Complications of acute myocardial infarction .all

2. ⚫ The term myocardial infarction should be used when there
is evidence of myocardial necrosis in a clinical setting
consistent with myocardial ischaemia. Under these
conditions any one of the following criteria meets the
diagnosis for myocardial infarction:
⚫ • Detection of rise and/or fall of cardiac biomarkers
(preferably troponin) with at leastonevalueabove the 99th
percentile of the upper reference limit (URL) together with
evidence of myocardial ischaemiawith at leastoneof
⚫ the following:
⚫ • Symptoms of ischaemia.
⚫ • ECG changes indicativeof new ischaemia (new ST-T
changesor new left bundle branch block [LBBB]).
⚫ • Developmentof pathological Q waves in the ECG.
⚫ • Imaging evidence of new lossof viable myocardium or new
regional wall motion abnormality. (Kristian Thygesen, et al
2007)

3. ⚫Complications
⚫Electrical Complications
⚫Mechanical complications
⚫Heart Failure
⚫Pericarditis
⚫Post Infarction Angina or ReInfarction .
⚫Take Home Message

5. ⚫Cardiogenicshock and heart failureare the most
common causes of death in patients hospitalized
with acute myocardial infarction.
⚫At least 75% of patientswith acute myocardial
infarction (MI) havean arrhythmia during the
periinfarct period.

6. Electrical Complications :
In acute M.I , Arrythmiasare mainlydue to reentry
caused by inhomogenicity of ischaemic myocardium .
While Reperfusion Arrythmiasare due towashout of the
accumlated ions and metabolites .
VentricularArrythmias
1. Ventricularpremature beats ( PVCs )
Nocorrelation to thedevelopment of primaryvent.
Fibrillation .
Treated by correction of the electrolyte or metabolic
disturbances . If associated with sinus tachycardia , Beta
Blockers are used tosuppress the sympatheticoverdrive.

7. 2. Accelerated idioventricularrhythm :
occurs in 20% of patientswith STEMI , mostoften
aftersuccessful reperfusion .
3. VentricularTachycardia :
Non-Sustained V.Tach. isn’tassociated with increase
mortalityduring hospitalizationoroneyearafter .
Sustained V.tachwith haemodynamicstability
should be treated immediately by amiodarone or
procainamide , while if it's notaborted orassociated
with chest pain or haemodynamicdeterioration ,
DC shock should be used forcardioversion .

8. 4. Ventricular fibrillation :
⚫ PrimaryV
.F
⚫ SecondaryV.F
⚫ Late V
.F
- Treatment Consistsof:
⚫
⚫
⚫ Unsynchronized DC shock with at least 200 – 300 joules
monophsic
⚫ Amiodarone I.V , helps interruptionof theattack and
prevent recurrence .
Treatmentof hypokalaemiaand magnesiumdeficits . ( aim K
≥ 4.5
Prophylactic Lidocaine is no longerrecommended .

9. SupraventricularArrythmias
1. Sinus Tachycardia :
very common in patients with acute M.I esp. Ant. M.I , it
may becaused byother post-infarctioncausesas anxiety ,
persistant pain , LVdysfunction , fever , hypotension ,
hypovolaemia , pericarditis , pulmonaryembolism , etc
…..
2. Premature Atrial beats :
may bedue toatrial ischaemiaor pericarditis .
No specific therapy is indicated .
3. Paroxysmal SVT :
usually transientand needs ratecontrol using carotid
massage , adenosine , verapamil , diltiazem or Beta
blockers .

10. 4. Atrial Flutterand Fibrillation :
both are usually transientand mayoccurwith patientswith
LVdysfunction , extensionof ischaemiaorpulmonary
embolism .
Bradyarrythmias
1. Sinus Bradycardia :
it’scommon especially in Inferiorand posterior Infarctions . If
heart rate is below 40-50 , Atropine is administered .
2. First Degree A-V block :
it may be caused by the useof Beta blockersor Calcium
channel blockers

11. 3. Second degree AV block :
Type I: Does not require treatment except if ventricular
rate is below 50 bpm , then atropine is indicated.
Type II: has a potential to progress to complete heart
block so temporary pacing is indicated and set at
about 60 bpm.
4. CompleteAV block :
⚫ If associated with Inferior infarctions , it’s usually transientand
resolveswithin 72 hrs . Pacing is indicated if Ventricularrate
is less than 40- 50 bpm
⚫ If associated with with anterior infarction , it usually occurs
suddenly , after 12-24 hrs , they have unstable escape rhythm
and awide complexesat a rate ≤ 40 bpm . Theyareassociated
with an extensiveseptal necrosisand may need permenant
pacing .

12. 5. Intraventricular block :
RBBB with ant. MI is associated with increased
mortality .

