Myocardial infarction, also known as a heart attack, results from prolonged lack of oxygen supply to heart muscle, causing cell death. It is usually caused by a blockage of a coronary artery from an atherosclerotic plaque rupture. Symptoms include chest pain and shortness of breath. Diagnosis involves evaluating symptoms, electrocardiogram changes, and cardiac enzyme levels. Treatment focuses on restoring blood flow, reducing workload and complications through medications like antiplatelets, anticoagulants, beta blockers, and ACE inhibitors.

2. MYOCARDIAL
INFARCTION

3. MUHAMMAD ADEEL
PHARM-D
G.C UNIVERSITY FAISALABAD

4. MYOCARDIAL INFARCTION
Definition:
Myocardial infarction (MI) also called (heart attack) is
the irreversible death (necrosis) of heart muscle due to prolonged
lack of oxygen supply (Ischemia) when blood flow ( enriched with
oxygen ) stops to a part of heart causing damage to heart muscles .
Mechanism Of Myocardial Infarction:
The mechanism of an MI
often involves the complete blockage of a coronary artery caused
by a rupture of an atherosclerotic plaque .

5. OTHER NAMES OF MYOCARDIAL
INFARCTION
Also called cardiac Infarction , Coronary attack Infarction of heart
, Myocardial Infarct .
Signs And Symptoms
• Most common sign and symptom is chest pain which travels into
shoulders , arms , back , neck and jaws . Often it occurs in the
center or left side of the chest and lasts for more than a few
minutes . ( 30 – 60 minutes ) .
• Patient Blood Pressure(BP) is initially elevated because of
peripheral arterial vasoconstriction.

6. SIGNS AND SYMPTOMS
• Patient heart rate (HR) is often increased (Tachycardia) .
• In some patient the symptom is epigastric with a feeling of
indigestion , fullness and gas .
• Respiratory rate also increased due to pulmonary congestion or
Anxiety .
• Other Signs And Symptoms are Fatigue , tiredness , Malaise ,
Coughing , Wheezing , Production of Frothy Sputum , Shortness of
Breath , Nausea , Cold sweats , Dizziness , Headache .

7. RISK FACTORS OF MYOCARDIAL
INFARCTION
• Commonly occur due to Coronary artery disease .
• High Blood Pressure .
• Smoking .
• Diabetes .
• Lack of Exercise .
• High Blood Cholesterol .
• Obesity .
• Poor diet
• Excessive Alcohol Intake .

8. LESS COMMON RISK FACTORS OF
MYOCARDIAL INFARCTION
Coronary artery spasm may occur due to :
 Cocaine .
 Emotional Stress .
 Extreme colds .
• Age ( Men are at higher risk of heart attack after age of 45 than
women ) .
• Family History .
• High blood pressure during pregnancy .

9. PREVENTION FROM MYOCARDIAL
INFARCTION
One way to lower the risk of heart attack is use of a healthy diet.
This diet should largely consist of :
• Whole grains
• Vegetables
• Fruits
• Lean protein
Reduce the amount of the following in your diet :
• Sugar
• Saturated fat
• Cholesterol

10. CLASSIFICATION OF MYOCARDIAL
INFARCTION
Type 1 :
Spontaneous MI related to ischemia due to a primary
coronary event such as plaque erosion or rupture, fissuring, or
dissection .
Type 2 :
MI secondary to ischemia due to either increased oxygen
demand or decreased supply, e.g. coronary artery spasm, coronary
embolism, anemia hypertension , or hypotension .

11. Type 3 :
Sudden unexpected cardiac death, including cardiac
arrest, often with symptoms suggestive of myocardial ischemia,
accompanied by new ST elevation or evidence of fresh thrombus in
coronary artery .
Type 4 :
Associated with coronary angioplasty or stents:
• Type 4a – MI associated with Percutaneous Coronary
Intervention (PCI) .
• Type 4b – MI associated with stent thrombosis as documented by
angiography or at Autopsy .
Type 5 :
MI associated with CABG

12. ETIOLOGY

13. LIFESTYLE
• Smoking (36%)
• Obesity (20%)
• Lack of exercise (7-12%)
• stress-related causes and chronic high stress levels (about 3%
)
• Tobacco smoking and short-term exposure to air pollution
• Other factors e.g lack of physical activity

14. LIFESTYLE
• Acute and prolonged intake of high quantities of alcoholic
drinks.

15. DISEASE
• Diabetes mellitus
• high blood pressure.
• high levels of blood cholesterol
• Endometriosis in women under the age of 40 and obesity
• A number of acute and chronic infections

16. GENETIC
• Family history
• genes CDKN2A & 2B at 9p21 genomic locus.

17. OTHERS
• Men are more at risk than women(before manupause)
• Family history of ischemic heart disease
• contraceptive pills
• Heart attacks appear to occur more commonly in the morning
hours(6am to noon)
• Old age increases risk of a heart attack.

