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ACUTE

CORONARY
SYNDROME

Objectives
At the end of this lecture, the PGIs will be
able to:
identify, diagnose, treat and manage cases
of UA, NSTEMI AND STEMI

Non-ST-Segment Elevation Acute Coronary Syndrome


(Non-ST-Segment Elevation Myocardial Infarction and
Unstable Angina)
IHD fall into two large groups:
Patients with chronic coronary artery disease (CAD)
with stable angina
Patients with acute coronary syndromes (ACSs)
Acute myocardial infarction with ST-segment elevation (STEMI) on
their presenting electrocardiogram and non-ST-segment
elevation acute coronary syndrome (NSTE-ACS) non-ST -segment
elevation myocardial infarction (NSTEMI) who by
definition have evidence of myocyte necrosis and those with
unstable angina (UA) who do not.

Pathophysiology
NSTE-ACS
- imbalance between oxygen
supply and oxygen demand

Other causes of NSTE-ACS


include:
( 1 ) dynamic obstruction
( 2 ) severe mechanical obstruction
( 3 ) increased myocardial oxygen
demand

NSTE-ACS studied at
angiography
10% have stenosis of the left main coronary
artery
35% have three-vessel CAD
20% have two-vessel disease
20% have single-vessel disease
15 % have no apparent critical epicardial
coronary artery stenosis;

Clinical PRESENTATION
chest discomfort is severe and has at least one of three features:
(1) it occurs at rest (or with minimal exertion) lasting > 10 minutes
(2) it is of relatively recent onset
(3) it occurs with a crescendo pattern
evidence of myocardial necrosis - elevated levels of biomarkers of
cardiac necrosis

History and Physical


Examination
The chest discomfort
- Severe - described as frank pain
- located in the substernal region or sometimes
in the epigastrium
- radiates to the left arm left shoulder and/or
neck.

Anginal "equivalents"
- Dyspnea
- epigastric discomfort
- Nausea
- weakness may occur instead of chest pain
appear to be more frequent in women, the elderly and
patients with diabetes mellitus.

Electrocardiogram
ST -segment depression occurs in 20 to 25% of
patients
it may be transient in patients without
biomarker evidence of myocardial necrosis, but
may be persistent for several days in NSTEMI.
T -wave changes are common but are less
specific signs of ischemia, unless they are new
and deep T-wave inversions (> or =0.3 mV).

Cardiac Biomarkers
elevated biomarkers of necrosis - cardiac troponin I
or T
- are specific, sensitive, and the preferred markers
of myocardial
necrosis.
The MB isoform of creatine kinase (CK-MB)
- is a less sensitive alternative.
- distinguish patients with NSTEMI from those with
UA.

DIAGNOSTlC EVALUATION
3 major noninvasive tools:
- electrocardiogram(ECG)
- cardiac biomarkers
- stress testing

Treatment
MEDICAL TREATMENT
Patients should be placed at bed rest with continuous ECG monitoring for
ST-segment deviation and cardiac arrhythmias.
Ambulation is permitted if the patient shows no recurrence of ischemia
(symptoms or ECG changes) and does not develop an elevation of a
biomarker of necrosis for 12-24 hrs.
Medical therapy involves simultaneous anti-ischemic and antithrombotic
treatments and consideration of coronary revascularization.

ANTISCHEMIC TREATMENT
- To provide relief and prevention of recurrence of chest
pain
- initial treatment should include bed
rest nitrates beta adrenergic blockers and inhaled
oxygen in the presence of hypoxemia.

Nitrates
These should first be given sublingually or by buccal spray (0.3-0.6 mg)
If pain persists after three doses given 5 min apart
- intravenous nitroglycerin (5- 10 g/min using non-absorbing tubing)
- The rate of the infusion may be increased by 10 g/min every 3-5min until symptoms
are
relieved systolic arterial pressure falls to <100 m m Hg or the dose reaches 200
g/min
Topical or oral nitrates can be used when the pain has resolved or they may replace
intravenous nitroglycerin when the patient has been pain free for 12-24 hr.
The only absolute contraindications - hypotension or the use of sildenafil or other
phosphodiesterase-5 inhibitors within the previous 24-48 h

Beta Adrenergic Blockers


intravenous route in patients with severe
ischemia
contraindicated in the presence of heart
failure.
oral beta blockade targeted to a heart rate of
50-60 beats/min

Calcium channel blockers


are recommended for patients who have
persistent symptoms
or ECG signs of ischemia

Additional medical therapy


ACE inhibitors or ARBs
Early administration of intensive HMG-CoA reductase
inhibitors
(statins such as atorvastatin 80 mg/d prior to
percutaneous coronary intervention (PCI) and
continued thereafter has been shown to reduce
complications of the procedure and recurrences of ACS.

ANTITHROMBOTIC THERAPY
This is the second major cornerstone of
treatment.
There are two components of antithrombotic
therapy:
- antiplatelet drugs and anticoagulants

Antiplatelet Drugs
Aspirin
Initial treatment should begin with the platelet
cyclooxygenase inhibitor.
initial dose is 325 mg/d with lower doses (75- 100 mg/d)
Contraindications a reactive bleeding or aspirin intolerance.
"Aspirin resistance" has been noted in 2-8% of patients but
frequently has been related to noncompliance.

Clopidogrel
Platelet P2Y12 receptor blocker
In the absence of a high risk for bleeding patients with
NSTE-ACS irrespective of whether an invasive or
conservative strategy is selected
to inhibit platelet activation.
is an inactive prodrug that is converted into an active
metabolite that causes irreversible blockade of the platelet
P2Y12 receptor.

Dual antiplatelet therapy


Clopidogrel + aspirin - shown to confer a 20% relative
reduction in cardiovascular death MI or stroke
compared to aspirin alone
BUT associated with a moderate (absolute 1%) increase
in major bleeding.
Beneficial - both in patients treated conservatively and in
those who underwent PCI
should continue for at least 1 year in patients with NSTEACS, esp. those with a drug-eluting stent - prevent stent
thrombosis

inadequate response - genetic variant of the


cytochrome P450 system
A variant of the 2C19 gene leads to reduced
conversion of clopidogrel into its active metabolite
Alternate P2Y12 blockers such as prasugrel or
ticagrelor used with aspirin should be
considered in patients with NSTE-ACS who develop
a coronary event while receiving clopidogrel and
aspirin or who are hyporesponsive to clopidogrel
as identified by platelet a n d/or genetic testing

Prasugrel
A second P2Y12 blocker also a thienopyridine
achieves a more rapid onset and higher level of
platelet inhibition than clopidogrel.
for ACS patients following angiography in whom
PCI is planned.
a loading dose of 60 mg followed by 10mg/d for
up to 15 months.

