Acute Coronary Syndrome

Dr Sunil Chaudhary
Resident, Internal Medicine
• ACS has evolved as a useful operational term
that refers to a spectrum of conditions
compatible with acute myocardial ischemia
and/or infarction that are usually due to an
abrupt reduction in coronary blood flow

2014 AHA/ACC NSTE-ACS Guideline

• Includes
– Unstable Angina
– Non STEMI
– STEMI
Pathophysiology
Clinical presentation
 Unstable Angina and NSTEMI
• chest discomfort is severe and has at least one
of three features:
– occurrence at rest (or with minimal exertion),
lasting >10 min;
– of relatively recent onset (i.e., within the prior 2
weeks); and/or
– a crescendo pattern, i.e., distinctly more severe,
prolonged, or frequent than previous episodes.
• Angina equivalents
• Diaphoresis, pale, cool skin, sinus tachycardia,
3rd and 4th heart sounds, basilar rales and
hypotension
 ECG
• New ST segment depression
• T waves inversions (≥0.3 mV)
 Cardiac Biomarkers
• The diagnosis of NSTEMI is established if a patient
with any of these features (without
electrocardiographic ST segment elevations)
develops evidence of myocardial necrosis, as
reflected in abnormally elevated levels of biomarkers
• UA no rise in cardiac biomarkers
Cardiac Respiratory
• MI • Pulmonary embolism
• Angina • Pneumothorax
• Pericarditis • Pneumonia
• Aortic dissection

Chest pain
GI Musculoskeletal
• Oesophageal spasm • Costochondriasis
• GORD • Trauma
• Pancreatitis
 Scoring systems
• GRACE scoring
• Predicts 6/12 mortality in
NSTEMI patients
– Age
– HR and systolic BP
– Killip class (CCF, pulmonary
oedema, shock)
– Cardiac arrest on admission
– Elevated cardiac markers
– ST segment change
• TIMI
• Risk of cardiac events in next
30 days
– Age >65
– Known coronary artery
disease
– Aspirin in last 7/7
– Severe angina (>2 in 24hr)
– ST deviation >1mm
– Elevated troponins
– > CAD risk factors
 Treatment
• ABCDE
• Medical treatment
• Anti-ischemic treatment
– Nitrates
– B blockers
• Antithrombotic therapy
– Antiplatelets
– Anticoagulants
• Invasive
 Long term management
• DAPT
• B-Blockers
• Statins
• ACEI/ ARB
• Lifestyle modification
 Prinzmetal’s Variant Angina
• severe ischemic pain that usually occurs at rest and is
associated with transient ST-segment elevation.
• Prinzmetal’s variant angina (PVA) is caused by focal
spasm of an epicardial coronary artery with resultant
transmural ischemia and abnormalities in left
ventricular function that may lead to acute MI,
ventricular tachycardia or fibrillation, and sudden
cardiac death
• Coronary angiography demonstrates transient
coronary spasm as the diagnostic hallmark of
PVA
• TRT:
– Nitrates and CCB
– Aspirin may increase severity
– Statins reduce risk of adverse effects
STEMI
 Definition
• The term acute myocardial infarction (AMI)
should be used when there is evidence of
myocardial injury (defined as an elevation of
cardiac troponin values with at least one value
above the 99th percentile upper reference
limit) with necrosis in a clinical setting
consistent with myocardial ischaemia
Pathophysiology
 Criteria for MI
• Detection of a rise and/or fall of cardiac biomarker values
(preferably cardiac troponin [cTn]) with at least one value
above the 99th percentile upper reference limit (URL) and
with at least one of the following:
– Symptoms of ischemia
– New or presumed new significant ST-segment T-wave (ST-T) changes
or new left bundle branch block (LBBB)
– Development of pathologic Q waves in the electrocardiogram (ECG)
– Imaging evidence of new loss of viable myocardium or new regional
wall motion abnormality
– Identification of an intracoronary thrombus by angiography or
autopsy
 Universal classification of MI
• Type 1: Spontaneous
• Type 2: MI secondary to ischemic imbalance
• Type 3: MI resulting in death when biomarkers
are unavailable
• Type 4: MI related to PCI
• Type 5: MI related to stent thrombosis
• Type 6: MI related to CABG
 Clinical presentation
• Similar to angina pectoris but pain occurs even
at rest, is more severe, and lasts longer
• Diaphoresis
• Anterior infarction: sympathetic hyperactivity
• Inferior infarction: parasympathetic
hyperactivty
• Temporal stages
– Acute- few hours to 7 days
– Healing-7-28 days
– Healed->28 days
ECG
• The current ECG standards for diagnosing
acute ischemia/infarction require that
– ST-segment elevation be present in 2 or more
contiguous leads and that the elevation of the ST
segment at the J point be
• greater than 0.2 mV (2 mm with standard calibration)
in leads V1, V2, and V3 and
• greater than 0.1 mV in all other leads
 ECG
• Recommendations
• For men 40 years of age and older, the threshold value for
abnormal J-point elevation should be 0.2 mV (2 mm) in
leads V2 and V3 and 0.1 mV (1 mm) in all other leads.
• For men less than 40 years of age, the threshold values for
abnormal J-point elevation in leads V2 and V3 should be
0.25 mV (2.5 mm).
• For women, the threshold value for abnormal J-point
elevation should be 0.15 mV (1.5 mm) in leads V2 and
V3 and greater than 0.1 mV (1 mm) in all other leads.

