ACS is one of the most important topics in medicine and yes you can SAVE A LIFE if you master this topic very well :)

1. Approach to
Acute Coronary
Syndrome
Sujood Hussien Khraisat
Hashemite University

2. Myocardial ischaemia :
• Reduced blood flow due to mechanical
obstruction .
• Due to decreased oxygenated Hemoglobin.
• Increased demand for oxygen .

3. • Myocardial ischaemia most commonly occurs
as a result of obstructive coronary artery
disease (CAD) in the form of coronary
atherosclerosis .

5. Pathogenesis Of Atherosclerosis

9. CAD can have the following clinical
presentations:
• Asymptomatic
• Stable angina pectoris
• Unstable angina pectoris
• Myocardial infarction (MI)—either NSTEMI
or STEMI
• Sudden cardiac death

12. Acute coronary syndromes
spectrum of clinical presentations ranging from those for
ST-segment elevation myocardial infarction (STEMI) to
presentations found in non–ST-segment elevation
myocardial infarction (NSTEMI) or in unstable angina.
In terms of pathology, ACS is almost always associated
with rupture of an atherosclerotic plaque and partial
or complete thrombosis of the infarct-related artery.

13. Unstable angina and NSTEMI
CRITERIA
• The diagnosis of UA is based largely on the
clinical presentation.
– (1) it occurs at rest (or with minimal exertion),
usually lasting >10 min;
– (2) it is severe and of new onset (i.e., within the
prior 4–6 weeks); and/or
– (3) it occurs with a crescendo pattern (i.e.,
distinctly more severe, prolonged, or frequent than
previously).
• The diagnosis of NSTEMI requires clinical
features of UA + elevated cardiac enzymes.

14. USA and non–ST segment
elevation MI are often considered
together because it
is very difficult to distinguish
the two based on patient
presentation. If cardiac
enzymes are elevated, then
the patient has non–ST segment
elevation MI

15. History
• The severity and duration of coronary artery
obstruction, the volume of myocardium
affected, the level of demand, and the ability
of the rest of the heart to compensate are
major determinants of a patient's clinical
presentation and outcome. A patient may
present to the ED because of a change in
pattern or severity of symptoms.

16. History
• Palpitations
• Pain, which is usually described as pressure,
squeezing, or a burning sensation across the
precordium and may radiate to the neck,
shoulder, jaw, back, upper abdomen, or either
arm
• Exertional dyspnea that resolves with pain or rest
• Diaphoresis from sympathetic discharge
• Nausea from vagal stimulation
• Decreased exercise tolerance

20. • Elderly !
• Diabetics !
• Women !

21. Cardiac vs Non-Cardiac chest pain

22. Causes of
chest
pain

23. Physical Examination
• frequently normal.
• patient will usually lie quietly in bed and may appear
anxious, diaphoretic, and pale.
• Hypotension - Indicates ventricular dysfunction due to
myocardial ischemia, infarction, or acute valvular
dysfunction
• Hypertension - May precipitate angina or reflect elevated
catecholamine levels due to anxiety or to exogenous
sympathomimetic stimulation
• Diaphoresis
• Pulmonary edema and other signs of left heart failure.

24. • (S3) , (S4), The latter is especially prevalent in
patients with inferior-wall ischemia .
• A new murmur may reflect papillary muscle
dysfunction. Rales on pulmonary examination
may suggest LV dysfunction or mitral
regurgitation.

25. ECG
• May be normal.
• ST depression and T wave inversion are highly
suggestive for an ACS. The ECG should be
repeated and continuous ST-segment monitoring
is recommended if the patient is in pain.
• Transient ST elevation is seen with coronary
vasospasm or Prinzmetal’s angina.
Workup

30. CARDIAC BIOCHEMICAL MARKERS
• Elevated CK-MB and troponin distinguish NSTEMI
from unstable angina.
• There is a direct relationship between the degree of
troponin elevation and mortality.
• In patients without a clear clinical history of ACS,
minor troponin elevations have been reported and
can be caused by CHF, myocarditis, or PE, or they
may be false-positive readings. Thus, in patients with
an unclear history, small troponin elevations may not
be diagnostic of an ACS.

