ABEL Chest pain & STEMI.ppt

2022/8/12
Approach to chest pain and
STEMI
Presenter –Dr. Abel B(IM-R1)
Moderator- Dr.Esubalew W.
(MD,Internist,consultant cardiologist)

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Outline
•Objectives
•Approach to chest pain
•Classification and epidemiology of STEMI
•Clinical and laboratory features of STEMI
•Diagnosis and Management of STEMI
•Complications of STEMI

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OBJECTIVES
At the end of this seminar we should be able to:
-Know the common & life threatening causes of
chest pain
- Describe the acute & long term treatment of
STEMI
- Describe the treatment approach of STEMI
- Know the principles of reperfusion therapies
- Know the complication of STEMI & its
managment

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APPROACH TO CHEST PAIN

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Epidemiology
• Chest discomfort is among the most common
reasons for which patients present for medical
attention at either an emergency department
(ED) or an outpatient clinic
• 7.6 million annual visits in USA.
• Chest pain is common in outpatient practice,
with a lifetime prevalence of 20–40% in the
general population
• Fewer than 15 % are eventually dx with ACS
• Less than 10 % have other serious conditions.

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Causes of chest pain
• It is helpful to frame the initial diagnostic
assessment and triage of patients with acute
chest discomfort around three categories:
i. Myocardial ischemia
ii.Other cardiopulmonary causes
iii.Non-cardiopulmonary causes

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Causes of chest pain...

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Approach to the patient
• The priorities in the initial clinical evaluation of
a patient with acute chest pain are:
1) the patient’s clinical stability and
2) the probability that the patient has an
underlying cause of the discomfort that may be
life-threatening

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Approach to the patient...
Life threatening causes:
• Acute coronary syndrome
• Acute aortic syndrome
• Pulmonary embolism
• Tension pneumothorax
• Pericarditis with Pericardial tamponade
• Oesophageal rupture

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 History
 Physical Examination
 ECG
 Chest radiography
 Cardiac Biomarkers
 Confirmatory Tests

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.History
• Characterization of the pain
• Quality
• Location (including radiation)
• Pattern (including onset and duration)
• Provoking or alleviating factors.
• Associated symptoms
Past Medical History
- Prior similar attack
- Conective tissue disease
- Prior panik attack

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•Physical examination
- General appearance
-anxious, uncomfortable, pale, cyanotic, or diaphoretic
-Levine sign
-Body habitus
- Vital signs
-BP( check in both arms), PR, Temprature, RR, Sao2
- Pulmonary
- respiratory distress,
- palpation.... tender area
- auscultatory findings
- Cardiac
- raised JVP, murmurs, S3 & S4 heart sounds, friction rub

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- Abdominal
- Localized tenderness
- Extremities
- Vascular pulse deficites........atherosclerosis
- Evidence of acute limb ischemia....aortic dissection
- Unilateral lower extrimity swelling...VTE
- Musculoskeletal & Intedumentary
- localized swelling, redness, or marked localized tenderness........costocondritis
- Vesicular rash....Herps zoster
- Subcutaneus emphysema
-Neurology
- Focal neurologic deficits.....CVA
- Sensory deficites......esp. in the upper limbs---Cervical disc disease

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•Ancillary tests
- ECG
- Chest radiography
- Cardiac biomarkers
- D-dimer
- CBC
- (BNP) and NT-pro BNP
- Coronary & myocardial stress imaging

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Approach to the patient

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Epidemiology
• IHD is the leading cause of death world wide.
• Develops on average 7–10 years later in women
compared with men.
• About half of AMI-related deaths occur before the
stricken individual reaches the hospital. Of note, the
in-hospital mortality rate after admission for AMI has
declined from 10 to ~5%.
• The 1-year mortality rate after AMI is ~15%.
Mortality is approximately fourfold higher in elderly
patients (aged >75) as compared with younger
patients.

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Pathophysiology
• STEMI usually occurs when coronary blood flow decreases abruptly after a
thrombotic occlusion of a coronary artery previously affected by
atherosclerosis
• Complete occlusion leading to transmural myocardial ischemia with ST-
segment elevation on the ECG and myocardial necrosis leading to a
diagnosis of ST elevation MI
• Unstable ischemic symptoms may also occur predominantly because of
increased myocardial oxygen demand (e.g. intense psychological stress or
fever) or because of decreased oxygen delivery due to anemia, hypoxia,
or hypotension.
• However, the term acute coronary syndrome, which encompasses
unstable angina, NSTEMI, and STEMI, is in general reserved for ischemia
precipitated by acute coronary atherothrombosis.

