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Back to Cardiovascular Diseases
Myocardial infarction
Revised: 13th November, 2004.
Clinical suspicion
The presence of sudden chest pain that lasts more than 30 minutes especially
in a patient with multiple risk factors. The pain is deep and visceral;
adjectives commonly used to describe it are heavy, squeezing, and crushing,
although occasionally it is described as stabbing or burning. It is often
accompanied by weakness, sweating, nausea, vomiting, anxiety, and a sense
of impending doom.
Although pain is the most common presenting complaint, it is by no
means always present. The proportion of painless AMIs is greater in patients
with diabetes mellitus, and it increases with age. In the elderly, AMI
may present as sudden-onset breathlessness, which may progress to pulmonary
edema.
The combination of substernal chest pain persisting for >30 min and
diaphoresis strongly suggests AMI.
Diagnosis
Myocardial infarction (MI) progresses through the following temporal
stages: (1) acute (first few hours to 7 days), (2) healing (7 to 28 days),and
(3) healed (29 days and beyond). When evaluating the results of diagnostic
tests forAMI, the temporal phase of the infarction process must be considered.
Diagnosed by the presence of at least 2 of the following:
- History of prolonged chest pain or anginal
equivalent.
- ECG changes consistent with ischemia or
necrosis.
- Elevated cardiac enzymes.
The laboratory tests of value in confirming the diagnosis may be divided
into 4 groups: (1) electrocardiogram (ECG), (2) serum cardiac markers,
(3) cardiac imaging, and (4) nonspecific indexes of tissue necrosis and
inflammation.
ECG (EKG)
During the initial stage of the acute phase of MI, total occlusion
of the infarct artery produces ST-segment elevation. Most patients initially
presenting with ST-segment elevation evolve Q waves on theECG and are
ultimately diagnosed as having sustained a Q-wave MI. A small proportion
may sustain only a non-Q-wave MI. When the obstructing thrombus is not
totally occlusive, obstruction is transient, or if a rich collateral network
is present, no ST-segment elevation is seen. Such patients are initially
considered to be experiencing either unstable anigna or a non-ST-segment
elevation MI (NSTEMI). Among patients presenting without ST-segment elevation,
if a serum cardiac marker is detected and no Q wave develops, the diagnosis
of non-Q-wave MI is ultimately made. A minority of patients who present
initially without ST-segment elevation may develop a Q-wave MI. Previously
it was believed that transmural MI is present if the ECG demonstrates
Q waves or loss of R waves, and nontransmural MI may be present if the
ECG shows only transient ST-segment and T-wave changes. However, electrocardiographic-pathologic
correlations are far from perfect; and therefore a more rational nomenclature
for designating electrocardiographic infarction is now commonly in use,
with the terms Q-wave and non-Q-wave MI replacing the terms transmural
and nontransmural MI, respectively.
Cardiac enzymes
Certain proteins, called serum cardiac markers, are released into the
blood in large quantities from necrotic heart muscle after AMI. The rate
of liberation of specific proteins differs depending on their intracellular
location and molecular weight, and the local blood and lymphatic flow.
The temporal pattern of protein release is of diagnostic importance,
but contemporary urgent reperfusion strategies necessitate making a decision
(based largely on a combination of clinical and ECG findings) before the
results of blood tests have returned from the central laboratory. Rapid
whole-blood bedside assays for serum cardiac markers are now available
and may facilitate management decisions, particularly in patients with
nondiagnostic ECGs.
-
CKMB: The MB isoenzyme of creatine phosphokinase is more specific to
AMI than
CK. However, it may still be elevated in skeletal muscle injury.
Rather than attempting to make the diagnosis ofAMI on the basis of a single
measurement of
CK and
CKMB, clinicians should evaluate a series of measurements
obtained over the first 24 h. Skeletal muscle release of
CKMB typically
produces a "plateau" pattern, whereas AMI produces a
CKMB elevation that
peaks approximately 20 h after the onset of coronary occlusion. When released
into the circulation, the myocardial form of
CKMB (CKMB2) is acted on
by the enzyme carboxypeptidase, which cleaves a lysine residue from the
carboxyl terminus to produce an isoform (CKMB1) with a different electrophoretic
mobility. A CKMB2:CKMB1 ratio of>1.5 is highly sensitive for the diagnosis
of AMI, particularly 4 to 6 h after the onset of coronary occlusion.
The MB-CK fraction appears in 4 hours after onset of infarction and
peaks at about 24hrs with a duration of 72 hours.
