This document discusses STEMI (ST-elevation myocardial infarction) in young patients. It covers the diagnosis of STEMI using ECG and cardiac biomarkers. Investigations discussed include echocardiography, coronary angiography, and cardiac imaging tests. Treatment focuses on rapid reperfusion through medications, PCI, or CABG. Complications and long-term management are also outlined. The document provides an overview of evaluating and treating STEMI in the young.

1. STEMI IN THE
YOUNG????
Dr Ikponmwosa Akhionbare
MBBS.
Cardiology Unit
Obafemi Awolowo University
Teaching Hospital Complex

2. OUTLINE
• INTRODUCTION
• INVESTIGATIONS
• TREATMENT
• COMPLICATIONS
• PROGNOSIS
• CONCLUSION

3. INTRODUCTION
• A working diagnosis of STEMI (called the ‘STEMI diagnosis’) must first
be made. This is usually based on symptoms consistent with
myocardial ischaemia (i.e. persistent chest pain) and signs [i.e. 12-
lead electrocardiogram (ECG)].
• Important clues are a history of CAD and radiation of pain to the neck,
lower jaw, or left arm.

4. INVESTIGATIONS
The objectives of laboratory testing and imaging include the following:
• To determine the presence or absence of myocardial infarction (MI) for diagnosis
and differential diagnosis (point–of-care testing and testing in central laboratory
of cardiac troponin levels)
• To characterize the locus, nature (ST-elevation MI [STEMI] or non–ST-elevation MI
[NSTEMI]), and extent of MI (ie, to estimate infarct size)
• To detect recurrent ischemia or MI (extension of MI)
• To detect early and late complications of MI
• To estimate the patient's prognosis

5. ECG
• The electrocardiogram (ECG) is the most important tool in the initial
evaluation and triage of patients in whom an acute coronary
syndrome (ACS) is suspected.

6. • Obtaining an ECG by emergency medical services (EMS) personnel at
the site of first medical contact in patients with symptoms consistent
with ST-elevation myocardial infarction (STEMI) not only confirms the
diagnosis in more than 80% of cases, but also helps to detect life-
threatening arrhythmias and allows early and prompt defibrillation
therapy, if indicated.

8. In the proper clinical context, ST-segment elevation (measured at the J-
point) is considered suggestive of ongoing coronary artery acute occlusion
in the following cases: at least two contiguous leads with
• ST-segment elevation > 2.5mm in men < 40 years, > 2mm in men >40
years, or > 1.5mm in women in leads V2–V3 and/or > 1mm in the other
leads [in the absence of left ventricular (LV) hypertrophy
• or left bundle branch block LBBB)].

9. Localization of the involved myocardium based on distribution of ECG
abnormalities in MI is as follows:
• Inferior wall - II, III, aVF
• Lateral wall - I, aVL, V4 through V6
• Anteroseptal - V1 through V3
• Anterolateral - V1 through V6
• Right ventricular - RV4, RV5
• Posterior wall - R/S ratio greater than 1 in V1 and V2, and T-wave changes in V1,
V8, and V9

10. Hyperacute Anteroseptal STEMI
•ST elevation is maximal in the anteroseptal leads (V1-4).
•Q waves are present in the septal leads (V1-2).
•There is also some subtle STE in I, aVL and V5, with
reciprocal ST depression in lead III.
•There are hyperacute (peaked ) T waves in V2-4.
•These features indicate a hyperacute anteroseptal STEMI

11. Extensive anterior MI (“tombstoning” pattern)
•Massive ST elevation with “tombstone” morphology is present throughout the
precordial (V1-6) and high lateral leads (I, aVL).
•This pattern is seen in proximal LAD occlusion and indicates a large territory
infarction with a poor LV ejection fraction and high likelihood of cardiogenic
shock and death

12. CARDIAC BIOMARKERS
• Cardiac markers are used in the diagnosis and risk stratification of
patients with chest pain and suspected acute coronary syndrome
(ACS). The cardiac troponins, in particular, have become the cardiac
markers of choice for patients with ACS.

13. CARDIAC BIOMARKERS
• Troponin is a contractile protein that normally is not found in serum.
It is released only when myocardial necrosis occurs. Of the three
troponin subunits, two (troponin I and troponin T) are derived from
the myocardium.