18. PATHOPHYSIOLOGY

19. SUB-TYPES
1. Non-ST Elevated MI
2. ST-Elevated MI

21. ATHEROSCLEROSIS ?

22. PLAQUE FORMATION

23. PATHOLOGICAL TYPES
1. Sub endocardial Myocardial
Infarction
2. Transmural Myocardial Infarction

24. EFFECT OF MI ON
HEART CELLS
1. Myocardial Cell Death
2. Evolution of MI and Ventricular
Remodeling

25. EFFECT OF MI ON
HEART CELLS
3. Reperfusion Injury
4. Stunned and Hibernating
Myocardium

26. DIAGNOSIS OF MYOCARDIAL
INFARCTION
A diagnosis of myocardial infarction can be done by:
1. Integrating the history of the presenting illness.
2. Physical examination
3. Electrocardiogram findings
4. Cardiac markers (blood tests for heart muscle cell damage).
5. A coronary angiogram allows visualization of narrowing or
obstructions on the heart vessels.
• A chest radiograph and routine blood tests may indicate
complications or precipitating causes and are often performed
upon arrival to an emergency department.

27. DIAGNOSTIC CRITERIA
WHO Criteria 2000:
According to the WHO criteria as revised in 2000, the diagnostic
of Myocardial Infarction are:
• A cardiac troponin rise accompanied by
• Typical symptoms (shortness of breath, chest pain, back pain,
anxiety etc.)
• Pathological Q waves
• ST elevation or depression
• Coronary intervention

28. PHYSICAL EXAMINATION
The general appearance of patients may vary according to the
experienced symptoms:
• The patient may be comfortable, or restless and in severe
distress with an increased respiratory rate.
• A cool and pale skin is common and points to vasoconstriction.
• Some patients have low-grade fever (38–39 °C).
• Blood Pressure may be elevated or decreased, and
the pulse can become irregular.

29. PHYSICAL EXAMINATION
If heart failure occurs, then:
• elevated jugular venous pressure and hepatojugular reflux(for
right ventricular failure).
• Swelling of the legs due to peripheral edema may be found on
inspection.

30. ELECTROCARDIOGRAM
• The primary purpose of the electrocardiogram is to
detect ischemia or acute coronary injury.
• A serial ECG may be used to follow rapid changes in time.
• The standard 12 lead ECG does not directly examine the right
ventricle, and is relatively poor at examining the lateral walls
of the left ventricle.

31. ELECTROCARDIOGRAM

32. ELECTROCARDIOGRAM
• A normal ECG does not rule out acute myocardial infarction.
• Mistakes in interpretation are relatively common, and the
failure to identify high risk features has a negative effect on
the quality of patient care.

33. CARDIAC MARKERS
• Cardiac markers or cardiac enzymes are proteins that leak out of
injured myocardial cells through their damaged cell membranes
into the bloodstream.
• Until the 1980s, the enzymes AST and LDH were used to assess
cardiac injury. Now, the markers most widely used in detection of
MI are Creatine kinase and Cardiactroponins T and I as they are
more specific for myocardial injury.
• The cardiac troponins T and I which are released within 4–6
hours of an attack of MI and remain elevated for up to 2 weeks,
have nearly complete tissue specificity and are now the preferred
markers for assessing myocardial damage.

34. CARDIAC MARKERS
• Heart-type fatty acid binding protein is another marker, used
in some home test kits.
• New markers such as glycogen phosphorylase isoenzyme BB
are under investigation.
• When damage to the heart occurs, levels of cardiac markers
rise over time, which is why blood tests for them are taken
over a 24-hour period. Because these enzyme levels are not
elevated immediately following a heart attack, patients
presenting with chest pain are generally treated with the
assumption that a myocardial infarction has occurred and
then evaluated for a more precise diagnosis.

