1. ST elevation myocardial infarction (STEMI) occurs when there is ST elevation or new left bundle branch block on ECG due to acute coronary artery occlusion. 2. Diagnosis is based on symptoms, elevated cardiac biomarkers, and ECG changes showing ST elevation. Treatment involves stabilization, pain control, and reperfusion therapy. 3. Prognosis depends on factors like age, previous MI history, infarct location and size, and presence of heart failure or hypotension. Early reperfusion, beta-blockers, ACE inhibitors and risk factor modification can limit damage.

1. Acute coronary syndromes
dr.Hussein Alshimary
Heba Fakhrulddin
ST elevation myocardial infarction
(STEMI)

2. ST elevation myocardial infarction
(STEMI)
Patients with ACS who have ST-segment
elevation or new left bundle branch block
(LBBB) on their presenting ECG benefit
significantly from immediate reperfusion and
are treated as one group under the term ST-
elevation myocardial infarction (STEMI).

3. LEFT BANDLE BRANCH BLOCK ANT.WALL STEMI

4. Presentation
• Chest pain is usually similar in nature to angina, but of greater severity
and longer duration and is not relieved by sublingual (SL) nitroglycerin.
Associated features are nausea and vomiting, sweating, breathlessness,
and extreme distress.
• The pain may be atypical (e.g., epigastric) or radiate to the back.
• Diabetics, elderly, women, or hypertensive patients may suffer painless
(“silent” infarcts) and/or atypical infarction. Presenting features
include breathlessness from acute pulmonary edema, syncope or coma
from arrhythmias, acute confusional states (mania/psychosis), diabetic
hyperglycemic crises.

5. STEMI: diagnosis
• STEMI diagnosis is based on a combination of
history, ECG, and biochemical markers of
cardiac injury.
• In practice, history and ECG changes are
diagnostic.
• Biochemical markers of cardiac injury usually
become available later and help reconfirm the
diagnosis and provide prognostic information
(magnitude of rise).

6. -- Aspects of Diagnosis of Myocardial Infarction by Different Techniques
Pathology Myocardial cell death
Biochemistry Markers of myocardial cell death recovered from blood samples
Electrocardiography Evidence of myocardial ischemia (ST and T wave abnormalities)
Evidence of loss of electrically functioning cardiac tissue (Q
waves)
Imaging Reduction or loss of tissue perfusion
Cardiac wall motion abnormalities

7. Revised Definition of Myocardial Infarction (MI)
Criteria for Acute, Evolving, or Recent MI
Either of the following criteria satisfies the diagnosis for acute, evolving, or recent MI:
1. Typical rise and/or fall of biochemical markers of myocardial necrosis with at
least one of the following:
a) Ischemic symptoms
b) Development of pathological Q waves in the ECG
c) ECG changes indicative of ischemia (ST segment elevation or
depression)
d) Imaging evidence of new loss of viable myocardium or new regional
wall motion abnormality
2. Pathological findings of an acute myocardial infarction

8. ECG changes
 ST-segment elevation occurs within minutes and may last
for up to
2 weeks. ST elevation of 2 mm in adjacent chest leads and 1
mm in
adjacent limb leads. Persisting
ST elevation after 1 month suggests formation of LV
aneurysm.
 Pathological Q waves indicate significant abnormal
electrical
conduction. In the context of a “transmural infarction” the Q
waves may
take hours or days to develop and usually remain indefinitely.
 T-wave inversion may be immediate or delayed and
generally persists after the ST elevation has resolved.

10. Anterior ST elevation and/or Q waves in V1–V4/V5
Anterseptal ST elevation and/or Q waves in V1–V3
Lateral ST elevation and/or Q waves in V5–V6 and T-wave
inversion/ST elevation/Q waves in I and aVL
Inferoseptal ST elevation and/or Q waves in II, III, aVF, and 5–V6
(sometimes I and aVL)
True posterior Tall R waves in V1–V2 with ST depression in V1–V3. T
waves remain upright in V1–V2. This can be confirmed with an esophageal
lead if available (method similar to an NG tube). This usually occurs in
conjunction with an inferior or lateral infarct
RV infarction ST-segment elevation in the right precordial leads (V3R–
V4R). Usually found in conjunction with inferior infarction. This may only
be present in the early hours of infarction
Localization of infarcts from ECG
changes

11. Conditions that may mimic ECG
changes of a STEMI
• Left or right ventricular hypertrophy
• LBBB or left anterior fascicular block
• Wolff–Parkinson–White syndrome
• Pericarditis or myocarditis
• Cardiomyopathy (hypertrophic or dilated)
• Trauma to myocardium
• Cardiac tumors (primary and metastatic)
• Pulmonary embolus
• Pneumothorax
• Intracranial hemorrhage
• Hyperkalemia
• Cardiac sarcoid or amyloid
• Pancreatitis

12. Biochemical markers of cardiac injury
CK (creatine kinase)
• Levels twice the upper limit of normal are considered abnormal.
• Serum levels rise within 4–8 hours post-STEMI and fall to normal within 3–4
days. The peak level occurs at about 24 hours but may be earlier (12 hours)
and higher in patients who have had reperfusion (thrombolysis or
percutaneous coronary intervention [PCI]).
• False-positive rates of ~15% occur in patients with alcohol intoxication, muscle
disease or trauma, vigorous exercise, convulsions, IM injections,
hypothyroidism, pulmonary embolism (PE), and thoracic outlet
syndrome.
CK-MB isoenzyme is more specific for myocardial disease. Levels may be
elevated despite a normal total CK. However, CK-MB is also present in
small quantities in other tissues (skeletal muscle, tongue, diaphragm,
uterus, and prostate) and trauma or surgery may lead to false-positive
results..

