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BELAJAR

BERSAMA KARDIO

RAGIL NUR ROSYADI


1. A 25-year-old male
developed sharp central chest
pain and palpitations after
drinking three cans of energy
drink whilst revising for
exams. The symptoms were
ongoing when he initially A. Admit for observations
attended the ED, and an ECG B. Exercise treadmill test
showed a sinus tachycardia
with no ST change. The pain C. Stress echocardiogram
subsided shortly afterwards. D. CT coronary angiogram
He is normally fit and well.
His father recently had a E. No further investigation
myocardial infarction at the
age of 62. All observations
and examination are normal.
Troponin and D-dimer tests
were negative. What would
you recommend?
2. One of your
patients has small
vessel coronary
disease which is not
suitable for
A. Amlodipine
revascularization.
They are still B. Ivabradine
experiencing class 2 C. Nicorandil
angina particularly in D. Bisoprolol 5 mg bd
the evening despite E. Ranolazine
bisoprolol 10 mg od.
Blood pressure is
135/90 mmHg.
What would you
recommend next?
3. One of your patients has
discrete
angiographically
significant lesions in the A. CABG will be associated with a greater
mid right coronary mortality benefit compared with PCI
artery and the mid left B. The risk of stroke will be significantly lower
anterior descending with PCI
coronary artery. He is C. Add a third oral antianginal and then reconsider
60 years old and is not revascularization
diabetic. He has D. The likelihood of repeat revascularization is
ongoing class 2 anginal higher with PCI
symptoms despite E. Revascularization is recommended for
optimal dose of a beta- prognostic reasons
blocker and a long-
acting nitrate. What do
you recommend?
In the Atorvastatin vs. Revascularization Treatment (AVERT)
trial, aggressive lipid lowering by high-dose atorvastatin was
marginaly better than PCI in reducing ischemic events.

OMT vs. PCI in One meta analysis reported a survival benefit for PCI over
OMT(respective mortalities of 7.4% vs. 8.7% at an average
CSA follow-up of 51 months).

The COURAGE RCT randomized 2287 patients with known


significant CAD and objective evidence of myocardial
ischaemia to OMT alone or to OMT + PCI. At a median
follow-up of 4.6 yrs, there was no significant difference in
the composite of death, MI, stroke, or hospitalization for UA
The superiority of CABG to
medical treatment in the
management of specific subsets
of CAD.
CABG vs. OMT
in CSA Survival benefit of CABG in pts
with LM or 3 vessel CAD. Benefits
were greater in those with severe
symptoms, early positive ETT.
5 year follow-up of the MASS II study
of 611 pts.
OMT vs. PCI vs.
CABG in multi-
vessel disease Composite primary endpoint (total
mortality, Q-wave MI or refractory
angina requiring revascularization) in
36% of OMT, 33% of PCI and 21% of
CABG.
Proximal LAD stenosis.

Two meta-analysis of >1900 & >1200 pts.


PCI vs.
CABG No significant difference in mortality, MI, CVA.