32. Other Investigations ?!
• CBC
• Basic metabolic profile
• CXR

34. Early Risk Stratification

35. • The first step in evaluating patients
with possible UA/NSTEMI is to
determine the likelihood that CAD is
the cause of the presenting
symptoms.

39. DIAGNOSTIC EVALUATION

40. DIAGNOSTIC EVALUATION
• For most patients, standard treadmill ECG stress testing is
used, but for patients with fixed abnormalities on the ECG
(e.g., left bundle branch block), perfusion or
echocardiographic imaging is used.
• For patients who cannot walk, pharmacologic stress is used.
• By demonstrating normal myocardial perfusion, sestamibi or
thallium imaging can reduce unnecessary hospitalizations by
excluding acute ischemia.
• CT angiography can also be used to exclude obstructive CAD

41. RISK STRATIFICATION AND PROGNOSIS
• Thrombolysis in Myocardial Infarction (TIMI)
score is useful both in predicting the risk of
recurrent cardiac events and in identifying
those patients who would derive the greatest
benefit from antithrombotic therapies more
potent than unfractionated heparin, such as
low-molecular-weight heparin (LMWH) and
glycoprotein (GP)IIb/IIIa inhibitors, and from
an early invasive strategy.

42. Used to estimate
percent risk at 14
days of MI, or
revascularization

43. RISK STRATIFICATION AND PROGNOSIS
• Other risk factors include DM, LV dysfunction,
and elevated levels of creatinine, ANP, and
CRP.
• CRP and BNP, a marker of increased
myocardial wall tension, correlate
independently with increased mortality (and,
in some studies, recurrent cardiac events) in
patients presenting with UA/NSTEMI.

46. Management of ACS
• General Measures
ECG , Nitroglycerine , Morphine , Beta-Blockers , ACE
Inhibitors , Atropine
• Parenteral Anti-coagulation ( UFH , Enoxaparin ,
Fondaparinux )
and Anti-platelets (Aspirin , Clopidogerl , Abciximab )
• Fibrinolytic therapy
• Anti-arrhythmic drug

47. Unstable angina and NSTEMI
ANTI-ISCHEMIC DRUGS
Nitrates
• Should first be given sublingually or by buccal spray (0.3–0.6
mg) if the patient is experiencing ischemic pain.
• If pain persists after 3 doses given 5 min apart, i.v. GTN 50 mg
in 50 ml 0.9% saline at 2-10 ml/h.
• The only absolute contraindications to the use of nitrates are
hypotension or the use of sildenafil (Viagra) or other drugs in
that class within the previous 24 h.

48. Unstable angina and NSTEMI
ANTI-ISCHEMIC DRUGS
ß-blockers
• I.V. metoprolol (Lopressor) 5 mg infusion over 1-2 minuets. It
is repeated every 5 min for a total dose of 15 mg. Followed in
1–2 h by 25–50 mg by mouth every 6 h continue for 48 hours;
then administer a maintenance dose of 100 mg twice daily.
• I.V. esmolol (Brevibloc)
• I.V. atenolol (Tenormin) 5 mg slow I.V. over 5 minutes; may
repeat in 10 minutes. Follow I.V. dose with 100 mg/day or 50
mg twice daily for 6 to 9 days postmyocardial infarction.

49. Unstable angina and NSTEMI
ANTI-ISCHEMIC DRUGS
ß-blockers
• Contraindications:
– PR interval (ECG) >0.24 s, 2° or 3° atrioventricular
block
– HR <60 beats/min, BP <90 mmHg
– Shock
– Left ventricular failure with congestive heart failure
– Severe reactive airway disease

50. Unstable angina and NSTEMI
ANTI-ISCHEMIC DRUGS
Morphine sulfate
• If pain persists despite intravenous
nitroglycerin and beta blockade, morphine
sulfate, 1–5 mg intravenously, can be
administered every 5–30 min as needed.

51. Unstable angina and NSTEMI
ANTITHROMBOTIC DRUGS
Aspirin and clopidogrel
• Aspirin blocks the formation of thromboxane
A2 and so prevents platelet aggregation. In
ACS patients 150-300 mg initially; then 75–
150 mg aspirin reduced the relative risk of
death or myocardial infarction by about 35–
50%.