14. • Serial measurement of cardiac troponins after the initial level is
obtained at presentation, 3 to 6 hours after symptom onset, is
recommended. If initial levels are negative, additional measurements
beyond the 6-hour mark should be obtained.

15. Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to
baseline over 5-14 days.

16. OTHER MARKERS
• Creatine Kinase MB
• Myoglobin
• Brain Naturietic Peptide
• C reactive protein
• Myeloperoxidase
• Ischemia modified albumin

17. Protein Molecular mass (kD) First detection Duration of detection Sensitivity Specificity
Myoglobin 16 1.5–2 hours 8–12 hours +++ +
CK-MB 83 2–3 hours 1–2 days +++ +++
Troponin I 33 3–4 hours 7–10 days ++++ ++++
Troponin T 38 3–4 hours 7–14 days ++++ ++++
CK 96 4–6 hours 2–3 days ++ ++
BIOCHEMICAL MARKERS

18. CARDIAC IMAGING
• The role of imaging in the work-up of acute myocardial infarction (MI)
is broad, but the procedures are primarily used to confirm or rule out
coronary artery disease (CAD).
• Furthermore, imaging may help to define the anatomy and degree of
myocardial perfusion abnormalities.

19. • CHEST XRAY
• ECHOCARDIOGRAPHY
• CORONARY ANGIOGRAPHY
• POSITRON EMISSION TOMOGRAPHY
• MAGNETIC RESONANCE IMAGING
• CT ANGIOGRAPHY

20. CHEST XRAY
Chest radiography is useful in determining the presence of
cardiomegaly,
• pulmonary edema,
• pleural effusions,
• Kerley B lines, and other criteria of HF.

21. ECHOCARDIOGRAPHY
• Echocardiography is indicated to evaluate regional and segmental
ventricular function, which influences therapy, to evaluate for
mechanical complications and intraventricular thrombosis, and to
provide prognostic information in acute myocardial infarction.

22. • Evaluation of wall motion while a patient is experiencing chest pain can
be useful when the ECG is nondiagnostic
• Evaluation of wall motion may also be useful if there is ECG or laboratory
evidence of MI even in the absence of chest pain
• Severe ischemia produces regional wall motion abnormalities (RWMAs)
that can be visualized echocardiographically within seconds of coronary
artery occlusion
• These changes occur prior to the onset of ECG changes or the
development of symptoms

23. Four chamber view from a 2-D echocardiogram shows a large area of
hypokinesis and akinesis of the anterior wall and apex of the left
ventricle. The left ventricular wall and interventricular septum are
thin and fail to thicken during systole.

24. There are a number of other causes of RWMAs, including a
• prior infarction,
• focal myocarditis,
• prior surgery,
• left bundle branch block,
• ventricular preexcitation via an accessory pathway, and
• cardiomyopathy.

26. Four-chamber view from a two-dimensional echocardiogram
shows a ventricular septal defect (VSD) near the left ventricular
apex. Blood flows through the VSD from left to right ventricle
during systole but not diastole.

27. Five chamber view from a 2-D echocardiogram with close up of
the left ventricle shows a large thrombus at the left ventricular
apex and interventricular septum. The apex and apical portion
of the septum are akinetic, suggesting a prior myocardial
infarction.

28. Subcostal view from a 2-D echocardiogram shows a large serofibrinous
pericardial effusion. Echos are seen within the effusion, suggesting the
presence of fibrous stands.

30. CORONARY ANGIOGRAPHY
• Coronary angiography is the criterion standard for identifying
coronary blockages
• Selective coronary angiography requires the injection of a material
that is opaque on radiography; typically, iodine is administered
through a catheter that is threaded through an artery to the aorta
and to the origin of each coronary artery.

