1. C O M P L I C AT I O N S O F
M Y O C A R D I A L
I N FA R C T I O N
B Y,
A B I M A N Y U K E S AVA N
F I N A L Y E A R
2. INTRODUCTION
• Myocardial Infarction is the irreversible necrosis
of heart muscle secondary to prolonged
ischemia.
• This usually results from an imbalance in oxygen
supply and demand, which is most often caused
by plaque rupture with thrombus formation in a
coronary vessel, resulting in an acute reduction
of blood supply to a portion of the myocardium
4. HEART FAILURE
• Cardiac failure can happen after MI if significant
myocardium is damaged. The Kilip classification is
used to assess patients with heart failure post-MI.
– Kilip I: No crackles and no third heart sound.
– Kilip II: Crackles in<50% of the lungs fields or a
third heart sound.
– Kilip III: Crackles >50% of the lungs fields.
– Kilip IV: Cardiogenic shock.
• Heart failure is treated with diuretics (furosemide or
terosemide or spironolactone) which reduce blood
volume and preload.
5. MYOCARDIAL RUPTURE AND
ANEURYSMAL DILATATION.
• Infarcted myocardium is weak and cannot tolerate
the pressure inside the ventricular chamber. This
may lead to rupture of the free wall of the left
ventricle or aneurysmal dilatation. Rupture is usually
an early, catastrophic and fatal event.
• Ventricle aneurysm impairs cardiac output because
of paradoxical motion of its wall. Double, diffuse, or
displaced apical impulse is noted on physical
examination.
6. VENTRICULAR SEPTAL DEFECT
• Infarcted septum may perforate and lead to VSD. It is
common in elderly and hypertensive patients and
after delayed thrombosis. It requires emergency
surgical repair.
7. MITRAL REGURGITATION.
• Severe mitral regurgitation can occur early in the course
of MI. Three mechanisms are responsible for mitral
regurgitation in MI, which are as follows,
– Left ventricular dysfunction and dilatation, causing
annular dilatation of the valve and subsequent
regurgitation.
– Infarction of the inferior wall, producing dysfunction of
the papillary muscle.
– Infarction and rupture of the papillary muscles,
producing sudden severe mitral regurgitation,
pulmonary edema and cardiogenic shock
• If there is rupture of papillary muscles, emergency
surgery should be taken.
8. CARDIAC ARRHYTHMIAS
• Ventricular tachycardia and ventricular
fibrillation(VT and VF)
– VF is the common cause cause for death after MI
in first 24 hours.
– Hemodynamically unstable VT and VF should be
treated with DC shock.
– Hemmodynamically stable VT should be treated
with IV beta blockers, IV lidocaine, IV
• Atrial Fibrillation
– Its common after MI and can be treated with beta
blockers and digoxin
– Amiodarone can be used daily to prevent
recurrence.
9. CARDIAC ARRHYTHMIAS
• Bradyarrhythmmias
– These are common following MI and may be due
to sinus node dysfunction and conduction
disturbances.
– AV block may occur during acute MI , especially
after inferior wall MI.
– Heart block, with hemodynamic compromise
requires treatment with atropine or a temporary
pacemaker.
10. ACUTE PERICARDITIS
• It happens with large, “transmural” infarctions cauing
pericardial inflammation and presents on days 2 to 4
after MI.
• Pericarditis developing later (2 to 10 weeks)after
acute MI may represent Dressler’s syndrome, which
is immune-mediated.
• Treatment includes aspirin or other NSAIDS
(indomethicin).
11. POST-MI DRUG THERAPY
• Aspirin--75-150 mg/day and Clopidogrel– 75 mg/day.
• Beta blockers e.g. metoprolol, carvedilol, atenolol , they
decrease myocardial oxygen demand and contraindicated
to asthma and severe LV dysfunction patients.
• Oral nitrates, e.g. isosorbide dinitrate . They improve the
symptoms of angina and heart failure.
• ACE inhibitors, e.g. enalapril, ramipril, lisinopril. They
prevent adverse myocardial remodeling after acute MI
and reduce heart failure and death. Contraindicated in
renal failure and hypotension.
• Calcium Channel Blockers They have negative inotropic
and are not routinely given. Short acting nifedipine should
be avoided as it cause reflex tachycardia.