TRITON-TIMI 38 trial
showed that relative to clopidogrel
prasugrel reduced the risk of cardiovascular
death MI or stroke significantly al beit
with an increase in major bleed ing.

Ticagrelor
is a novel potent reversible platelet P2Y12 inhibitor
has been shown in the PLATO trial to reduce the risk of cardiovascular
death MI or stroke compared with clopidogrel in ACS patients
who a retreated by either an invasive or a conservative strategy.
This agent reduced mortality but increased the risk of bleeding not
associated with coronary artery bypass grafting.
a loading dose of 180 mg and maintenance dose of 90 mg bid

Intravenous GPIlb/IIla inhibitors


Their benefit however has been small (only
a 10% reduction in death or MI with a
significant increase in major bleeding).
Two recent studies failed to show a benefit of
routine early initiation of a drug in this class
compared with their use only in patients who
undergo PCI.

Anticoagulants
Four options to be added to antiplatelet agents:
(1) unfractionated heparin (UFH) long the mainstay
of therapy;
(2) the low-molecular-weight heparin (LMWH)
enoxaparin
(3) bivalirudin
(4) the indirect factor Xa inhibitor, fondaparinux

Excessive bleeding
is the most important adverse effect of all
antithrombotic agents including both antiplatelet
agents and anticoagulants.
Therefore attention must be directed to the doses of
antithrombotic agents, accounting for body
weight creatinine clearance and a previous
history of excessive bleeding
Patients who have experienced a stroke are at higher
risk of intracranial bleeding with potent antiplatelet
agents and combinations of antithrombotic drugs

LONG.TERM MANAGEMENT
The time of hospital discharge - "teachable
moment" for the patient
Risk-factor modification is key

There is evidence of benefit with long-term therapy with five classes of drugs that are
directed at different components of the atherothrombotic process.
Beta blockers statins and ACE inhibitors or angiotensin receptor blockers - recommended
for long-term plaque stabilization.
Antiplatelet therapy now recommended to be the combination of low-dose (75-100 mg/d)
Aspirin and a P2Y12 inhibitor (clopidogrel prasugrel or ticagrelor) for 1 year with
aspirin continued thereafter prevents or reduces the severit of any thrombosis that would
occur if a plaque were to rupture
Registries have shown that women and racial minorities as well as patients with NSTE-ACS
at high risk including the elderly and patients with diabetes or chronic kidney disease are
less likely to receive evidence-based pharmacologic and interventional therapies with
resultant poorer clinical outcomes and quality of life. Special attention should be directed to
these groups.

PRINZMETAL'S VARIANT ANGINA


described a syndrome of severe ischemic pain that usually occurs
at rest and is associated with transient ST segment elevation.
is caused by focal spasm of an epicardial coronary artery
leading to severe transient myocardial ischemia and occasionally
infarction.
cause of the spasm is not well defined but it may be related to
hypercontractility of vascular smooth muscle due to adrenergic
vasoconstrictors leukotrienes or serotonin.

Manifestations Patients with PVA are generally younger


and have fewer coronary risk factors (with the exception
of cigarette smoking) than do patients with NSTE-ACS.
Cardiac examination is usually unremarkable in the
absence of ischemia.
The clinical diagnosis of PV A is made by the detection of
transient ST segment elevation with rest pain.
Many patients also exhibit multiple episodes of
asymptomatic ST-segment elevation (silent ischemia ) .
Small elevations of troponin may occur in patients with
prolonged attacks.

Coronary angiography
demonstrates transient coronary spasm as the
diagnostic hallmark of PVA.
Hyperventilation or intracoronary acetylcholine
has been used to provoke focal coronary stenosis
on angiography or to provoke rest angina with ST
-segment elevation to establish the diagnosis.

Nitrates and calcium channel blockers


- are the main therapeutic agents.
- Aspirin may actually increase the severity of ischemic
episodes possibly as a result of the sensitivity of coronary tone
to modest changes in the synthesis of prostacyclin. The
response to beta blockers is variable.
- Coronary revascularization may be helpful in patients who also
have discrete flow-limiting proximal fixed obstructive lesions

Prognosis
Many patients with PVA pass through an acute active phase with frequent
episodes of angina and cardiac events during the first 6 months after
presentation.
Survival at 5 years is excellent (-90-95%).
Patients with no or mild fixed coronary obstruction tend to experience a more
benign course than do patients with associated severe obstructive lesions.
Nonfatal MI occurs in up to 20% of patients by 5 years.
Patients with PVA who develop serious arrhythmias during spontaneous episodes
of pain are at a higher risk for sudden cardiac death. In most patients who survive
an infarction or the initial 3- to 6-month period of frequent episodes there is a
tendency for symptoms and cardiac events to diminish over time.

ST-Segment Elevation Myocardial


Infarction
Acute myocardial infarction (AMI) is one of the most
common diagnoses in hospitalized patients in
industrialized countries.
In the United States approximately 525000 patients
experience a new AMI and 190,000 experience a
recurrent AMI each year.
More than half of AMI related deaths occur before the
stricken individual reaches the hospital.
The 1 -year mortality rate after AMI is about 1 5%.
Mortality is approximately fourfold higher in elderly
patients (over age 75) as compared with younger patients.

clinical diagnosis - prolonged ischemic discomfort


at rest
diagnostic and triage tool 12-1ead
electrocardiogram (ECG)

PATHOPHYSIOLOGY: ROL E
OF ACUTE PLAQUE RUPTURE
usually occurs when coronary blood flow
decreases abruptly after a thrombotic occlusion
of a coronary artery previously affected by
atherosclerosis.
development of a rich collateral network over
time.
occurs when a coronary artery thrombus
develops rapidly at a site of vascular injury.

surface of an atherosclerotic plaque becomes


disrupted (exposing its contents to the blood)
and conditions (local or systemic) favor
thrombogenesis.
A mural thrombus forms at the site of plaque
disruption and the involved coronary artery
becomes occluded.
Histologic studies indicate that the coronary
plaques prone to disruption are those with a
rich lipid core and a thin fibrous cap.

The coagulation cascade


exposure of tissue factor in damaged
endothelial cells at the site of the disrupted
plaque.
Factors VII and X are activated
prothrombin to thrombin
converts fibrinogen to fibrin

The amount of myocardial damage caused by coronary occlusion depends on


(1) the territory supplied by the affected vessel
(2) whether or not the vessel becomes totally occluded
(3) the duration of coronary occlusion
(4) the quantity of blood supplied by collateral vessels to the affected tissue
(5) the demand for oxygen of the myocardium whose blood supply has been
suddenly limited
(6) endogenous factors that can produce early spontaneous lysis of the occlusive
thrombus
(7) the adequacy of myocardial perfusion in the infarct zone when flow is restored
in the occluded epicardial coronary artery.

