Pathophysiology/Epidemiology of

Acute Coronary Syndromes

2 November 2019 1
 Reference
s
– 2014 AHA/ACC Guideline for the Management of
Patients with Non-ST-Elevation Acute Coronary
Syndromes. Circulation 2014;130:e344-e426.
– 2013 ACC/AHA Guideline for the Management for
the management of patients with STEMI
– 2016 ACC/AHA Guideline Focused Update on
Duration of Dual Antiplatelet Therapy in Patients
With Coronary Artery Disease
 Acute coronary syndromes (ACSs)
• Is a term that includes all clinical syndromes compatible
with acute myocardial ischemia or infarction resulting
from an imbalance between myocardial oxygen
demand and supply due to an abrupt reduction in
coronary blood flow secondary to an occlusive
coronary artery thrombus.

• Prolonged decrease in oxygen delivery to a region of

cardiac muscle resulting in injury/necrosis of the
affected heart muscle.
 Comparison of ACSs
Unstable NSTEMI STEMI
Angina

Symptoms + + +
present
ECG changes Usually None, ST segment ST segment
ST segment depression, T wave elevation
depression, T inversion, or no
wave inversion changes

Biochemical No changes Increased troponins & Increased troponins

marker CK MB & CK MB

Extent of No myocardial Myocardial injury; Myocardial necrosis;

Injury injury partial occlusion of total occlusion of
coronary artery coronary artery
 Complications
• The most serious complication is cardiogenic shock,
– occurring in approximately 10% of hospitalized MI
patients. Mortality in cardiogenic shock patients with
MI is high, approaching 60%.
• Heart failure, Valvular dysfunction, Bradycardia, Heart
block, Pericarditis, LV free wall rupture,
• Venous thromboembolism,
• Stroke secondary to left ventricular (LV) thrombus
embolization,
• Ventricular and atrial tachyarrhythmias,
– In fact, more than one-quarter of MI patients die, presumably
from ventricular fibrillation, prior to reaching the hospital.
 Clinical presentation: Case 1
• RR is a 65-year-old, 85-kg (187-lb) woman who developed chest
heaviness/tightness at 10:15 hours while she was watching TV .
She described the pain as crushing and as if an elephant is setting
on her chest (10/10 intensity). The pain didn’t respond to 3 NTG
Tablets at home. Local paramedics were summoned and she was
given three 0.4 -mg sublingual nitroglycerin tablets by mouth,
325 mg ASA by mouth, and morphine 2-mg IV push without
relief of chest discomfort. RR presented to the hospital at 11:00
hours. The hospital has a cardiac catheterization laboratory and
primary PCI was selected as a treatment strategy for STE MI.
• PMH: HTN, DL, TIA. Meds: Amlodipine. Echo: Anterior wall
dyskinesis, LVEF 35%. troponin I 1.8 ng/ml, oxygen saturation 99%.
ECG: NSR, 3 mm ST elevation anterior leads.
 Presentation of Acute Coronary Syndromes
General
• The patient typically is in acute distress and may develop or present with acute
heart failure, cardiogenic shock, or cardiac arrest
Subjective criteria:
• classic symptoms
– Chest pain described as (tightness, pressure, heaviness) in sensation in
70-80% of patients (>20 min)
– Also the pain may be felt in epigastrium,
arms, shoulders & may in jaw or back.
– Not relieved by nitrates, Movement, deep
breathing or change in body position doesn’t
affect the pain.
• Other symptoms include:
– Diaphoresis, Nausea and vomiting, Shortness of
breath, Arm tingling/ numbness.
–
– Weakness,
Patients less Light headedness
likely to present withorclassic
syncopesymptoms include elderly patients,
diabetic patients, and women  May be silent in 15-20% of the patients
 Presentation of Acute Coronary Syndromes
Objective criteria:
Signs
– No signs are classic for ACS. Many appear pale & cold.
– Abnormal heart sounds: S4 heard in most pts, S3 may indicate heart failure
– patients with ACS may present with signs of acute heart failure, including jugular
venous distension, rales, and S3 sound on auscultation.
– HR: Patients may present with arrhythmias and therefore may have tachycardia,
bradycardia, or heart block.
12 lead ECG: The 12-lead ECG is the first step in management, within 10 min
followed by serial ECGs
Angiography: in High risk patients to determine the presence and extent of
coronary artery stenosis.
Echocardiogram to determine LV function
• LV function: best predictor of mortality after MI
• LVEF < 40% = higher risk of death
Selected low-risk patients may undergo early stress testing to diagnose CAD
 Presentation of Acute Coronary Syndromes
• Laboratory Tests
– Troponin I or T and CK-MB are measured. at the time of first
assessment and repeated at least once, 6 to 9 hours
– Blood chemistry tests are performed with particular attention
given to potassium and magnesium, which may affect heart
rhythm.
– The serum creatinine is measured to identify patients who may
need dosing adjustments for some medications, as well as those
who are at high risk of morbidity and mortality.
– Baseline complete blood count (CBC) and coagulation tests
(activated partial thromboplastin time and International
Normalized Ratio) should be obtained, as most patients will
receive antithrombotic therapy, which increases the risk for
bleeding.
– Fasting lipid panel.
 Clinical Assessment and Initial Evaluation

