Aims
- If a person at risk of a myocardial infarction (MI) has an acute coronary
syndrome lasting over 20 minutes, an imminent MI must be suspected. Instead of
chest pain, acute dyspnoea may be the primary symptom.
- An acute coronary syndrome without myocardial damage is often unstable
angina, which calls for active treatment.
- The diagnosis should be made without delay since early therapy improves the
prognosis decisively.
- Thrombolytic therapy is given as early as possible in all cases with a
clinical picture of imminent MI and corresponding electrocardiogram (ECG)
changes. See the Finnish Medical Society Duodecim guideline "Thrombolytic
Therapy in Acute Myocardial Infarction."
- Acute angioplasty (percutaneous transluminal coronary angioplasty [PTCA],
percutaneous coronary intervention [PCI]) is an alternative or a complementary
procedure to thrombolytic therapy ("Primary angioplasty versus intravenous,
thrombolysis" 2002; Sim, et al., 1995; DARE-953385, 1999; Grines, et al., 1999)
[A]. Angioplasty is probably preferred, at least in ST
elevation MI (Keeley, Boura, & Grines, 2003).
- If there are no contraindications, aspirin and a beta-blocker should be
started for all patients and, for most patients, also an angiotensin-converting
enzyme (ACE) inhibitor and a statin on the first days of treatment.
- Health care system should include a planned care pathway for coronary
patients.
Diagnosis
- The diagnostic criteria change in the course of treatment.
- During first aid, pain is the primary symptom in younger patients.
Presentation in the elderly is often atypical.
- When thrombolytic therapy is considered, an ST elevation on the ECG or a
recent left bundle branch block (LBBB) should be taken into account. See the
Finnish Medical Society Duodecim guideline "Thrombolytic Therapy in Acute
Myocardial Infarction."
- In addition to pain and ECG findings, myocardial enzyme levels are needed
for definite clinical diagnosis.
- For differential diagnosis of chest pain, see the National Guideline
Clearinghouse (NGC) summary of the Finnish Medical Society Duodecim guideline Differential
Diagnosis of Chest Pain.
- The pain in MI lasts over 20 minutes and is localized widely in the
retrosternal area, with radiation to the arms, back, neck, or lower jaw. The
pain is squeezing and is experienced as tightness, heaviness, and pressure or
pressing. Breathing or changing posture does not influence the intensity of
pain. The pain is usually severe and consistent. It may be localized in the
upper abdomen, in which case, if nausea and vomiting are also present, it
simulates acute abdominal disease. The patient is often pale, in a cold sweat,
and anxious.
- MI may also present as acute pulmonary oedema, unconsciousness, or sudden
death.
- Thrombolytic therapy is indicated
- if the pain has lasted less than 6 to 12 (24) hours and there is at least a
2-mm elevation in the ST segment in at least two chest leads, or
- a 1-mm elevation of ST in at least two leads in the extremities, or
- a reciprocal ST depression in V1–V4, or
- a recent left bundle branch block
- The contraindications for thrombolytic therapy must always be considered.
See the Finnish Medical Society Duodecim guideline "Thrombolytic Therapy in
Acute Myocardial Infarction."
- In clinical investigation, remember that the ECG and myocardial markers
change with the course of the disease: first there is an ST elevation, after
that development of the Q-wave, and finally T-wave inversion. Complications must
also be recognized. In a T-wave infarction (non-Q-wave infarction), no classical
Q waves are present, but the diagnosis is based on an increase of myocardial
enzymes, chest pain, or ST-T changes. Classical Q-wave changes, ST elevations,
and T inversions may be caused by various other diseases, which should be
remembered in the differential diagnosis. An old infarction, bundle branch
block, and early repolarization make the diagnosis difficult, in which case the
change in ECG is important and an old ECG recording valuable. When added to
other criteria, "minor" signs of infarction are also important.
- The European Society of Cardiology and the American College of Cardiology
have agreed on a new definition of MI ("Myocardial infarction redefined," 2000):
- Typical increase in the concentration of serum cardiac troponins or creatine
kinase isoenzyme containing M and B subunits (CK-MB) associated with at least
one of the following:
- symptoms of cardiac ischaemia
- recent pathological Q waves in the ECG
- ischaemic ST segment changes in the ECG
- coronary artery revascularization
ECG Diagnosis
- Points for taking an ECG: acute care, emergency room, 12 hours later, on day
2, upon discharge from hospital, and thereafter as deemed necessary.
