STEMI

"Last updated:"Wednesday, May 28, 2014

STEMI is a shorthand medical term for ST-segment elevation myocardial infarction. It is one
type of heart attack that can be defined as a development of full thickness cardiac muscle
damage resulting from an acute interruption of blood supply to a part of the heart and can be
demonstrated by ECG (electrocardiography) change of ST-segment elevation.
Here, ST-segment elevation appears in ECG due to full thickness damage of cardiac muscle.
Therefore, STEMI is more severe type of myocardial infarction compared to NSTEMI (nonST segment elevation myocardial infarction) in which partial thickness damage of heart
muscle develops.

Pathophysiology:
STEMI usually develops by formation of an occlusive thrombus (blood clot) in a major
coronary artery previously affected by atherosclerosis. Cholesterol deposition within the wall
of the artery is the main mechanism of atherosclerosis. This deposited cholesterol ultimately
forms a plaque in the wall of the artery called atherosclerotic plaque. Atherosclerotic plaque
formation is a long term process, required many years to establish. Sometimes this
plaque may rupture or erode, and can trigger platelet aggregation and fibrin deposition, which
lead to formation of an occlusive thrombus in a coronary artery. This occlusive thrombus
completely block a coronary artery and interrupts blood supply to part of the myocardium
(heart muscle), profound changes take place in the myocardium that lead to irreversible
changes and death of myocardial cells, and ultimately ST-segment elevation myocardial
infarction develops.

Symptoms:
Chest pain: Chest pain is the cardinal symptom of STEMI. Pain is often described by
patients as a tightness, heaviness or constriction in the chest. It is usually located in the center
of the chest, but may radiate to neck, jaw, shoulder, back, and arms (most commonly left
arms). Occasionally, pain may be felt only at the sites of radiation.
Breathing difficulty: Sometimes breathing difficulty develops due to left ventricular
dysfunction or dynamic mitral regurgitation.
Profuse sweating, nausea and vomiting may occur due to nervous upset.
Syncope (sudden loss of consciousness): Sometimes patients may present with syncope,
usually due to an arrhythmia or severe hypotension.
Tachycardia (high pulse rate): Due to sympathetic nerve activation.
Bradycardia (low pulse rate): Patients with inferior STEMI may present with bradycardia
due to vagus nerve activation.
Cardiogenic shock: Some patients may present with shock due to impaired myocardial
function.

Diagnosis:
Diagnosis of STEMI is done by clinical symptoms and signs with following investigations:
Electrocardiography (ECG):
The typical ECG findings of STEMI are ST-segment elevation with pathological Q-wave
formation. Sometimes T-wave inversion may be found but it is a non-specific feature. STsegment elevation indicates full thickness cardiac muscle injury, pathological Q-wave
indicates muscle necrosis and T-wave inversion indicates muscle ischemia.

Figure: ECG of STEMI

Cardiac markers:
Troponin T and troponin I, and CK-MB (creatine kinase myocardial band) are rises in blood
in STEMI. Troponin T and troponin I start to rise at 4-6 hours and remain high for up to two
weeks. CK-MB starts to rise at 4-6 hours and falls to normal within 48-72 hours. Cardiac
markers should rise above two times the upper limit of the reference range.
Full blood count:
Elevation of White blood cell (WBC) count is usual. Erythrocyte sedimentation rate (ESR)
and C-reactive protein (CRP) may elevate.
Chest X-ray:
It is done for assessing pulmonary edema.
Echocardiography:
Immediate echocardiography is not essential, but is helpful if the ECG cannot evaluate the
diagnosis of STEMI. A regional wall motion defect is found in infarct area of the heart. It also
can assess ventricular function and can detect important complications.