1. 12-lead ECG should be done within 10 min of ED

arrival (Class 1) 1st step in management
• Key findings indicating myocardial damage
– T-wave inversion: indicates ischemia. earliest change in
ECG
– ST-segment depression
– ST-segment elevation: indicates myocardial injury. location
of ST elevation in the ECG provides information on the
location of the MI (anterior, inferior, septal, lateral, etc.).
this location also allows for prediction of which coronary
artery is the infarct-related vessel. For example, anterior
MI usually involves the LAD, inferior MI usually involves
the RCA. ~20% of MIs are STEMI.
 Clinical Assessment and Initial Evaluation
2. Troponin I or T : levels should be measured at presentation and 3 to 6 hours after
symptom onset to identify a rising and/or falling pattern and confirm MI (class1)
• CK-MB : If CK-MB  3-5% of total CK, MI occurred. Begins to rise within 4-6 hours
after symptom onset, usually peaks within 18-24 hours after symptom onset and
is undetectable by 48 hours.
• Cardiac Troponin I & T (most preferred & sensitive one, replaced CK-MB in most
centers for routine diagnosis of MI, bedside test available), but can not detect
early MI & reinfarction. Onset 2-4 hrs, duration for Tropnin I is 7 days and Tropnin
T is 10 –14 days. Elevations in Tn I associated with higher mortality risk even in pts
with normal CK-MB
• With contemporary troponin assays, creatine kinase myocardial isoenzyme (CK-
MB) and myoglobin are not useful for diagnosis of ACS. (class 3)
• MI diagnosis:
– > 1 one troponin value greater than MI decision limit set by lab
or
– 2 CK MB values greater than MI decision limit set by lab
CK MB: good for early reinfarction, Low sensitivity during very
early Ml (less than 6 h after symptom onset) or later after
symptom onset (more than 36 h) and for minor myocardial
damage (detectable with troponins)
Question:
1. What is the preferred lab test for early reinfarction?
 Case1
• Identify your acute treatment goals for RR.
• What adjunctive pharmacotherapy should be
administered to RR in the emergency
department prior to proceeding to the cardiac
catheterization laboratory?
• What additional pharmacotherapy should be
initiated on the first day of RR’s hospitalization
following successful PCI/intracoronary stenting?
 Treatment of
ACS’s Desired
outcomes
Short-term desired outcomes in a patient with ACS are:
1. Relief of ischemic chest discomfort
2. Early restoration of blood flow to the infarct-related artery to
prevent infarct expansion (in the case of MI) or prevent
complete occlusion and MI (in unstable angina)
3. Prevention of death and other complications
4. Prevention of coronary artery reocclusion

Long-term desired outcomes are:

5. control of risk factors,
6. prevention of additional cardiovascular events,
7. improvement in quality of life.