Discussed myocardial infarction in general. Great article.

1. MANAGEMENT OF
ACUTE MYOCARDIAL
INFARCTION
BY
DR UBOGUN O. EFE MD.
HOUSE OFFICER, CARDIOLOGY.
DEPARTMENT OF MEDICINE, DELSUTH

2. OUTLINE
• Introduction
• Epidemiology
• Aetiology
• Pathogenesis
• Classification
• Risk factors
• Clinical features
• Management
• Complications
• Prognosis
• Conclusion

3. INTRODUCTION
• Myocardial infarction (MI), commonly known as a heart attack, is defined
pathologically as the irreversible death of myocardial cells caused by ischemia.
• Myocardial infarction is a medical emergency.
• There is an imbalance between oxygen supply and demand to the myocardium
• It occurs when there is blockage in one of the arteries which supply the heart
musculature
• Part of the Acute Coronary Syndrome complex together with unstable angina
because they cause loss of cardiac myocytes if intervention is delayed.

4. EPIDEMIOLOGY
• Cardiovascular disease is the leading cause of death in the United States;
approximately 500,000-700,000 deaths related to the coronary artery occur each
year.
• Approximately 1.5 million cases of myocardial infarction occur annually in the
United States; the yearly incidence rate is approximately 600 cases per 100,000
people

5. CONT'D
• The incidence of ACS in Nigeria is put at 59.1 people per 100 000 hospitalized
adults per year, and comprised ST‐segment–elevation myocardial infarction
(48.7%), non–ST‐segment–elevation myocardial infarction (24.5%), and unstable
angina (26.8%)

6. AETIOLOGY
Mainly by Atherosceloris
Nonatherosclerotic causes of MI include the following:
• Coronary occlusion secondary to vasculitis
• Ventricular hypertrophy (eg, hypertrophic cardiomyopathy,aortic stenosis)
• Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
• Coronary trauma
• Primary coronary vasospasm (variant angina)
• Drug use (eg, cocaine, amphetamines, ephedrine)
• Arteritis
• Coronary anomalies, including aneurysms of coronary arteries

7. CONT'D
• Factors that increase oxygen requirement, such as heavy exertion, fever, or
hyperthyroidism
• Factors that decrease oxygen delivery, such as hypoxemia of severe anemia,
hypotension.
• Aortic dissection, with retrograde involvement of the coronary arteries

8. PATHOGENESIS

11. CLASSIFICATION

12. • Can also be classified according to ECG Findings into:
• STEMI ( ST elevated MI)
• NSTEMI (Non ST elevated MI)

14. RISK FACTORS
Non Modifiable Modifiable
• Age
• Gender
• Family history
• Previous history of CAD
• Smoking
• Diabetes control
• Hypertension
• Hyper/dyslipidemia
• Sedentary life style
• Increased levels of C-reactive proteins
• Menopause
• Obesity
• Drug use e.g cocaine
• Alcohol use

15. CLINICAL FEATURES
SYMPTOMS
• Chest – Pain, discomfort, tightness which last for 20mins and is not relieved by rest
with radiation to the neck and left arm.
• G. I – Heartburn, indigestion, nausea and vomiting
• Neck – discomfort , tightness
• Sweating
• Nausea and Vomiting
• Palpitations
• Shortness of breath
• Fainting
• Back pain/ left arm pain

16. CONT'D
SIGNS
• Fever usually mild
• Pallor
• Tachycardia/ bradycardia
• Arrhythmias
• Narrow pulse pressure
• Raised JVP
• Basal crepitations
• Rales or wheezes
• Peripheral cyanosis

17. INVESTIGATIONS
• ECG – single most important investigation. Used for diagnosing, eliminating
differentials and locate infarct
• Cardiac biomarkers – Cardiac troponins , Cardiac Creatinine Kinase- MB
• CBC
• Electrolyte urea and creatinine
• Lipid profile

