Acute chest pain is one of the most common reason for seeking care in the emergency department (10% of all visits) Only 10-15% of patients with chest pain actually have ACS.

1. ACUTE CORONARY
SYNDROME
DR SHADAB AHMAD

2. • Acute chest pain is one of the most common reason for seeking care in
the emergency department (10% of all visits)
• Only 10-15% of patients with chest pain actually have ACS.
• The diagnosis of ACS is missed in approx. 2% of patients

3. CARDIAC CAUSES OF ACUTE CHEST PAIN
CAUSES CLINICAL DESCRIPTION
ANGINA • Retrosternal chest pain, burning or heaviness, radiating occasionally to the neck,
jaw, epigastrium, shoulder, left arm
• Precipitated by exercise, cold weather, or emotional stress
• Duration of 2-10 min
UNSTABLE ANGINA • Same as angina, but may be more severe
• Typically <20 min, lower tolerance for exertion, crescendo pattern
ACUTE MI • Same as angina, but may be more severe
• Sudden onset, usually lasting ≥30 min, often associated with shortness of breath,
weakness, nausea, vomiting
PERICARDITIS • Sharp, pleuritic pain aggravated by changes in position, highly variable duration
• Pericardial friction rub

4. NON-CARDIAC CAUSES OF ACUTE CHEST PAIN
VASCULAR
• Aortic dissection
• Pulmonary embolism
• Pulmonary hypertension
PULMONARY
• Pleuritis and/or pneumonia
• Tracheobronchitis
• Spontaneous pneumothorax
GASTROINTESTINAL
• Esophageal reflux
• Peptic ulcer disease
• Pancreatitis
MUSCULOSKELETAL
• Costochondritis
• Cervical disc disease
• Trauma & strain
INFECTIOUS
• Herpes zoster
PSYCHOLOGICAL
• Panic disorder

5. MYOCARDIAL ISCHEMIA OR INFARCTION
• The most common serious causes of acute chest discomfort is myocardial
ischemia or MI, which occurs when the supply of myocardial O2 is in
adequate for the demand.
• Myocardial ischemia usually occurs in the setting of coronary
atherosclerosis, but it may also reflect dynamic components of coronary
vascular resistance.
• Coronary spasm can occur in normal coronary arteries, or in patients with
CAD, near atherosclerotic plaque and in smaller coronary arteries.
• Other less common causes of impaired coronary blood flow include
syndromes that compromise the orifices or lumina of the coronary arteries,
such as coronary arteritis, proximal aortitis, spontaneous coronary artery
dissection, proximal aortic dissection, coronary emboli from infective
endocarditis or thrombus in LA or LV, myocardial bridge, or a congenital
abnormality of the coronary arteries.

6. CLASSIC MANIFESTATION OF ISCHEMIA
• The classic manifestation of ischemia is angina, which is usually
described as a heavy chest pressure or squeezing, a burning feeling, or
difficulty breathing.
• The discomfort often radiates to the left shoulder, neck, or arm.
• It typically builds in intensity over a few minutes.
• The pain may begin with exercise or psychological stress, but ACS
most frequently occurs without obvious precipitating factors.

7. PAIN DESCRIPTIONS UNCHARACTERISTIC OF MYOCARDIAL
ISCHEMIA (ACC/AHA GUIDELINES)
• Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory movements or
coughing)
• Primary or sole location of the discomfort in the middle or lower abdominal region
• Pain that may be localized by the tip of one finger, particularly over the LV apex
• Pain reproduced with movement or palpitation of the chest wall or arms
• Contact pain that persist for many hours
• Very brief episodes of pain that last a few seconds or less
• Pain that radiate into the lower extremities
Clinicians should be mindful of “angina equivalents” such as jaw or shoulder pain in
the absence of chest pain; nausea or vomiting; and diaphoresis.
In particular women, older persons, and individuals with diabetes may be more
likely to report atypical symptoms of myocardial ischemia or MI.