- ECG is the most important diagnostic procedure. To start with, the positions
of the chest leads must be marked on the skin to allow detection of meaningful
changes on the ECG. By monitoring the ECG, the efficacy of the treatment can be
assessed. However, in the early stages there may be no changes in ECG, and the
changes may be first evident after hours or even days. An ECG diagnosis is made
more difficult by an old infarction, left bundle branch block, or posterior
infarction.
- In posterior wall infarction, a reciprocal ST segment depression in V1–V4
simulates ischaemia. A posterior infarction is, however, often inferoposterior
and, in addition to ST segment depression, ST segment elevations are found in
leads III and aVF.
- ST depression is suggestive of ischaemia and/or unstable angina pectoris.
Extensive ST depressions in connection with a clinical picture of MI can
indicate subendocardial damage.
Tests Following the ECG
- Troponin is the most important new marker and is replacing creatine kinase
(CK).
- CK and CK-MB or CK-MB mass (CK-MBm).
- A negative troponin T, troponin I, or CK-MBm result 9 to 12 hours after the
onset of symptoms practically rules out MI.
- Troponin T test is also valuable, if the time lapse since the beginning of
the symptoms is more than 24 hours (the concentration remains elevated longer
than that of CK). An elevated troponin T or troponin I concentration predicts
adverse events irrespective of ECG findings (Olatidoye, et al., 1998;
DARE-981100, 2000) [A].
- The tests should be performed 3 times in case of suspected infarction: on
arrival of the patient and 12 and 24 hours after arrival.
- Blood haemoglobin, leukocytes, erythrocyte sedimentation rate (ESR), and
C-reactive protein (CRP)
- Serum sodium and potassium, and chest radiograph if needed
Troponin-T or Troponin-I
- Principal indicators of myocardial damage, which can also be determined by
means of rapid testing methods suited for primary health care. A reading device
facilitates the interpretation.
- Troponin is more myocardium-specific than CK-MB and is also very sensitive.
- The concentration increases rapidly (in 4 to 6 hours) after myocardial
damage, and the elevated levels persist for at least one week.
- Indications:
- To verify or exclude MI (or myocarditis) when at least 6 hours have elapsed
from the onset of pain. Unstable angina pectoris may give positive results,
indicating slight myocardial damage, which means that the prognosis is serious
regardless of the ECG findings and active treatment is necessary. The normal
reference concentration is zero, or the method-dependent threshold is often
given as <0.5 micrograms/L.
- A negative result within 12 hours after the onset of pain excludes
infarction.
- Also used for the diagnosis of infarction when the patient's arrival for
treatment is delayed, and CK and aspartate aminotransferase (AST) have returned
to normal.
- Troponin verifies MI in cases where high CK concentration from skeletal
muscle increases the CK-MB concentration over normal limits.
- Mild elevations in the concentration that exceed the threshold are often
seen in cardiac surgery. The threshold level that would verify the diagnosis of
MI has not been defined for the situations. Mild elevations may also occur in
connection when prolonged tachycardia causes a strain on the sick
heart.
Serum CK-MB Mass
- More specific and sensitive than CK-MB
- Abnormal within 6 to 8 hours from the beginning of the pain, and remains
abnormal for 1 to 2 days.
- Slightly positive values may indicate mild myocardial damage that requires
active treatment. Unlike with troponin, the normal concentration of CK-MB is not
zero. There is an uncertain borderline area of 5 to 10 micrograms/L between the
positive and negative result.
Myoglobin
- Reacts most rapidly to myocardial damage and is positive from the first
hours onward
- Not a specific indicator of myocardial damage. Negative myoglobin is
valuable in exclusion diagnosis.
- Lack of reference values limits use.
Differential Diagnosis
- The most important differential diagnoses include
- myopericarditis
- aortic dissection
- pulmonary embolism
- unstable angina pectoris
- oesophageal pain
- See the NGC summary of the Finnish Medical Society Duodecim guideline Differential
Diagnosis of Chest Pain.
Treatment
- Oxygen, if there are problems in oxygenation (pulmonary oedema)
- For treating pain
- Glyceryl nitrate: mouth spray or sublingual tablet
- Morphine 4 to 6 mg intravenously (i.v.), additionally 4 mg 1 to 3 times at
5-minute intervals, if necessary. Oxycodone 3 to 5 mg i.v. is an alternative.
- A beta-blocker (metoprolol, atenolol, practolol) 2 to 5 mg i.v. may
sometimes ease the pain.
