Myocardial infarction, also known as a heart attack, results from a critical imbalance between oxygen supply and demand in the heart muscle. The primary cause is coronary artery occlusion due to atherosclerosis, vasospasm, or embolism. Symptoms may include chest pain, dyspnea, sweating, and anxiety. Diagnosis is made based on elevated cardiac enzyme levels and ECG changes. Initial treatment focuses on pain relief, oxygen, fluids, and aspirin while long-term prevention includes medications like beta-blockers, ACE inhibitors, antiplatelets, and statins to reduce risk of future heart attacks and heart failure.

1. MANAGEMENT OF MYOCARDIAL INFARCTION
SAMEEH SAIFUDHEEN

2. INTRODUCTION
• Rapid development of myocardial necrosis due to a
critical imbalance between O2 supply & myocardial
demand.
• Also known as “Heart attack”.
• The most important form of IHD.
• One of the major cause of mortality around the
world.

3. CAUSES
• The primary cause for MI is CORONARY ARTERY
OCCLUSION.
• Factors responsible are:
– Coronary atherosclerosis
– Vasospasm
• Platelet aggregation
• Cocaine abuse.
– Emboli
• AF
• Lt. sided mural thrombus
• Vegetations of inf. endocarditis

4. – Ischemia without detectable CA & thrombosis
• Vasculitis of intramural vessels
• Sickle cell disease
• Amyloidosis
• Vascular dissection
• Low systemic BP(shock)

5. CLINICAL FEATURES
Clinical symptoms:
– May or may not present with angina pectoris.
– Dyspnoea
• due to pulmonary congestion caused by impaired
contractility .
– Diaphoresis(profuse sweating).
– Rapid, weak pulse.
– Anxiety.

6. Cardiac markers:
• Enzymes
– Creatine kinase(MB fraction)
– Aspartate transaminase(AST)
– Lactate dehydrogenase
• Non-enzyme proteins
– Troponin T & I
– Myoglobin

7. Marker Abnormal activity
detectable(hr)
Peak value of
abnormality(hr)
Duration of
abnormality(days)
CK-MB 3-8 10-24 2-3
LD 8-12 72-144 8-14
AST 6-12 24-48 4-6
MYOGLOBIN 1-3 6-9 1
TROPONIN I
TROPONIN T
3-8
3-8
24-48
72-100
3-5
5-10
CARDIAC MARKERS & TIME COURSE AFTER ONSET OF
MI

8. WHO DIAGNOSIS OF MI
Requires atleast 2 of the following criteriae:
– Prolonged ischemic-type chest discomfort.
– Serial ECG changes.
– Elevation of cardiac markers in serum.

9. TREATMENT
Initial treatment:
1.Morphine(2.5-5.0 mg i.v) - For sudden relief of pain
& anxiety.
2.Aspirin(162-325 mg orally) - For prevention of
thrombus extension, embolism, venous thrombosis.
3.O2 inhalation & assisted respiration, if needed.
4.I.V fluids - Maintain blood volume & perfusion.

10. Subsequent Management:
– Treatment of complications:
•Arrhythmias
•Pump failure
•Thromboembolism
•Acidosis – NaHCO3 i.v infusion
– Secondary prevention of further consequences
& future MI.

11. Prevention & Treatment of Arrhythmia
1. β-blocker
– Prophylactic i.v infusion
• Inj. Atenolol(50 mg)
– oral administration for few days
• Tab. Atenolol(50 mg)
– Reduce incidence of arrhythmia & mortality
Note: β-blockers used early in evolving MI can reduce the infarct
size & subsequent complications.

12. 2. Other Antiarrhythmics
– Lidocaine, Procainamide for tachyarrhythmia
Note: Bradycardia & Heart block may be managed with
Atropine or electrical pacing.

13. Pump Failure
– The objective is to C.O and/or filling pressure without
unduly increasing cardiac work or reducing B.P.
– The drugs include:
• Furosemide: Reduce preload & pulm. edema.
• Vasodilators:
–GTN, Sod. Nitroprusside
– Reduce venous return, cardiac work load.
• Inotropic agents:
–Dopamine, Dobutamine
–Augment the pumping action of heart.

14. Thrombolysis & Reperfusion
– First infarct patient
• Inj. Streptokinase – 15,00,000 units i.v infusion over 1
hour.
– Subsequent infarcts
• Recombinant tissue plasminogen activator(Alteplase).
• Regimen for coronary thrombolysis is 15 mg i.v
followed by 0.75 mg/kg over 30 min. & 0.5mg/kg over
following hour.

15. Fibrinolysis
Plasminogen
in blood
Plasmin
Fibrinolysis
Fibrinolytics
Streptokinase
Urokinase
Alteplase

16. Adverse reactions:
• Bleeding
• Nausea, vomiting
• Multiple micro emboli
• Allergic reactions – Streptokinase is
antigenic – cause anaphylaxis

17. Contraindications:
• Haemorrhagic diathesis
• Pregnancy
• Recent symptoms of peptic ulcer / GI
bleeding
• Recent stroke (Previous 3 mths)
• Recent surgery (Previous 10-14 days)
• Proliferative Diabetic retinopathy
• Severe uncontrolled hypertension
• Aortic dissection
• Acute pancreatitis

18. Long term Treatment
The objectives include:
• Prevention of remodeling & subsequent CHF.
– ACE inhibitors / ARBs are of proven efficacy & afford
long term survival benefit.
• Prevention of future attacks.
– Platelet inhibitors:
– Aspirin or Clopidogrel given on long term basis are
routinely prescribed.

19. – β blockers :
– Reduces risk of reinfarction, CHF & mortality
– Given for at least 2 years unless contraindicated.
– Control of hyperlipidemia
– Hypolipidemic drugs, especially statins.
– Dietary substitution with unsaturated fats.