8. CLINICAL EVALUATION
• Guidelines from ACC/AHA emphasize that
• Patients with symptoms consistent with ACS should not be evaluated solely
over the telephone but should be referred to facilities that allow evaluation by
a physician and recording of ECG
• Strong consideration of immediate referral to an ED or a specialized chest pain
unit for patients with suspected ACS who experience chest discomfort at rest
for longer than 20 minutes, hemodynamic instability or recent syncope or
near-syncope.
• Transport as a passanger in a private vehicle is considered an acceptable
alternative to an emergency vehicle only if the wait would lead to a delay
longer than 20-30 minutes.

9. HISTORY
• History of acute events:
• Characteristics of the patient’s pain , including its quality, location, and
radiation;
• The time and tempo (abrupt or gradual) of onset, the duration of symptoms;
• Provoking or palliating activities; and
• Any associated symptoms, particularly pulmonary or GI symptoms.
• Risk factors for atherosclerosis (eg., advanced age, male sex, diabetes)
• Younger patients have a lower risk for ACS but should be screened
with greater care for a history of recent cocaine use.

10. PHYSICAL EXAMINATION
Should begin with
• Identification of potential precipitating causes of myocardial ischemia (eg.,
uncontrolled hypertension),
• Important comorbid conditions (eg., COPD), and
• Evidence of hemodynamic complications (eg., CHF, new MR,
hypotension).
• Examination of peripheral pulses (presence of bruit or absent pulse, suggest
extracardiac vascular disease)
• For patients whose clinical findings do not suggest myocardial ischemia, the
search for noncoronary causes of chest pain should focus on potentially life-
threatening issues (eg., aortic dissection, pulmonary embolism) and then
turn to the possibility of other cardiac diagnoses( eg., pericarditis) and
noncardiac diagnoses.

11. ECG
• An ECG should be obtained within 10 minutes after arrival for individuals with ongoing chest
discomfort, and
• as rapid as possible in those who have a history of chest discomfort consistent with ACS, but whose
discomfort has resolved by the time of evaluation, to identify patients who might benefit from immediate
reperfusion therapy.
• Obtaining a prehospital ECG decreases the door-to-diagnosis time and, for STEMI, the door-
to-balloon time.
• New persistent or transient ST-segment abnormalities (≥0.05mV) that develop during a
symptomatic episode at rest and resolve when the symptoms resolve strongly suggest acute
ischemia and severe CAD.
• A completely normal ECG does not exclude ACS, however, patients with normal or near
normal findings on ECG have a better prognosis than those with abnormal ECG at initial
evaluation.
• The availability of a previous ECG improves diagnostic accuracy and reduce admission rates
for patients with abnormal baseline tracings.
• Serial ECG tracings improve the clinician’s ability to diagnose AMI, if combined with serial
measurements of cardiac biomarkers.
• Posterior leads can help identify ischemia in the territory supplied by LCX, an otherwise
relatively silent zone on ECG.

12. CHEST X-RAY
• Chest radiograph is usually nondiagnostic in patients with ACS but
can show pulmonary edema secondary to ischemia-induced diastolic
or systolic dysfunction.

13. CARDIAC BIOMARKERS
• The preferred biomarker is cardiac troponin T(cTnT) or I (cTnI); CK-MB is less sensitive.
TOPONINS:
Causes of elevated troponins
• Causes of reduced myocardial O2 supply (eg., hypotension, vasospasm, severe anemia);
• Increased myocardial O2 demand (eg., hypertensive crisis, tachycardia, critical aortic
stenosis, severe HCM, extreme exercise);
• Direct myocardial injury (eg., myocarditis, myocardial contusion, cardioversion or
defibrillation);
• RV injury (eg., pulmonary embolism or other causes of acute pulmonary hypertension)
• Non cardiac causes- renal disease, severe sepsis
Current US guidelines recommended measurement at presentation and 3-6 hours after
symptom onset.
Elevations in cTnI may persist for 7-10 days and cTnT may persist for up to 10-14 days
after MI

14. High-sensitivity Troponin(hsTn)
• More recently, high-sensitivity troponin(hsTn) assay now enable even lower
limits of detection (eg., <0.001 ng/ml) and allow at least 50% of healthy
individuals below the 99th percentile to have a measurable level of troponin.
• These assays can shorten the time interval to the next measurement to 1-2
hours and still achieve negative predictive value ≥99.5%
• May also permit the safe discharge of patients based on a single troponin
value at presentation.
• Serial sampling with hsTn assays also offers the ability to examine the
change in troponin concentration between two time points, with relative and
particularly increases above certain thresholds offering the potential for
greater specificity fro MI
• Studies evaluating hsTn support the concept of accelerated diagnostic
protocols that demonstrate a high NPV of very low concentrations in
patients presenting with suspected ACS.