33. INDICATIONS FOR ANGIOGRAPHY
Class I
• Class I indications are as follows:
• Spontaneous myocardial ischemia or ischemia provoked with minimal
exertion
• Presurgical therapy for acute MI, ventricular septal defect, true aneurysm,
or pseudoaneurysm
• Persistent hemodynamic instability

34. CONTRAINDICATIONS
• No absolute contraindications are
described for coronary arteriography.
• Relative contraindications include the
following:
• Unexplained fever
• Untreated infection
• Severe anemia with hemoglobin level
less than 8 g/dL
• Severe electrolyte imbalance
• Severe active bleeding
• Uncontrolled systemic hypertension
• Digitalis toxicity

35. ACCESS
Access is easiest from right
side of patient due to aortic
bend
• Puncture is generally done
via the femoral artery
• Alternative sites include the
radial and
brachial arteries of the arm

36. FLUOROSCOPY MACHINE
• The x-ray machine is suspended from the ceiling. It can be
manipulated in multiple angles and views to achieve a desired
picture.
• The x-ray comes from the bottom of the machine and the image
intensifier that transmits the image is above the patient

39. Tight stenosis noted involving the
mid segment of right coronary
artery. Distal branches are normal
A partially obstructive
narrowing noted in the
proximal segment of the
LAD

40. • POSITRON EMISSION TOMOGRAPHY
• MAGNETIC RESONANCE IMAGING
• Computed TOMOGRAPHY
• CT ANGIOGRAPHY

41. TREATMENT
• The first goal for healthcare professionals in management of acute myocardial
infarction (MI) is to diagnose the condition in a very rapid manner.
• As a general rule, initial therapy for acute MI is directed toward restoration of
perfusion as soon as possible to salvage as much of the jeopardized myocardium
as possible.
• This may be accomplished through medical or mechanical means, such as
percutaneous coronary intervention (PCI), or coronary artery bypass graft
(CABG) surgery.

42. PREHOSPITAL CARE
Specific prehospital care includes the following:
• Supplemental oxygen by a mask or nasal cannula is indicated only for patients who are
breathless, hypoxic (oxygen saturation < 90% or PaO2< 60 mm Hg [70] ), or who present
with heart failure.
Reduction of cardiac pain
• Nitrates are usually given as a 0.4 mg dose in a sublingual tablet, followed by close
observation of the effect on chest pain and the hemodynamic response. If the initial
dose is well tolerated, further nitrates can be administered

43. Analgesia
• Refractory or severe pain should be treated symptomatically with IV
morphine.
• The initial dose of morphine of 2 to 4 mg as an IV bolus can be given, with
increments of 2 to 4 mg repeated every 5 to 10 minutes until the pain is
relieved or intolerance is manifested by hypotension, vomiting, or depressed
respiration.
• The patient's blood pressure and pulse must be monitored; the systolic blood
pressure must be maintained above 100 mm Hg and, optimally, below 140 mm
Hg

45. Aspirin
• All patients presenting with ACS should receive nonenteric-coated
chewable aspirin in a dose of at least 162 to 325 mg, unless there is a
clear history of aspirin allergy. Patients with aspirin intolerance still
should receive aspirin at presentation.
• Patients undergoing primary PCI should receive DAPT, a combination of
aspirin and a P2Y12 inhibitor, and a parenteral anticoagulant

46. • The preferred P2Y12 inhibitors are prasugrel [60mg loading dose and
10mg maintenance dose once daily per os (p.o.)] or ticagrelor (180
mg p.o. loading dose and 90mg maintenance dose twice daily.
• These drugs have a more rapid onset of action, greater potency, and
are superior to clopidogrel in clinical outcomes.

50. Inhibitors of the renin-angiotensin-aldosterone (RAA) system
• Initiate angiotensin-converting enzyme (ACE) inhibitors and continue
administration indefinitely in all patients with a left ventricular
ejection fraction that is less than 40% and in those with hypertension,
diabetes mellitus, or stable chronic kidney disease, unless
contraindicated.

51. Beta blockers
• All patients should be maintained on a beta blocker. Current clinical
practice guidelines recommend use of one of three beta blocker
agents proven to reduce mortality in patients with heart failure:
metoprolol, carvedilol, or bisoprolol.

52. Statins
• All patients with an acute MI should be started on high-potency statin
therapy and continued indefinitely.
• Current clinical practice guidelines, high potency statins such as
atorvastatin 40 mg or 80 mg, or rosuvastatin 20 mg are
recommended.

53. Percutaneous coronary intervention PCI
• Early mechanical intervention (primary PCI) or pharmacologic reperfusion should
be performed as soon as possible for patients with clinical presentation of STEMI
within 12 hours of symptom onset and who have persistent ST-segment elevation
or new or presumed new left bundle branch block (LBBB)..
• Primary PCI is the preferred reperfusion strategy in patients with STEMI within
12hrs of symptom onset, provided it can be performed expeditiously.

