Cardiology JC012: Sudden Severe Chest Pain: Acute MI And Aortic Dissection

Question 1

ST elevation MI: Pathophysiology and Clinical features

Answer 1

Pathophysiology:
Plaque with fibrous cap
—> Cap rupture
—> Blood clots form around rupture
—> Block coronary artery
—> Death of cardiac tissue

Predisposing factors
1. **Unusual heavy exercise
2. **Emotional stress
3. Progression from unstable angina
4. **Surgical procedures
5. **Infection e.g. pneumonia
6. Circadian periodicity (peak incidence between 0600-1200)

Clinical features:
1. Chest pain
- severe, intolerable
- prolonged > 30 mins
- constricting, crushing, compressing, heavy weight
- radiation to left arm (ulnar aspect) / jaw

2. Others
   - SOB, weakness, dizziness, palpitations, N+V (Bezold-Jarisch reflex)

Question 2

Acute Coronary Syndrome (ACS)

Answer 2

ACS: Plaque rupture leading to occlusion of vessels
—> If **complete occlusion —> **ST elevation

ACS: STEMI + NSTEMI

ACS with persistent ST elevation
- **Complete occlusion
- **↑ Troponin
- Medical emergency

ACS without persistent ST elevation
- ***Incomplete occlusion
- ↑/- Troponin
- ST depression / non-ST elevation MI

STEMI have worse 1 month survival but ***similar prognosis overall

Question 3

Acute MI

Answer 3

Pathology:
- Myocardial cell death ∵ prolonged myocardial ischaemia

Prognosis:
- 40% mortality in first 4 weeks
- 90% of patients with transmural infarct have total occlusion of relevant artery within 4 hours of pain, secondary to plaque fissure

Question 4

Myocardial response during AMI

Answer 4

Myocardial cells will not die / necrotic immediately after ischaemia —> ***12 hours

1. Evolving phase
   - first 6 hours from time of pain (up to **12h)
   - potential for recovery of heart muscle
   —> ↑ Blood supply (via revascularisation)
   —> ↓ Oxygen demand (↓ HR + BP)
   - infarcted muscles are **acidotic, with Ca loss + K influx —> Arrhythmia
2. Convalescence phase
   - infarcted muscles will not recover
   - treatment can still improve mortality / morbidity by
   —> Avoid remodelling of infarct (Thinning of infarct wall + **Dilation of infarct zone —> can cause Aneurysm, Ventricular septal rupture, HF)
   —> Improve **collateral circulation

Question 5

Features NOT characteristic of MI

Answer 5

1. Pleuritic pain
   - sharp pain by respiratory movement / cough
2. Primary / Sole location in middle / lower abdominal region
3. Localised at 1 finger tip, particularly over LV apex
4. Pain on movement / palpitation
5. Very brief episodes
6. Radiate to lower limbs

Question 6

DDx of life-threatening chest pain

Answer 6

1. Acute pericarditis
   - aggravated by respiratory movement, sharp pain
   - radiate to ***trapezius ridge (characteristic site)
   - may have fever
2. Pulmonary embolism
   - haemoptysis
3. Aortic dissection
   - radiate to back
   - tearing sensation

Question 7

***Classification of AMI

Answer 7

Type 1 (most common): Atherothrombotic CAD —> ***Plaque rupture, erosion, fissuring, dissection —> spontaneous MI related to ischaemia

Type 2: **Coronary spasm / **Anaemia / **Hypotension / **CHF —> imbalance of O2 demand and supply —> ischaemia
- unrelated to Atherothrombotic CAD

Type 3: **Sudden cardiac death with symptoms of ischaemia (patient死左)
- **before determination of elevation of cardiac biomarker
- accompanied by new ST elevation / LBBB
or
- verified coronary thrombosis by angiography / autopsy
—> for epidemiological study purpose only

