STEMI

ACUTE ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

STEMI: definition:
Myocardial necrosis caused by thrombotic occlusion of a coronary artery. Occlusive thrombus is formed at the site of rupture of atherosclerotic plaque. Myocardial necrosis occurs over the course of several hours, so most patients present within the time window when it is still possible to salvage the myocardium.

CLINICAL PRESENTATION

Pain: felt in the chest, back, abdomen, neck, throat, mandible, arms, or hands. It is prolonged, severe and is not relieved.
Other features: severe anxiety, nausea and vomiting, breathlessness, collapse, syncope.

PHYSICAL SIGNS

The patient is usually pale, sweaty, restless and anxious.
There may be signs of sympathetic activation: pallor, sweating, tachycardia. Or signs of vagal activation: vomiting and bradycardia.
Signs of impaired myocardial function: hypotension, oliguria, cold sweat, narrow pulse pressure, raised JVP, S3, faint S1, diffuse apical impulse, lung crepitations.
Signs of tissue damage: fever
Signs of complications e.g. MR or pericarditis.

DIFFERENTIAL DIAGNOSIS:

Aortic dissection: in which pain is abrupt and severe from the start, tearing in nature.
Pulmonary embolism
Acute pericarditis: important to differentiate, as thrombolytic therapy may cause tamponade
Non cardiac chest pain: peptic ulcer, acute cholecsystitis, acute pancreatitis or esophageal problems.


INVESTIGATIONS

ECG
Biochemical markers
Other blood tests
Chest X-ray
Echocardiography

The diagnosis of STEMI depends on the demonstration of biochemical evidence of tissue necrosis in the presence of ECG or clinical background of the condition.

 ECG

Often helpful in establishing the diagnosis, but may be difficult to interpret in the presence of LBBB or previous MI.
Sequence of changes in STEMI:
Acute ST elevation (the current of injury)
Loss of amplitude of the R wave
Development of a Q wave
T wave inversion
Reduction in the magnitude of the ST elevation (ST resolution)
Deepening of Q waves


Twelve weeks after MI, the ST segment returns completely to normal. Persistent ST elevation beyond 12 weeks indicates LV aneurysm.

Biochemical Markers:

These are the most important in establishing the diagnosis of acute ST elevation MI.

Creatinine phospho kinase (CK):

Found in skeletal muscles (MM isoenzyme), in the brain (BB isoenzyme) and in the myocardium (MB isozyme). It starts to rise at 4-6 hours, peaks at 12 hrs, and disappears in 36-48 hrs after the incidence of myocardial infarction.
CK is not specific for cardiac muscle; it may rise in intramuscular injection, physical exercise, and defibrillation. CK-MB is more specific and sensitive for cardiac muscle injury. It is not elevated with the administration of DC shock or skeletal muscle injury.

Cardiac troponins: Tn T & Tn I:

More specific than CK & CK-MB. They start to rise in 4-6 hours and persist in the circulation for 2 weeks. Troponins are elevated in unstable angina but to less severe degree.

Other Blood Tests

Leukocytosis (neutrophilia). Increased erythrocyte sedimentation rate (ESR), and increased C-Reactive Protein (CRP)

Chest X-Ray:

The manifestations depend on the extent of myocardial damage and the duration of the infarction. In the early stages the CXR may be normal, later on there may be features of pulmonary edema. The heart size is usually normal, but cardiomegaly may occur due to old myocardial infarctions

Echocardiography

It can be performed at the bedside, and is useful to assess the status of the LV & RV. It detects mechanical complications, LV mural thrombus, ventricular septal rutpture, mitral regurgitation, and pericardial effusion.


MANAGEMENT OF STEMI
THE KEY TO PROPER MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION IS THE TIMELY AND IMMEDIATE REMOVAL OF THROMBUS OBSTRUTION AND RESTORATION OF BLOOD FLOW TO THE INFARCTED SEGMENT. THIS IS EXPECTED TO PREVENT LOSS OF MYOCARDIUM, IMPROVE LV FUNCTION, IMPROVE QUALITY OF LIFE, AND PROLONG SURVIVAL.

