APPROACH TO A CASE OF
ACUTE CORONARY SYNDROME
AND ITS MANAGEMENT
BY:
DR. AMMAR SABIR SIDDIQUI
JR-3
DEPARTMENT OF MEDICINE, KGMU
ACUTE CORONARY SYNDROME
• The term acute coronary syndrome (ACS) is a unifying
construct representing a pathophysiologic and clinical spectrum
culminating in acute myocardial ischemia
• Unstable angina (UA), Non ST Elevation Myocardial Infarction
(NSTEMI) and ST Elevation Myocardial Infarction (STEMI)
collectively constitute the diagnosis of Acute Coronary
Syndrome (ACS).
HISTORY
• Chest pain - the classical symptom but not always present
• Described by the patient as heaviness, pressure, squeezing, smothering
or choking and only rarely as frank pain
• Site of pain- Retrosternal, may radiate to back, interscapular region, root
of neck, jaw, teeth and epigastrium
( Rarely below the umbilicus or above the mandible)
Duration- Variable. May last for 2 mins to > 30 mins
If pain ends in <10 mins it is highly unlikely of ACS
Pain lasting for >10 mins that occurs at rest or with minimal exertion-
possibility of ACS
• Onset of pain- Within prior 2 weeks
• Pattern- Crescendo-decrescendo- Mostly stable angina(not included
in ACS)
• Crescendo pattern- more severe, prolonged or frequent than previous
episodes- suggestive of ACS
• Dyspnea
Anginal equivalents- may be
• Palpitations present with or without chest
• Nausea discomfort
• Epigastric discomfort
• Fatiguability
• Sweating
• Family history: h/o CAD, DM, sudden cardiac deaths
• Past history: DM, hypertension, CAD, hyperlipidemia, sudden cardiac
deaths, peripheral arterial diseases( h/o intermittent claudication,
stroke/TIA)
• Personal history: Smoking, high fat and energy rich diet
SIGNS
• Levine’s sign- Patient typically placing hand over the sternum,
sometimes with a clenched fist to indicate the chest discomfort
On examination: Patient may have pallor, sweating Sympathetic
hyperactivity
Signs of tissue damage : Fever
Pulse rate: Bradycardia- possibly inferior wall MI
Tachycardia- Anterior wall MI
Blood pressure: Hypertension- Anterior infarction
Hypotension- Inferior infarction
Parasympathetic
hyperactivity
JVP- Raised RVMI
Palptation
Apex: May be
(a) Normal
(b) Diffuse- due to weak ventricular contractions
(c) Double- due to LV aneurysm as a complication of MI
Auscultation:
S1- Soft- due to weak ventricular contractions
S2- wide(variable) split—late P2 in RVMI
reverse/paradoxical split—late A2LVMI
S3 and S4- presence is suggestive of ventricular dysfunction
• Murmur: A transient mid-systolic or late systolic murmur may be
heard
Respiratory—Rales due to LV dysfunction—pulmonary edema
INVESTIGATIONS
• 1. ECG : Should be done in all patients presenting with chest
discomfort.
Possible findings
(a) Normal
(b) New ST segment depression and T wave inversions
(c) ST segment elevation
(i)Transient: Prinzmetal’s angina( due to coronary vasospasm)
(ii)Sustained: STEMI
ST Elevation MI ( in absence of
LBBB)
• ST elevation in two contiguous leads with following cut points
0.1 mV in all leads (except v2-v3)
In leads v2-v3
> 0.2 mV in men > 40 years
> 0.25 mV in men < 40 years
> 0.15 mV in women
ECG manifestations of ischemia in
presence of LBBB
ECG criteria
• ST-segment elevation >1 mm
and concordant with the QRS
complex
• ST-segment depression >
1mm in lead V1,V2 or V3.
• ST-segment elevation > 5 mm
and discordant with the QRS
complex.
• Score > 3 had a specificity of
98% for acute MI.
LOCATION LEAD WITH AFFECTED
OF MI ST CHANGES CORONAR
Y ARTERY
ANTERIOR V1,V2,V3,V4 LAD
SEPTUM V1,V2 LAD
LATERAL I,aVL, V5,V6 Left
with ST Circumflex
depression in
II,III,aVF
INFERIOR II,III,Avf RCA
withST
depression in
I,aVL
POSTERIOR V7,V8,V9 RCA
with ST
depression in
V2,V3,V4
RIGHT V4R with ST RCA
VENTRICLE depression in
I,aVL
ANTEROSEPTAL STEMI- ST elevation is maximal in the anteroseptal leads (V2-4)
LATERAL STEMI- ST elevation is present in the lateral leads (I and aVL). Subtle
elevations in lead V5 as well
INFERIOR STEMI- Marked ST elevation in II, III and aVF
POSTERIOR WALL MI- Suggested by ST depression in V2-3. If extended chest
leads i.e. V7,V8,V9 are placed ST elevation will be seen in V7,V8,V9
2. Cardiac biomarkers:
• Troponin-I is most sensitive
• To detect reinfarction between 3-10 days- CK-MB is preferred
Note: h-FABP(heart type specific fatty acid binding protein) has a
high potential as marker for early diagnosis of acute MI—rises as
early as 2 hours following an event.
