ACUTE MYOCARDIAL INFARCTION

(ACUTE CORONARY SYNDROME)

 Following disruption of a vulnerable plaque, patients experience ischemic discomfort

resulting from a reduction in flow through the affected epicardial coronary artery.
 Acute coronary syndrome incudes unstable angina and myocardial infarction.

ETIOLOGY & PATHOGENESIS

Myocardial ischemia results from:

 decreased myocardial oxygen supply : severe coronary artery narrowing, acute

atherosclerotic plaque rupture and superimposed thrombus formation, in-stent
restenosis or bypass graft disease.

 Increased demand : severe anemia, hypertensive crisis, acute decompensated HF or

surgery.

 Less common causes include coronary vasospasm (Prinzmetal angina) coronary artery
dissection, coronary vasculitis and embolus.

CLINICAL FEATURES

 Retro sternal chest pain (dull/constricting) radiating to left arm/forearm, lower jaw, back
and neck that is increased on exertion/cold and decreased on rest/sublingual nitrate.

Note: painless/silent MI occur in diabetic individuals and in elderly due to autonomic

dysfunction. They present with angina equivalents symptoms.

 Angina equivalents symptoms : unexplained sweating, nausea, vomiting, unexplained

anxiety and a sense of impending doom.

 Less commonly sudden loss of consciousness, appearance of arrhythmia, confusional

state, evidence of peripheral embolism or an unexplained drop in atrial pressure.

PHYSICAL FINDINGS

 Signs of sympathetic activation : pallor, sweating, tachycardia

 Sign of vagal activation : vomiting, bradycardia

 Sign of impaired myocardial function :

-Hypotension, oliguria, cold peripheries
-Narrow pulse pressure
-Raised JVP
-3rd heart sound
 -Basal crepitation
-Pulses alterans (LVF, LBBB (2:1 block))
-Quick first heart sound
-Diffuse apical impulse

 Sign of tissue damage : fever

 Signs of complications:
-Early systolic murmur: acute MR due to papillary muscle rupture
-Pansystolic murmers: VSD due to interventricular septal rupture

INVESTIGATION

- LOCALISING SITE OF MI FROM ECG -

ECG leads Heart Territory Coronary Artery

I, aVL, V4 – V6 Lateral Circumflex
V1 – V3 Anterior septal Lt Anterior descending
II, III, aVF Inferior Rt coronary artery/circumflex
VT-9 Posterior Circumflex

1) ECG : Should be done within 10 minutes of arrival to the hospital

Sequence of changes :
 Tall T wave : Hyperacute MI , earliest change
 Gravestone/tombstone ST elevation : acute MI
 Pardees sign - ST elevation + T wave inversion : evolving MI
 Pathological Q wave : evolved MI

*Repeat ECGs required for diagnosis. (Localisation of site in Table 1)

2) Plasma cardiac biomarkers

 Best marker : Cardiac troponins

Most sensitive and specific marker (Troponin I>T)

Note: D/D of ↑ cardiac troponin: Acute MI, Pulmonary embolus, Septic shock, acute pulmonary
edema.

Cardiac biomarkers Time of elevation Peak Back to (N)

cTnT 4 – 6 hrs 5 – 14 days
cTnI 4 – 6 hr 24 hrs 5 – 10 days
CK - MB 4 – 6 hrs 12 hrs 48 – 72 hrs
  Marker for reinfarction : BEST- CPK - MB (fall and subsequent rise is suggestive)
Or > 20% rise of tropT/I from initial value (levels will remain elevated for two weeks
post infarction)
 BNP : suggestive of large infarction and need for urgent angiography
 LDH flip : LDH 1/ LDH 2 > 1 ( normal < o.5 ) is a finding

3) CBC (to find out contributory factors like anemia and conditions that may alter management like
thrombocytopenia)
Findings include : Leucocytosis usually peak on 1st day, ESR, CRP raised

4) CXR : May show pulmonary edema that is not evident in clinical examination.
Heart size usually normal; but cardiomegaly in pre-existing myocardeal disease.