aha 2009, esc 2017

• For men and women, the threshold for abnormal J-point
elevation in V3R and V4R should be 0.05 mV (0.5 mm),
except for males less than 30 years of age, for whom 0.1 mV
(1 mm) is more appropriate.
• For men and women, the threshold value for abnormal J-
point elevation in V7 through V9 should be 0.05 mV (0.5
mm).
• For men and women of all ages, the threshold value for
abnormal J-point depression should be −0.05 mV (−0.5 mm)
in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads

aha 2009, esc 2017

 Causes of ST elevation
• Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular
tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (MI or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetal’s
angina)
• When ST-segment elevation is present in I and
aVL, as well as in leads V1 through V4 and
sometimes in V6, and ST-segment depression is
present in leads II, III, and aVF, the automated
interpretation should suggest an extensive
anterior wall or anterobasal
ischemia/infarction due to occlusion of the
proximal portion of the left anterior
descending coronary artery
• When ST-segment elevation is present in leads
V3 through V6, and ST-segment depression is
not present in leads II, III, and aVF, the
automated interpretation should suggest
anterior wall ischemia/infarction due to
occlusion of the mid or distal portion of the
left anterior descending coronary artery.
•  ST-segment elevation in only leads II, III, and
aVF may be the result of occlusion of either the
right coronary artery (RCA) or the left
circumflex coronary artery (LCx), depending on
which provides the posterior descending branch
– RCA:
• greater ST- segment elevation in lead III than in lead II
and will often be associated with ST-segment depression
in leads I and aVL
• Absence of ST depression in V1,V2,V3
• When the RCA is occluded in its proximal
portion, ischemia/infarction of the right
ventricle may occur, which causes the spatial
vector of the ST-segment shift to be directed
to the right and anteriorly, as well as inferiorly.
This will result in ST-segment elevation in
leads placed on the right anterior chest, in
positions referred to as V3R and V4R, and often
in lead V1
 Prior MI
• Any one of the following criteria meets the diagnosis for prior MI:
• Pathologic Q waves with or without symptoms in the absence of
nonischemic causes.
• Imaging evidence of a region of loss of viable myocardium that is
thinned and fails to contract, in the absence of a nonischemic
cause.
• Pathologic findings of a prior MI.
Cardiac Biomarkers
 Imaging
• Regional wall motion abnormalities
• Radionucleotide imaging
– Myocardial perfusion imaging with [ Tl] or [ Tc],
201 99m