3. Echocardiogram(ECHO)- To detect the presence or absence of wall
motion abnormalities and value of ejection fraction
4. Magnetic resonance imaging ( MRI ) - The most accurate method for
diagnosing MI or non-ischemic cardiomyopathies, quantifying the scar,
assessing viability and evaluating thrombus
- Hyper-enhancement is seen as bright area of tissue against background of
dark normal myocardium
- Gadolinium is administered, images obtained after 10 mins
5.Blood investigations
Leukocytosis with a peak on 1st day
Raised ESR that remains elevated for some days
Elevated C- reactive protein
6. Chest radiography :
- Heart size usually normal
- Enlargement of cardiac shadow indicate previous myocardial damage or pericardial
effusion
- Evidence of pulmonary edema
7. Radionuclide scanning -Shows site of necrosis and extent of impairment of
ventricular function (lack of sensitivity and specificity)
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 in
form of dipyridamole or adenosine is used.
• CT angiography can also be used to exclude obstructive
CAD
MANAGMENT
ANTI ISCHEMIC TREATMENT:
1. 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, intravenous nitroglycerin
(5–10 μg/min) is recommended.
• The rate of the infusion may be increased by 10 μg/min every 3–5 min
until symptoms are relieved, systolic arterial pressure falls to <90 mmHg,
or the dose reaches 200 μg/min.
• The only absolute contraindications to the use of nitrates are hypotension
or the use of PDE-5 inhibitors within the previous 24 h.
2. Beta blockers: To be given to all patients with ACS
• Target HR- 50-60/min
• I.V. metoprolol 5 mg infusion over 1-2 minutes. 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 continued for 48 hours; then administer a
maintenance dose of 100 mg twice daily.
3. CCB- Added when ischemic discomfort is not relieved by adequate
doses of nitrates and beta blockers or patients in whom either agent is
contraindicated.
• Non DHP(Verapamil or Diltiazem) are used to decrease heart rate
3. 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.
ANTITHROMBOTIC THERAPY FOR ACS
REPERFUSION THERAPY
Primary percutaneous coronary (PCI)
• Usually angioplasty
• Applicable to patients with contraindication to fibrinolytics.
• Preferred when diagnosis is in doubt, cardiogenic shock is
present, bleeding risk increased, or symptoms has been
present at least 2-3 hours when clot is more mature and harder
to lyse
2. Fibrinolysis - Should be initiated within 30 min of presentation.
• Tissue plasminogen activator (t-PA), streptokinase, tenecteplase (TNK),
reteplase (rPA).
• t-PA – 15mg bolus followed by 50mg IV over 30 min, 35mg next 60 min.
• Streptokinase – 1.5 million units (MU) IV over 1 hr.
• rPA – 10 MU bolus over 2-3 min, followed by 2nd 10 MU bolus after 30
min.
• TNK – IV bolus 0.53mg/kg over 10 seconds.
CONTRAINDICATIONS OF FIBRINOLYTIC
THERAPY
ABSOLUTE RELATIVE
Cerebrovascular hemorrhage at any time Current use of anti-coagulants (INR ≥2)
A non-hemorrhagic stroke or other Recent (<2 weeks) invasive or surgical
cerebrovascular event within the past year procedure
Marked hypertension (systolic arterial pressure Prolonged (>10 min) cardiopulmonary
>180 mmHg and/or a diastolic pressure >110 resuscitation
mmHg) at any time during the acute
presentation
Suspicion of aortic dissection Known bleeding diathesis, pregnancy, a
hemorrhagic ophthalmic condition (e.g.,
hemorrhagic diabetic retinopathy),
Active internal bleeding (excluding menses). Active peptic ulcer disease
History of severe hypertension that is currently
adequately controlled
3. Integrated Reperfusion therapy: Cardiac catherization and coronary
angiography to be carried out after fibrinolytic therapy if there is evidence of
a) Failure of reperfusion(persistent chest pain and ST-segment elevation
>90 min) consider rescue PCI
b) Coronary artery re-occlusion or development of recurrent ischemia
consider urgent PCI
4. Coronary Artery Bypass Graft (CABG) -When PCI fails to prevent
further ischemia, CABG is considered.