Management of STEMI

Early management
Maintaining vessel patency
Adjunctive therapy

Early Management

Management before transmission to hospital: advanced life support
Transferring the patient to hospital
Management inside hospital

Management at the site:

This includes providing advanced life support, reassurance, and if available, locally held DC shock devices if needed.

Rapid transfer of the patient to hospital: ambulance

Thrombolytic therapy should be administered in the ambulance.

Early management: immediate measures

Cannula
Oxygen
ECG monitoring
Standard (12-lead) ECG
Analgesia: morphine sulphate
Aspirin (300 mg)


The patient should be admitted to the intensive coronary care unit (CCU)
Mobilized the next day
Discharged from hospital on the 6th day

Reperfusion: either with thrombolytic therapy or primary angioplasty

Reperfusion: Thrombolytic therapy
It restores coronary patency, helps in resolution of acute ST elevation, reduces myocardial infarct size, relieves pain, preserves LV function, improves survival, and
may reduce arrhythmias, but may exacerbate these arrhythmias (reperfusion injury). It should be administered as soon as possible to achieve maximal salvage of myocardium (minutes mean muscle)
Thrombolysis is of no benefit (and may be harmful) if given > 12 hours from the onset of STEMI (preferably given within the first 6 hours), and in cases on NSTEMI or unstable angina.

Complications of thrombolytic therapy:

Bleeding: the most serious site is cerebral hemorrhage. So it may be wise to withhold treatment if there is significant risk of bleeding.
With streptokinase: the development of antigens to the drug that render future administration of the drug ineffective. Streptokinase may cause hypotension

Absolute contraindications to thrombolytic therapy:

Active bleeding (except menstruation)
History of bleeding tendency
History of thrombotic or embolic CVA during the past year
Any history of intracranial hemorrhage
Suspected or definite diagnosis of aortic dissection
Cerebral or spinal tumor


Reperfusion therapy: primary PCI
It is associated with better results than thrombolytic therapy, but it requires specialized experience and expensive equipment. It should be performed as soon as possible. It is indicated in cases of failure of thrombolytic therapy or when such therapy is contraindicated.

Maintaining Vessel Patency

Aspirin
Clopidogrel
Anticoagulants

Aspirin:

Given orally in a dose of (75-350 mg/day). It reduces mortality, should be continued for life. Combination with clopidogrel improves outcome.

Maintaining Patency: Anticoagulants

Heparin: both unfractionated heaprin and LMWH. It improve survival of patients with STEMI at a slightly increased risk of intracranial bleeding

Antithrombotic therapy: Warfarin

Indications:
Atrial fibrillation
Extensive anterior wall MI with LV dysfunction
The demonstration of mobile thrombus on echocardiography

Adjunctive Therapy: including β-blockers and nitrates.

β-blockers
During the acute presentation: i.v. administration of atenolol or metoprolol reduce pain, reduce arrhythmia, and improve short term survival
Contraindicated in congestive heart failure, heart block, and bradycardia


Long term use of β-blockers :
Should be given to ALL patients unless contraindicated
Improve long term survival

Nitates

In the form of intravenous GTN or isosorbide dinitrate. They're useful for the treatment of LV failure and relieve ischemic pain. However, they have NOT been shown to improve long- or short term survival

COMPLICATIONS OF STEMI

Short-term complications
Arrhythmias
Mechanical complications
Residual ischemia
Pericarditis
Embloism
Long term complications
Recurrnet ischemia
LVdysfunction
Complications:
Arrhythmias: tachyarrhythmias (ventricular, atrial)
brady arrhythmias


Tachyarrhythmias
Ventricular:
Premature ventricular ectopics (PVCs)
Accelerated idioventricular rhythm
Ventricular tachycardia
Ventricular fibrillation
Atrial
Atrial fibrillation

Ventricular fibrillation:

The major cause of death in patients with STEMI before reaching hospital
Occurs in 5-10% of patients who reach hospital
Lethal arrhythmia unless treated by prompt defibrillation
Does not affect the long term prognosis of acute MI.

