DIAGNOSIS AND MANAGEMENT

OF MYOCARDIAL INFARCTION.

BY-
Dr. Sanjana GK
Intern
 Definition of myocardial infarction.
The term acute MI should be used when there is an evidence of myocardial
necrosis in a clinical setting consistent with acute myocardial ischemia. Under
these conditions, any of the following criteria meets the diagnosis of MI :-
• Detection of a rise and/or fall in cardiac biomarker values (preferably cTn) with
one value above 99th percentile URL and with at least 1 of the following :-
• Symptoms of ischemia
• New or presumed new significant ST segment-T wave changes
• Development of new pathologic Q waves on ECG
• Imaging evidence of new loss of viable myocardium or new regional wall motion
abnormality
• Identification of an intracoronary thrombus by angiography or autopsy
Algorithm for evaluation and management of patients
with suspected Acute Coronary Syndrome(ACS)
1. Non cardiac diagnosis
• Treatment as indicated by alternative diagnosis.

2. Chronic stable angina

• Treat accordingly
3. Possible ACS
(Non diagnostic ECG
Normal initial cTn)
No recurrent pain and negative follow up studies

Stress study to provoke ischemia

NEGATIVE POSITIVE

Non ischemic discomfort Diagnosis of ACS confirmed

Low risk ACS or Highly likely
 4. Definite ACS
No ST segment elevation ST segment elevation

Possible
ACS Admit to hospital and manage via acute
ischemic pathway
1. ST or T wave changes
2. elevated cTn
3. hemodynamic changes
4. ongoing pain
Acute coronary syndromes
Diagnostic approach to ACS
• History and examination
• ECG
• biomarkers
History
• Pain
• Nausea
• Vomiting
• Giddiness
• Epigastric discomfort
• Sweating
• Weakness
• In up to one-half of cases, a precipitating factor appears to be present
before STEMI, such as vigorous physical exercise, emotional stress, or a
medical or surgical illness. Although STEMI may commence at any time
of the day or night, circadian variations have been reported such that
clusters are seen in the morning within a few hours of awakening.
• The pain of STEMI may radiate as high as the occipital area but not
below the umbilicus
Pain is the most common presenting complaint in patients
• Typically, chest pain has at least one of three features:
1. occurrence at rest (or with minimal exertion), lasting >10 min
2. relatively recent onset (i.e., within the prior 2 weeks)
3. a crescendo pattern, i.e., distinctly more severe, prolonged, or frequent than
previous episodes.
• The pain is deep and visceral. adjectives commonly used to describe it are heavy,
squeezing, and crushing
• Typically, the pain involves the central portion of the chest and/or the
epigastrium, and, on occasion, it radiates to the arms. Less common sites of
radiation include the abdomen, back, lower jaw, and neck.
• It is often accompanied by a sense of impending doom.
 Levine sign
• Clenching the fist in front of the chest while describing the chest pain is
typical of ischaemic chest pain
• However, pain is not uniformly present in patients with STEMI. The
proportion of painless STEMIs is greater in patients with diabetes mellitus,
and it increases with age.
• In the elderly, STEMI may present as
1. sudden-onset breathlessness, which may progress to pulmonary edema.
2. sudden loss of consciousness
3. a confusional state
4. a sensation of profound weakness
5. The appearance of an arrhythmia
6. evidence of peripheral embolism
7. Merely an unexplained drop in arterial pressure.
Examination
• Perspiration associated with pallor
• Coolness of extremities
• within the first hour of STEMI, about one-fourth of patients with
anterior infarction have manifestations of sympathetic nervous
system hyperactivity (tachycardia and/or hypertension), and up to
one-half with inferior infarction show evidence of parasympathetic
hyperactivity (bradycardia and/or hypotension).
• Precordium is usually quiet
• Apical impulse is difficult to palpate
• In patients with anterior wall infarction, an abnormal systolic pulsation
caused by dyskinetic bulging of infarcted myocardium may develop in the
periapical area within the first days of the illness and then may resolve.