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Pathophysiology...
• The amount of myocardial damage caused by coronary
occlusion depends on:
1) the territory supplied by the affected vessel
2) whether or not the vessel becomes totally occluded
3) the duration of coronary occlusion
4) the quantity of blood supplied by collateral vessels to the
affected tissue
5) the demand for oxygen of the myocardium whose blood
supply has been suddenly limited
6) endogenous factors that can produce early spontaneous
lysis of the occlusive thrombus and
7) the adequacy of myocardial perfusion in the infarct zone
when flow is restored in the occluded epicardial coronary
artery

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Risk factors
• Age
• Family history – Multiple gene inheritance
• Lipid abnormalities – Leading to atherosclerosis – LDL > 160
mg/dl, HDL < 40 mg/dl
• Environmental – Smoking, lifestyle, drugs (cocaine) –
hypertension & diabetes.
• Others include hypercoagulability, collagen vascular disease,
and intracardiac thrombi or masses that can produce coronary
emboli.

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Clinical presentation
• Predisposing Factors
– 50% of patients with STEMI have an identifiable
precipitating factor.
• Unusually heavy exercise
• Emotional stress
• Hypoxemia from any cause
• Pulmonary embolism
• Administration of Ergot preparations, Cocaine use,
Sympathomimetic.

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Clinical presentation...
• Pain is the most common presenting complaint in patients with STEMI.
-deep and visceral
- heavy, squeezing, and crushing; although, occasionally, it is described
as stabbing or burning
- occurs at rest, is usually more severe, and lasts longer
- involves the central portion of the chest and/or the epigastrium, and it
radiates to the arms.
- may radiate as high as the occipital area but not below the umbilicus
- often accompanied by weakness, sweating, nausea, vomiting, anxiety,
and a sense of impending doom.
 Painless STEMI is greater in patients with diabetes mellitus, female &
elderly

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-General Appearance:
- Anxious and in considerable distress
- Often massage or clutch their chests
- Clenched fist held against the sternum (Levine sign)
-Vital signs:
-BP & PR...Tachycardia &/or hypertension.....Anterior MI
Bradycardia &/or hypotension.....Inferior MI
-Temperature:
• Fever develops in most patients with extensive STEMI within 24 to 48 hours.
– usually resolves by the fourth or fifth day after infarction.
– Respiration:
• Rate rises slightly soon after the development of STEMI (from anxiety & pain)
• Pts. with LV failure: Respiratory rate as severity of the failure

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Chest
– Rales - in LV failure and/or a
reduction of LV compliance.
– Diffuse wheezing - can occur
with severe LV failure.
– Killip Classification :
Prognostic classification scheme
on the presence and severity of
rales
Cla
sse
s
Description
Clas
s I
No Signs of Congestion
Clas
s II
Rales, only to a mild to
moderate degree (<50% of
lung fields), ± S3 gallop
Clas
s III
Rales in more than half of
each lung field and
frequently have pulmonary
edema.
Clas
s IV
Cardiogenic shock

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Laboratory Findings
• The laboratory tests of value in confirming the
diagnosis may be divided into four groups:
1. ECG,
2. serum cardiac biomarkers,
3. cardiac imaging , and
4. nonspecific indices of tissue necrosis and inflammation.

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Loboratory findings
CBC
• Leuococytosis: develops within 2 hours after the onset of chest pain
– Peak 2 to 4 days after infarction, and returns to normal in 1 week;
– Generally 12-15×103/mL, occasionally up to 20×103/mL in patients
with large STEMI
– Predominantly PMN leucocytes
ESR: normal during the first day or two after infarction,
 rises to a peak on the first week and may remain elevated for
1-2 weeks

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Loboratory findings...
– Serum Markers of Cardiac Damage
• Circulating proteins released from damaged myocardial cells.
• CK-MB
– rises within 4–8 h and generally returns to normal by 48–72 h
– Best alternative, if a cardiac-specific troponin assay is not
available
– May be increased in cardiac surgery, myocarditis & electrical
cardioversion.
– Found in other tissues in small quantities, (Lacks Specificity)
» Small Intestine, Tongue, Diaphragm, Uterus, & Prostate.
– Inaccurate in circumstances involving skeletal muscle injury