Atrial fibrillation:

Common in acute MI
Frequently transient
May be serious if it occurs in the context of LV failure:
muscle fiber stretching
May be transient and needs no treatment
Indications to treat:
Rapid ventricular rate
Hemodynamic deterioration (hypotension, CHF, pulmonary edema)
Emergency treatment:
Synchronized DC shock
Non-emergency situation:
Infusion of β-blocker or digoxin


Bradyarrhythmia: AV block
In the setting of inferior MI:
Usually temporary
Resolves with thrombolytic therapy
May need atropine if persists
If there is hemodynamic deterioration: temporary pacemaker insertion
AV block in the setting of anterior wall MI:
More serious than in inferior MI
May be complicated by sudden asystole
Prophylactic temporary pacemaker should be inserted

Mechanical complications

Papillary muscle rupture
Interventricular septal rupture
Ventricular free wall ruputre

Papillary muscle rupture

Sudden severe mitral regurgitation (MR)
Presents with pulmonary edema & shock
O/E: pansystolic murmur at the apical area radiating to the axilla or back. S3 & S4
The murmur is frequently faint or even absent
Dx: echo and Doppler
Treatment: urgent surgery


Ventricular Septal rupture
Sudden deterioration: hypotension, right ventricular failure, shock
Clinically: pansystolic murmur at the left sternal border
Diagnosis: echo and Doppler
Treatment: surgery

Acute circulatory failure(Cardiogenic Shock)

Indicates extensive myocardial damage
Usually fatal without intervention
Mortality of 90% if untreated
With primary PCI: can be reduced to 25%

Residual Ischemia

Presents as post infarction angina
Causes of residual ischemia:
Significant stenosis of an artery after successful thrombolysis
Blockage of an artery that was responsible for the collateral supply of another coronary artery
Occurs in ~ 50% of patients with AMI

Residual Ischemia: Management

High risk group of unstable angina
i.v. nitrates
β-blockers
Aspirin
Clopidogrel
Anticoagulation
Invasive strategy (PCI or CABG)
PCI is done under cover of GP IIb-IIIa antagonist


Acute Pericarditis
Usually occurs in the 2nd & 3rd days
Chest pain of different quality than ischemic:
Sharp
Localized
Positional (changes severity with posture)
Related to breathing: worse on inspiration
Pericardial friction rub
ECG changes of acute pericarditis
The use of steroids or NSAID is contraindicated in AMI as it may cause weakening of scar and increase the risk of aneurysm formation. So acute pericarditis is treated with aspirin in high dose or opiate-based analgesia.

Post-MI-Pericarditis(Dresslers syndrome)

Auto-immune reaction
May occur 6 days-6 months after MI
Pain (pleuro-pericarditis)
Pyrexia
Pericarditis
Pleurisy
Treatment: High dose ASA, NSAID, or even steroids

Ventricular Remodelling

Infarct expansion: thinning & stretching of the infarcted segment
Compensatory hypertrophy of the remaining muscle
Increased myocardial wall tension
Eventual dilatation and dysfunction of LV, with the formation of aneurysm


Management after discharge from hospital
Risk stratification
Secondary prevention
Rehabilitation

Risk Stratification after MI

Assessment for
Residual ischemia
Left ventricular function
arrhythmias

Residual Ischemia

Symptomatic patient (i.e. angina): Coronary angio is done with a view to revascularization
Asymptomatic:
Exercise testing: routinely done after 4 weeks
If high risk criteria : coronary angio should be done
If not , then repeat ETT every year or if new symptoms appear

Assessment of LV function

Clinically
ECG
CXR
Echo
Radioisotope study


In patients with LV dysfunction:
Look for reversible ischemia: coronary angio
ACE inhibitors (captopril, enalapril, lisinopril )
Angiotensin receptor blocker (valsartan, losartan, candisartan etc) in patients who can’t tolerate ACEI
β-blockers: metoprolol, bisoprolol, & carvedilol
Aldosterone receptor antagonist: spironolactone, eplerenone

Arrhythmias

Recurrent ventricular arrhythmias are caused by:
Residual ischemia
LV dysfunction
The presence of scar tissue
Significant ventricular arrhythmias: mangement
Treatment of LV dysfunction, residual ischemia
Electrophysiological study
Specific anti-arrhythmic therapy
Implantable cardiovertor-defibrillator (ICD)

Determinants of poor prognosis

Poor LV function
Arrhythmias
Persistent AV block
Anterior infarction > inferior infarction
Old age
Depression
Social isolation









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