• Other physical signs of ventricular dysfunction include

1. fourth and third heart sounds
2. decreased intensity of the first heart sound
3. paradoxical splitting of the second heart sound

• A transient midsystolic or late systolic apical systolic murmur due to

dysfunction of the mitral valve apparatus may be present.
• The carotid pulse is often decreased in volume, reflecting reduced
stroke volume.
• Temperature elevations up to 38°C may be observed during the first
week after STEMI.
• The arterial pressure is variable; in most patients with transmural
infarction, systolic pressure declines by ~10–15 mmHg from the
preinfarction state
Differential diagnosis based on history and
examination.
• Chest wall pain
At least 2 of the following
1. localised muscle tension
2. stinging pain
3. pain reproducible by palpation
• GERD : burning retrosternal pain, sour or bitter taste in mouth, acid
regurgitation. One week trial of high dose proton pump inhibitors relieves the
symptoms.
• Anxiety disorder/panic attack : single question – have you had an
anxiety attacks in the past few weeks?
• Pericarditis : clinical triad of pleuritic chest pain (increases with respiration
or reclining and lessens on leaning forward), pericardial friction rub, ECG
changes (diffuse ST segment elevation, PR interval depression without T wave
inversion). Radiation of discomfort to the trapezius.
• Pneumonia : egophony , fever , dullness to percussion and clinical
impression.
• Heart failure : history of heart failure
history of acute MI
pulmonary edema on chest xray
clinical impression
• Acute thoracic aortic dissection : acute chest or back pain and
pulse differential in the upper extremities.
12 lead ECG changes

STEMI NSTEMI
• ECG leads are useful in localising regions of ST elevation than non ST
elevation ischemia.
1. Acute transmural anterion wall ischemia is reflected by ST elevation or
increased t wave positivity in one or more of the precordial leads (V1 –
V6) and leads I and aVL.
• Inferior wall ischemia produces changes in leads II, III and aVF.
• Posterior wall ischemia (usually associated with lateral or inferior
involvement) may be indirectly recognized by reciprocal ST depressions
in leads V1 to V3 (thus constituting an ST elevation “equivalent” acute
coronary syndrome).
• Right ventricular ischemia usually produces ST elevations in rightsided
chest leads
ECG changes and its evolution in STEMI

A. Normal ECG
B. Hyper acute phase of MI
C. Evolved phase of acute MI
D. Chronic stabilised phase of MI
• Sclarowsky birnbaum score for grading of
severity of ischaemia
grade 1 tall,peaked,symmetrical T waves
grade 2 slope elevation of ST segment
grade 3 distortion of terminal qrs complex in form of J point
elevation of >50% of the preceding R wave or loss of S waves (
TOMBSTONE appearance)
Differential diagnosis of ST segment elevation

• Left ventricular hypertrophy/left bundle branch blocka.

• Acute pulmonary embolism
• Brugada patterns (right bundle branch block–like pattern with ST elevations
in right precordial leads)
• Class 1C antiarrhythmic drugs
• Hypercalcemia
• Hyperkalemia
(but theses are localised to V1 - V2 or V3)
NSTEMI
ST depression takes one of the 4 forms :
1. Horizontality of ST segment : earliest sign
 2. Upward sloping ST segment depression