15. CKMB ISOENZYMES
• CKMB has less specificity than cardiac troponins because of its production
by skeletal muscle, tongue, diaphragm, small intestine, uterus, and prostate.
• Use of the CKMB relative index (ratio of CKMB to total CK) partially
addresses this limitation for skeletal muscle as a source.
• The amount of CKMB in skeletal muscle, however, increases in patients
with conditions that cause chronic muscle destruction and regeneration (eg.,
muscle dystrophy), those who participate in high performance athletics (eg.,
marathon running), and those with rhabdomyolysis.
• CKMB elevation are particularly common in alcohol abuse or trauma
patients.
• One advantage of CKMB is a shorter half life in the circulation, which
makes it useful for gauging the timing of an MI and for diagnosing
reinfarction in a patient who had an MI in the past week, however, hsTn
assays offer similar value.

16. OTHER BIOMARKERS
• COEPTIN: It is secreted from the pituitary gland early in the course of
MI.
• In the CHOPTIN study, both a negative coeptin and a sensitive troponin assay
in patients presenting within 6 hours of symptom onset had NPV of 99.2%.
• Myoglobin, heart type fatty acid-binding protein, and ischemia-
modified albumin(IMA) have been studied as diagnostic biomarkers,
but none is specific to myocardial tissue.
• Many patients with ACS have elevated concentrations of inflammatory
biomarkers such as CRP, serum amyloid A, myeloperoxidase, or IL-6.
• D-dimer testing is useful for chest pain patients to rule out PE or aortic
dissection, because a negative ELISA has NPV >99% in patients with
a low clinical probability (patients with a higher clinical probability
should undergo an imaging study).

17. • BNP and NT-pro BNP reflects increased ventricular wall stress
• BNP level can rise in the setting of transient myocardial ischemia, and the
magnitude of elevation in patients with ACS is related to prognosis
• Circulating microRNAs have been evaluated in studies but have not
yet been shown to provide incremental diagnostic or prognostic value
in patients presenting with suspected AMI

18. BIOMARKERS TESTING STRATEGY
• Current practice guidelines recommend measurement of biomarkers of
cardiac injury in patients with symptoms that suggest ACS.
• Patients with a very low probability of ACS should not undergo
measurement of biomarkers because false positive results could lead to
unnecessary hospitalization
• The ACC/AHA/ESC guidelines recommend cTnI or cTnT as the
preferred first line marker, although CKMB is an acceptable
alternative.
• If the initial set of marker is negative, another sample should be drawn 3-6
hours later
• If a hsTn assay is used, a 1 hour algorithm can be considered.

19. LIKELIHOOD FEATURES OF ACS

21. CHEST PAIN PROTOCOLS
• According to the ACC/AHA recommendations, patients with a low risk for
ACS can be observed for several hours while undergoing ECG monitoring
and serial measurements of cardiac markers.
• Patients in whom evidence of ischemia or other indicators of increased risk
develop should be admitted to a cardiology service/CCU
• Patients in whom recurrent pain or other predictors of increased risk do not
develop can be discharged.
• Patients with normal troponin levels, no ECG abnormalities concerning for
ischemia, and a TIMI risk score of 0 or a HERAT score of ≤3 have
extremely low risk of adverse cardiac events and can be discharged to
home.
• Outpatient stress testing is a reasonable option if the patient is at low risk
for ACS and if the testing can be accomplished within 72 hours
• Such patient can receive aspirin and possibly beta-blockers and sublingual
nitroglycerin.

22. MANAGEMENT OF PATIENTS SUSPECTED TO HAVE ACS

23. A 65y/m chronic smoker, NT, ND presented in emergency department
with first time acute retrosternal persistent chest pain radiating to jaw,
6 hour duration, associated with sweating.
Vitals
PR-120/min
BP-150/90 DIAGNOSIS ???
SpO2-97%
Examination-unremarkable
Trop-t- twice negative 4 hours apart

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