JC 12 (Medicine) - Acute Myocardial Infarction and Aortic Dissection

Question 1

Difference in troponin levels between ACS with/ without ST elevation

Answer 1

ACS + ST elevation = Troponin elevated

ACS without ST elevation/ with ST depression/ T wave inversion = Troponin normal/ marginally elevated

Question 2

Pathophysiology of acute myocardial infarction

Difference between myocardial ischemia and infarction

Answer 2

Fibrous cap of plaque ruptures
» blood clot forms around the rupture
» blocked coronary artery
» death of heart tissue due to prolonged ischemia

o Ischemia = lack of blood supply, no myocardial cell death, reversible
o Myocardial infarction = cell death, cannot regenerate, irreversible

Question 3

Phases of myocardial infarction

Which phase is salvageable?

Answer 3

1. Evolving phase (first 6 hours to 12 hours from the time of pain)
    Infarcted muscles are acidotic, with loss of Ca and influx of K+ → arrhythmia
    Potential for recovery of heart muscle if:
   a) Improve blood supply by revascularization
   b) Decrease oxygen demand (lower BP, HR)
2. Convalescence phase
    Infarcted muscles will not recover, irreversible

Question 4

Treating myocardial infarct during convalescence phase is not useful. T or F?

Answer 4

False

treatment during convalescence phase can improve mortality and morbidity by:

a) Avoiding remodeling of infarct (thinning of the infarct wall and dilation of
infarct zone) → avoid aneurysm, ventricular septal rupture, heart failure

b) Improving collateral circulation

Question 5

ST elevation myocardial infarction

• Predisposing factors/ triggers

Answer 5

 Unusual heavy exercise
 Emotional stress (including surgery, infection, exercise)
 Progression from unstable angina
 Surgical procedures
 Infection e.g. pneumonia
 Circadian periodicity (peak incidence between 0600-1200)

Question 6

ST elevation myocardial infarction:

Presentation

Answer 6

 Severe (maybe intolerable)
 Prolonged (usually > 30 minutes, not relieved by rest)
 Nature: constricting, crushing, compressing, heavy weight
 Radiation: left arm (ulnar aspect), lower jaw
 Other symptoms: SOB, weakness, dizziness, palpitation, nausea, vomiting (Bezold-Jarisch reflex)

Question 7

ST elevation myocardial infarction

Differential diagnosis

Answer 7

1. Acute pericarditis
    Sharp (knifelike)
    Aggravated by respiratory movement
    Radiates to the trapezius ridge (= characteristic site of pericardial pain)
2. Pulmonary embolism: hemoptysis
3. Aortic dissection:
    Ripping / tearing sensation
    Radiation to back

Question 8

Diagnostic criteria for acute myocardial infarction (type 1 and 2) **

Answer 8

1. Detection of rise and/or fall of cardiac biomarkers above 99th percentile of ULN
2. Evidence of ischemia:
   - Clinical symptoms of ischemia
   - ECG changes: New St-T wave changes/ New LBBB/ New Pathological Q waves
   - Cardiac imaging evidence: New loss of viable myocardium/ new loss of wall motion

Question 9

Types of cardiac imaging for diagnosis of myocardial infarction

Answer 9

Echocardiogram

Angiogram + PTCA (percutaneous transluminal coronary angioplasty)

Nuclear imaging (Tc-99m)

Question 10

List ECG changes associated with myocardial infarction

Answer 10

New ischemia:
- ST elevation in any leads (e.g. II, III, aVF for inferior infarct, V2-V6 for anterior infarct)
- New Pathological Q waves: Any Q wave or QS complex in V2-V3
- Hyperacute T waves
- Pseudonormalization of T waves
- Wellen syndrome: Deep inverted/ Biphasic T wave in V2-3
- ST elevation in aVR: left main stem occlusion

Question 11

Causes of false positive ST- elevation

Answer 11

Electrical dysfunctions
 Metabolic disturbances (e.g. hyperkalemia)

Cardiac disease:
 Peri-/myocarditis
 Benign early repolarization
 LBBB
 Pre-excitation
 Brugada syndrome
 LVH with strain pattern
 Post- cardioversion
 Ventricular apical aneurysm

Acute Infarct/ Hemorrhage:
 Pulmonary embolism (e.g. long haul flight)
 Subarachnoid hemorrhage

Question 12

Causes of false-negative ST elevation (check)