which are distributed in proportion to myocardial

blood flow and concentrated by viable myocardium,
reveals a defect (“cold spot”) in most patients during
the first few hours after development of a transmural
infarct
• High resolution Cardiac MRI- late enhancement
 Management
• Initial Diagnosis
• Prehospital Care
• Control in ED
• Control of discomfort
• Limitation of infarct size
• Reperfusion Therapy
• Pharmacotherapy
 Primary PCI
• Compared with fibrinolysis, primary PCI is
generally preferred when the diagnosis is in
doubt, cardiogenic shock is present, bleeding
risk is increased, or symptoms have been
present for at least 2–3 h when the clot is
more mature and less easily lysed by
fibrinolytic drugs
 Fibrinolysis
• act by promoting the conversion of plasminogen to
plasmin, which subsequently lyses fibrin thrombi.
• ideally be initiated within 30 min of presentation
(i.e., door-to needle time ≤30 min)
• Agents
– tissue Plasminogen Activator (tPA),
– streptokinase,
– tenecteplase (TNK), and
– reteplase (rPA)
 TIMI FLOW GRADE
• grade 0 indicates complete occlusion
of the infarct-related artery;
• grade 1 indicates some penetration
of the contrast material beyond the
point of obstruction, but without
perfusion of the distal coronary bed;
• grade 2 indicates perfusion of the
entire infarct vessel into the distal
bed, but with flow that is delayed
compared with that of a normal
artery; and
• grade 3 indicates full perfusion of
the infarct vessel with normal flow.
 ABSOLUTE
CONTRAINDICATIONS
• History of cerebrovascular
hemorrhage at any time
• Nonhemorrhagic stroke or other
cerebrovascular event within the
past year,
• marked hypertension (a reliably
determined systolic arterial
pressure >180 mmHg and/or a
diastolic pressure >110 mmHg) at
any time
• during the acute presentation,
suspicion of aortic dissection, and
active internal bleeding
(excluding menses).
RELATIVE
CONTRAINDICATIONS
• Current use of anti-coagulants
(international normalized ratio ≥2),
• Recent (<2 weeks) invasive or
surgical procedure or prolonged
(>10 min) cardiopulmonary
resuscitation,
• Known bleeding diathesis,
pregnancy, a hemorrhagic
ophthalmic condition (e.g.,
hemorrhagic diabetic retinopathy),
• Active peptic ulcer disease, and
• History of severe hypertension that
is currently adequately controlled.
 Pharmacotherapy
• Antithrombotic Agents
• B blockers
• ACEI/ARB
• Others
 Complications
• Ventricular dysfunction
• Cardiogenic Shock
• Right Ventricular Infarction
• Arrythmias
– Ventricular Premature Beats
– Ventricular Tachycardia and fibrillation
– Accelerated Idioventricular Rhythm
– Supraventricular Rhythm
• Left Ventricular Aneurysm
• Mechanical Complications
• Pericarditis
 Hospital Phase Management
• Activity
• Diet
• Bowel Management
• Sedation
CABG
 Long term Therapies
• Lifestyle Modification
• Antithrombotic therapy
• Beta blockers
• Lipid lowering agents
• Nitrates
• Calcium antagonists
• ACEI/ARB
• MRA
 DAPT
• Undergoing PCI: upto 1 year
• Only fibrinolysis: upto 1 month can be
extended upto 1 year
• Fibrinolysis and subsequent PCI: 1 year
• High ischemic risk (e.g., those with prior MI,
diabetes mellitus, vein graft stent, congestive
heart failure) who are also at low risk of
bleeding upto: 3 years

esc 2017
Special Subsets
 MINOCA
(Myocardial Infarction with Non Obstructive Coronary Arteries)