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– Cardiac Troponins
• Preferred biomarkers to detect myocardial injury
• Begin to rise by approximately 3 hrs. after the onset of chest
pain
– B/c of continuous release from necrotic myocytes, level
remain high for days
» cTnI may persist for 7 to 10 days after MI;
» cTnT may persist for up to 10 to 14 days

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• Conditions Associated With Elevated Cardiac Troponin Levels in the
Absence of IHD
• Acute neurologic disease
• Myocardial infiltrative diseases
• Inflammatory cardiac diseases
• Drug toxicity
• Respiratory failure
• Sepsis
• Burns
• Extreme exertion (e.g.,
endurance athletes)
 Cardiac contusion
 Cardiac procedures
 Acute or chronic CHF
 Aortic dissection
 Aortic valve disease
 Hypertrophic cardiomyopathy
 Arrhythmias
 Apical ballooning syndrome
 Rhabdomyolysis with cardiac injury
 Pulmonary hypertension
 Pulmonary embolism

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Criteria for myocardial injury
• The term myocardial injury should be used
when there is evidence of elevated cardiac
troponin values (cTn) with at least one value
above the 99th percentile upper reference
limit (URL).
• The myocardial injury is considered acute if
there is a rise and/or fall of cTn values.

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Criteria for type 1 MI
Detection of a rise and/or fall of cTn values with at least one
value above the 99th percentile URL and with at least one of the
following:
• Symptoms of acute myocardial ischaemia;
• New ischaemic ECG changes;
• Development of pathological Q waves;
• Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality in a pattern consistent with
an ischaemic aetiology;
• Identification of a coronary thrombus by angiography including
intracoronary imaging or by autopsy.

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Criteria for Type 2- MI
≥ 1 of the following
• Symptoms of acute myocardial ischemia;
• New ischemic ECG changes;
• Development of pathological Q waves;
• Imaging evidence of new loss of viable myocardium or new RWMA in a pattern
consistent with an ischemic etiology
• Detection of a rise &/or fall of cTn values with at least one value above 99th
percentile URL.
• Evidence of an imbalance between myocardial oxygen supply and demand
unrelated to acute coronary atherothrombosis.

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– Precordium is usually quiet, and the apical impulse may be
difficult to palpate.
Murmur: Transient mid-systolic or late systolic apical murmur
20 to dysfunction of the mitral valve apparatus (Papillary muscle
dysfunction, LV dilation)
Friction rub: in those sustaining large transmural infarctions.
• Occur most commonly on the 2nd or 3rd day (1st 24hrs. to 2 Weeks)

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Criteria for Type 3- Myocardial Infarction
• Patients who suffer cardiac death,
• with symptoms suggestive of myocardial ischemia and
• Presumed new ischemic ECG changes or ventricular fibrillation,
• DEATH occurred-
• before blood samples for biomarkers can be obtained, or
• before increases in cardiac biomarkers can be identified, or
• MI is detected by autopsy examination.

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Criteria for Type 4 Myocardial Infarction
• Cardiac procedural myocardial injury
– Related to coronary revascularization procedures (PCI or CABG)
• Early or late stent thrombosis or
• In-stent re-stenosis for PCI, or
• Graft occlusion or stenosis with CABG
– Baseline cTn determination is important.
• If elevated, it has to be stable for correct diagnosis, post
procedure.
• Repeat after 3-6hrs post procedure.

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Type 4a- Myocardial Infarction
PCI-related MI: ≤ 48 hrs. after the index procedure.
– Elevation of cTn values (to >5 × the 99th percentile of the URL) in patients
with normal baseline values Or
– A rise in cTn values >20% if the baseline values are elevated and are
stable(≤ 20% variation) or falling
– New ischemic changes on the ECG,
– Development of pathological Q waves
– Angiographic findings consistent with a procedural complication, or
– Imaging evidence of new loss of viable myocardium or new RWMA
consistent with an ischemic etiology.