18. CONT'D
• ECG is the most important tool in the initial evaluation and triage of patients in
whom an acute coronary syndrome (ACS) is suspected
• Early ECG in patients with symptoms consistent with ST-elevation myocardial
infarction (STEMI) not only confirms the diagnosis in more than 80% of cases, but
also helps to detect life-threatening arrhythmias and allows early and prompt
defibrillation therapy, if indicated

19. CONT'D
• An ECG will show the following characteristics for an NSTEMI:
• depressed ST wave or T-wave inversion
• no progression to Q wave
• partial blockage of the coronary artery
• A STEMI will show:
• elevated ST wave
• progression to Q wave
• full blockage of the coronary artery

20. CONT'D
CARDIAC BIOMARKERS
Cardiac Troponins
• Troponin is a contractile protein that normally is not found in serum. It is released
only when myocardial necrosis occurs
• Of the three troponin subunits, two (troponin I and troponin T) are derived from
the myocardium.
• Highly sensitive and specific
• Used for diagnostic and prognostication purposes in patients with symptoms
suggestive of acute MI.
• CK-MB and myoglobins are other importants markers but they are not specific

22. CONTD
IMAGING
• Echocardiography
• Chest Radiographs
• MRI
• Multidetector Computed Tomographic (MDCT) angiography

23. DIAGNOSIS
• HISTORY +/- PHYSICAL EXAMINATION
• Either one of the following criteria satisfies the diagnosis for an acute, evolving,
recent myocardial infarction:
1. Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of
biochemical markers of myocardial necrosis with at least one of the following:
a. Ischemic symptoms
b. Development of pathologic Q waves on the electrocardiogram..
c. Electrocardiographic changes indicative of ischemia (ST segment elevation or
depression)

25. DIFFERENTIAL DIAGNOSIS
• There are many causes of chest pain, which can originate from the heart, lungs,
gastrointestinal tract, aorta, and other muscles, bones and nerves surrounding the chest
• Angina
• PUD, GERD, Heartburn
• Pulmonary embolism
• Heart failure
• Tumors of the lungs
• Pneumonia
• Rib fracture, costochondritis, and other musculoskeletal injuries.
• Pulmonary edema
• Allergic reactions
• Asthma
• Acute respiratory distress syndrome.

26. MANAGEMENT
• Treatment can be Medical or Surgical
• Surgical –
• Percutaneous intervention
• Coronary artery bypass graft

27. MEDICAL MANAGEMENT
• M- morphine
• O- oxygen
• N- Nitrate
• A- Acei/ARB
• B- Beta blockers
• A- Aspirin/ clopidogrel
• S- statin/spironolactone
• H- heparin

28. • T- thrombolytics.

29. • Acute MI is a medical emergency and must be treated as such
• Goals of treatment are to
1. Prolong life
2. Minimize infarct size
3. Reverse ischemia
4. Reduce cardiac work
5. Prevent and treat complications

30. INITIAL RESUSCITATION
• Quick history
• ABC of resusucitation
• Establish intravenous access
• Give supplemental oxygen if saturation < 90%
• Close vital sign monitoring
• Collect samples for investigations – Cardiac enzymes, CBC, Electrolyes and lipid profiles
• QUICK ECG – STEMI or NSTEMI

31. TREATMENT
PAIN CONTROL
• Nitroglycerin (NITRATES) – potent vasodilators, reduce preload thereby reducing
workload
• Usually Sublingual @ 0.4mg/dose, then IV Nitrates @ 5-10 microgram/min if
chest pain persists
• IV Morphine indicated in refractory chest pain @ 2-4mg bolus with increments
until pain is relieved or intolerance occurs… Naloxone must be present to reverse
toxicity