5) ECHOCARDIOGRAPHY : For assessing ventricular function and for detecting complications

like : Mural thrombus
Cardiac rupture
Ventricular septal defect
Mitral regurgitation
Pericardial effusion

INITIAL TREATMENT

 Aspirin 325mg non enteric coated tablet : essential in all cases of ACS
 O2 inhalation : if saturation < 90%
 Morphine 2-4mg IV : Analgesic,also causes venodilation and hence reduce preload I/c/o
pulmonary edema, C/I in RVMI
 ACE inhibitors : essential in all cases of ACS, reduce ventricular remodeling and
mortality
 NTG infusion 10mcg/min : coronary vasodilation and hypertensive control, C/I in RVMI
and STEMI
 Metoprolol 5mg IV : to decrease workload and prevent arrhythmia, C/I in RVMI
 Atorvastatin 80mg : atheromatous plaque stabilizing agent
 Clopidogrel : if patient is undergoing PCI where dual antiplatelet therapy is critical

DEFINITIVE TREATMENT of:

(I) STEMI
 PCI : initial choice as it is associated with better short term and long term outcomes and
can be used where fibrinolysis is C/I.
- should be done < 24 hours of onset of symptoms
- if there is delay for PCI > 120 min, do thrombolysis
- if patient is in shock shift for PCI irrespective of delay in time
- types : 1) angioplasty without stent
2) bare metal stents
3) drug eluting stent - most commonly used
- C/l : 1) left main coronary thrombus
2) multivessel disease
TOC - CABG
  Thrombolysis : should be done<12 hours of symptom onset
- types : 1) infusion : streptokinase,urokinase,alteplase
2) bolus : tenecteplase( max fibrin So and max reperfusion rate) , reteplase

Ii) STEMI with hypotension

 RVF due to RVMI : IV fluids to improve preload, PCI when hemodynamically stable
 LVF due to LVMI : IABP( intraaortic balloon pulsation), PCI when hemodynamically
stable

III) NSTEMI/Unstable Angina

 Our body can lyse small clots and hence never thrombolyse.
 Conservative management : (1) aspirin + clopidogrel
(2) LMWH
(3) SL Dinitrate 5mg 3doses; IV NTG if no relief
(4) oral Metoprolol 25-50mg/d
 If ECG is still unsettled/ recurrent chest pain : PCI

IV) Prinzmetal/Variant Angina(idiopathic vasospasm of epicardial coronary vessel in young)

 Emergency : Nitrate
 Maintenance : CCB
 Aspirin is C/I as it inhibit local vasodilatory PG


COMPLICATIONS (of Acute Coronary Syndrome) (or MI)

(Often only seen with transmural MI)

1. Cardiac arrest – Management : ACLS guidelines for cardiac arrest.

2. Cardiogenic shock
3. Left ventricular failure
4. Arrhythmias – General Management : Pam relief, Rest correction of hypokalaemia
Bradycardia – If deterioration - atropine (0.6 – 1.2 mg iv)
AV block complicating inf. Infact resolves itself
2nd degree/complete AV block – Temporary pace maker
Atrial fibrillation – digoxin/βblocker/DC shock
Ventricular fibrillation – Defibrillation
Sinus tachycardia - treat cause Pain
hypoxia
Sepsis
add β blocker – if not contraindicated
5. Right ventricular failure (low cardiac output, ↑JVP)
Fluid is key
Vasodialators (nitrates)
Diuretics
6. Pericarditis : Opiates (1st line) Ionotropes in some cases)
Can ↑ chance of aneurysm NSAIDs / ECHO to check effusion
7. System k embolism → Anticoagulation with warfarin x 3 months
8. Cardiac tamponade → Pericardial aspiration, surgery
(Temporary relief)
9. Mitral regurgitation → Treat LVF ; valve replacement if indicated.
10. Ventricular septal defects → Surgery
11. Late malignant ventricular arrhythmia (1-3 wk post MI)
Avoid hypokalaemia, 24 hr ECG monitoring prior to discharge
12. Dressler’s syndrome (recurrent pericarditis, pleural effusion, fever, anaemia, ↑ESR 1-3 wk
post MI)
13. Left ventricular aneurysm (4-6 wk post MI)
Mx – anticoagulate ; consider excision

POST MORTEM HISTOPATHOLOGY OF ACUTE MYOCARDIAL INFARCTIOIN

Staining : Triphengl tetra sodium chloride.

Principle : Intact non-infarcted myocardium has LDH activity preserved ; in infarcted area
due to damaged membranes LDH leaks out.
Appearance : Noninfarct : Brick red colour
Infarct areas: unstained pale zone.
(staining +ve if infarct occurred 2-3 hr before death)

Davidson’s
Principles & Practice of MEDICINE

OXFORD HANDBOOK OF CLINICAL MEDICINE

Robbins & Cotran

Pathologic Basis of Disease
South Asia Edition

19th Edition
HARRISON’S
MANUAL OF
MEDICINE

KASPER
FAUCI
HAUSER
LONGO
JAMESON
LOSCALZO