• Early and mild manifestation of ST depression

• Only proximal part of ST segment i.e junction with the QRS complex is
depressed
• ST depression: Normal / Abnormal
• Normal: unbroken parabola
• Abnormal/ pathological –
Broken parabola sign
3. Plane ST segment depression
4. T wave inversion
Cardiac biomarkers for diagnosis of MI
• Myoglobin
• Cardiac specific Troponins
• High sensitivity cardiac troponin
• Creatine kinase MB isozyme
Other causes of raised troponin
Killip classification
• Class 1 – signs of heart failure
• Class 2 – rales and diffuse wheezing in the lungs
• Class 3 – acute pulmonart edema
• Class 4 – cardiogenic shock
 Management of ACS
General measures :
• Patients with new or worsening chest discomfort or an anginal
equivalent symptom suggestive of ACS should be transported rapidly to
the ED by ambulance, if possible, and evaluated immediately.
• The initial evaluation should include a directed history and physical
examination and ECG performed within 10 minutes of arrival.
• Blood specimens for cTn should be obtained. Also,CBC, S. electrolytes,
creatinine, and glucose, can help guide early management treatments and
strategy
• Patients with elevated cTn or new ST-segment abnormalities should be
admitted to a specialized cardiovascular intensive care unit.
• In these settings, continuous ecg monitoring detects tachyarrhythmias,
alterations in atrioventricular and intraventricular conduction, and
changes in ST-segment deviation.
• Patients should be placed on bed rest and inhaled oxygen provided to
patients with arterial oxygen saturation (SaO2) less than 90% and
those with HF and pulmonary rales.
Management of NSTEMI :
Anti - platelets
• Initial treatment should begin with the COX inhibitor aspirin with a
dose of 325 mg. Lower doses (75–100 mg/d) are recommended
thereafter. Contraindications are severe active bleeding or aspirin
allergy.
• P2Y12 inhibitors - clopidogrel loading dose of clopidogrel is 600 or
300 mg while the maintenance dose is 75 mg daily
• When clopidogrel is added to aspirin, so called dual antiplatelet
therapy (DAPT) has been shown to confer a 20% relative reduction in
cardiovascular death, MI, or stroke, compared to aspirin alone, but to
be associated with a moderate (absolute 1%) increase in major
bleeding
Anticoagulants
Factors Associated with Appropriate Selection of Early
Invasive Strategy
Management of STEMI :
• Initial management: Prehospital care
major elements of prehospital care of patients with suspected STEMI include
(1) recognition of symptoms by the patient and prompt seeking of medical
attention
(2) rapid deployment of an emergency medical team capable of performing
resuscitative maneuvers, including defibrillation
(3) transportation of the patient to a hospital facility that is continuously
staffed by physicians and nurses skilled in managing arrhythmias and
providing advanced cardiac life support
(4) implementation of reperfusion therapy
• Management in the emergency department : the goals for the
management of patients with suspected STEMI include
A. control of cardiac discomfort
B. rapid identification of patients who are candidates for urgent
reperfusion therapy
Control of cardiac discomfort
• Aspirin 325 mg followed by 75 mg OD
• Supplemental oxygen if SpO2 is low
• Sublingual nitroglycerin.Up to three doses of 0.4 mg should be
administered at about 5-min intervals. IV can be given for persistent
pain unless contraindicated
• Morphine
• Beta blockers
Reperfusion therapy :
• Primary Coronary Intervention
• Fibrinolysis
Selection for reperfusion therapy :
• When performed rapidly after arrival at an experienced center, primary
PCI is superior to pharmacologic reperfusion therapy.
• Prehospital fibrinolysis may be as effective as PCI in patients early
after symptom onset but requires significant infrastructure with direct
physician support
• In patients taken to centers that are not PCI capable, the primary
consideration is time required for transportation to a PCI-capable
center.
• If the time from primary care to PCI is expected to be more than
120 minutes, fibrinolysis is recommended
• Otherwise, transfer for primary PCI is generally favored even if the
delay to revascularization will be greater than 120 minutes
Fibrinolysis
• If no contraindications are present, fibrinolytic therapy should ideally
be initiated within 30 min of presentation (i.e., door to needle time ≤30
min).
• pharmacologic reperfusion also involves adjunctive antiplatelet and
antithrombotic drugs
• Fibrinolysis can recanalize the thrombotic occlusion associated with
STEMI, and when achieved, restoration of coronary flow reduces
infarct size and improves myocardial function and survival over
both the short and the long term .
Indications for PCI :
• Arterial access is obtained via the femoral or radial artery

