acute Mi for students

1. Acute Myocardial Infarction
Rasheed Ibdah ,MD, FACC
Associate Professor of Cardiology /JUST
Interventional Cardiologist/KAUH

2. O BJECTIVES
•Define
•Classification
•Diagnosis
•Treatment

3. DEFINITION
Myocardial infarction (MI), commonly known
as a “heart attack,” is defined as acute
myocardial injury and tissue death resulting
from ischemia.

4. Epidemiology
• One of the leading causes of death in the world
80% of deaths from cardiovascular disease worldwide
• Prevalence:
3% in Americans > 20 years of age
• Incidence in the United States:
600 cases per 100,000 people
1.5 million cases annually
• More common in older patients:
Approximately 60%–65% of MIs occur in patients > 65 years of age.
Approximately 33% of MIs occur in Patients > 75 years of age.
80% of all MI-related deaths occur in Patients > 65 years of age.
• Men > women
• The survival rate for those hospitalized due to MI has reached
approximately 95%

5. RISK FACTORS
NOT MODIFIABLE
• Age
• Gender
• Family history
MODIFIABLE
• Smoking:X2-6TIMES
• Diabetes 2-4 folds
• Hypertension
• Hyperlipidemia
• Obesity
• Physical Inactivity

6. Classification of MI based on
ECG findings and pathology:
STEMI:
• Due to a major occlusion of a coronary artery, causing transmural infarction
(through the heart muscle wall)
• Produces ECG changes with ST elevation and Q waves.
NSTEMI:
• Due to less severe occlusion of a coronary artery , causing a subendocardial
MI (not through the entire heart muscle wall)
• ECG does not show ST elevation

7. CONTINUED …..
Classification of MI according to the assumed cause:
Type 1: acute thrombus on a ruptured atherosclerotic plaque
Type 2: ↑ oxygen demand in the Myocardium without adequate oxygen supply (whether
or not there is underlying atherosclerotic CAD)
Type 3: clinical symptoms of MI with
ECG changes, but with death of the patient occurring before lab tests are performed
Type 4a: MI associated with percutaneous coronary intervention
(PCI) or from procedure-related complications associated with ↓ coronary blood flow
Type 4b: intervention-related MI with stent/scaffold thrombosis
Type 5: MI related to coronary artery bypass graft (CABG) surgery

8. Acute Coronary Syndrome ACS

9. Pathophysioloy

10. Characteristics of unstable versus stable plaque:
Unstable plaque:
Thin fibrous cap
Massive inflammatory cell infiltrate
↑ Activity of metalloproteinase enzymes (weakens the fibrous cap)
↑ Lipid content
Rupture of unstable plaque in a coronary artery→ thrombosis
Stable plaque:
Thick fibrous cap
Narrowing of an artery → inability to meet oxygen demand with ↑ exertion May lead to stable
angina(symptoms only with exertion)
Coronary artery occlusion → ischemia → death of the tissue (infarction) in the area of the heart
supplied by that artery
Partial occlusion of the coronary artery→ affects the inner myocardium(subendocardium) → may
cause:
NSTEMI
Unstable angina
(if the ischemia does not result in cell death)
Complete occlusion → transmural infarction → STEMI

11. • Ischemia can develop within 10 seconds and if it lasts
longer than 20 minutes,irreversible cell and tissue death
occurs
• As vessel occlusion continues cell death spreads to the
myocardium and eventually to the epicardium.
• Severity of the MI depends on three factors.
• Level of occlusion,length of time of occlusion and presence or
absence of collateral circulation

12. DIAGNO STIC TRIAGE
• History
• ECG
• Biomarkers (Serial measurement)

13. Clinical Presentation
The classic symptom of MI in most patients is acute chest pain.
However, some patients may present with more vague symptoms.
Diaphoresis
Dyspnea
Nausea and vomiting
Associated symptoms:
Dizziness
“Indigestion” and/or vomiting
Syncope
Epigastric Pain (with inferior-wall MI)
Palpitations

14. Chest Pain
PQRST assessment for chest pain
analysis
• P- Precipitating events
• Q- Quality of pain
• R- Radiation of pain
• S- Severity ofpain
• T-Timing

15. Patient gestures indicate origin of pain: a patient demonstrating A (the Levine sign), B (palm
sign) or C (arm sign) is more likely to be experiencing ischaemic cardiac pain than one showing D
(pointing sign) .

16. Typical Chest Pain
Retrosternal
Dull, squeezing/pressure-like pain
May radiate to the left arm, shoulder, or jaw
Usually constant, lasting ≥ 20–30 minutes

17. Atypical Presentation
• Atypical presentation more common in women, the
elderly, or patients with diabetes:
Absence of chest pain or atypical locations/quality
• May present with only the usual associated symptoms

18. Physical examination
Vitals:
• Tachycardia
• Bradycardia :with right coronary artery (RCA) occlusion (supplies the
sinoatrial (SA) and atrioventricular (AV) nodes)
• Hypotension
Cardiovascular:
S3 heart sound (early diastolic sound heard at the end of rapid
ventricular filling)
S4 heart sound (late diastolic sound heard at the onset of atrial contraction)
Jugular venous distention: RCA occlusion → right-sided heart failure (HF)
Hepatic congestion: RCA occlusion → right-sided HF
Pulmonary edema
Skin:
Cool
Pale or cyanotic
Diaphoretic