- Aspirin 250 mg, chewable tablet or dissolved in water, unless there are
contraindications (active ulcer, hypersensitivity to aspirin, anticoagulation)
("Collaborative overview of randomised trials of antiplatelet therapy" 1994;
DARE-948032, 1999) [A].
- A beta-blocker (Danchin, DeBenedetti, & Urban, 2002)
[A] is always instituted, unless there are contraindications
(asthma, hypotension, heart insufficiency, conduction disturbance, bradycardia).
The first dose can be given intravenously if the patient is in pain, or orally
if the patient is pain-free and time has passed since the infarction.
Beta-blockers are useful especially in patients who are tachycardic and
hypertensive but do not have heart failure.
- i.v. dose: metoprolol or atenolol 5 mg
- Orally: metoprolol or atenolol 25 to 50 mg x 2
- Thrombolytic therapy, unless there are contraindications ("Indications for
fibrinolytic therapy," 1994; DARE-948029, 1999) [A].
- Immediate percutaneous transluminal angioplasty (PTCA)
("Primary angioplasty versus intravenous thrombolysis," 2002; Sim, et al., 1995;
DARE-953385, 1999; Grines, et al., 1999) [A] if available. May
be performed when thrombolytic therapy is contraindicated. The effect is better
than that of thrombolysis in the acute phase (Vaitkus, 1995; DARE-988078, 1999;
"Primary angioplasty versus intravenous thrombolysis," 2002; Weaver, et al.,
1997; DARE-988115, 1999) [B] and also in long-term follow-up.
Stenting probably improves the outcome (Meads, et al, 2000; DARE-20018012, 2002;
Grines, et al., 1999) [A]. Further treatment with clopidogrel
for 3 months.
- An ACE inhibitor to all patients with signs or symptoms of heart failure or
ejection fraction (EF) <40, anterior wall infarction, or reinfarction
(Domanski et al., 1999; DARE-990660, 2000; Danchin, De Benedetti, & Urban,
2002) [A]. Therapy is not usually started on the first day.
- For example: captopril. Start with 6.25 mg and increase the dose
rapidly.
- Continuous nitrate therapy (Mehta & Yusuf, 2000) [A]
- Administered as an infusion, if the patient has ischaemic pain and pain
medication has no effect. Nitrate infusion.
- Orally (e.g., isosorbide dinitrate 10 to 20 mg x 2 to 3)
- Heparinization is often indicated, if the patient
- Needs prolonged bed rest and is clearly obese (thrombosis prophylaxis)
- Has atrial fibrillation (also permanent warfarin therapy)
- Has ventricular aneurysm (also permanent warfarin therapy)
- Has unstable angina pectoris
- Has embolic complications
- Anticoagulation with warfarin is often started in massive anterior
infarction and when transient ischemic attack (TIA) or stroke (mural thrombosis)
occurs with MI.
Arrhythmias in Myocardial Infarction
Objectives
- To prevent sudden death and treat severe arrhythmias immediately
- To prevent arrhythmias by treating the underlying conditions
Causes of Arrhythmias
- Myocardial damage, ischaemia, and sympathetic stimulation are associated
with ventricular arrhythmias.
- Ejection failure causes supraventricular tachyarrhythmias and atrial
fibrillation.
- Vagal stimulation causes bradyarrhythmias and atrioventricular (AV)
conduction disturbances, especially in cases of inferior-posterior wall
infarction.
- Reperfusion often causes benign ventricular rhythm; however, it also causes
severe ventricular arrhythmias.
Ventricular Fibrillation
- Often occurs within 2 to 4 hours of infarction. After 12 hours, a primary
ventricular fibrillation is rare.
- An early ectopic beat may initiate ventricular fibrillation in an ischaemic
myocardium. Ectopic beats are not treated if cardiac monitoring is effective.
- Treatment
- Acute ventricular fibrillation is treated by immediate defibrillation
starting with 200 joules. Prolonged ventricular fibrillation frequently calls
for cardiopulmonary resuscitation (CPR).
- To prevent recurrence of fibrillation, lidocaine is given: initially as
bolus of 100 mg, which can be repeated if necessary. Thereafter, a continuous
infusion of 3 to 4 mg/min is given. Amiodarone is a modern and more effective
alternative to lidocaine: infuse a 150 to 300 mg bolus in 20 minutes. Thereafter
infusion at 800 to 1200 mg/24 hours.
- A beta-blocker is usually added to the therapy.
Ventricular Tachycardia
- More than three ectopic beats and a heart rate over 120 bpm.