Three fold increase in recurrent angina & a five


fold increase in repeat TVR with PCI at up to 5
years of follow-up.
4. A 45-year-old diabetic male
patient has returned to clinic
following a recent
angiogram. He has stable A. Titrate the beta-blocker and add a calcium-
class 2 angina and is
currently on aspirin 75 mg channel blocker or long-acting nitrate reassess
od, atorvastatin 40 mg nocte, symptoms
and bisoprolol 2.5 mg as B. Titrate the beta-blocker and add an ACE
antianginal treatment. His
symptoms have improved
inhibitor—reassess symptoms and LV function
since starting the beta- C. CABG for prognostic and symptomatic
blocker. The angiogram improvement
showed severe plaque in the
proximal left anterior D. PCI guided by ischaemia via a functional
descending artery and imaging test
discrete simple lesions in the
mid circumflex and right
E. Multivessel PCI or CABG for symptomatic
coronary arteries. The treatment
echocardiogram has shown
moderate LV impairment.
What do you recommend?
A. It is an acute inflammatory disease of the
5. Which vascular intima
one of the B. It is characterized by the accumulation and
modification of cholesterol esters on the
following luminal surface of the endothelium
is true of C. Macrophages bind and phagocytose
oxidized LDL to form foam cells
atheroscler D. Typically form away from branch points
otic plaque E. Endothelial dysfunction as a result of an
formation? insult to the endothelium is characterized by
increased nitric oxide release
A. Thin-capped fibroatheromas are most prone
to cap disruption and thrombus formation
6. Atherosclerotic B. Fracture of the fibrous cap allows platelets,
plaque rupture is the clotting factors, and inflammatory cells to
most common event come into contact with the thrombogenic
leading to clinically necrotic lipid core, leading to thrombus
relevant ischaemia. C. Disrupted plaques can be accurately
Which one of the identified by optical coherence tomography
following statements D. Plaque rupture will always result in some
regarding this degree of clinical ischaemia (ACS)
process is not true? E. Patients presenting with an ACS who have a
ruptured plaque identified during angiography
can be managed without stenting
A. Clopidogrel, prasugrel, and ticagrelor all
inhibit the same receptor (P2Y12 ADP
receptor)
7. Which one of B. Clopidogrel and prasugrel are irreversible
the following inhibitors, whereas ticagrelor is reversible
statements C. Clopidogrel and prasugrel are both prodrugs
which are metabolized to the active form,
regarding the new whereas ticagrelor acts directly
generation of D. Ticagrelor requires twice daily
antiplatelet drugs maintenance, whereas clopidogrel and
prasugrel are once daily
is not true? E. All are converted to the active metabolite by
the hepatic cytochrome enzyme (CYP3A4)
pathway
8. You are called by the CCU nurses.
They are concerned that one of a post
primary angioplasty patient’s blood A. This is likely to be a spurious result; continue with the
results has returned with platelets of current treatments but repeat the
12 × 109/L. Bloods taken at the time blood result urgently and watch for bleeding
of procedure revealed platelets of 179
B. This degree of platelet inhibition is to be expected with
× 109/L. The patient has no signs of the current regime; reassure but
bleeding and all other blood results,
including haemoglobin, are stable watch for bleeding and repeat the bloods
and consistent. They have been C. This is a sign of early heparin-induced
loaded with aspirin 300 mg, prasugrel thrombocytopenia; stop the abciximab and replace
60 mg, heparin 8000 units, and platelets until >50 × 109/L
abciximab as a weight-adjusted bolus
and current infusion for 12 hours. D. This may represent an immune-mediated
thrombocytopenic reaction to abciximab; stop the infusion
They had not previously received and repeat the bloods
these agents. GP 2b/3a was
recommended as the patient had a E. The patient is at significant risk of bleeding; stop all
highly thrombotic right coronary antiplatelets until the platelet count is
artery occlusion with evidence of >50 × 109/L
microvascular distal embolization
and required a long length of drug-
eluting stent. What do you advise?
Abciximab with
thrombocytopenia
The platelet count should gradually recover on stopping
the agent, but the platelets should not be replaced
unless there were signs of signifcant bleeding.

heparin-induced thrombocytopenia usually occurs after


a few days with repeated exposure.

Pseudo-thrombocytopenia (clumping) is possible and


would be obvious on a blood flm, but this should be
excluded rather than assumed.
9. A patient
arrives directly in A. A single administration of unfractionated
the catheterization heparin in this situation should be safe
laboratory for B. Avoid all anticoagulants as a precaution and
primary angioplasty. complete the procedure with Gb2b/3a cover
They volunteer a C. Bivalarudin is safe and effective in this
previous serious situation
allergic reaction to D. A single administration of fondaparinux in
heparin called ‘HIT’ this situation should be safe and effective
as you are E. There is a risk with all anticoagulants in this
consenting them. situation, and so the balance of benefit is
What would be your shifted to thrombolysis over primary
anticoagulation angioplasty
strategy?
Heparin-Induced
Thrombocytopenia
Heparin induced thrombocytopenia (HIT) is an immune‐mediated event that can
have severe life‐ and limb‐threatening complications.