20. ECG in STEMI
Findings in STEMI and their evolution:
• Tall, peaked (hyperacute) T waves may be seen early in the course.
• ≥ 1-mm ST elevation in ≥ 2 contiguous leads
• Reciprocal ST depression
• New left bundle branch block(LBBB) and symptoms → STEMI until
proven otherwise
• Pathologic Q waves typically emerge between 6 and 16 hours after
symptom onset
• T-wave inversion follows ST-segment normalization
• T-wave normalization over several hours to days

21. ECG in NSTEMI
ST depression (not elevations)
Nonspecific changes
Inverted T waves
Normal ?

22. Localization of STEMI on ECG

27. Laboratory evaluation
Cardiac enzymes:
Structural proteins that are released as a result of myocardial injury
Troponin I: only cardiac , gold standard
• Start to ↑ within 2–3 hours after the onset of chest pain
• Peak levels at 12–48 hours
• Return to baseline over 4–10 days
• Highest sensitivity and specificity (compared to other cardiac
enzymes
• Serial lab draws are used to assess for a rise and fall in levels
(recheck in 1–3 hours).
• The degree of ↑ correlates with the size of the infarct

28. Troponinitis
Can be ↑ as the result of causes of coronary ischemia other than acute MI:
Arrhythmia
Cocaine
PCI
Coronary embolism
Aortic dissection
Can be ↑ with non-coronary ischemia or myocardial injury:
Electrical shock
Hypoxia
Myocarditis
Takotsubo cardiomyopathy
CKD
Pericarditis
Stroke
Pulmonary embolism

29. CK-MB isoenzyme
• Less sensitive and specific than troponin
• ↑ within 3–6 hours after chest pain
• Peaks within 12–24 hours
• Normalizes 48–72 hours after MI
• Continued ↑ after 72 hours is diagnostic of
reinfarction.
• The degree of ↑ in CK-MB correlates with the size of
the infarct, a total CPK is not
• CK-Mb: Ck ratio

30. Supporting labs
• LDH and AST→ may be ↑, but no longer used in the
diagnosis of MI.
• BNP→ ↑ in heart failure
• Drug screen to evaluate for cocain or methamphetamine
use.

31. Imaging
Chest X-ray:
Should be done to evaluate for other causes of chest pain, such as:
Pneumonia
Pneumothorax
Mediastinal widening → aortic dissection
May show pulmonary edema → heart failure
Transthoracic echocardiography:
• Left ventricular ejection fraction(LVEF) is the best predictor of
survival in STEMI.
• New regional wall motion abnormalities can be visualized
• Can evaluate for complications of MI:
Free-wall rupture
Ventricular septal rupture
Mitral regurgitation
Aneurysm formation
Presence of a thrombus

32. Management
• Prompt recognition of the diagnosis of acute MI is imperative in
order to realize the benefit from reperfusion therapy.
• Time is muscle

33. O2 Therapy
Oxygen: previously used with every patient, currently used only if:
O2 saturation < 90%
Respiratory distress present
Heart failure present
Other high-risk features of hypoxia

34. Aspirin
• Prevents thrombus formation/expansion
• ↓ Mortality
• 300 mg crushed ,immediately after diagnosis

35. Nitroglycerin (sublingual)
• Start if the patient still has chest pain, hypertension, or heart failure
• Vasodilation→ ↓ preload → ↓ oxygen demand → ↓ symptoms
• Add IV nitratesif symptoms persist after 3 sublingual doses
Avoid in patients with:
• Hypotension
• Right ventricular infarction ( use IV saline to ↑ cardiac output )

36. Morphine i.v
• Provides relief of ischemic pain(↓ preload)↓ Anxiety
and the adrenergic drive that causes further vasoconstriction
• Can ↑ mortality
• Can cause respiratory depression

37. ADP Antagonists
• Clopidogrel, prasugrel and ticagrelor are all
adenosine diphosphate (ADP) antagonists.
• Bind selectively to the P2Y12 receptor to inhibit
platelet function .
• Assess risk for bleeding
• Timing of invasive strategy

38. Beta-Blockers
• ↓ Heart rate and contractility → ↓ oxygen demand→ ↓ symptoms
• ↓ Mortality
Contraindicated if the patient has:
• Heart failure
• Bradycardia
• Severe reactive airway disease
• Cocaine-induced MI

39. Anticoagulation
Recommendations vary with the clinical situation and
plan for PCI or thrombolytic therapy:
• Heparin
• Low-molecular-weight heparin (LMWH)

40. Statin
Start high-dose statin therapy (e.g., atorvastatin) as
early as possible and before PCI.

41. Reperfusion
1. Percutaneous coronary intervention PCI
Indications:
• STEMI
• NSTEMI with TIMI score > 3
↓ Amount of myocardial damage
↓ Mortality
2. Thrombolysis Therapy If PCI is not available

42. • Tenecteplase and reteplase (fibrin-specific) are preferred.
• Streptokinase and alteplase are other options.
• Consider fibrinolytic therapy in patients with ≤ 12 hours of symptoms
All are contraindicated with active bleeding, recent stroke, or
suspected aortic dissection

43. STRATEGY
• INVASIVE
• NON-INVASIVE (ISCHEMIA-GUIDED)
• THE CHOICE OF EARLY INVASIVE MANAGEMENT IS
BASED ON RISK .

44. Complications
Early : in the first 1–3 days post-MI:
Ventricular arrhythmia (most common cause of death)
Acute heart failure
Cardiogenic shock
Early pericarditis
Late : 3–14 days post-MI
• Free-wall rupture
• Papillary muscle rupture
• Ventricular septal rupture
• Mural thrombus formation with potential embolization
• Dressler syndrome