Types:
According to wall of cardiac muscle involvement, STEMI may be different types. To read
about specific type click on the link below.
Anterior STEMI
Antero-septal STEMI
Lateral STEMI
High lateral STEMI
Antero-lateral STEMI
Inferior STEMI
Posterior STEM
RV (right ventricular) infarction

Complications:
Both early and late complications may occur in STEMI.
Early complications:
These develop within one week. Early complications of STEMI are as followings:
Heart arrhythmias
Arrhythmias are disturbance of the electrical rhythm of the heart in which heartbeat may be
too fast, too slow or irregular. In most of cases arrhythmias are mild and transient. But, life
threatening arrhythmias may develop that are the major cause of death during the first 24
hours after an attack. Arrhythmias that may develop in STEMI are ventricular fibrillation,
ventricular tachycardia, ventricular ectopics, accelerated idioventricular rhythm, atrial
fibrillation, atrial tachycardia, atrioventricular block and sinus bradicardia.
Acute heart failure
It may occur due to left ventricular dysfunction.
Cardiogenic shock
It is due to extensive left ventricular damage.
Percarditis

Pericarditis develops on second or third days after attack. Patient may feel a different type of
chest pain that tends to be worse or sometimes only feel on inspiration.
Embolism
The endocardial surface (inner surface) of infarcted heart muscle is rough that may triggers
platelet aggregation and often forms thrombus. This thrombus may dislodged from heart and
may cause stroke (if reach in the brain) or ischemic limb (if reach in the limb).
Mechanical complications
It is due to tear or rupture of infarcted heart muscle. It includes1. Severe mitral regurgitation it is due to rupture of papillary muscle.
2. Cardiac tamponate it is due to rupture of ventricle.
3. Right heart failure it is due to rupture of interventricular septum.
Late complications:
These develop after one week of attack and include:
Post MI syndrome (Dresslers syndrome)
It usually occurs 1-3 weeks after STEMI, and is characterized by fever, pericarditis and
pleuritis, and is probably due to myocardial antigens released after infarction. Management is
with NSAIDs (pain killer), high dose aspirin or even corticosteroids.
Left ventricular aneurysm
Aneurysm means abnormal dilatation. In STEMI, aneurysm may develop in left ventricular
wall due to full thickness cardiac muscle damage in which infarcted heart muscle may dilate
and moves paradoxically during systole (when heart pump). Left ventricular aneurysm can be
minimized by early use of ACE inhibitor and beta-blocker.
Chronic heart failure
It develops gradually over time after an attack in which the heart muscle cannot pump enough
blood to meet the bodys demand.

Treatment:
STEMI is more serious form of heart attack. Therefore, patients need immediate
hospitalization, preferably to a cardiac care unit.
Basic treatment:
(1) Complete bed rest with continuous monitoring by ECG.

(2) Inhaled high flow oxygen therapy.

(3) Aspirin.
A 300 mg tablet of aspirin is given orally as early as possible. It can be given intravenously to
patients who cannot swallow or who are unconscious. Aspirin reduces the mortality rate of
STEMI by approximately 25%.
(4) Clopidogrel.
In combination of aspirin, clopidogrel 300 mg should be given orally as early as possible.
Small mortality benefit is seen in combination of aspirin and clopidogrel. Ticagrelor 150 mg
orally may be given instead of clopidogrel.
(4) Relief of pain by opiate analgegic
Intravenous morphine 10 mg or diamorphine 5 mg is usually used along with anti-emetic
drug and may have to be repeated to relieve severe pain.
Reperfusion therapy:
All patients with STEMI should be considered for primary PCI (percutaneous coronary
intervention) immediately. It is treatment of choice for ST-segment elevation myocardial
infarction. It reduces a significant mortality, infarct size and further infarction. Where PCI is
not available or primary PCI cannot be achieved within 120 minutes of diagnosis,
thrombolytic therapy should be given.
Drug used for thrombolysis is alteplase, tenecteplase, reteplase, or streptokinase. These drugs
break the occlusive thrombus within the coronary artery and clear the arterial lumen. The
benefit of thrombolytic therapy is very time dependent. Major benefit is seen in those patients
who are present within three hours of onset of chest pain. It may also be given in patients
who present within 12 hours of pain. Thrombolytic therapy reduces hospital mortality by 25
to 50% and also reduces infarct size. The survival benefit of thrombolytic therapy is
maintained for at least 10 years. The main hazard of this therapy is hemorrhage. Therefore, it
should be avoided for patients with active bleeding, previous hemorrhagic stroke or
subarachnoid hemorrhage, uncontrolled hypertension, any major surgery within one month,
recent major trauma, active peptic ulcer and pregnancy. Among the thrombolytic therapy,
tissue plasminogen activators such as alteplase, tenecteplase and reteplase are best. Among
the tissue plasminogen activators, tenecteplase have a lower incidence of hemorrhage.
In patients who fail to achieve coronary arterial reperfusion following thrombolytic therapy
or thrombolytic therapy is contraindicated, early (within 6 hours of symptom onset)
emergency PCI may be considered, particularly who develop cardiogenic shock.
Treatment for maintaining arterial patency:
Further occlusion of coronary artery following reperfusion therapy is common in ST-segment
elevation myocardial infarction. Therefore, maintaining arterial patency after successful
reperfusion is essential.