When a diagnosis of HIT is suspected immediate cessation of all forms of


heparin, including UFH and LMWH, is imperative.

A direct thrombin inhibitor, such as bivalirudin or fundaparinux, is considered


the agent of choice for treatment of HIT.

Warfarin should not be used until the platelet count has recovered.
10. You review a patient in
clinic who has previously A. The left wrist would be the preferred route
had bypass surgery and a here
recurrence of angina. They
have three grafts (LIMA to B. The right wrist would be the preferred route
LAD, vein graft to OM, and here
vein graft to RCA). You C. The left leg would be the preferred route,
recommend a coronary but you will need to obtain further information
angiogram. The patient asks
you if the procedure will be
regarding the vascular procedures
carried out from the wrist or D. The right leg would be the preferred route,
the leg as they have had but you will need to obtain further information
vascular procedure to both regarding the vascular procedures
groins. You can see bilateral E. On further thought an angiogram is not
inguinal scars, but the possible and a non-invasive test should be
procedures were carried out utilized
at another hospital.
What do you advise?
11. Which of the A. Initial mortality of NSTE-ACS is higher
following statements
is true regarding non- B. Six-month mortality of STEMI is higher
ST elevation acute C. Long-term mortality of NSTE-ACS is
coronary syndromes higher
(NSTE-ACS) D. STEMI patients are older with more
compared with ST comorbity
elevation myocardial
E. STEMI is more frequent
infarctions (STEMI)?
12. On your ward round you review a
patient who is 48 hours post anterior
STEMI treated successfully with primary
angioplasty. He has type 2 diabetes and
hypertension. He is gradually improving,
A. Add furosemide 40 mg od
having initially suffered with heart failure.
B. Reduce the bisoprolol
He still feels ‘chesty’ and auscultation
reveals minimal basal crepitations. C. Further titrate the ramipril
Echocardiography has revealed an ejection D. Add Eplerenone 25 mg
od
fraction of 40%. Blood pressure is 110/70
E. Add isosorbide
mmHg with heart rate 55 bpm at rest. mononitrate MR 30 mg od
Ramipril has been titrated to 2.5 mg bd
with bisoprolol 2.5mg od. U&Es have
remained normal.
How would you improve his medical
treatment?
13. You are asked to review a 32-
year-old smoker in the ED. He
A. Activation of the primary
has presented with an hour of angioplasty team
ongoing chest pain. The pain is B. Await troponin tests and
described as left-sided and sharp give analgesia
but not focal. There is no postural C. Non-steroidal anti-
change and no change with inflammatory analgesia
inspiration. He appears clinically D. Urgent bedside echo to
rule out a regional wall
well. The emergency team are motion abnormality
concerned because he has anterior E. CT pulmonary angiogram
ST elevation and show you his
ECG. What do you recommend?
14. Which of the following should not be used as a
procedural antiacoagulant for primary angioplasty?