• aspirin 325 mg
• platelet P2Y12 inhibitor such as clopidogrel ,prasugrel , ticagrelor
before the procedure. Cangrelor, an IV P2Y12 inhibitor, is approved
for use in patients who have not received an oral agent prior to the
procedure.
• During the procedure, anticoagulation is achieved by administration of
unfractionated heparin, enoxaparin or bivalirudin
• intravenous glycoprotein IIb/IIIa inhibitor (abciximab, tirofiban, or
eptifibatide) may also be given, though cangrelor may be as effective
with less bleeding risk.
• PCI is performed under local anesthesia and mild sedation, it requires
only a short (1-day) hospitalization or less.
Uses of stents in PCI
• Stents are currently used in >90% of coronary angioplasty procedures.
• wire meshes (made of stainless steel or other metals, such as cobalt
chromium or nitinol) that are compressed over a deflated angioplasty
balloon.
• When the balloon is inflated, the stent is enlarged to approximate the
“normal” vessel lumen.
• The balloon is then deflated and removed, leaving the stent behind to
provide a permanent scaffold in the artery.
• Stents are rigid enough to prevent elastic recoil of the vessel and have
dramatically improved the success and safety of the procedure as a result
Drug eluting stents
• These elute antiproliferative drugs over 3 months or longer duration
• shown to reduce clinical restenosis by 50%
• symptomatic restenosis occurs in 5–10% of patients
• currently 80–90% of all stents implanted are drug-eluting
• 1st generation : coated with sirolimus or paclitaxel
• 2nd generation : everolimus, biolimus, and zotarolimus
Stent thrombosis
• All types of stents are prone to stent thrombosis (1–3%)
• Acute(<24 hours)
• Subacute(1-30 days)
• Late( 30 days-1 year)
• Very late( >1 year)
• Acute & subacute are common with 1st generation DES.
• This necessitates DAPT for up to 1 year or longer
• Use of the second- generation stents is associated with lower rates of late and very late
stent thromboses, and shorter durations of DAPT (6 months) are recommended
• Premature stoppage of DAPT increases risk of stent thrombosis 3 to 9 fold.
• Stent thrombosis results in death in 10–20% and myocardial infarction in 30–70% of
patients
Restenosis
• renarrowing of the dilated coronary stenosis,occurs in 20–50% of patients
with balloon angioplasty alone and 5–15% of patients with des within the
first year
• recognized by recurrence of angina or symptoms within 12 months of the
procedure
• Less frequently, patients with restenosis can present with NSTEMI (10%)
or STEMI (2%)
• management of clinical restenosis is usually to repeat the PCI with balloon
dilatation and placement of another drug-eluting stent.
• The risk factors for restenosis are diabetes, myocardial infarction, long
lesions, small-diameter vessels, and suboptimal initial PCI result
Hospital phase management post reperfusion
• Activity
• STEMI patient should be kept at bed rest for the first 6–12 h.
• encouraged, under supervision, to resume an upright posture by
dangling their feet over the side of the bed and sitting in a chair within
the first 24 h
• by the second or third day, patients typically are ambulating in their
room with increasing duration and frequency
• By day 3 after infarction, patients should be increasing their
ambulation progressively to a goal of 185 m (600 ft) at least three
times a day
• Diet
typical coronary care unit diet should provide ≤30% of total calories as
fat and have a cholesterol content of ≤300 mg/d. Complex
carbohydrates should make up 50–55% of total calories. Portions should
not be unusually large, and the menu should be enriched with foods that
are high in potassium, magnesium, and fiber, but low in sodium
• Laxatives
• Sedation
Complications of MI
• Ventricular dysfunction
• Hypovolemia and cardiogenic shock
• Arrhythmias
• Pericarditis
• Thromboembolism
• LV aneurysm
Reference
• Harrison’s principles of internal medicine.
Thank you.