Type 4a: ***PCI associated
Type 4b: Verified stent thrombosis associated

Type 5: ***CABG associated

Question 8

***Diagnosis of AMI type 1 and 2

Answer 8

Detection of ↑ / ↓ of cardiac biomarkers (***Troponin)
- at least 1 value > 99th percentile of URL
AND
- evidence of ischaemia with >=1 following:

1. Symptoms of ischaemia
2. ECG changes of new ischaemia (***New ST-T changes / New LBBB)
3. Development of ***pathological Q waves (∵ transmural infarct)
4. Imaging evidence of new **loss of viable myocardium / new **regional wall motion abnormality

Question 9

Investigations of STEMI

Answer 9

1. Biomarkers
2. ECG
3. Cardiac imaging
   - Echocardiogram
   - Angiogram + PTCA
   - Nuclear imaging

Question 10

Biomarkers for AMI

Answer 10

1. ↑ 2x CPK (creatinine phosphokinase)
   - **MB isoenzyme, CPK MM - skeletal muscle (may be confusing if give imi)
   - high sensitivity but NOT specific
   - good for detecting **reinfarction
2. SGOT (i.e. ***AST) (serum glutamic oxaloacetic transaminase)
   - ↑ also in liver disease, pulmonary congestion, skeletal muscle injury
3. LDH
   - ***LDH1: cardiac, RBC
   - LDH4, 5: liver, skeletal muscle
4. Troponin T / I
   - not normally present —> more sensitive + specific than CK-MB/CK
   - **long lasting: good for diagnosis of MI with **delayed presentation (not good for reinfarction)
   - “stick” test available
   - Elevated: STEMI, NSTEMI, Myocarditis, Acute decompensated HF, Pulmonary embolism
   - ***Not-elevated: Pericardial effusion
5. Myoglobin
   - ***first marker to ↑ in MI
   - non-specific
   - eliminated quickly

Question 11

***ECG of AMI

Answer 11

Anterior MI:
- ST elevation in ***V2-V6

Inferior MI:
- ST elevation in Lead 2, 3, aVF
- ST depression in **V2-V6 (*reciprocal change of ST elevation in MI)

RV infarction:
- Right side chest leads
- ST elevation in V4R, V5R

Pitfalls:
**False positive
- Benign early repolarisation (in young patients)
- **LBBB
- Pre-excitation (Wolff-Parkinson-White)
- Brugada syndrome
- **Peri/Myocarditis
- **Pulmonary embolism
- Subarachnoid haemorrhage

**False negative
- Prior Q waves / persistent ST elevation
- **Paced rhythm
- ***LBBB

Question 12

Cardiac imaging for AMI

Answer 12

1. Echocardiogram
   - ***abnormal wall motions
   - ventricular function: determine need for use of ACEI
   - assess complications of MI: VSD, PE, ventricular thrombus, RV infarct
2. Coronary Angiogram + PTCA (Percutaneous transluminal coronary angioplasty)
3. Nuclear imaging
   - assess **new loss of viable myocardium / **new regional wall motion abnormality with biomarker criteria for MI in absence of non-ischaemic cause

Question 13

Criteria for Prior MI

Answer 13

Prior MI:
- Q wave in V2, V3 >=0.02s
or
- Q wave >=0.03s and >=0.1 mV deep
or
- QS complex in any two contiguous leads of lead 1, aVL, V6; V4-V6; lead 2, 3, aVF

1. Development of ***new pathological Q waves with / without symptoms
2. Imaging evidence of region of **loss of viable myocardium
   - **thinned, fails to contract
   - in absence of non-ischaemic cause
3. Pathological findings post-mortem of a ***healed / healing MI

Question 14

***Treatment of MI

Answer 14

Occlusive coronary thrombus treatment

1. ***Antiplatelet
   - Aspirin + Clopidogrel / Prasugrel / Ticagrelor or GP2b/3a inhibitors (usually not given e.g. Abciximab, Eptifibatide)
2. Antithrombin
   - Heparin
   - ***LMWH
   - Fondaparinux
   - Bivalirudin
3. ***Plasminogen activators (causes fibrinolysis)
   - tPA (Alteplase)
   - rPA (Reteplase)
   - nPA (Lanoteplase)
   - TNK-tPA (Tenecteplase)
   - Streptokinase (old days)