Answer 12

 Prior Q waves and/or persistent ST- elevation
 Paced rhythm
 LBBB

Question 13

Classification of acute myocardial infarction (5 classes)

Answer 13

Question 14

Types and subtypes of cardiac biomarkers for myocardial infarction **

Answer 14

1. CPK (creatinine phosphokinase):
   - CK-MB isoenzyme – short half-life and good for detecting reinfarction
   - CK-MM – also in skeletal muscle
2. SGOT (serum glutamic oxaloacetic transaminase)
3. LDH-1 (Lactic dehydrogenase) *
4. Troponin T or I **
5. Myoglobin **

Question 15

Compare the timing of cardiac biomarkers after myocardial infarction

Answer 15

Myoglobin = FIRST biomarker, but non-specific and fast elimination

CK-MB = Second, short half-life, good for reinfarction

Troponin T or I = Third, long half-life, more sensitive and specific than CK-MB, good for MI with delayed presentation

Question 16

List acute treatment options for acute myocardial infarction

Answer 16

General:
 Bed rest, O2, morphine
 Coronary care unit +/- resuscitation

Fibrinolytic therapy***

• Non-specific: Streptokinase, Urokinase
• Tissue-type plasminogen activator (t-PA)
• TPA derivatives: TNK-tPA, lanoteplase, reteplase

PTCA (percutaneous transluminal coronary angioplasty)***

• Angiogram and PCI
• Emergency coronary artery bypass graft (CABG)

Question 17

Indication for fibrinolytic therapy for acute myocardial infarction

Answer 17

o AMI – pain + ST elevation in 2 contiguous chest leads

o Time of onset of pain < 12 hours **

o Absence of contraindications (absolute and relative c/i)

Question 18

Absolute contraindications to fibrinolytic therapy for myocardial infarction

Answer 18

Cerebral:

• Prior intracranial hemorrhage
• Structural cerebral vascular lesions
• Malignant cerebral neoplasms
• Recent ischemic stroke (3 months)

Vascular:

• Aortic dissection
• Bleeding/ bleeding tendency

Trauma:
Recent closed head/ facial trauma (3 moinths)

Question 19

Relative contraindications to fibrinolytic therapy for myocardial infarction

Answer 19

CVD History:

• Chronic severe hypertension/ uncontrolled hypertension on presentation
• History of ischemic stroke, intracranial pathologies
• Anticoagulant use

Surgical risk:

• Major surgery, long CPR
• Recent internal bleeding
• Allergy to streptokinase

Miscellaneous:

• Pregnancy
• Peptic ulcers

Question 20

Criteria for successful fibrinolysis after myocardial infarction

Answer 20

Clinical: decrease pain

ECG criteria:
 Early resolution of ST elevation at 90min
 Preservation of R wave

Biochemical evidence – early peaking of CPK (11-12h)
 Vs. normal peak: 22-24h

Imaging: radionuclide imaging, angiography

Question 21

MoA of fibrinolysis therapy for myocardial infraction

Answer 21

Streptokinase
 Activates plasminogen to plasmin&raquo_space;> plasmin lyses fibrin in clots

Tissue-type plasminogen activator (t-PA)
 In the presence of fibrin, t-PA is activated and activates
plasminogen at the site of the clot
 More rapid lysis, fewer bleeding complications
 Administered with heparin

(TPA derivatives: TNK-tPA, lanoteplase, reteplase)

Question 22

Limitations of fibrinolytic therapy for myocardial infarction

Answer 22

1. Only 50% of patients receiving fibrinolysis achieved optimal myocardial perfusion
2. 1/3 re-occlusion by 3 months
3. Delayed presentation and undiagnostic ECGs

Question 23

MoA of percutaneous transluminal coronary angioplasty

Answer 23

PCI:
- Balloon angioplasty and stent insertion into coronary artery to restore blood flow

CABG:
- Coronary artery bypass graft: graft from saphenous artery, radial artery, internal thoracic arteries

Question 24

Indications for PCI over fibrinolytic therapy

Answer 24

• presented 3-12 hrs after onset
• contraindicated against fibrinolysis: cardiogenic shock, stroke …etc
• Unclear diagnosis
• Previously failed fibrinolysis/ Rescue PCI
• Post-thrombolysis PCI to increase efficacy of treatment
• Ischemia-driven PCI after thrombolysis