Patients at increased risk for developing STEMI


include those
with multiple coronary risk factors and those with
UA
Less common underlying medical conditions
predisposing
hypercoagulability collagen vascular disease
cocaine abuse and intracardiac thrombi or
masses that can produce coronary emboli.

C L l N ICAL PRESENTAT I
ON
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.

Pain
is the most common presenting complaint in patients with STEMI
is deep and visceral; heavy squeezing and crushing
occasionally it is described as stabbing or burning
occurs at rest is usually more severe and lasts longer.
Typically the pain involves the central portion of the chest and/or
the epigastrium and on occasion it radiates to the arms.
It is often accompanied by weakness sweating
nausea vomiting anxiety and a sense of impending doom.
The pain may commence when the patient is at rest but when it
begins during a period of exertion it does not usually subside with
cessation of activity in contrast to angina pectors.

simulate pain from acute pericarditis


(Chap.288) pulmonary embolism (Chap.
300) acute aortic dissection (Chap.30 1 )
costochondritis and gastrointestinal disorders.
The proportion of painless STEMIs is greater in
patients with diabetes mellitus and it
increases with age.
In the elderly STEMI may present as suddenonset breathlessness which may progress to
pulmonary edema.

PHYSICAL FINDINGS
The combination of substernal chest pain persisting for
>30 min and diaphoresis strongly suggests STEMI.
Although many patients have a normal pulse rate and
blood pressure 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)
up to one-half with inferior infarction show evidence of
parasympathetic hyperactivity (bradycardia and/or
hypotension)

The precordium is usually quiet


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 fourth and third heart sounds decreased
intensity of the first heart sound and paradoxical
splitting of the second heart sound(Chap. 267)

transient midsystolic or late systolic apical systolic


murmur - valvular
pericardial friction rub - transmural STEMI
The carotid pulse is often decreased in volume
reflecting reduced stroke volume.
Temperature elevations up to 38C may be observed
during the first week after STEMI. The arterial
pressure is variable; in most patients with transmural
infarction systolic pressure declines by appro
mately 10 1 5 mmHg from the preinfarction state.

LABORATORY FINDINGS

STEMI progresses through the following


temporal stages:
(1) acute (first few hours-7 days)
(2) healing (7-28 days)
(3) healed ( 29 days).

The laboratory tests of value in confirming the


diagnosis may be divided into four groups:
(1) ECG
(2) serum cardiac biomarkers
(3) cardiac imaging
(4) nonspecific indices of tissue necrosis and
inflammation.

ELECTROCARDIOGRAM

The electrocardiographic manifestations of STEMI


initial stage - total occlusion of an epicardial coronary artery produces ST -segment
elevation.
A small proportion of patients initially presenting with ST -segment elevation will
not develop Q waves when the obstructing thrombus is not totally occlusive,
obstruction is
transient or if a rich collateral network is present.
with ischemic discomfort but without ST -segment elevation if a serum cardiac biomarker
of necrosis is detected the diagnosis of NSTEMI is ultimately made.
A minority of patients who present initially without ST -segment elevation may develop a Qwave MI. Previously it was believed that transmural myocardial infarction (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 terms such as Q-wave
MI non-Q-wave MI transmural MI and nontransmural MI have been replaced by
STEMI and NSTEMI (Fig. 295 - 1 ) .
Contemporary studies using magnetic resonance imaging (MRI) suggest that the
development of a Q wave on the ECG is more dependent on the volume of infarcted tissue
rather than the transmurality of infarction

SERUM CARDIAC
BIOMARKERS
are released from necrotic heart muscle after
STEMI.
The rate of liberation of specific proteins differs
depending on their intracellular location their
molecular weight and the local blood and
lymphatic flow.
become detectable in the peripheral blood once
the capacity of the cardiac lymphatics to clear
the interstitium of the infarct zone is exceeded
and spillover into the venous circulation occurs.

Cardiac-specifiC troponin T (cTnT) and cardiac-specific troponin 1 (cTnI)


amino-acid sequences different from those of the skeletal muscle forms of these
proteins.
Detected by highly specific monoclonal antibodies.
Since cTnT and cTnl are not normally detectable in the blood of healthy individuals but
may increase after STEMI to levels many times higher than the upper reference limit
(the highest value seen in 99% of a reference population not suffering from MI) the
measurement of cTnT or cTnl is of considerable diagnostic usefulness preferred
biochemical markers for MI
With improvements in the assays for the cardiac-specific troponins it is now possible
to detect concentrations < 1 ng/L in patients without ischemic-type chest discomfort.
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 creatine
phosphokinase (CK) and its MB isoenzyme (CK-MB) measurements and they are
therefore of particular value in distinguishing UA from NSTEMI.
Levels of cTnl and cTnT may remain elevated for 7- 1 0 days after STEMI.

CK rises within 4-8 h and generally returns to normal by 48-72 h


An important drawback - is its lack of specificity for STEMI as
CK may be elevated with skeletal muscle disease or trauma
including intramuscular injection.
The MB lsoenzyme of CK has the advantage over total CK that it
is not present in significant concentrations in extracardiac tissue
and therefore is considerably more specific. However
cardiac surgery myocarditis 1 601 and electrical
cardioversion often result in elevated serum levels of the MB
isoenzyme.
A ratio (relative index) of CK-MB mass to CK activity ???2.5
suggests but is not diagnostic of a myocardial rather than a
skeletal muscle source for the CK-MB elevation

Many hospitals are using cTnT or cTnl rather than CKMB as the routine serum cardiac marker for
diagnosis of STEMI although any of these analytes
remain clinically acceptable.
not cost -effective to measure both a cardiac-specific
troponin and CK-MB at all time points in every
patient.
While it has long been recognized that the total
quantity of protein released correlates with the size
of the infarct the peak protein con centration
correlates only weakly with infarct size.

The nonspecific reaction to myocardial injury is


associated with polymorphonuclear
leukocytosis which appears within a few
hours after the onset of pain and persists for 37 days; the white blood cell count often reaches
levels of 1 2OOO- 1 5 OOOmg/dL.
The erythrocyte sedimentation rate rises more
slowly than the white blood cell
count peaking during the first week and
sometimes remaining elevated for 1 or 2
weeks.