Question 15

***Management of MI

Answer 15

1. General measures
   - Bed rest
   - **O2
   - **Morphine
   - CCU care +/- resuscitation
2. Early presentation (**<12h)
   - Opening of infarct related artery
   - **Fibrinolytic therapy
   - Primary PTCA / ***PCI
3. Antiplatelets / Anticoagulants
   - Aspirin
   - Heparin
   - Warfarin
   - Clopidogrel
4. Other non-thrombolytic therapy
   ***↓ Myocardial O2 consumption
   - β-blockers
   - CCB (Diltiazem)
   - Nitrates

↓ LV remodeling
- ACEI / ARB
- β-blockers
- Aldosterone receptor antagonist

5. Complications management + Rehabilitation
   - Secondary prevention: **Aspirin, β-blockers, ACEI / ARB
   - Complications: **HF, Arrhythmia, **VSD (esp. anterior / septal wall infarction), **MR, Pericarditis, Frozen shoulder

Question 16

Fibrinolytic therapy

Answer 16

Used when no equipment for PCI

Indication:
1. AMI: Pain + ST elevation in 2 contiguous chest leads
2. Time of onset of pain **< 12 hours
3. Absence of CI: **bleeding tendency, cardiogenic shock, recent head injury, stroke

Successful fibrinolysis:
1. Decrease pain

2. ECG criteria
   - early resolution of ST elevation at 90 mins
   - preservation of R wave (i.e. without Q wave)
3. Biochemical evidence
   - e.g. early peaking of CPK
   - normal peak: 22-24 hours
   - successful thrombolysis 11-12 hours
4. Imaging
   - Radionuclide imaging
   - Angiography

Types:
1. Streptokinase
- Non-specific
- activation of plasminogen to plasmin in whole circulation
—> plasmin digest fibrin —> FDP (fibrinogen degradation product)

2. Tissue type plasminogen activator (tPA) (Alteplase)
   - activated when fibrin present —> activates plasminogen —> rapid lysis
   - lower bleeding complications (∵ inactive without fibrin)
   - administered with ***Heparin
3. tPA derivatives
   - TNK-tPA (Tenecteplase)
   - nPA (Lanoteplase)
   - rPA (Reteplase)

Question 17

Contraindications for Fibrinolytics

Answer 17

Absolute CI:
1. **Prior ICH
2. Structural cerebral vascular lesion e.g. **AVM
3. Malignant intracranial neoplasm (primary / metastatic)
4. Ischaemic stroke within 3 months (except acute ischaemic stroke within 3 hours)
5. Suspected aortic dissection
6. ***Active bleeding / bleeding diathesis (exclude menses)
7. Significant closed head / facial trauma within 3 months

Relative CI:
- poorly controlled chronic severe HT
- pregnancy
- active peptic ulcer
etc.

Question 18

Limitations of current Fibrinolytic Regimens

Answer 18

1. ***Not 100% successful
   - only 50% achieved optimal myocardial perfusion
   —> Thrombin inhibition (Anticoagulant) + Platelet inhibition (Antiplatelet) needed
2. 1/3 reocclusion by 3 months
   —> PTCA needed (Mechanically open the occluded artery is the best)
3. Delayed presentation + undiagnostic ECG
   —> Treatment in ambulance + A/E
   —> Education
4. Fibrinolytic therapy ↓ in-hospital mortality by 50% compared to placebo (real world only 20%)

Question 19

***Flowchart of Management

Answer 19

STEMI ***< 12 hours of chest pain onset —>

If hospital have PCI —> PCI

If hospital no PCI
—> **< 3 hours —> Thrombolysis / immediate transfer to hospitals have PCI
—> **>=3 hours —> immediate transfer to hospitals have PCI