Question 25

Long-term prophylaxis treatment after myocardial infarction

Answer 25

Antiplatelet therapy: lower acute mortality and re-infarction - Aspirin + Clopidogrel / prasugrel / ticagrelor or GP IIb/IIIa inhibitors Anti-thrombin therapy (anticoagulants): prophylaxis vs DVT - Heparin, LMWH - Fondaparinux - Bivalirudin - Warfarin: Only if LV thrombus/ venous thrombosis or embolization

Question 26

Long-term cardio-protective treatment after myocardial infarction

Answer 26

Lower oxygen demand: - Betablockers e.g. metoprolol, timolol, oral or IV - CCB e.g. diltiazem - Nitrates Lower remodeling/ dilatation - Beta-blockers - ACEi/ ARB - Aldosterone receptor antagonist

Question 27

Complications of acute myocardial infarction (limited to the heart alone)

Answer 27

```  Heart failure  Arrhythmias  VSD (anterior MI)  Mitral regurgitation complicating papillary muscle dysfunction  Pericarditis ```

Question 28

Follow-up tests and secondary prevention of acute myocardial infarct

Answer 28

Tests:  Residual ischaemia – exercise test, angiogram  Electrical instability – 24h ECG for ventricular tachycardia or arrhythmia Secondary prevention:  Risk factors modulation: exercise, stop alcohol and smoking, lipid (aggressive lipid lowering with statin)  Beta blocker (oral), aspirin, ACEI/ARB  Cardiac rehabilitation and prevention

Question 29

Aortic dissection Pathophysiology

Answer 29

Blood violates aortic intimal and adventitial layers (intimal tears) >> blood goes into media >> separates wall of aorta >> False lumen is created Dissection may extend proximally, distally, or in both directions

Question 30

Difference between aortic dissection and anuerysms

Answer 30

o Vs. true aneurysm: permanent dilatation of aorta (all layers) o Vs. false aneurysm: adventitia is covered but wall of intima and media are damaged

Question 31

Classification of aortic dissection

Answer 31

Stanford Classification: o Type A: ascending aorta involved o Type B: all dissections not involving the ascending aorta

Question 32

Complications of Type A and Type B aortic dissection

Answer 32

Type A (emergency surgery needed, rapidly fatal)  Coronary artery >> MI  Pericardial sac >> cardiac tamponade  Damage aortic valve >> acute severe aortic regurgitation and congestive heart failure  CVA, syncope Type B (medical treatment unless severe)  Acute ischemic lower limb, paraplegia (femoral artery, iliac artery)  Renal infarct (renal artery)  Mesenteric infarct (celiac artery)

Question 33

Causes of aortic dissection

Answer 33

o Coexisting hypertension (80%) o Genetic disease: Marfan’s syndrome, familial aortic aneurysm/dissection, Ehlers-Danlos, Loeys- Dietz aneurysm syndrome o Bicuspid aortic valve o Trauma

Question 34

Aortic dissection Presentation

Answer 34

Symptoms: o Chronic: asymptomatic o Acute: severe tearing pain, radiates to anterior chest or interscapular/ abdominal area Signs: o BP: high or low (tamponade) o Pulse deficits (radiofemoral delay) o Complications: aortic regurgitation (collapsing pulse, early diastolic decrescendo murmur)

Question 35

First-line investigations for aortic dissection

Answer 35

CXR: abnormal widening of mediastinum CT thorax (& CT aortogram): thrombosed false lumen MRI: for chronic dissection follow-up Transesophageal echocardiogram: rapid imaging

Question 36

Prognosis of aortic dissection

Answer 36

o Mortality rates approach 1% per hour within first 48 hours (within 2 days: 50% patients die) o Survival >90% with prompt diagnosis and management o Death in aortic dissection results from progression of dissection

Question 37

Transoesophageal echocardiogram (TEE) for aortic dissection - Advantages and disadvantages

Answer 37

Advantages:  Combining transthoracic and TEE demonstrate sensitivities and specificities >95%  Very rapid (~10 minutes)  Done at bedside with minimal risk Problems:  Limited visualization of the distal aorta  False-positive results are possible

Question 38

Management of aortic dissection

Answer 38

1. Haemodynamic stabilization: Control BP: SBP 100-120mmHg E.g. IV nitroprusside, pre-treated with IV Labetalol Surgical drainage of cardiac tamponade 2. Definitive treatment: - Resection and graft surgeries DO NOT give anticoagulants (giving heparin generates more dissection)