CARDIAC IMAGIN G
Abnormalities of wall motion on two-dimensional echocardiography are almost universally present.
Although acute STEMI cannot be distinguished from an old myocardial scar or from acute severe
ischemia by echocardiography the ease and safety of the procedure make its use appealing as a
screening tool in the Emergency Department setting.
When the ECG is not diagnostic of STEMI early detection of the presence or absence of wall
motion abnormalities by echocardiography can aid in management decisions such as whether
the patient should receive reperfusion therapy (e.g. fibrinolysis or a percutaneous coronary
intervention [PCI] ) .
Echocardiographic estimation of left ventricular (L V) function is useful prognostically; detection of
reduced function serves as an indication for therapy with an inhibitor of the renin-angiotensinaldosterone system.
Echocardiography may also identify the presence of right ventricular (RV) infarction ventricular
aneurysm pericardial effusion and LV thrombus. In addition Doppler echocardiography is
useful in the detection and quantitation of a ventricular septal defect and mitral regurgitation
two serious compliations of STEMI.

Several radionuclide imaging techniques are available for evaluating


patients with suspected STEMI. However these imaging modalities are
used less often than echocardiography because they are more cumbersome
and lack sensitivity and speificity in many clinical circumstances.
Myocardial perfusion imaging with [201Tl] or 99mTc] sestamibi, which are
distributed in proportion to myocardial blood flow and concentrated by
viable myocardium reveals a defect (" cold spot") in most patients during
the first few hours after development of a transmural infarct.
Radionuclide ventriculography carried out with [99mTc ] -labeled red
blood cells, frequently demonstrates wall motion disorders and reduction in
the ventricular ejection fraction in patients with STEMI. While of value in
assessing the hemodynamic onsequences of infarction and in aiding in the
diagnosis of RV infarction when the RV ejection fraction is depressed this
technique is nonspecific as many cardiac abnormalities other than MI
alter the radionuclide ventriculogram.

MI can be detected accurately with high-resolution cardiac MRI


(Chap. 270e) using a technique referred to as late enhancement. A
standard imaging agent (gadolinium) is administered and images
are obtained after a l O-min delay. Since little gadolinium enters
normal myocardium where there are tightly packed myocytes
but does percolate into the expanded intercellular region of the
infarct zone there is a bright signal in areas of infarction that
appears in stark contrast to the dark areas of normal myocardium.
An Expert Consensus Task Force for the Universal Definition of
Myocardial Infarction has provided a comprehensive set of criteria
for the definition of MI that integrates the clinical and laboratory
findings discussed earlier (Table 295- 1 ) as well as a classification
of MI into five types that reflect the clinical circumstances in which
it may occur

INITIAL MANAGEMENT
PREHOSPITAL CARE
The prognosis in STEMI is largely related to the occurrence of two
general classes of complications:
( 1 ) electrical complications (arrhythmias)
(2) mechanical complications ("pump failure").
Most out of-hospital deaths from STEMI are due to the sudden
development of ventricular fibrillation. The vast majority of deaths
due to ventricular fibrillation occur within the first 24 h of the onset
of symptoms and of these over half 0ur in the first hour.

Therefore the 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

General guidelines for initiation of fibrinolysis in


the prehospital setting include the ability to
transmit 1 2-1ead ECGs to confirm the
diagnosis the presence of paramedics in the
ambulance training of paramedics in the
interpretation of ECGs and management of
STEMI and online medical command and
control that can authorize the initiation of
treatment m e field

MANAGEMENT IN THE
EMERGENCY DEPARTMENT
In the Emergency Department
the goals with suspected STEMI
control of cardiac discomfort
rapid identification who are candidates for urgent reperfusion therapy
triage of lower-risk patients to the appropriate location in the hospital
avoidance of inappropriate discharge of patients with STEMI
The overarching goal is to minimize the time from first medical contact to
initiation of reperfusion therapy.
This may involve transfer from a non-PCI hospital to one that is PCI capable
with a goal of initiating PCI within 120 min of first medical contact

Aspirin
is essential in the management of patients with suspected
STEMI and is effective across the entire spectrum of acute coronary
syndromes (Fig. 295- 1 ) . Rapid inhibition of cyclooxygenase- 1 in
platelets
followed by a reduction of thromboxane A2 levels is achieved by
buccal absorption of a chewed 160-325-mg tablet in the Emergency
Department. This measure should be followed by daily oral adminis
tration of aspirin in a dose of 75- 162 mg.

In patients whose arterial 0?? saturation is normal


supplemental 0
is of limited if any clinical benefit and therefore is not cost
-effective.
However when hypoxemia is present O2 should be
administered by
nasal prongs or face mask (2-4 L/min) for the first 6 1
2 h after infarction;
the patient should then be reassessed to determine if
there is a
ontinued need for such treatment.

CONTROL OF
DISCOMFORT
Sublingual nitroglycerin
can be given safely to most patients with STEMI.
Up to three doses of 0.4 mg should be administered at about 5-min
intervals.
nitroglyerin may be capable of both decreasing myocardial oxygen
demand (by lowering preload) and increasing myocardial oxygen supply
(by dilating infarct-related coronary vessels or collateral vessels).
In patients whose initially favorable response to sublingual nitroglyerin is
followed by the return of chest discomfort particularly if accompanied
by other evidence of ongoing ischemia such as further ST-segment or Twave shifts the use of intravenous nitroglycerin should be considered.

Contraindications
low systolic arterial pressure (<90 mmHg)
clinical suspicion of RV infarction (inferior infarction on
ECG elevated jugular venous pressure clear lungs and
hypotension).
phosphodiesterase-5 inhibitor for erectile dysfunction within the
preceding 24h (hypotensive effects of nitrates)
An idiosyncratic reaction to nitrates consisting of sudden marked
hypotension sometimes occurs but can usually be reversed
promptly by the rapid administration of intravenous atropine

Morphine

is a very effective analgesic for the pain associated with STEMI.


But..it may reduce sympathetically mediated arteriolar and venous constriction
and the resulting venous pooling may reduce cardiac output and arterial pressure.
These hemodynamic disturbances usually respond promptly to elevation of the
legs but in some patients volume expansion with intravenous saline is
required.
The patient may experience diaphoresis and nausea but these events usually
pass and are replaced by a feeling of well-being associated with the relief of pain.
vagotonic effect and may cause bradycardia or advanced degrees of heart
block particularly in patients with inferior infarction. These side effects usually
respond to atropine (0.5 mg intravenously).
routinely administered by repetitive (every 5 min) intravenous injection of small
doses (2-4 mg) rather than by the subcutaneous administration of a larger
quantity because absorption may be unpredictable by the latter route.

Intravenous beta blockers


control pain effectively in some patients presumably by diminishing
myocardial 02 demand and hence ischemia.
More important - reduce the risks of reinfarction and ventriular
fibrillation
Oral beta blocker
initiated in the first 24 h for patients who do not have any of the
following:
(1) signs of heart failure
(2) evidence of a low-output state
(3) increased risk for cardiogenic shock

Relative contraindications to beta blockade


PR interval greater than 0.24 seconds
second- or third-degree heart block
active asthma or reactive airway disease .