(1) Antiplatelet therapy

Aspirin 75 mg daily should be taken indefinitely if there are no side effects occur. In
combination of aspirin, clopidogrel 75 mg daily should be given orally. Both aspirin and
clopidogrel inhibit platelet aggregation and prevent further occlusion. Ticagrelor 90 mg two
times daily may be given instead of clopidegrol. Patients with STEMI who undergo primary
PCI, glycoprotein IIb/IIIa receptor blocking drug such as tirofiban, abciximab, or eptifibatide
are the best antiplatet drug.
(2) Anticoagulant therapy
In general, anticoagulant therapy is not required after PCI (Glycoprotein IIb/IIIa inhibitor is
infused for 18 hours after PCI). Usually, anticoagulant therapy is given for 48 hours
following thrombolytic therapy with tissues plasminogen activator because a rebound
procoagulant effect may appear following thrombolysis. In contrast, streptokinase has
persistant anticoagulant effect for 24-48 hours after administration due to its different
pharmacological mechanism. Therefore, anticoagulant therapy following streptokinase has no
additional benefits.
If patients with STEMI not treated with PCI or thrombolytic therapy, anticoagulant therapy
should be given for 5-8 days. These drugs prevent reinfarction and reduce the risk of
thromboembolic complications. Available anticoagulation drugs are unfractionated heparin,
fractionated heparin also called low molecular weight heparin (enoxaparin, dalteparin) or a
pentasaccharide (fondaparinux). Comparatively low molecular weight heparin is more safety
and efficacious than unfractionated heparin, and pentasaccharide is more safety and
efficacious than low molecular weight heparin. The dose regimens are:
1. Enoxaparin: 1 mg/kg body weight two times a day by subcutaneous injection.
2. Dalteparin: 120 units/kg body weight two times a day by subcutaneous injection.
3. Fondaparinux: 2.5 mg daily by subcutaneous injection.
(3) Beta-blockers
In the absence of bradycardia, heart failure, heart block or hypotension, all patients with STsegment elevation myocardial infarction should be considered for beta-blocker. Beta-blockers
reduce arrhythmias, relive pain and further attack. Atenolol 25-50 mg twice daily, bisoprolol
5 mg once daily or metoprolol 25-50 mg twice daily may be given orally. Initially
intravenous beta-blocker (atenolol 5-10 mg or metoprolol 5-15 mg over 5 minutes) can be
given if heart rate 90 beats/minute, or systolic blood pressure 150 mmHg or diastolic 90
mmHg.
ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensive receptor
blockers):
An ACE inhibitor such as enalapril, ramipril, lisinopril or captopril is started 1 or 2 days after
attack. An ACE inhibitor reduces ventricular remodeling, reduce recurrent infarction and
prevent the onset of heart failure. An ARB such as valsartan, olmesartan candesartan, or
losartan is suitable alternatives in patients who are intolerant of ACE inhibitors.

Statins:
All patients with STEMI should receive statin such as atorvastatin, simvastatin or
rosuvastatin irrespective of their serum cholesterol level.
Nitrates:
Nitrate spray may be used sublingually or buccally if patients feel chest pain.

Prognosis:
Approximately 25% of patients die within a few minutes after an attack without medical care.
The prognosis is much better of those who survive to reach hospital, with a 28-day survival
of more than 85%. Of those patients who survive an acute episode, more than 80% survive
for 1 year, about 75% for 5 years, 50% for 10 years and 25% for 20 years. The prognosis is
better for inferior than anterior STEMI.
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