35. CORONARY INTERVENTION
(ANGIOGRAPHY)
• In difficult cases or in situations where intervention to restore
blood flow is appropriate, coronary angiography can be
performed.
• A catheter is inserted into an artery (usually the femoral
artery) and pushed to the vessels supplying the heart.
• A radio-opaque dye is administered through the catheter and
a sequence of x-rays (fluoroscopy) is performed.
• Obstructed or narrowed arteries can be identified,
and angioplasty applied as a therapeutic measure.

36. PHARMACOTHERAPY
Treatment of disease with drugs is called
pharmacotherapy

37. MEDICATION SUMMARY
• The goals of pharmacotherapy for myocardial infarction
are to reduce morbidity and to prevent complications.
The main goals of emergency department medical
therapy are rapid intravenous thrombolysis,
optimization of oxygenation, reduction of cardiac
workload, and pain control.

38. 1. ANTIPLATELET AGENTS
• Antiplatelet agents are member of a class of a
pharmaceuticals that decrease platelet aggregation and
inhibit the thrombus formation. They are effective in the
arterial circulation, where anticoagulants have little effect.
• It include the drugs:
1. Aspirin
2. Clopidogrel (Plavix)
3. Ticagrelor (Brilinta)
4. Prasugrel (Effient)
5. Vorapaxar (Zontivity)

39. 2. ANTITHROMBOTIC AGENTS
• Antithrombotic agents prevent the formation of thrombi
associated with myocardial infarction and inhibit
platelet function by blocking cyclooxygenase and
subsequent platelet aggregation. Unfractionated
intravenous heparin and fractionated low-molecular-
weight subcutaneous heparins are the 2 choices for
initial anticoagulation therapy.
• It include the drugs:
1. Bivalirudin (Angiomax)
2. Heparin
3. Enoxaparin (Lovenox)
4. Dalteparin (Fragmin)

40. 3. GLYCOPROTEIN IIB/IIIA
INHIBITORS
• They work by preventing platelet aggregation and thrombus
formation. They do so by inhibition of GpIIb/IIIA receptors on
the surface of platelets.
• Glycoprotein IIb/IIIa inhibitors prevent acute cardiac ischemic
complications that is unresponsive to conventional therapy.
It include the drugs:
1. Tirofiban (Aggrastat)
2. Eptifibatide (Integrilin)

41. 4. VASODILATORS
• Vasodilators relieve chest discomfort by improving myocardial
oxygen supply, which in turn dilates epicardial and collateral
vessels, improving blood supply to the ischemic myocardium.
• It include the drugs:
Nitroglycerine

42. 5. BETA-ADRENERGIC BLOCKERS
• This category of drugs has the potential to suppress
ventricular ectopy due to ischemia or excess
catecholamines. In the setting of myocardial ischemia,
beta-blockers have antiarrhythmic properties and
reduce myocardial oxygen demand.
• It include the drugs:
1. Metoprolol
2. Esmolol
3. Atenolol

43. 6. ANGIOTENSIN-CONVERTING
ENZYME INHIBITORS
• ACE inhibitors may prevent the conversion of angiotensin I to
angiotensin II, a potent vasoconstrictor. ACE inhibitors reduce
mortality rates after myocardial infarction. Administer ACE
inhibitors as soon as possible as long as the patient has no
contraindications and remains in stable condition. ACE
inhibitors have the greatest benefit in patients with
ventricular dysfunction.
• It include the drugs:
1. Captopril
2. Enalapril
3. Quinapril
4. Lisinopril

44. 7. ANGIOTENSIN-RECEPTOR
BLOCKER
• Angiotensin-receptor blockers may be used as an
alternative to ACE inhibitors in patients who develop
adverse effects, such as a persistent cough. An
angiotensin-receptor blocker should be administered to
patients who are intolerant of ACE inhibitors.
• It include the drugs:
1. Irbesartan
2. Candesartan
3. Valsartan
4. Azilsartan
5. Eprosartan mesylate
6. Losartan

45. 8. ANALGESICS
Pain control is essential to quality patient care. Analgesics
ensure patient comfort and have sedating properties, which are
beneficial for patients who experience pain.
It include the drugs:
Morphine sulfate