Metoprolol
5 mg every 2-5 min for a total of three doses
provided the patient has a heart rate >60 beats/min
systolic pressure > 100 mmHg
a PR interval <0.24 s
and rales that are no higher than 10 cm up from the
diaphragm
Fifteen minutes after the last intravenous dose an oral
regimen is initiated of 50 mg every 6 h for 48 h followed
by 1 00 mg every 12 h.

Calcium antagonists
evidence that short-acting dihydropyridines may
be associated with an increased mortality risk

MANAG E M E N T
STRATEG I ES
The primary tool for screening patients and
making triage decisions
initial 12-lead ECG.

LIMITATION OF INFARCT
SIZE
The quantity of myocardium - necrotic as a
consequence of a coronary artery occlusion
While the central zone of the infarct contains
necrotic tissue that is irretrievably lost the
fate of the surrounding ischemic myocardium
(ischemic penumbra) may be improved

Glucocorticoids and nonsteroidal antiinflammatory agents with


the exception of aspirin should be avoided in
patients with STEMI.
They can impair infarct healing and increase
the risk of myocardial rupture and their use
may result in a larger infarct scar.
In addition they can increase coronary
vascular resistance

PRIMARY PERCUTANEOUS
CORONARY INTERVENTION
PCI ( angioplasty and/or stenting without
preceding fibrinolysis)
is effective in restoring perfusion in STEMI
when carried out on an emergency basis in the
first few hours of MI.
patients who have contraindications to
fibrinolytic therapy

FIBRINOLYSIS

Fibrinolytic therapy should ideally be initiated within


30 min of presentation
The principal goal - prompt restoration of full coronary
arterial patency.
tissue plasminogen activator (tPA) streptokinase
tenecteplase (TNK) and reteplase (rP A)
Administration for intravenous use in patients with
STEMI.
promoting the conversion of plasminogen to plasmin
Iyses fibrin thrombi.

Angiographically flow in the culprit coronary artery is described


by a simple qualitative scale called the Thrombo 515 m
Myocardial Infarction (TIMI) grading system:
grade 0 indicates complete occlusion of the infarct-related artery
grade 1 indicates some penetration of the contrast material
beyond the point of obstruction but without perfusion of the
distal coronary bed
grade 2 indicates perfusion of the entire infarct vessel into the
distal bed but with flow that is delayed compared with that of
a normal artery
grade 3 indicates full perfusion of the infarct vessel with normal
flow.

tPA rPA and TNK are more effective than streptokinase at restoring full
perfusion
The current recommended regimen of tPA
- 15-mg bolus followed by 50 mg intravenously over the first 30
min followed by
35 mg over the next 60 min.
Streptokinase is administered as 1.5 million units (MU) intravenously over 1h.
rPA
- double-bolus regimen consisting of a 10-MU bolus given over 2-3
min followed
by a second 10-MU bolus 30 min later.
TNK
- single weight-based intravenous bolus of 0.53 mg/kg over 10s.
In addition to the fibrinolytic agents discussed earlier pharmacologic
reperfusion typically involves adjunctive antiplatelet and antithrombotic
drugs as discussed subsequently.

Clear contraindications
history of cerebrovascular hemorrhage at any time
a nonhemorrhagic stroke or other cerebrovascular
event within the past year
Marked hypertension (systolic arterial pressure >
180mmHg and/or a diastolic pressure >110mmHg)
at any time during the acute presentation
suspicion of aortic dissection
active internal bleeding (excluding menses)

Relative contraindications
current use of anti coagulants (international normalized ratio
2) a recent (<2 weeks)
invasive or surgical procedure
prolonged (> 10 min) cardiopulmonary Resuscitation
known bleeding diathesis pregnancy a hemorrhagic
ophthalmic condition (e.g. hemorrhagic diabetic
retinopathy) active peptic ulcer disease and a history of
severe hypertension that is currently adequately controlled
risk of an allergic reaction streptokinase not used if
received within the preceding 5 days to 2 years.

Allergic reactions to streptokinase occur in -2%


minor degree of hypotension occurs in 4- 1 0%
marked hypotension occurs
although rarely association with severe allergic reactions.
Hemorrhage is the most frequent and potentially the most
serious complication.
Hemorrhagic stroke is the most serious complication and
occurs in -0.5-0.9% of patients being treated with these
agents.

INTEGRATED
REPERFUSION STRATEGY
Cardiac catheterization and coronary angiography
should be carried out after fibrinolytic therapy if there is evidence of either
(1) failure of reperfusion (persistent chest pain and ST -segment elevation >90min) in which
case a rescue PCI should be considered;
(2) coronary artery reocclusion (re-elevation of ST segments and/or recurrent chest pain) or the
development of recurrent ischemia (such as recurrent angina in the early hospital course or a
positive exercise stress test before discharge) in which case an urgent PCI should be
considered.
Routine angiography and elective PCI even in asymptomatic patients following administration of
fibrinolytic therapy are used with less frequency given the numerous technologic advances
that have occurred in the catheterization laborator and the increasing number of skilled
interventionalists.
Coronary artery bypass surgery should be reserved for patients whose coronary anatomy is
unsuited to PCI but in whom revascularization appears to be advisable because of extensive
jeopardized myocardium or recurrent ischemia.

HOSPITAL PHASE
MANAGEMENT
CORONARY CARE U N ITS
routinely equipped with a system that permits
continuous monitoring of the cardiac rhythm of each
patient and hemodynamic monitoring in selected
patients. Defibrillators respirators noninvasive
transthoracic paemakers and facilities for
introducing pacing catheters and flow-directed
balloon-tipped catheters are also usually available.

The duration of stay in the coronary care unit is


dictated by the ongoing need for intensive care.
If symptoms are controlled with oral therapy
patients may be transferred out of the coronary
care unit.
Also patients who have a confirrmed STEMI
but who are considered to be at low risk (no
prior infarction and no persistent chest
discomfort CHF hypotension or cardiac
arrhythmias) may be safely transferred out of
the coronary care unit within 24 h.

Activity Factors that increase the work of the heart during the initial
hours of infarction may increase the size of the infarct.
kept at bed rest for the first 6- 12 h.
encourage 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 reduction in the pulmonar capillary wedge
pressure
absence of hypotension and other complication
by the 2nd or 3rd day patients typically are ambulating in their
room with increasing duration and frequency and they may shower
or stand at the
sink to bathe
by day 3 after infarction, increasing their ambulation
progressively to a
goal of 185 m (600 ft) at least three times a day.