Failed thrombolysis
—> Rescue PCI

Successful thrombolysis
—> PCI within up to 24 hours available —> Post-thrombolysis PCI
—> PCI within up to 24 hours unavailable —> Predischarge ischaemia —> Ischaemia-driven PCI

Question 20

Early intervention is important

Answer 20

Every 10 min delay to PCI
—> 1% reduction in mortality difference

Question 21

Emergency CABG

Answer 21

Indication:
- Complicated coronary occlusion not amenable by traditional coronary stenting
- Less common now due to advancement in stenting technique

Question 22

Antiplatelets and Anticoagulants

Answer 22

1. Aspirin
   - ↓ Acute mortality (in conjunction with Thrombolysis)
   - ↓ Reinfarction in long term follow up
2. Heparin
   - SC heparin (prophylaxis against DVT, aPTT not changed)
   - IV heparin (prophylaxis against embolisation, mural thrombosis)
   - Adjunct to tPA
3. Warfarin
   - Established VT / Embolisation
   - Echocardiographic evidence of LV thrombus
4. Clopidogrel
   - 75mg >=14 days
   - after PCI / stenting

Question 23

Other non-thrombolytic therapy: ***↓ Myocardial O2 consumption

Answer 23

1. **β-blockers
   - Use β-blockers **without intrinsic sympathomimetic activities e.g. Metoprolol (β-1 selective), Timolol (non-selective)
   - IV: ↓ mortality by 15% with 12 hours of infarct
   - IV: hypotension, ***carcinogenic shock risk
   - Oral: ↓ long term mortality by 25%
2. Ca blockers
   - Diltiazem (non-Q-wave infarct —> ↓ reinfarction, ↑ survival in patients without HF)
   - ***NO outcome performance, only ↓ chest comfort
3. Nitrates
   - IV: ↓ infarct size if mean BP > 80mmHg
   - Oral: neutral effect
   - ***NO outcome performance, only ↓ chest comfort

Question 24

Other non-thrombolytic therapy: ***↓ LV Remodeling

Answer 24

1. ***β-blockers
   - ALL patients with LV dysfunction
2. ***ACEI
   - ALL patients with LVEF <40%, DM, HT, Renal dysfunction
3. ARB
   - patients intolerant to ACE-1
4. Aldosterone receptor antagonist
   - adjunct: patients on ACE-1 / BB + LVEF <40% + HF without significant renal dysfunction / hyperK

Question 25

Post-MI management

Answer 25

1. Risk stratification
   - Residual ischaemia: **Exercise test, Angiogram, PCI
   - Electrical instability: **24 hr ECG for VT / Ventricular arrhythmia, Anti-arrhythmic, ICD
2. Secondary prevention
   - ***Aspirin, β-blockers, ACEI / ARB
   - Risk factor modulation: exercise, smoking, statin (aggressive lipid lowering)
   - Cardiac rehabilitation + prevention: exercise, work, sex, alcohol, travel
   —> Reduce symptoms (SpC FM)
   —> Improve cardiac function
   —> Reduce sudden cardiac death
   —> Slow down atherosclerosis process

Question 26

Complications of AMI

Answer 26

1. ***HF
2. Arrhythmia
3. ***VSD (esp. anterior / septal wall infarction)
4. ***MR (∵ Papillary muscle dysfunction in inferior wall infarction)
5. Pericarditis
6. Frozen shoulder

Question 27

Flowchart summary

Answer 27

Admission:
- Chest pain

Working diagnosis:
- Suspicion of ACS

ECG:
- Persistent ST elevation
- ST/T abnormalities —> Biochemistry test
- Normal / Undetermined ECG —> Biochemistry test

Biochemistry:
- Troponin: Positive / Negative (need x2)

