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Acute myocardial infarction (AMI) – aetiology, pathogenesis, risk factors, clinical presentation, biomarker
Definition
Ischemic necrosis of the cardiac muscle, caused by the abrupt diminishing or total stop of blood flow in one or more epicardial coronary
arteries
Aetiology
1. Coronary atherosclerosis
2. Non coronary reasons
a. Emboli
b. Spasm
c. Coronaritis
d. Aortic dissection
e. Shock
Pathogenesis
(a) Main reason for acute myocardial infarction is coronary thrombosis due to activated plaque (where increased o2 consumption
and spasm are added)
(b) 10% caused by high degree coronary stenosis  Total occlusion
(c) Atherosclerotic plaque can be complicated by rupture
(d) When coronary vessel is partially/totally occluded, coronary blood flow diminishes/blocked
(e) After 20 mins of ischemia  Irreversible necrosis of subendocardial cardiac muscle
(f) Several h  Pericardial necrosis
(g) After reperfusion (opening) of infarcted artery, corresponding myocardium remains “stunned”
(h) Takes days to one week to regain contractility
(i) When blood flow is restored  “reperfusion injury” + acute cellular oedema follows

Risk factors (RF)

1. Unmodifiable RF
a. Age
b. Male
c. Postmenopausal women
d. Family predisposition with early CAD development
e. Social and economic status
2. Modifiable RF
a. Arterial hypertension
b. Diabetes
c. Smoking
d. Dyslipidemia
e. Obesity
f. Lack of physical activity
g. Pyscho emotional stress

Predisposing factors for AMI

1. Physical overstrain
2. Exhaustion/psycho-emotional stress
3. Accelerating angina/angina at rest
4. Non cardiac surgery
5. Extreme hypotension, fever, tachycardia
6. Pulmonary infections

Clinical Presentation
1. Basic symptom pain lasting more than 20 mins
2. Squeezing, pressing with feeling of weight over thorax
3. Stabbing, burning accompanied by vagal symptoms (nausea, vomiting sweating)
4. Angina lasting hours localized behind sternum propagating over whole pericardium, to left shoulder and ulnar side of hand
Atypical forms of clinical presentation
1. Gastralgic
a. Pain localized in epigastrium
2. Asthmatic
a. No pain but symptoms of acute LV failure and pulmonary congestion
3. Cerebral
a. Central symptomatics resulting from diminished LV output and co existing cerebrovascular disease
4. Peripheral
a. Pain not concentrated in propagated areas
Physical symptoms (always present)
1. Rhythm and conduction disorders
a. Richer the physical sign the larger ischemic zone
2. Can register
a. Mitral insufficiency
b. Gallop rhythms
c. Pericardial friction rub
d. Newly appeared murmurs
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3 Basic direct ECG sings of AMI

1. (a) Pathological broad (>0.04 sec) and deep Q wave (b) Smaller amplitude or disappearance of R wave with formation of QS
from myocardial necrosis
2. ST segment elevation from currents of injury
3. Deep negative, symmetric peaked T wave a sign of ischemia
Main direct signs of AMI in leads against infarction zone

3 Basic Indirect ECG sings of AMI (mirror image of direct)

1. Increase of R wave amplitude
2. ST segment depression
3. Positive, tall, symmetrical and peaked R wave

Biomarkers/ laboratory tests

1. Creatinkinase, especially MB is the fraction with highest specificity
2. Glutamate oxalacetic transaminase (SGOT)
a. Rises 6-12h after beginning of AMI
b. Reaches max 2-10 fold over normal values after 18-36h
c. Normal after 3-4 days
3. Lactatdehydrogenase
a. Rises after 24-48h
b. Peaks 2-10 fold at day 3-6
c. Normal at 8-14 days
d. Its isoenzyme alpha-hydroxybutyrate is more specific
4. Gama glutaryl transpeptidase latest enzyme
a. + at 60-100h
b. Max activity at 120-240h
c. Normalizes after 20-35 days
5. Myokinase earliest enzyme
a. 0.5-6h after onset
b. Normalizes at 1-3 days
Coagulation status is a must

Echocardiography 
1. Establishes presence of segment wall motion
a. Hypokinesia of infarcted wall
b. dyskinesia of infarcted wall
c. Localization
d. Extensiveness

Diagnosis 3 basic criteria

1. Anterior chest pain lasting more than 30min
2. Typical ECG changes
3. Rise of cardio-specific enzyme activity

Complications Early/Late
There are no AMI without complications. They are rhythm and conduction disorders
1. In the infarct related artery (IRA)
a. Recurrent ischemia
b. Thrombus growth engaging branches of IRA
c. Distal embolization
2. At a distance from IRA
a. Diminished collateral blood flow from IRA
b. New intracoronary thrombus hypercoagulability
c. Decreased systemic perfusion pressure
Treatment
1. Pre hospital
a. Quick transport
b. Pain relief
c. Prophylaxis of sudden cardiac death
d. Defibrillation in ventricular fibrillation
e. Thrombolysis
2. In hospital
a. Morphinum 2,5-10mg I.V
b. Oxygen 2-5 L/min
i. In refractory pulmonary edema
c. Nitrates sublingually or I.V for pain
d. Correction of ions
e. To decrease infarction zone:
i. B blockers
ii. Ace inhibitors
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iii. Reperfusion (Primary Percutaneous coronary intervention PCI)

f. Thrombolysis patients
i. Anticoagulants
ii. Antiplatelet drugs
3. Post discharge treatment (ABC2)
a. Aspirin
b. B blocker
c. Converting enzyme inhibitor (ACE)
d. Co enzyme A reductase inhibitor (statin)
i. Aiming constant LDL cholesterol level of <1.8mmol/L