Diet - risk of emesis and aspiration soon after STEMI


NPO or only clear
liquids by mouth for the first 4- 12
h.
30% of total calories as fat and have a cholesterol
content of :0;300mg/d.
Complex carbohydrates should make up 50-55% of total
calories.
foods high in potassium magnesium and
fiber but low in sodium
Diabetes mellitus and hypertriglyceridemia - restriction
of concentrated sweets in the diet

Bowel Management - Bed rest and narcotics


constipation
bedside commode rather than a bedpan a diet
rich in bulk and the routine use of a stool
softener such as dioctyl sodium sulfosuccinate
(200 mg/d) are recommended.
laxative can be prescribed
safe to perform a gentle rectal examination on
patients with STEMI

Sedation
to withstand the period of enforced inactivity
with tranquility.
Diazepam (5 mg) oxazepam ( 1 5-30 mg)
or lorazepam (0.5-2 mg) given three to four
times daily
An additional dose - at night to ensure
adequate sleep.

PHARMACOTHERAPY
ANTI THROMBOTIC AGENTS
initial phase of STEMI thrombosis plays an important role in the
pathogenesis
The primary goal to maintain patency of the infarct-related artery in
conjunction with reperfusion strategies.
A secondary goal to reduce the patient' s tendency to thrombosis and
the likelihood of mural thrombus formation or deep venous thrombosis
pulmonary embolization
The degree to which antiplatelet and anticoagulant therapy achieves these
goals partly determines how effectively it reduces the risk of mortality from
STEMI.
aspirin is the standard antiplatelet agent for patients with STEMI.

Inhibitors of the P2Y12 ADP receptor


- prevent activation and aggregation of platelets.
- clopidogrel + aspirin reduces the risk of clinical events (death
reinfarction stroke) and in patients receiving fibrinolytic therapy
has been shown to prevent reocclusion of a successfully reperfused
infarct artery.
- New P2Y12 ADP receptor antagonists such as prasugrel and
ticagrelor are more effective than clopidogrel in preventing ischemic
complications in STEMI patients undergoing PCI but are associated
with an increased risk of bleeding.
- Glycoprotein IIb/IIIa receptor inhibitors appear useful for preventing
thrombotic complications in patients with STEMI undergoing PCI

The standard anticoagulant agent used in clinical


practice is unfractionated heparin (UFH).
UFH + aspirin and a non-fibrin-specific
thrombolytic agent such as streptokinase
additional mortality benefit occurs (about 5 lives
saved per 1000 patients treated).
intravenous UFH + aspirin and relatively fibrin
-specific fibrinolytic agents (tPA rPA or TNK)
helps to maintain patency of the infarctrelated artery.

Alternatives to UFH the low-molecular-weight heparin (LMWH) preparations


- a synthetic version of the critical pentasaccharide sequence (fondaparinux)
direct antithrombin bivalirudin.
Advantages of LMWHs - high bioavailability permitting administration subcutaneously, reliable
anticoagulation without monitoring and greater antiXa:IIa activity.
Enoxaparin has been shown to reduce significantly the composite end points of death/nonfatal
reinfarction and death/nonfatal reinfarction/ urgent revascularization compared with UFH in STEMI
patients who receive fibrinolysis.
- higher rates of serious bleeding but net clinical benefit-a composite endpoint that combines
efficacy and safety- still favors enoxaparin over UFH.
Fondaparinux appears superior to placebo in STEMI patients not receiving reperfusion therapy but
its relative efficacy and safety compared with UFH is less certain.
- risk of catheter thrombosis - not be used alone at the time of coronary angiography and PCI
but
should be combined with another anticoagulant with antithrombin activity such as
UFH or bivalirudin.

Patients with an anterior location of the


infarction severe LV Dysfunction heart
failure a history of embolism twodimensional echocardiographic evidence of
mural thrombus or atrial fibrillation are at
increased risk of systemic or pulmonary
thromboembolism.
Such individuals should receive full therapeutic
levels of anticoagulant therapy (LMWH or UFH)
while hospitalized followed by at least 3
months of warfarin therapy.

COM P L lCAT I O N S A N D
THE I R MANAG E M E N T
VENTRICULAR DYSFU NCTION

H EMODYNAMIC
ASSESSMENT
Pump failure is now the primary cause of inhospital death from STEMI

A classification originally proposed by Killip divides patients


into four groups:
class 1 no signs of pulmonary or venous congestion;
class 11 moderate heart failure as evidenced by rales at the
lung bases S3 gallop tachypnea or signs of failure of the
right side of e heart including venous and hepatic
congestion;
class III severe heart failure pulmonary edema; and
class IV shock with systolic pressure <90 mmHg and
evidence of peripheral vasoconstriction peripheral
cyanosis mental confusion and oliguria. When this
classification wasestablished in 1967

Hemodynamic evidence of abnormal global L V function appears


contraction is seriously impaired in 20-25% of the left ventricle.
Infarction of 40% of the left ventricle usually results in cardiogenic
shock (Chap. 326) . Positioning of a balloon flotation (Swan-Ganz)
catheter in the pulmonary artery permits monitoring of L V filling
pressure; this technique is useful in patients who exhibit hypotension
and/or clinical evidence of CHF. Cardiac output can also be determined
with a pulmonary artery catheter. With the addition of intra-arterial
pressure monitoring systemic vascular resistance can be calculated
as a guide to adjusting vasopressor and vasodilator therapy. Some
patients with STEMI have markedly elevated L V filling pressures (>22
mmHg) and normal cardiac indices (2.6-3.6 L/ [min/m' while others
have relatively low LV filling pressures (<15 mmHg) and reduced
cardiac indices. The former patients usually benefit from diuresis
while the latter may respond to volume expansion

HYPOVOLEMIA

This is an easily corrected condition that may contribute to


the hypo
tension and vascular collapse associated with STEMI in some
patients.
It may be secondary to previous diuretic use to reduced
fluid intake
during the early stages of the illness and/or to vomiting
associated
with pain or medications. Consequently hypovolemia
should be identified
and corrected in patients with STEMI and hypotension before

CARDIOG E N IC SHOCK

Prompt reperfusion efforts to reduce infarct size and treatment of


ongoing ischemia and other complications of MI appear to have
reduced the incidence of cardiogenic shock from 20% to about 7%.
Only 10% of patients with this condition present with it on admission
while 90% develop it during hospitalization. Typically patients who
develop cardiogenic shock have severe multivessel coronary artery
disease with evidence of "piecemeal" necrosis extending outward from
the original infarct zone. The evaluation and management of
cardiogenic
shock and severe power failure after STEMI are discussed in
detail in Chap. 326.