13. ⚫Indicationsof Temporary Pacing in Acute M.I :
1. Asystole
2. Symptomatic bradycardia not responsive toatropine
3. Complete Heart Block
4. Second degree H.B ( Mobitz type II )
5. New Bifasicular block
6. Bilateral Bundle branch block
7. Sinus pauses > 3 sec. , not resposive toatropine
8. Incessant Vent. Tachycardia ( overdrive pacing )

14. Mechanical complications
1. Acute Mitral Regurge :
Papillary muscledysfunction:
⚫ Caused by posteromedial papillary ms dysfunction , It’susually
transientduring ischaemia .
⚫ It usually presents with an apical systolic murmur , confirmed by
echocardiography .
⚫ It requires no specific therapy , in intermediate cases it may require
antifailuretreatment , while in severecases it requires treatment like
thatof papiilary ms rupture .
Papillary ms Rupture :
⚫ It occurs with Inferior Infarction 6-12 times more than Anterior
infarctions .
⚫ It may presentwithacutepulmonaryoedemaoreven sudden cardiac
death , itcan occurupto 2-7 days post infarction .
⚫ Intra-Aortic Balloon , vasodilators or inotropic therapy may be
required fortemporarystabilization before surgery ( CABG + Mitral
Valve Repairor Replacement )

15. Papillary muscle rupture complicating acute inferior myocardial infarction;
magnified four-chamberview. The ruptured head of the posteromedial papillary
muscle (arrow) prolapses freely into the leftatrium; the posterior mitral valve
leaflet (arrowhead) is flail.

16. 2. Ventricular Septal Rupture
⚫ It occurs within the first week post-Infarction .
⚫ Itoccurs equally with Inferiorand Anterior infarctions.
⚫ Rupture with Anterior Infarctions tend to be apical while
it’s basal and has aworse prognosis with inferiorinfarctions
.
⚫ Itusually presentswith a new onset murmur ( new harsh
holosystolic murmur along the left sternal border ) . The
patient is usually stable and develops sudden clinical
deterioration .
⚫ Patientswith acute VSR usually lie flat , while patientswith
acute MR develop pulmonaryoedema & cann’t Lie flat .
⚫ Medical therapy is ineffective , Emergency Surgical
Intervention is the treatmentof choice .

17. Transthoracic sub-costal 4-chamberechocardiographic findings
showing a largeventricular septal rupture (VSR)

18. 3. Free wall Rupture :
⚫ Occurs within 2 weeks , and mostcommoncauseof death after
cardiogenicshock and arrythmias .
⚫ Early useof thrombolytic therapy appears toreduce the incidence
of cardiac rupture , while late use appears to increase the
incidence .
⚫ Itusually presents bysudden Death.
⚫ Fewcases can be salvaged by immediatepericardiocentesis ,
emergencyThoracotomyand surgical repair .

19. Cardiac freewall rupture post
myocardial
infarction.
Pericardial tamponade from left
ventricular free
wall ruptureand hemopericardium.

20. 4. Ventricular Aneurysm :
Diff. between True and Pseudo-aneurysm .
True Aneurysm Pseudo-Aneurysm

21. ⚫ Clinically : abnormal precordial impulse in the 3rd left intercostal space
⚫ ECG : ST Seg. Elevation persists more than 2 weeks . ( it may indicatea
large infarctionwith RWMA not necessarilyAneurysm ) .
Other Mechanical Complications
5. Pulmonary Embolism :
• Post-infarction patients havegreatertendancies for Pulmonary
embolism ( P.E ) due to decreased cardiac output and
immoblization ,
• Early mobilizationand treatmentaiming to increase Cardiac
outputare the mosteffective prophylactic methods .

22. 7. Systemic embolism :
⚫ LV thrombi occurs in 20-40 % of ant. Infarction Patients .
⚫ If LVthrombus is clearly demonstrated in Echocardiography ,
Systemicanticoagulationshould begiven for 3-6 months .

23. Heart Failure and Cardiogenic shock:
⚫Heart Failureoccurs when LV function decrease by 30% of
normal function .
⚫Killip Class: Clinical Examination
I. No S3 or rales
II.Rales in less than half of lung field III
Rales in more than half of lung field
IV Cardiogenicshock
⚫Maypresentacutelyafter MI ( killipclass II or III ) oras a
delayed presentation ( NYHA II-IV) .

24. ⚫Cardiogenic shock is persistent hypotension with a
systolicpressure <80 mm Hg for more than 30 minutes
in the absence of hypovolemia. It occurs when ≥ 40 %
of myocardium is affected .
⚫The mostcommoncausesof cardiogenic shock
include
1) large leftventricularinfarct (usually >40% of
left ventricle) seen in about 80% of shock patients
2)rightventricular infarct in 10% of shock patients
3) mechanical complications of myocardial infarction
(ventricular septal defect, acute mitral regurgitation,
tamponade) in 10% of shock patients.

25. ⚫Pericarditis :
1. Earlypost-infarction Pericarditis
⚫ Occurs 2-4 days following acute infarction .
⚫ Patientswhodevelop this condition usually have largerinfarcts ,
lower EF and higher incidence of CHF .
⚫ Presented by Fever , Chestpain and friction rub .
⚫ Pain is aggrevated by movementand inspiration , Radiated to the
trapezius .
⚫ Treated by Aspirin 160 – 325 mg daily ( although higher doses
may be required 650 mg / 4-6 hrs ) , Anticoagulantsare relatively
contraindicated .

26. 2. Post MI syndrome ( Dressler’s Syndrome )
⚫Fever , chest pain , friction Rub .
⚫Occurs after 1 week up to several weeks of MI .
⚫Treatment as that of early post-MI pericarditis except
that an oral corticosteroid course maybe required .
⚫Anti-Coagulants should be stopped .
⚫May cause pericardial effusion but rarely tamponading .

27. ⚫Take Home Message
⚫Cardiac Rehabilitationand extended follow upof the
post-Infarction patient clinically and by imaging
modalitiesareas importantas theearly follow up.
⚫Anticipatecomplications in every patient , soyou won’t
miss itwhen itoccurs .