embolization
(Anticoagulant therapy  ↓ rate of embolic
events by 33% เทียบกับไม่ได้ anticoagulation)
• most common presentation  Stroke (within
the first 10 days after AMI)
Left ventricular mural thrombus
• Transthoracic echocardiography  modality
of choice (92% sensitivity, 88% specificity)
• Management  heparin treatment followed
by oral warfarin therapy for 3-6 months,
lifelong anticoagulation if a mural clot persists.
Left ventricular mural thrombus
Apical LV
thrombus
Pericarditis
• ≈10%, ภายใน 24-96 hr
• inflammation of pericardial tissue overlying
infarcted myocardium
• severe chest pain (pleuritic) & pericardial
friction rub
• ECG  diffuse ST-segment ↑ in all or nearly
all of leads
• Echocardiography may reveal a small
pericardial effusion
Pericarditis & Dressler syndrome
• Treatment  aspirin & NSAIDs
• Colchicine  in recurrent pericarditis
• Post-MI syndrome (Dressler syndrome) 
autoimmune process, fever, chest pain, signs &
symptoms of pericarditis เกิด 2-3 weeks after AMI.
• incidence 1-5%, ลดลงหลังมีการรักษาด้ วย thrombolysis
และ coronary angioplasty
• Management: hospitalization & observation for
any evidence of cardiac tamponade, rest, NSAIDs,
and/or steroids