CK MB: 4h - 24h - 72h
-
Cardiac-specific troponin T (cTnT) and
cardiac-specific troponin I
(cTnI) have amino acid sequences different from those of the skeletal
muscle forms of these proteins. These differences have permitted the development
of quantitative assays for
cTnT and
cTnI with highly specific monoclonal
antibodies. Since
cTnT and
cTnI are not normally detectable in the blood
of healthy individuals but may increase afterAMI to levels over 20 times
higher than the cutoff value (usually set only slightly above the noise
level of the assay), the measurement of
cTnT or
cTnI is of considerable
diagnostic usefulness, and they are now the preferred biochemical markers
for MI.
The cardiac troponins are particularly valuable when there is clinical
suspicion of either skeletal muscle injury or a small MI that may be below
the detection limit for
CK and
CKMB measurements. Levels of
cTnI may remain
elevated for 7 to 10 days after AMI, and
cTnT levels may remain elevated
for up to 10 to 14 days. Thus, measurement of
cTnT or
cTnI has replaced
measurement of
lactate dehydrogenase (LDH) and its isoenzymes in patients
with suspected MI who come to medical attention more than 24 to 48 h after
the onset of symptoms.
- LDH on the other hand appears 12 hours after the infarct and peaks
2 days later to last 14 days.
LDH has been largely replaced with the more
specific cardiac
troponin
for patients with suspected AMI presenting after
the initial 48 hours have passed.
LDH: 12h - 48h - 14 days
-
CK: Creatine phosphkinase has been replaced by
CKMB due to lack of
specificity of
CK in AMI.
- SGOT, SGPT
Imaging
Two-dimensional echocardiography (Chap. 227) is the most frequently
employed imaging modality in patients with AMI. Abnormalities of wall
motion are almost universally present.
Several radionuclide imaging techniques are available for evaluating
patients with suspected AMI. However, these imaging modalities are used
less often than echocardiography because they are more cumbersome and
they lack sensitivity and specificity in many clinical circumstances.
Myocardial perfusion imaging with201Tl or99mTc-sestamibi, which are distributed
in proportion to myocardial blood flow and concentrated by viable myocardium
(Chap. 244) reveal a defect ("cold spot") in most patients during the
first few hours after development of a transmural infarct. However, although
perfusion scanning is extremely sensitive, it cannot distinguish acute
infarcts from chronic scars and thus is not specific for the diagnosis
of acute MI.
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Management of MI
Recognize patients that are candidates
for reperfusion therapy.
Patients presenting with new ST elevation or presumed new LBBB is indicative
of transmural infarction and are indicated for thrombolytic therapy within
30mints of admission or 1ry PTCA within 60mints of arrival
to hospital.
Initial treatment for all patients with chest pain and suspected
myocardial infarction ( whether or not they are indicated for reperfusion
therapy they should all receive the following):
-
Sublingual nitroglycerin 0.4mg q
5mints should be administered to all patients in the absence of hypotension
or marked tachycardia or inferior infarction complicated by right ventricular
infarction.
-
Analgesics: very important as it
reduces the circulating catecholamines and myocardial oxygen consumption.
Morphine sulfate is choice and given only if symptoms persist after
0.4mg sublingual nitroglycerin q 5mints.
-
Antiplatelets: 165-325mg PO reduces
mortality from myocardial infarction.
-
Anticoagulation: as in
ischemia.
-
Beta-antagonists: reduce myocardial
ischemia and may limit infarct size.
Contraindications to beta blockers are:
- rales over > 1/3 of lung fields.
- HR < 60/mint
- Sys BP <90.
- PR >250msec
- advanced heart block.
- bronchospastic lung disease.
- severe PVD.
Therapy is initiated with IV metoprolol 5mg. Can be repeated q5mints
till total 15mg (loading). Patients tolerating the loading dose are
switched to oral 50mg q6-12hrs then 100 mg PO bid (/ atenolol 100mg
qd).
-
IV fluids for those in shock
-
ACE-inhibitors in all normotensive patients especially if there is
clinical evidence of heart failure.
-
Oxygen: arterial O2 is
obtained at admission only if the patient is in respiratory distress
and is not a candidate for thrombolytic therapy. 2-4 L/mint via nasal
cannulation. If patients do not have hypoxemia they can be discontinued
after 6hrs. increasing O2 to supranormal levels is not indicated
as this increases the BP and resistance.
Thrombolytic therapy
Patients should be stratified into those that are candidates for thrombolytic
therapy and those that are candidates for angiography and PTCA. Thrombolytic
therapy is the first choice for restoring coronary
perfusion in patients with acute MI, assuming the absence of contraindications
for its use.