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Type 4b- Myocardial Infarction
Type 4b: Stent/scaffold thrombosis associated with PCI:
– Subcategory of PCI-related MI.
– Diagnosed by angiography or autopsy using the same criteria utilized
for type 1 MI.
Acute: 0 - 24 hrs.-Subacute: > 24 hrs. to 30 days
Late: > 30 days to 1 year-Very late: > 1 year after stent/scaffold
implantation.
Type 4c: focal or diffuse restenosis, or a complex lesion associated with a rise and/or
fall of cTn values above the 99th percentile URL applying, the same criteria utilized for
type 1 MI.

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CABG-related MI: ≤ 48 hrs. after the index procedure.
- Elevation of cardiac biomarker values (to >10 × the 99th percentile of the
URL) in patients with normal baseline cTn values.
Or
–A rise in cTn values >20% if the baseline values are elevated and are
stable(≤ 20% variation) or falling
New pathologic Q waves
–Angiographically documented new graft or new native coronary artery
occlusion, or
–Imaging evidence of new loss of viable myocardium or new RWMA
consistent with an ischemic etiology.
Type 5- Myocardial Infarction

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Criteria for Prior or Silent/Unrecognized MI
• Any one of the following criteria meets the diagnosis for
prior or silent/ unrecognized MI:
- Abnormal Q waves with or without symptoms in
the absence of nonischemic causes
- Imaging evidence of loss of viable myocardium in a
pattern consistent with ischemic etiology
- Pathoanatomical findings of a prior MI

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ECG criteria for Diagnosis of STEMI
• ST-segment elevation
On at least two contiguous leads
Leads
Men Women
<40 yrs. ≥ 40 yrs.
V2 and V3
ST elevation ≥
2.5mm
ST elevation ≥
2 mm
ST elevation ≥
1.5 mm
OR
In the other
leads
ST elevation ≥ 1 mm [in the absence of LVH
or LBBB]

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Atypical ECG presentation

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Localization of ischemia

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Echocardiography
 Abnormalities of wall motion almost universally present.
 When the ECG is not diagnostic of STEMI, early detection of
the presence or absence of wall motion abnormalities can aid
in management decisions.
 Estimation of LV function is useful prognostically & for
initiation of therapy.
 Identify the presence of RV infarction, ventricular aneurysm,
pericardial effusion, and LV thrombus.
 Doppler echo is useful in the detection and quantitation of a
VSD and MR

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Prehospital Management
• The public and Pre-hospital Care personnel should be
educated on the importance of early diagnosis and the
benefits of early treatment.
• Most out-of-hospital deaths from STEMI are due to the
sudden development of ventricular fibrillation.
• The vast majority of deaths due to ventricular fibrillation
occur within the first 24 h of the onset of symptoms, and of
these, over half occur in the first hour.

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Prehospital management...
1. recognition of symptoms by the patient and prompt seeking of
medical attention;
– The greatest delay usually occurs between the onset of pain and the
patient’s decision to call for help.
(2) rapid deployment of an emergency medical team capable of
performing resuscitative maneuvers;
(3) expeditious transportation of the patient to a hospital
(4) expeditious implementation of reperfusion therapy.

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Management at ED
-Goals
-control of cardiac discomfort,
-rapid identification of patients who are candidates for urgent
reperfusion therapy,
-triage of lower-risk patients to the appropriate location in the hospital,
and
-avoidance of inappropriate discharge of patients with STEMI.
• The overarching goal is to minimize the time from first medical contact to
initiation of reperfusion therapy. This may involve transfer from a non-PCI
hospital to one that is PCI capable, with a goal of initiating PCI within 120
min of first medical contact

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Management at ED...
• DAPT
ASPIRIN
MOA
– Irreversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in
decreased formation of prostaglandin precursors
– irreversibly inhibits formation thromboxane A2 thus inhibiting platelet aggregation
• Aspirin is recommended indefinitely in all patients with STEMI.
• 160–325-mg (chewed) followed by low aspirin doses (75–100mg)
– low aspirin doses has similar anti-ischaemic and less adverse events than higher doses
Clopidogrel
Loading 300mg followed by 75mg po/d
• High dose statin

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Control of discomfort
• SUBLINGUALNITROGLYCERIN
• MOA
– Diminish or abolish chest discomfort
– decreasing myocardial oxygen demand (by lowering preload) and
– increasing myocardial oxygen supply (by dilating infarct-related
coronary vessels or collateral vessels).
• Up to 3 doses of 0.4 mg at about 5-min intervals.
• If symptoms persists, IV nitroglycerin 5–10 μg/min is
recommended.
• The rate of the infusion may be increased by 10 μg/min every
3–5 min until symptoms are relieved, SBP falls to <90 mmHg,
or the dose reaches 200 μg/min.