RIGHT VENTRICULAR I N
FARCTION
Approximately one-third of patients with inferior infarction demonstrate
at least a minor degree of RV necrosis. An occasional patient with
inferoposterior L V infarction also has extensive RV infarction and rare
patients present with infarction limited primarily to the RV.
Clinically significant RV infarction causes signs of severe RV failure
(19u1ar venous distention Kussmaul's sign hepatomegaly [Chap.
267] ) with or without hypotension. ST -segment elevations of right
sided precordial ECG leads particularly lead V4R are frequently
present in the first 24 h in patients with RV infarction. Two-dimensional
echocardiography is helpful in determining the degree of RV
dysfunction. Catheterization of the right side of the heart often reveals a
distinctive hemodynamic pattern resembling constrictive pericarditis
(steep right atrial "y" descent and an early diastolic dip and plateau in
RV waveforms) (Chap. 288). Therapy consists of volume expansion to
maintain adequate RV preload and efforts to improve L V performance

ARRHYTHMIAS
The incidence of arrhythmias after STEMI is higher in patients seen
ea a r the onset of symptoms.
The mechanisms responsible for infarction-related arrhythmias
include autonomic nervous system imbalance electrolyte
disturbances ischemia and slowed conduction in zones of
ischemic myocardium. An arrh hmia can usually be managed
successfully if trained personnel and appropriate equipment are
available when it develops. Since most deaths from arrh hmia
occur during the first few hours after infarction the effectiveness
of treatment relates directly to the speed with which patients come
under medical observation. The prompt management of
arrhythmias constitutes a significant advance in the treatment of
STEMI.

Ventricular Premature Beats Infrequent sporadic ventricular premature depolarizations occur in


almost all patients with STEMI and do not require therapy. Whereas in the past frequent
multifocal or early diastolic ventricular extrasystoles (so-called warning arrhythmias) were
routinely treated with antiarrhythmic drugs to reduce the risk of development of ventricular
tachycardia and ventricular fibrillation pharmacologic therapy is now reserved for patients with
sustained ventricular arrhythmias. Prophylactic antiarrhythmic therapy (either intravenous
lidocaine early or oral agents later) is contraindicated for ventricular premature beats in the
absence of clinically important ventricular tachyarrhythmias because such therapy may
actually increase the mortality rate. Beta -adrenoceptor blocking agents are effective
in abolishing ventricular ectopic activity in patients with STEMI
and in the prevention of ventricular fibrillation. As described earlier
(see "Beta-Adrenoceptor Blockers") they should be used routinely
in patients without contraindications. In addition hypokalemia and
hypomagnesemia are risk factors for ventricular fibrillation in patients
with STEMI; to reduce the risk the serum potassium ncentraton
should be adjusted to approximately 4.5 mmol/L and magnesium to
about 2.0 mmol/L.

Ventricular Tachycardia and Fibrillation Within the first 24 h of


STEMI
ventricular tachycardia and fibrillation can occur without prior
warning arrhythmias.
reduced by prophylactic administration of intravenous lidocaine
- not been shown to reduce overall mortality from STEMI.
lidocaine may predispose to an excess risk of bradycardia and
asystole.
-For these reasons and with earlier treatment of active
ischemia more frequent use of beta-blocking agents, and the
nearly universal success of electrical cardioversion or defibrillation,
routine prophylactic antiarrhythmic drug therapy is no longer
recommended

Sustained ventricular tachycardia that is well tolerated hemody namically should be


treated with an intravenous regimen of amiodarone (bolus of 150 mg over 10
min allowed by infusion of 1.0 mg/min for 6 h and then 0.5 mg/min) or procainamide
(bolus of 15 mg/kg over 20-30 min; infusion of 1-4 mg/min);
if it does not stop promptly electroversion should be used (Chap. 276).
An unsynchronized discharge of 200-300 J (monophasic waveform; approximately 50% of
these energies with biphasic waveforms) is used immediately in patients with ventricular
fibrillation or when ventricular tachycardia causes hemodynamic deterioration.
Ventricular tachycardia or fibrillation that is refractory to electroshock may be more
responsive after the patient is treated with epinephrine (1 mg intravenously or 10 mL of a
1 : 1 0 000 solution via the intracardiac route) or amiodarone (a 75-150-mg bolus).
Ventricular arrhythmias including the unusual form of ventricular tachyardia known as
torsades des pointes (Chaps. 276 and 277) may occur in patients with STEMI as a
consequence of other concurrent problems (such as hypoxia hypokalemia or other
electrolyte disturbances) or of the toxic effects of an agent being administered to the
patient (such as digoxin or quinidine).
A search for such secondary causes should always be undertaken.

Although the in-hospital mortality rate is increased the long-term survival is


excellent in patients who survive to hospital discharge after primary ventricular
fibrillation; i.e. ventricular fibrillation that is a primary response to acute ischemia
that occurs during the first 48 h and is not associated with predisposing factors
such as CHF shock bundle branch block or ventricular aneurysm.
This result is in sharp contrast to the poor prognosis for patients who develop
ventricular fibrillation secondary to severe pump failure. For patients who develop
ventricular tachycardia or ventricular fibrillation late in their hospital course (i.e.
after the first 48 h) the mortality rate is increased both in-hospital and during
long-term follow-up. Such patients should be considered for electrophysiologic
study and implantation of a cardioverter defibrillator (ICD) (Chap. 276).
A more challenging issue is the prevention of sudden cardiac death from ventricular
fibrillation late after STEMI in patients who have not exhibited sustained ventricular
tachyarrhythmias during their index hospitalization. An algorithm for selection of
patients who warrant prophylactic implantation of an ICD is shown in

Accelerated Idioventricular Rhythm Accelerated


idioventricular rhythm (AIVR "slow ventricular
tachycardia)
a ventricular rhythm with a rate of 60- 100 beats/min
often occurs transiently during fibrinolytic therapy at the
time of reperfusion.
whether it occurs in association with fibrinolytic therapy or
spontaneously is benign and does not presage the
development of classic ventricular tachycardia.
Most episodes of AIVR do not require treatment if the
patient is monitored carefully as degeneration into a
more serious arrhythmia is rare.