52. ANTITHROMBOTIC DRUGS
Aspirin and clopidogrel
• Clopidogrel (Plavex), which blocks the platelet P2Y12
(adenosine) receptor (in combination with aspirin), was
shown in the CURE trial to confer a 20% relative reduction in
cardiovascular death, MI, or stroke, compared with aspirin
alone in both low- and high-risk patients with UA/NSTEMI, but
to be associated with a moderate (absolute 1%) increase in
major bleeding, which is more common in patients who
undergo coronary artery bypass grafting, so it is best avoided
if urgent CABG is likely.
• Clopidogrel should be given (preferably more than 6 hours)
after planned PCI, but may be omitted if coronary
angiography is planned immediately.

53. ANTITHROMBOTIC DRUGS
• Intravenous GP IIb/IIIa inhibitors (abciximab, tirofiban,
and eptifibatide) reduce cardiac complications in
patients undergoing percutaneous coronary
intervention (PCI).
• Small molecule inhibitors eptifibatide and tirofiban
show benefit, while the monoclonal antibody abciximab
appears not to be effective in patients treated
conservatively, (i.e., in those not undergoing coronary
angiography or PCI).
• Concomitant tirofban is particularly useful in diabetic
patients.
• Patients receiving GP IIb/IIIa inhibitors should be
monitored for 24 hours for bleeding and
thrombocytopenia.

54. ANTITHROMBOTIC DRUGS
Anticoagulants
• Unfractionated heparin (UFH) is the mainstay of
therapy.
• The LMWH enoxaparin (Clexane ®) is superior to UFH
in reducing recurrent cardiac events, especially in
conservatively managed patients.
• The Factor Xa inhibitor fondaparinux is equivalent
with enoxaparin but appears to have a lower risk of
major bleeding and thus may have the best benefit
risk ratio.

55. ANTITHROMBOTIC DRUGS
Anticoagulants
• However, UFH, LMWH, or a direct thrombin
inhibitor such as bivalirudin should be used
during cardiac catheterization or PCI.
• Bivalirudin is a direct thrombin inhibitor as effective as
heparin plus GPIIb/IIIa inhibitors in reducing ischaemic
events in patients pretreated with a thienopyridine and
undergoing diagnostic angiography or percutaneous
intervention, but with less bleeding.

56. ANTITHROMBOTIC DRUGS

58. INVASIVE THERAPY
• In high-risk patients, following treatment with
anti-ischemic and antithrombotic agents,
coronary arteriography is carried out within
~48 h of admission, followed by coronary
revascularization (PCI or coronary artery
bypass grafting), depending on the coronary
anatomy.

59. LONG-TERM THERAPY
• Risk factor modification: smoking cessation, achieving optimal
weight, daily exercise following an appropriate diet, blood
pressure control, tight control of hyperglycemia, and lipid
management.
• Beta blockers.
• Statins (at a high dose, e.g., atorvastatin 80 mg/d) and ACE
inhibitors are recommended for long-term plaque
stabilization.
• Antiplatelet therapy: combination of aspirin and clopidogrel
for at least 9–12 months, with aspirin continued thereafter.

61. STEMI
• Primary PCI is generally more effective than fibrinolysis and is
preferred, especially when diagnosis is in doubt, cardiogenic
shock is present, bleeding risk is increased, or if symptoms
have been present for >3 h.

62. STEMI
Fibrinolytic drugs
• Proceed with IV fibrinolysis if PCI is not available or if logistics would
delay PCI >1 h longer than fibrinolysis could be initiated.
• Door-to-needle time should be <30 min for maximum benefit.
• Those treated within 1–3 h benefit most; can still be useful up to 12
h if chest pain is persistent or ST remains elevated in leads that have
not developed new Q waves.
• Complications include bleeding, reperfusion arrhythmias, and, in
case of streptokinase (SK), allergic reactions.

63. STEMI
INITIAL THERAPY
Fibrinolytic drugs
• Coadmnister enoxaparin or heparin and maintain activated
partial thromboplastin time (aPTT) at 1.5–2.0 × control (~50–
70 s).
• If chest pain or ST elevation persists >90 min after fibrinolysis,
consider referral for rescue PCI.
• Later coronary angiography after fibrinolysis generally
reserved for pts with recurrent angina or positive stress test.

67. Thank You !
:D