* those in need of thrombolytic therapy:
- all patients presenting within 12hrs of a prolonged ischemic attack
(>30mints that is associated with new
ST segment elevation of at least 0.1 mV (>1 mm) in at least two
contiguous leads).
- therapy is also indicated in patients with marked ST segment depression
(>2 mm) in the anterior leads that is indicative of posterior wall infarction
and
- those with prolonged chest pain and presumed
new LBBB.
Fibrinolytic agents will induce clot lysis in 60-90% of patients and will
normalize coronary blood flow in 30-40% of infarct-related arteries by
90 minutes, depending on the agent used.
Absolute Contraindications to Fibrinolytic Therapy
- Active internal bleeding
- CNS neoplasm, AV malformation, or aneurysm.
- CNS procedure or CVA within two months.
- Severe uncontrolled hypertension (over 200/130 or complicated
by retinovascular disease or encephalopathy)
- Known bleeding diathesis
- MI due to aortic dissection
- Allergy to either streptokinase or anistreplase, if streptokinase
or anistreplase will be used
Relative Contraindications to thrombolytic therapy
- Age over 75
- Cerebrovascular disease
- Pregnancy or early postpartum
- Recent major surgery (less than 10 days), noncompressable vessel
puncture, or organ biopsy
- Recent trauma, including CPR of over 2 minutes duration
- Recent GI bleeding or active ulcer disease (less than 10 days)
- Acute pericarditis or subacute bacterial endocarditis
- Septic thrombophlebitis
- High likelihood of left heart thrombus (eg. mitral stenosis with
atrial fibrillation)
- Known coagulation defects, including anticoagulant therapy
- Significant liver dysfunction
- Conditions associated with bleeding risks, such as diabetic retinopathy.
- Menstruation
- Terminal cancer or other end-stage disease
- Recent streptococcal infection, if streptokinase or anistreplase
will be used
Adjuncts to thrombolysis:
Antithrombotic
therapy in the form of anti-patelets and anti-thrombotics in addition
to beta adrenergic blockers.
Those in need of emergency
angiography and possible PTCA are: (within 60mints of admission)
- (1) those with chest
pain and persistent ST elevation who present more than 12 hours
after the onset of acute MI,
- (2) those with persistent ST depression, and
- (3) those with refractory angina symptoms and nondiagnostic ECG changes.
- (4) Patients with contraindications to thrombolysis usually are candidates
for primary PTCA.
Those in need of emergency CABG:
Emergency CABG is indicated in patients with refractory
ischemia or cardiogenic shock whose coronary anatomy is not suitable for
PTCA, in patients in whom PTCA has failed, and in patients with mechanical
complications of MI. Insertion of an intra-aortic balloon pump usually
is indicated to stabilize these patients before the surgical procedure.
Risk stratification & subsequent management of MI:
This is done by clinical assessment and echocardiography
at 24 hours.
1. High risk patients (patients with any of the following):
-
Heart failure, heart block
-
Previous myocardial infarction
-
Recurrent myocardial infarction or angina during the 24 hours.
These should remain hospitalized for several days after stabilization
and undergo a coronary angiography to determine if in need of PTCA/ CABG.
2. Low risk patients (those without any of the above criteria).
These patients can be transferred to a monitored telemetry floor after
24-36 hours. If ambulatory without recurrent ischemia they can be discharged
within 4 days and undergo subsequent symptom limited stress testing as
outpatients within 10 -14 days. Those with induceable ischemia are subsequently
sheduled for PTCA / CABG. If stress testing goes well then another one
is usually performed at 6-8 weeks before going to work.
Secondary prevention:
After all the above is accomplished patients are put on a diet and exercise
program to reduce co-existing risk factors e.g. lipid lowering drugs in
hypercholestrolemia, estrogens in postmenopausal patients.
-
Coexisting medical conditions are treated appropriately.
-
Antiplatelets (Aspirin 75-325mg) given daily indefinitely
(reduces vascular events by 30%).
-
Warfarin for 6 months if large anterior infarct, aneurysm or mural thrombus.
It is given for life if co-existing atrial fibrillation and severe left
ventricular failure.
-
Beta blockers are given indefinitely unless contraindicated or very low
risk group and young (reduces mortality from all causes by ~25%).
-
Calcium channel blockers are given if beta blockers are contraindicated.
-
Angiotensin converting enzyme (ACE) inhibitors are given to all patients
for the first 6 weeks. It is given indefinitely if left ventricular failure
or if the ejection fraction is less than 40% (decreases 2 year
mortality by 30%).
-
Nitrates in symptomatic ischemia or heart failure.
Prognosis
33% of patients will die from their 1st
myocardial infarction.
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