32. STEMI
• Rapid Recognition and timely reperfusion
• All patients with STEMI should receive an empiric loading dose of aspirin (150. to 325
mg) as early as possible and prior to reperfusion, regardless of the reperfusion
method
• Ideally, revascularization is done within 90-120mins of patients presentation.
• However, since most centres are not PCI capable, fibrinolysis is the reperfusion
strategy of choice
• Tenecteplase (TNK-tPA), Reteplase (rPA) and Alteplase (tPA) are fibrin specific
fibrinolytic agents that can be used. Streptokinase (Non Specific)
• Usually given IV bolus

33. • Coronary artery bypass grafting (CABG)
• Anti coagulants e.g Unfractionated heparin, LMW heparin (Enoxaparin) are
important adjuvants
• Antiplatelets like aspirin, clopidogrel can be used for dual antiplatelet therapy

34. NSTEMI
• Nonenteric-coated chewable aspirin 150 to 325 mg should be given to all patients with
NSTEMI as soon as possible after presentation.
• A maintenance dose of aspirin 75-100 mg daily should be continued indefinitely.
• Early PCI or CABG can be done
• Alternatively, conservative medical management + use of non invasive imaging
• Beta blockers - metoprolol, carvedilol, or bisoprolol preferably oral given in the first
24hours lower HR, BP and myocardial contractility thereby reducing O2 consumption
• Antiplatelets – P2Y12 receptor inhibitors – Clopidogrel, Ticagrelor, Prasugrel given daily
has ben associated with beteer outcomes
• Enoxaparin and other anticoagulants are also recommended in addition to anti platelet
therapy

35. • AcE Inhibitors or ARBs are recommended as cardioprotectives especially in
patients with ejection fraction <40% with other co-morbidities
• Aldosterone antagonists like eplenerone are also indicated provided the patient
has no renal impairment.
• Statins (Atorvastatin 40mg dly) are indicated in all patients who have had an
acute MI indefinitely

38. COMPLICATIONS
• Cardiogenic shock
• Heart failure
• Ventricular and atrial tachyarrrhythmias
• Stroke secondary to LV thrombus embolization
• Heartblocks
• Valvular dysfunction
• Pericarditis
• Venous thromboembolism
• Dressler syndrome

39. • False ventricular aneurysm
• True ventricular aneurysm
• Interventricular septal perforation

41. PREVENTION
LIFESTYLE MODIFCATIONS
• Cessation of smoking ( reduces risk of MI by 50% after wo years)
• No illicit drug use
• Alcohol moderation or cessation
• Physical activities and exercise
• Weight reduction
• Diets rich is soluble fibers, vegetables, whole grains and low in saturated fats should
be encouraged
Adequate management of co-morbid ailments – DM, HTN
Patient education

42. PROGNOSIS
• The prognosis after myocardial infarction varies greatly depending on the extent and
location of the affected heart muscle, and the development and management of
complications.
• Prognosis is worse with older age, social isolation, diabetes, previous vascular disease
(ie, cerebrovascular disease or peripheral vascular disease), delayed or unsuccessful
reperfusion and a elevated B-type natriuretic peptide (BNP) levels.
• Anterior infarcts, persistent ventricular tachycardia or fibrillation, development of
heart blocks, and left ventricular impairment are all associated with poorer prognosis.
• Without treatment, about a quarter of those affected by MI die within minutes and
about forty percent within the first month

43. CONCLUSION
• Prompt diagnosis and early intervention are the hallmark of effective therapy.
• Adequate Clinical education and provision of basic tools for investigation will
help in saving the lives of patients who develop this emergency.
• Prevention will always be the safer option hence proper education of the at risk
population.

44. REFERENCES
• Wikipedia. (2022). Myocardial infarction. [online] Available at:
https://en.wikipedia.org/wiki/Myocardial_infarction#Pain_2.
• Zafari, M. (2019). Myocardial Infarction: Practice Essentials, Background, Definitions. [online]
Medscape.com. Available at: https://emedicine.medscape.com/article/155919-overview.
• Davidson’s Principles And Practice Of Medicine. (2022). S.L.: Elsevier Health Sciences.