Risk stratification:
- Troponin +ve: High risk
- Troponin -ve: Low risk

Diagnosis:
- STEMI
- NSTEMI
- Unstable angina

Treatment:
- STEMI —> Reperfusion (∵ complete occlusion)
- NSTEMI / Unstable angina —> Invasive / Non-invasive

Question 28

Aortic dissection

Answer 28

Pathology:
- Tunica ***Media collagen + elastin degeneration

Pathophysiology:
- Blood violates aortic **intimal and **adventitial layers
—> ***False lumen created
—> Dissection may extend proximally / distally / both

Causes:
- **Coexisting HT (80%)
- Genetic: **Marfan, Familial aortic aneurysms / dissection, ***Ehlers-Danlos, Loeys-Dietz aneurysm syndrome
- Biscuspid aortic valve
- Trauma

Question 29

Aortic dissection vs Aortic aneurysm

Answer 29

True aneurysm:
- dilated aorta
- 3 layers all intact

False aneurysm:
- ruptured intima / media
- still enclosed by adventitia

Dissection:
- dissection into medial layer

Question 30

S/S, Complications of Aortic dissection

Answer 30

Symptoms:
- Chronic: can be asymptomatic
- Acute: severe pain (maximum at onset)
—> Tearing
—> Anterior chest (ascending aorta)
—> Interscapular, Abdomen (descending aorta)

Signs:
- BP: High (Tamponade if dissection involve pericardium) / Low
- ***Pulse deficits (Pulse not reaching periphery) (Radio-radial delay, measure 2 arm BP (SpC Medicine))
- Complications

Complications:
- **Syncope
- CVA (i.e. stroke)
- **Acute AR (∵ dilation of aortic root) —> CHF
- **Ischaemic limb
- Paraplegia
- **Renal, Intestinal failure

Question 31

Classification of Aortic dissection

Answer 31

Stanford:
- Type A (life-threatening): Ascending aorta
—> Can involve Coronary artery, Aortic valve, Dissect into pericardium
—> **Acute MI , **Acute AR, ***Acute pericardial effusion

• Type B: All parts except Ascending aorta
  —> can be medically managed, surgery might not be needed

DeBakey:
- I: Stanford A
- II: Stanford A
- III: Stanford B

Question 32

Investigations

Answer 32

1. CXR
   - widening of mediastinum
2. ***CT thorax (preferred over MRI)
   - quicker
   - ~100% specificity / sensitivity
   - ability to identify thrombosed false lumen
   - less invasive
3. MRI
   - ~100% specificity / sensitivity
   - identify intimal flaps, great vessel anatomy, Type A vs B, degree of aortic insufficiency
   - useful test for serial FU of patients with chronic dissections
   - unsuitable for confused / claustrophobic patients
   - unsuitable for pacing wire
   - CI in some life supporting equipment
   - time-consuming
   - need to be disconnected from monitoring devices, IV pumps
4. Transthoracic (TTE) + Transesophageal Echocardiogram (TEE)
   - suitable for patients with renal failure (unsuitable for contrast injection)
   - >95% sensitivity / specificity
   - very rapid
   - done at bedside with minimal risk
   - limited visualisation of distal aorta
   - false positive possible

Question 33

Prognosis of Aortic dissection

Answer 33

Not good overall
- mortality rates approach 1% per hour within 1st 48 hours (i.e. 50% mortality if not treated within 2 days)
- survival >90% with prompt diagnosis / management

Death:
- Progression of dissection&raquo_space; Vascular compromise / rupture

Question 34

Management of Aortic dissection

Answer 34

1. Haemodynamic stabilisation
   - Control BP (SBP: 100-120)
   —> **Labetalol
   —> **Nitroprusside (may ↑ dP/dt, ***pretreated with β-blockers)
   - Surgical drainage (Tamponade)
2. Resection + Graft (definitive)
   - Acute Type A dissection
   - Distal usually ***not require surgery unless: Involve distal organ, rupture, retrograde dissection, Marfan, concomitant aneurysm
   - Stent graft (newer treatment)