55. FIBRINOLYSIS
• Fibrinolytic therapy is an important reperfusion strategy in settings
where primary PCI cannot be offered in a timely manner.
• The later the patient presents (particularly after 3 h), the more
consideration should be given to transfer for primary PCI (as opposed to
administering fibrinolytic therapy) because the efficacy and clinical
benefit of fibrinolysis decrease as the time from symptom onset
increases.

60. CORONARY BYPASS SURGERY(CABG)
• CABG remains indicated for cardiogenic shock, failed PCI, high-risk
anatomy, surgical repair of a mechanical complication of STEMI (eg,
ventricular septal rupture, free-wall rupture, or severe mitral
regurgitation from papillary muscle dysfunction or rupture).

61. Long-term therapies for ACS
• Antithrombotic therapy –
• Aspirin - CURRENT-OASIS 7 trial, TRANSLATE – ACS study,
• Ticagrelor - TREAT trial, PLATO trial, PEGASUS-TIMI 54,
• Prasugrel - TRITON - TIMI trial,
• Ticagrelor or Prasugrel – PRAGUE – 18 study,
• Rivaroxaban - ATLAS ACS 2–TIMI 51 trial.
• Beta-blockers - METOCARD-CNIC trial, EARLY-BAMI trial
• Lipid-lowering therapy - IMPROVE-IT, FOURIER trial
• Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers -
VALIANT trial
• Mineralocorticoid/aldosterone receptor antagonists - ALBATROSS trial,
REMINDER

62. LIFESTYLE MODIFICATION/POST MI CARE
• SMOKING CESSATION
• DIET, ALCOHOL AND WEIGHT CONTROL
Salt intake of< 5 g per day;30–45 g fibre per day; 200 g fruits and 200 g
vegetables per day; fish 1–2 times per week (especially oily varieties);
30 g unsalted nuts daily; limited alcohol intake [maximum of 2 glasses
(20 g of alcohol) daily for men and 1 for women.

63. COMPLICATIONS
Mechanical complications
The three major mechanical complications of MI, each of which can
cause cardiogenic shock, are as follows:
• Ventricular free wall rupture
• Ventricular septal defect
• Papillary muscle rupture with severe mitral regurgitation

64. • Ventricular septal defect
• Right ventricular infarction
• Ventricular pseudoaneurysm
• Left ventricular mural thrombus
• Pericarditis

65. PROGNOSIS
Better prognosis is associated with the following factors:
• Successful early reperfusion (ST-elevation MI [STEMI] goals: patient
arrival to fibrinolysis infusion within 30 minutes OR patient arrival to
percutaneous coronary intervention [PCI] within 90 minutes)
• Preserved left ventricular function
• Short-term and long-term treatment with beta-blockers, aspirin, and
angiotensin-converting enzyme (ACE) inhibitors

66. Poorer prognosis is associated with the following factors:
• Advanced age
• Diabetes mellitus
• Previous vascular disease (eg, cerebrovascular disease or peripheral vascular disease)
• Delayed reperfusion
• Involvement of lead aVR on ecg
• Depression

67. • Return to work after AMI represents an important indicator of
recovery. Younger women in particular are at greater risk of not
returning to work, given evidence of their worse recovery after MI
than similarly aged men.
• Extended sick leave is usually not beneficial and light-to-moderate
physical activity after discharge should be encouraged.

68. CONCLUSION
• Cannabis use in the world is rising with increased legalization. It has
been noted that there is a five-fold increase risk of Myocardial
Infarctions (MI) in the first hour after cannabis use.
• The rising use of cannabis may have ushered in an additional MI risk
factor to be added to the list; that is cannabis

69. CONCLUSION
• Patients with active symptoms of acute coronary syndrome (ACS)
should be instructed to call emergency services
• Patients should be instructed to go to the emergency department
immediately if the suspected ACS symptoms last longer than 20
minutes at rest or are associated with near syncope/syncope or
hemodynamic instability.

70. THANK YOU
FOR LISTENING.
For good heart’s sake, run jump and shake!
And do not smoke cannabis! Drink water!