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Contraindications to nitroglycerine
• SBP <90 mmHg
• phosphodiesterase-5 inhibitor within the preceding 24 -48
hours
– it may potentiate the hypotensive effects of nitrates.
• In whom there is clinical suspicion of RV infarction (inferior
infarction on ECG, elevated JVP, and hypotension).
• An idiosyncratic reaction to nitrates
– Can be reversed by the rapid administration of IV atropine

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Morphine
• a very effective analgesic for the pain associated with
STEMI.
• 2–4 mg IV, every 5 min
• Side effects
– it may reduce sympathetically mediated arteriolar and venous constriction, and the
resulting venous pooling may reduce CO and BP.
• respond promptly to elevation of the legs,
• volume expansion with saline is required (in some patients).
– has a vagotonic effect and may cause bradycardia or advanced degrees of
heart block, particularly in patients with inferior infarction.
• respond to atropine (0.5 mg IV).

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Beta Blockers
• control of the pain of STEMI by diminishing myocardial O2
demand and hence ischemia.
• reduce the risks of reinfarction and ventricular fibrillation
• metoprolol, 5 mg every 2–5 min for a total of three doses,
provided the patient has
– HR>60 beats/min,
– SBP >100 mmHg,
– PR interval <0.24 s, and
– rales that are no higher than 10 cm up from the diaphragm
• 15 minutes after the last IV dose, an oral regimen is initiated
of 50 mg QID for 48 h, followed by 100 mg BID.

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Beta Blockers
• Oral beta blocker therapy should be initiated in the first 24 h
for patients who do not have any of the following:
1) signs of heart failure,
2) evidence of a low-output state,
3) increased risk for cardiogenic shock
4) other relative contraindications to beta blockade (PR interval >0.24 s,
second- or third-degree heart block, active asthma, or reactive airway
disease).

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Reperfusion therapy...
Fibrinolysis
• an important reperfusion strategy in settings where
primary PCI can’t be offered in a timely manner
– Recommended within 12 h of symptom onset
• if primary PCI cannot be performed within 120 min from
STEMI diagnosis and there are no contraindications.
– The goal is to inject the bolus of fibrinolytics within 10 min
from STEMI diagnosis

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• Associated with risk of stroke
– Largely cerebral hemorrhage more on the first day after treatment.
• Predictors of significant Intracranial hemorrhage
– Advanced Age, Lower Weight, Female Sex,
– Previous Cerebrovascular Disease, & Hypertension on
admission

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Contraindications to fibrinolytic therapy

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• ST-segment
resolution > 50% at
60–90min; and
disappearance of
chest pain
• TIMI Flow Grade
Successful reperfusion

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Percutaneous Coronary Intervention

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Percutaneous Coronary Intervention...
• PCI, usually angioplasty and/or stenting is effective in
restoring perfusion in STEMI when carried out on an
emergency basis in the first few hours of MI
• 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

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• Reperfusion therapy is indicated in all patients with symptoms
of ischaemia of<_12h duration and persistent ST-segment
elevation.
• A primary PCI strategy is recommended over ﬁbrinolysis
within indicated timeframes
• If timely primary PCI cannot be performed after STEMI
diagnosis, ﬁbrinolytic therapy is recommended within 12h of
symptom onset in patients without contraindications.
• In patients with time from symptom onset >12h, a primary PCI
strategy is indicated in the presence of ongoing symptoms
suggestive of ischaemia, haemodynamic instability, or life-
threatening arrhythmias

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• In the absence of ST-segment elevation, a primary PCI
strategy is indicated in patients with suspected ongoing
ischaemic symptoms suggestive of MI and at least one of the
following criteria present:
- haemodynamic instability or cardiogenic shock
- recurrent or ongoing chest pain refractory to medical
treatment
- life-threatening arrhythmias or cardiac arrest
- mechanical complications of MI
- acute heart failure
- recurrent dynamic ST-segment or Twave changes,
particularly with intermittent ST-segment elevation.