A. Unfractionated
B. Enoxaparin (±
heparin (± GP C. Fondaparinux
GP 2b/3a)
2b/3a)

E. Bivalarudin +
D. Bivalarudin
GP 2b/3a
15. You review a patient in the CCU who
was admitted earlier with a large anterior
myocardial infarction treated with primary
angioplasty. He has no bystander disease
but the presentation was late. The A. Call an anaesthetist to
echocardiogram shows severe LV consider ventilation
impairment. There is pulmonary oedema B. Start a dopamine infusion
which you have been treating with C. Give a fluid challenge
furosemide boluses and continuous positive D. Start a nitrate infusion
airway pressure non-invasive ventilation. E. Start a furosemide
Blood pressure is now 85/50 mmHg and infusion
urine output in the last hour is 10 mL.
Oxygen saturations are maintained at 94%
with high-flow oxygen. He remains alert.
What treatment should you consider next?
PERKI,2015
16. 24. A 45-year-old diabetic
A. Acute stent thrombosis of
man is admitted directly to the the right coronary artery
catheterization laboratory with B. Acute stent thrombosis of
chest pain and ST elevation. He the left anterior descending
had elective angioplasty a week artery
previously for stable angina. He C. Acute stent thrombosis of
the circumflex artery
received drug-eluting stents and is
taking aspirin and clopidogrel. D. Acute stent thrombosis of
a saphenous vein graft
The relevant angiographic image
E. Catheter-induced
is shown in below. coronary dissection
What is the diagnosis?
17. You are
completing the
discharge summary
for a patient who has A. Dual antiplatelets for 12 months and then
aspirin long term
undergone primary
angioplasty with a B. Ticagrelor for 1 month and aspirin long
bare metal stent for an term
anterior myocardial C. Aspirin for 1 month and ticagrelor long
infarction. The term
pharmacist questions D. Ticagrelor alone is adequate long term
you regarding the E. Dual antiplatelets long term
duration of
antiplatelets. What do
you advise?
18. What is the
most common a. Triggered activity
mechanism b. Abnormal automaticity
involved in c. Reentry
clinically
d. Early afterdepolarizations
important
cardiac e. Parasystole
arrhythmias?
Arrhythmia
mechanism
• Triggered activity
• Abnormal automaticity
• Reentry
a. Results from triggered activity (early
afterdepolarizations) that occurs during
19. Torsades
phase 2 or 3 of the cardiac action potential
de pointes is
b. Prolonged QT interval
characterized
c. Exacerbation by bradycardia with short-long
by all of the coupling intervals
following d. Polymorphic VT
except: e. Often provoked during amiodarone
administration
• prolonged QT intervals
• exacerbation by bradycardia
Torsades de • short-long couple intervals
• “salvos” of nonsustained polymorphic
pointes VT before degeneration into a
sustained ventricular arrhythmia
• polymorphic VT with characteristic
“twisting around the axis” morphology
• Although amiodarone often prolongs
the QT interval, it rarely causes
torsades de pointes.
20. Which one of the
following currents is
responsible for a. I f
maintaining stable resting b. I Na
membrane potential in
the atrial and ventricular c. I Kl
cells? d. I K
e. I Ca
Membrane potential
21. The IKATP a. A consequence of If activation that enhances
pacemaker activity
is a potassium
channel that b. Physical opening of the channel pore by the N-
terminal portion of the channel
is inhibited by
physiologic c. Chemical ligand binding in response to
intracellular depletion of ATP from ischemia
concentration
d. Conformational changes in channel structure
s of ATP. How
is this channel e. The channel is only inhibitory and is not
activated? activated
22. The sinus
node is • a. Phase 0
predominantly • b. Phase 1
characterized by • c. Phase 2
depolarization in
• d. Phase 3
which phase of
• e. Phase 4
the action
potential?
23. A 26-year-old man is referred to the
arrhythmia clinic for evaluation of
exerciseinduced palpitations. He denies
presyncope or syncope during these episodes. a. RVOT tachycardia
He had no other significant medical history. b. Wolff-Parkinson-White
He has no family history of cardiomyopathy, syndrome
arrhythmia, or sudden death. An ECG, c. Atrial flutter with rapid
echocardiogram, and 24 hour ambulatory ventricular response
Holter monitor were all within normal limits. d. Sinus tachycardia with
aberrancy
During TMET, the wide complex tachycardia
was induced. The 12 lead ECG is shown. The e. Scar-mediated VT
patient reports palpitations without
lightheadedness.
What is the most likely clinical diagnosis?
a. ICD
b. Beta blocker
24. What
treatment should c. Digoxin
be considered for d. Referral for catheter ablation of a
ventricular arrhythmogenic focus
this patient?
e. Referral for catheter ablation of the caval-
tricuspid isthmus
The treatment decision depends on the symptoms

Symptoms are infrequent and mild  no treatment

Severe symptoms (presyncope or syncope or low


RVOT VT quality of life) catheter ablation
Pharmacologic therapy (beta blocker) improves
symptoms in up to 50% of patients.
Digoxin increases intracellular calcium and can
potentially promote triggered activity.
25. Which one of a. Quinidine
the following b. Lidocaine
antiarrhythmic c. Sotalol
agents does not
d. Procainamide
prolong the QT
e. Ibutilide
interval?

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