- Brief, spontaneously ending bursts are seen in over 50% of patients with
infarction during the first two days. They occur mainly 8 to 14 hours after, not
immediately after the infarction, as ventricular fibrillation does.
- Ventricular tachycardia leads to haemodynamic collapse or ventricular
fibrillation. The severity depends on the duration, variability, frequency, and
timing of tachycardia.
- Ventricular tachycardia may be monomorphic or polymorphic
- Treatment
- Beta-blocker
- Lidocaine boluses and infusion as in ventricular fibrillation, if
haemodynamics is compromised. Amiodarone may be a better alternative.
- If necessary, synchronized cardioversion shock with 50 joules is performed.
- Late in infarction, ventricular tachycardia is, like ventricular
fibrillation, a serious problem that requires further
examination.
Ventricular Ectopic Beats
- Occur in nearly all patients with painful MI
- May cause complications if they are frequent (more than 5/min), are
variable, or occur concomitantly with an early T wave
- Treatment is usually not necessary if cardiac monitoring is effective. A
beta-blocker may be indicated. Potassium level should be kept above
4.0.
Idioventricular Rhythm
Idioventricular rhythm is an arrhythmia often associated with MI. In the
reperfusion phase, it may even indicate that thrombolysis has been successful.
The frequency is often 70 to 80 bpm and drug therapy is not necessary.
Supraventricular Tachyarrhythmias
- Atrial fibrillation in a patient with infarction is often associated with
cardiac insufficiency and worsens the prognosis. Atrial fibrillation increases
the risk of stroke, which is why low molecular weight (LMW) heparin and warfarin
therapy are indicated.
- Atrial fibrillation is often associated with the thrombosis of the right
coronary artery or the circumflex branch: reperfusion also often corrects atrial
fibrillation.
- Atrial function is important in MI. In cardiac insufficiency, rapid atrial
fibrillation requires active direct current (DC) cardioversion. Often, the
achieved sinus rhythm does not last. In such a case, haemodynamics must be
stabilised (oxygenation, treatment of pulmonary oedema, controlling of
ventricular response with a beta-blocker and digitalis) after which spontaneous
reversal of the rhythm is waited for. The effect of the beta-blocker is seen
rapidly but that of digitalis not before several hours. Rapid ventricular
response may be controlled even if cardiac insufficiency is present: the benefit
often outweighs the disadvantage.
- Selective beta-blockers are best suited for maintaining the achieved sinus
rhythm.
- Intravenous amiodarone will not reduce the contraction of the myocardium. It
is effective in prophylaxis of atrial fibrillation (together with a
beta-blocker) and it may be used in cardioversion of atrial fibrillation and/or
slowing down the ventricular response.
- Ibutilide is a new class III drug with a single indication: treatment of
atrial fibrillation and flutter. There are limited data on its use in patients
with infarction.
- Note: A broad QRS complex tachycardia in a patient with infarction must
always be treated as a ventricular tachycardia.
Bradyarrhythmias
- A strong vagal reaction in the early stages of infarction may lead to a
circulatory collapse.
- Posteroinferior wall infarction is often associated with a functional
atrioventricular block. The QRS complex is narrow and the heart rhythm is 50 to
60 even in cases of a total block. A pacemaker is rarely needed.
- In anterior wall infarction, the proximal conduction system may be blocked:
the QRS complex is wide, the substituting rhythm is slow (30-40), the patient is
in a poor condition, and pacing is necessary. Prognosis is poor even with
pacing.
- Drug treatment
- Atropine 0.5 mg i.v., repeated as necessary, for treatment of functional
bradycardia.
Pacemaker
- In anterior wall infarction, pacing is indicated if there is a 2nd or 3rd
degree block. Pacing should be anticipated in case of a trifascicular block,
alternating right and left bundle branch block, or if an extensive infarction is
associated with left anterior hemi-block (LAFB) or left posterior hemi-block
(LPFB).
- Posteroinferior wall infarction associated with a 3rd degree
atrioventricular block requires pacing if bradycardia is detrimental to
haemodynamics and not responsive to treatment with atropine.
- Sinus bradycardia may be temporarily controlled with i.v.
atropine.