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Hospital phase management
• Activity :-bed rest for first 12hrs,sited by the side of the bed in the first
24hrs, ambulation by 3rd day
– By day 3 patients should be increasing their ambulation progressively
to a goal of 185 m at least three times a day.
• Diet:- NPO or clear liquid diet for 4-12hrs(Because of the risk of emesis
and aspiration soon after STEMI)
• Bowel management:- stool softeners, laxatives, gentle PR
• Sedation:- Diazepam (5 mg), oxazepam (15–30 mg), or lorazepam (0.5–2
mg), given 3–4 times daily, to withstand the period of enforced inactivity
with tranquility.

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Pharmacotherapy
• Antithrombotic
• Anticoagulant
• B-blockers
• ACE inhibitors/ ARBs
• MRA
• Statins

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Pharmacotherapy...
• ANTITHROMBOTIC AGENTS
– Aspirin
– P2y12 ADP receptor antagonists- clopidogrel, Prasugrel,ticlaglor
• Anticoagulant
– UFH
• an initial bolus of 60 U/kg (maximum 4000 U) followed by an initial
infusion of 12 U/kg per h (maximum 1000 U/h). The aPTT during
maintenance therapy (1.5–2 times the control value).
– LMWH (Enoxaparin)
– Fondaparinux
– Direct thrombin inhibitors:- Bivaluridi

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Pharmacotherapy...
Indications for anticoagulants
– an anterior location of the infarction,
– severe LV dysfunction,
– heart failure,
– a history of embolism,
– mural thrombus,
– atrial fibrillation.
• Such individuals should receive full therapeutic levels of
anticoagulant therapy (LMWH or UFH) while hospitalized,
followed by at least 3 months of warfarin therapy.

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Beta Blockers
-Acute IV beta blockade
-improves the myocardial O2 supply-demand relationship,
-decreases pain,
-reduces infarct size, and
-decreases the incidence of serious ventricular arrhythmias.
-In patients who undergo fibrinolysis soon after the onset of
chest pain, no incremental reduction in mortality rate is seen
with beta blockers, but recurrent ischemia and reinfarction
are reduced.

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• ACE inhibitors
– reduce the mortality rate after STEMI
– The maximum benefit is seen in high-risk patients (those who are
elderly or who have an anterior infarction, a prior infarction, and/or
globally depressed LV function).
– short-term benefit occurs when ACE inhibitors are prescribed
unselectively to all hemodynamically stable patients with STEMI
– The mechanism involves a reduction in ventricular remodeling after
infarction with a subsequent reduction in the risk of CHF.

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• ACE inhibitors should be continued indefinitely
– in patients whohave clinically evident CHF,
– in patients in whoman imaging study shows a reduction in LVEF ora largeregional wallmotion abnormality, or
– in those whoare hypertensive.
• Angiotensin receptor blockers (ARBs) should be administered toSTEMIpatients who
– areintolerantofACEinhibitorsandwhohaveheartfailure.
– HaveLV ejectionfraction≤40%,and
– HavesymptomaticheartfailureorDM
• Contraindication
– renaldysfunction(Scr.≥2.5mg/dLinmenand≥2.0mg/dLin women)or
– hyperkalemia(potassium≥5.0mEq/L)

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Life style modification & risk factor control
• Smoking cessation
• Dietary modification
• Weight reduction
• Alcohol reduction
• Exercise based cardiac rehabilitation
• BP control
• Adherence to treatment

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Special patient subsets
• Patients taking oral anticoagulants
• Elderly
• Renal dysfunction
• Non-reperfused patients
• Diabetic patients

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Complications
Mechanical complication
•Ventricular dysfunction
•Cardiogenic shock
•Wall rupture
•Papillary muscle rupture
•Pericarditis
Electrical complication
•Supraventricular
arrhythmia
– Atrial flutter, Atrial
fibrillation , Sinus
tachycardia,Sinus
bradycardia
•AV block
•Pvc
•Ventricular tachycardia
•Ventricular fibrillation

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Poor Prognostic Factors
• Age >65
• ECG features (Infarct size)
• LVEF
• 3 or more risk factors
• Elevated troponin
• Chronic use of ASA
• DM
• CKD

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References
Harrison’s Principles of Internal Medicine, 21st Ed.
2017 ESC Guidelines for the management STEMI
2018 ESC 4th Universal Definition of MI
Braunwald’s Heart Disease, 12th Ed.
UpToDate 2021

ABEL Chest pain & STEMI.ppt

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