13. Cardiac troponins ( Tn T ,Tn I )
• Both TnT and TnI are highly sensitive and specific markers of cardiac injury.
• Serum levels start to rise by 3 hours post-MI and elevation may persist up to 7–14 days. This is
advantageous for diagnosis of late MI.
• In most STEMI cases, the diagnosis can be made using a combination of the clinical picture
and serial CK/CK-MB levels. In the event of normal CK-MB levels and suspected noncardiac
sources of CK, troponins can be used.
• Troponins can also be elevated in non ischemic myocyte damage, such as myocarditis,
cardiomyopathy, and pericarditis.
Other markers
There are multiple other markers, but with increasing clinical availability of Troponin,
measurements of these markers are not recommended. These include aspartamine
transferase (AST) (rise 18–36 hours post-MI) and lactate dehydrogenase (LDH) (rise 24–36
hours post-MI).

14. Biomarker Begins to rise Peak value Returns to
normal
Myoglobin 1-2 hours 6-8 hours 1-2 days
CK-MB 2-6 hours 16-20 hours 1-2 days
CK 4-8 hours 16-24 hours 3-4 days
Trop T 4-6 hours 12-24 hours 7-10 days
AST 12-24 hours 36-48 hours 3-4 days
LDH 24-48 hours 72 hours 8-10 days

16. Factors associated with a poor
prognosis
• Age >70 years
• Previous MI or chronic stable angina
• Anterior MI or right ventricular infarction
• Left ventricular failure at presentation
• Hypotension (and sinus tachycardia) at
presentation
• Diabetes mellitus
• Mitral regurgitation (acute)
• Ventricular septal defect

17. Treatment of STEMI
All patients with STEMI should be admitted to an intensive care unit (ICU),
e.g., coronary ICU (CICU).
Stabilizing measures are generally similar for all ACS patients.
 • All patients with suspected STEMI should have continuous ECG
monitoring in an area with full resuscitation facilities.
 • Patients should receive immediate aspirin 325 mg po plus one of
thyenopyridine antiplatlets (if no contraindications) , analgesia, and
oxygen. Secure IV access.
 • Conduct rapid examination to exclude hypotension, note the presence
of murmurs, and identify and treat acute pulmonary edema.
Right ventricular failure (RVF) out of proportion to left ventricular failure
(LVF) suggests RV infarction.
Diagnosis is normally made on presentation (history and ECG changes of ST –
elevation /new LBBBB )followed by rapid stabilizing measures to ensure institution
of reperfusion therapy without delay.
This is in contrast to NSTEMI/UA, where diagnosis may evolve over a period of
24–72 hours. (Reperfusion must not be delayed to wait for biochemical markers.)

18. Control of cardiac pain
• Morphine 2.5–10 mg IV is the drug of choice and may be repeated
to ensure adequate pain relief, unless there is evidence of emerging
toxicity (hypotension, respiratory depression). Nausea and vomiting
should be treated with metoclopramide (10 mg IV) or a phenothiazine.
• Oxygen should be administered at 2–5 L/min for at least 2–3 hours.
Hypoxemia is frequently seen post-MI due to ventilation–perfusion
abnormalities secondary to LVF. In patients with refractory pulmonary
edema, endotracheal intubation may be necessary. Beware of CO2
retention in patients with COPD.
• Nitrates may lessen pain and can be given (sublingual or IV) provided
that the patient is not hypotensive. These drugs should be used
cautiously in inferior STEMI, especially with right ventricular infarction,
as venodilation may decrease RV filling and precipitate hypotension.
Nitrate therapy has no demonstrated effect on mortality (ISIS-4).
Correction of electrolytes
Both low potassium and low magnesium may be arrhythmogenic and must
be supplemented, especially in the context of arrhythmias.

19. Strategies to limit infarct size
 B-Blockade
Early B-blockade has been shown to be beneficial by limiting infarct size,
reducing mortality, and decreasing early malignant arrhythmias.
All patients (including primary PCI and thrombolysis patients) should have
early B-blockade.
Patients with the following features may benefit most from B-blocker therapy:
• Hyperdynamic state (sinus tachycardia, hypertensive)
• Ongoing or recurrent pain or reinfarction
• Tachyarrhythmias such as AF
Use a short-acting agent IV initially (metoprolol 5 mg at a time repeated at
5-minute intervals to a maximum dose of 15 mg) under continuous ECG
and BP monitoring. Aim for a HR of 60 beats per minute (bpm) and SBP
100–110 mmHg. If hemodynamic stability continues 15–30 minutes after
the last IV dose, start metoprolol 50 mg po bid. Esmolol is an ultra-short
acting IV B-blocker, which may be tried if there is concern whether the
patient will tolerate B-blockers.

20. CONTRAINDICATIONS TO THE USE OF B- BLOCKERS
Absolute contraindications: heart rate (HR) <50, systolic blood
pressure (SBP) <90 mmHg, moderate to severe heart failure, AV
conduction defect, severe airways disease.
Relative contraindications: asthma, current use of calcium
channel blocker and/or B-blocker, severe peripheral vascular
disease with critical limb ischemia, large inferior MI involving the
right ventricle.

21. ACE inhibitors
After receiving aspirin, B-blockade (if appropriate), and reperfusion, all
patients with STEMI/LBBB infarction should receive an ACE inhibitor
within the first 24 hours of presentation.
• Patients with high risk or large infarcts, particularly with an
anterior STEMI, a previous MI, heart failure, and impaired LV
function on imaging, will benefit most.
• The effect of ACE inhibitors appears to be a class effect; therefore,
one may use the drug that the physician is familiar with.