Table 1. Circulatory Conditions and Their Treatment after
Myocardial Infarction
| Condition and Treatment |
Symptoms and Signs |
Normal circulation
- Monitoring
- i.v. line (saline drop)
|
- Heart rate and blood pressure normal
- No arrhythmias
- No heart insufficiency
|
Hyperdynamic state
- Beta-blocker (metoprolol, atenolol, practolol 2 to 5 mg i.v.)
|
- Increased heart rate, high blood pressure
|
Neurovascular reflex (bradycardia-hypotension)
- Atropine 0.5 mg i.v., repeated ad 2 mg
- Dopamine infusion, if necessary
|
- Usually in connection with posteroinferior infarction
- Bradycardia, hypotension
|
Hypovolemia
- 0.9% saline 200 mL in 5 to 10 minutes according to the
response
|
- Low blood pressure, low central venous pressure (CVP), tachycardia
- Cold extremities
- Decreased venous distension (also jugular veins)
|
Severe heart failure
- Nitrate infusion
- Dopamine infusion
- Continuous positive airway pressure (CPAP)
- Treatment of pulmonary oedema
|
- Low blood pressure
- Cold extremities
- Engorged neck veins
- Chest crackles
- Chest radiograph
|
Treatment in Hospital
Follow-up and Treatment
- Pain: morphine, nitro, beta-blocker
- Blood pressure
- Skin, peripheral circulation
- Increased respiratory rate suggests cardiac insufficiency.
- Monitoring of arrhythmias
- ST segment changes
- Oxygen saturation; oxygen or continuous positive airway pressure
- A comfortable posture
- Informing and reassuring the patient
- Nicotine replacement therapy is started already in the hospital. Nicotine
addiction may be evaluated by using the Fagerstrom test, and the planning of
further treatment may be based on it.
- In an uncomplicated infarction, patients are allowed to sit as soon as they
want, they can eat unassisted, and they can be helped to a portable toilet at
the bedside. Intensive monitoring is usually needed for 1 to 2 days.
- The infarction is complicated and treatment lasts longer if the patient has
had
- Shock
- Hypotension
- Obvious cardiac insufficiency (usually requires thrombosis prophylaxis or
anticoagulation, especially if in connection with atrial fibrillation)
- Prolonged chest pain
- Serious ventricular arrhythmias
- Thromboembolic complications
- Anatomical complications (papillary muscle dysfunction or rupture)
- Pericarditis on days 2 to 4
- Treatment of the patient in primary health care (in a primary health care
hospital) is justifiable if the patient's prognosis is otherwise poor: those who
are permanent inpatients or otherwise severely disabled and for whom invasive
treatment has not been planned.
Assessment of Risk Factors in a Patient with Myocardial
Infarction
- The most important causes of mortality are
- Reinfarction
- Cardiac insufficiency
- Arrhythmias
- During hospitalization, a poor prognosis is indicated by
- Cardiac insufficiency and extensive infarction (ejection fraction [EF]
<25%)
- Chest pain and ischaemic ST changes (send to angiography)
- In connection with non-Q-wave infarction, risk factors for coronary heart
disease (CHD) and especially diabetes mellitus
- Evaluation of ischaemia and need for active treatment
- Risk is highest during the first few weeks and months after infarction.
Therefore, at the end of the hospital treatment, an early symptom-limited
exercise test is performed on many patients to estimate the need for angioplasty
and coronary surgery in particular. Refer to Table 2 in the original guideline
document for more information on the assessment of risk of reinfarction and
patient’s prognosis.
- For indications of coronary angiography, see the NGC summary of the Finnish
Medical Society Duodecim guideline Coronary
Angiography and Indications for CABG or Angioplasty.
Care after Myocardial Infarction
Drug Treatment
- Aspirin, beta-blocker (Freemantle, et al., 1999; DARE-999336, 2001; Sudlow
et al., 2002) [A], ACE inhibitors, and statins have been shown
to improve the prognosis. Glycaemic control is also important.
- Unnecessary drugs instituted during the initial phase should be discontinued
already towards the end of hospital treatment or when the patient comes to the
first check-up, not on the last day in hospital.
- Only those with cardiac insufficiency or poorly controlled blood pressure
need a diuretic.
- Aspirin 50 to 100 (-250) mg is given unless there are contraindications
("Collaborative overview of randomised trials of antiplatelet therapy," 1994;
DARE-948032, 1999) [A].
- Patients with hypertension, angina pectoris, ventricular arrhythmias,
ischaemia during an exercise test, previous infarction, an enlarged heart, low
ejection fraction, or a cardiac insufficiency need a beta-blocker. In practice,
these drugs are given to all patients who have no contraindications. Adequate
beta-blockade is achieved when the heart rate at rest is about 60 bpm.
- Nitrate plus a beta-blocker are given to all patients with angina pectoris
or ischaemia during an exercise test. Nitrate is a drug used for symptom relief
that can often be discontinued.