Supraventri(ular Arrhythmias Sinus tachycardia is the most common supraventricular


arrhythmia. If it occurs secon (such as anemia fever heart failure or a metabolic
derangement) the 1 609 primary problem should be treated first. However if it
appears to be due to sympathetic overstimulation (e. as part of a hyperdynamic
state) then treatment with a beta blocker is indicated. Other common arrhythmias in
this group are atrial flutter and atrial fibrillation which are en secondary to L V
failure. Digoxin is usually the treatment of choice for supraventricular arrhythmias if heart
failure is present.
If heart failure is absent beta blockers verapamil or diltiazem are suitable
alternatives for controlling the ventricular rate as they may also help to control
ischemia. If the abnormal rhythm persists for >2 h with a ventricular rate > 1 20
beats/min or if tachycardia induces heart failure shock or ischemia (as manifested
by recurrent pain or ECG changes) a synchronized electroshock ( 1 00-200 J
monophasic waveform) should be used.
Accelerated junctional rhythms have diverse causes but may occur in patients with
inferoposterior infarction. Digitalis excess must be ruled out. In some patients with severely
compromised L V function the loss of appropriately timed atrial systole results in a
marked reduction of cardiac output. Right atrial or coronary sinus pacing is indicated in such
instances.dary to another cause

Sinus Brady(ardia Treatment of sinus


bradycardia is indicated if hemodynamic
compromise results from the slow heart rate.
Atropine is the most useful drug for increasing
heart rate and should be given intravenously in
doses of 0.5 mg initially. If the rate remains
<50-60 beats/min additional doses of 0.2
mg up to a total of 2.0 mg may be given.
Persistent bradycardia (<40 beats/min) despite
atropine may be treated with electrical pacing.
Isoproterenol should be avoided.

Atrioventri(ular and Intraventricular Conduction Disturbances


Both the in-hospital mortality rate and the postdischarge mortality rate of patients who have
complete atrioventricular (A V) block in association with anterior infarction are markedly
higher than those of patients who develop AV block with inferior infarction.
This difference is related to the fact that heart block in inferior infarction is commonly a result
of increased vagal tone and/or the release of adenosine and therefore is transient. In anterior
wall infarction however heart block is usually related to ischemic malfunction of the
conduction system which is commonly associated with extensive myocardial necrosis.
Temporal electrical pacing provides an effective means of increasing the heart rate of
patients with bradycardia due to A V block. However acceleration of the heart rate may
have only a limited impact on prognosis in patients with anterior wall infarction and complete
heart block in whom the large size of the infarct is the m or factor determining outcome. It
should be carried out if it improves hemodynamics. Pacing does appear to be beneficial in
patients with inferoposterior infarction who have complete heart block associated with heart
failure hypotension marked bradycardia or significant ventricular ectopic activity. A
subgroup of these patients those with RV infarction often respond poorly to ventricular
paing beause of the loss of the atrial contribution to ventricular filling. In such patients
dual-chamber A V sequential pacing may be required.

External noninvasive pacing electrodes


should be positioned in a "demand" mode for patients with
sinus bradycardia (rate <50 beats/min) that is unresponsive
to drug therapy Mobitz II second-degree A V block thirddegree heart block or bilateral bundle branch block (e.g.
right bundle branch block plus le anterior fascicular block).
Retrospective studies suggest that permanent pacing may
reduce the long-term risk of sudden death due to
bradyarrhythmias in the rare patient who develops combined
persistent bifascicular and transient third -degree heart block
during the acute phase of MI.

OTHER COMPLlCATIONS
Recurrent Chest Discomfort - recurrent or persistent
ischemia often heralds extension of the original infarct
or reinfarction in a new myocardial zone and is
associated with a near tripling of mortality after
STEMI
patients with these symptoms should be referred for
prompt coronary arteriography and mechanical
revascularization
Administration of a fibrinolytic agent is an alternative
to early mechanical revascularization.

Pericarditis
Pericardial friction rubs and/or pericardial pain are frequently
encountered in patients with STEMI involving the epicardium.
managed with aspirin (650 mg four times daily).
failure to recognize it may lead to the erroneous diagnosis of recurrent
ischemic pain and/or infarct extension with resulting inappropriate use
of anticoagulants nitrates beta blockers or coronary arteriography.
complaints of pain radiating to either trapezius muscle is helpful
because such a pattern of discomfort is typical of pericarditis but rarely
occurs with ischemic discomfort.
Anticoagulants potentially could cause tamponade in the presence of
acute pericarditis (as manifested by either pain or persistent rub) and
therefore should not be used unless there is a compelling indication.

Thromboembolism
complicates STEMI in -10% of cases but embolic lesions are found in 20% of patients
in necropsy series suggesting that thromboembolism is often clinically silent.
contributing cause of death in 25% of patients with STEMI who die after admission to the
hospital.
Arterial emboli originate from L V mural thrombi while most pulmonary emboli arise in
the leg veins
typically occurs in association with large infarcts (especially anterior) CHF and an LV
thrombus detected by echocardiography.
The incidence of arterial embolism from a clot originating in the ventricle at the site of
an infarction is small but real.
Two-dimensional echocardiography reveals L V thrombi in about one-third of patients
with anterior wall infarction but in few patients with inferior or posterior infarction.
presents as a major complication such as hemiparesis when the cerebral circulation is
involved or hypertension if the renal circulation is compromised.

Left Ventricular Aneurysm


The term ventricular aneurysm is usually used to describe
dyskinesis or local expansile paradoxical wall motion.
Normally functioning myocardial fibers must shorten more if stroke
volume and cardiac output are to be maintained in patients with
ventricular aneurysm; if they cannot overall ventricular function
is impaired.
True aneurysms are composed of scar tissue and neither
predispose to nor are associated with cardiac rupture.
The complications of L V aneurysm do not usually occur for weeks
to months after STEMI; they include CHF arterial embolism
and ventricular arrhythmias. Apical aneurysms are the most
common and the most easily detected by clinical examination.

The physical finding of greatest value is a double


diffuse or displaced apical impulse. Ventricular
aneurysms are readily deteted by two-dimensional
echocardiography which may also reveal a mural
thrombus in an aneurysm
Rarely myocardial rupture may be contained by a local
area of pericardiu along with organizing thrombus and
hematoma. Over time this pseudoaneurysm
enlarges maintaining communication with the L V
cavity through a narrow neck. Because a
pseudoaneurysm often ruptures spontaneously it
should be surgically repaired if recognized.

POST INFARCTION RISK


STRATIFICATION AND
MANAGMENT
persistent ischemia (spontaneous or provoked)
depressed LV ejection fraction (<40%)
rales above the lung bases on physical examination or congestion on chest radiograph
symptomatic ventricular arrhythmias.
Other features associated with increased risk include
a history of previous MI
age >75
diabetes mellitus
prolonged sInus tachycardia hypotension
ST-segment changes at rest without angina (silent ischemia abnormal signal-averaged ECG
nonpatency of the infarct-related coronary artery (if angiography is undertaken
persistent advanced heart block or a new intraventricular conduction abnormality on the ECG.

Exercise tests also aid in formulating an individualized exercise prescription


which can be much more vigorous in patients who tolerate exercise without any
of the previously mentioned adverse signs.
In many hospitals a cardiac rehabilitation program with progressive exercise
is initiated in the hospital and continued after discharge.
programs should include an educational component that informs patients about
their disease and its risk factors.
The usual duration of hospitalization for an uncomplicated STEMI is about 5
days. The remainder of the convalescent phase may be accomplished at home.
During the first 1 -2 weeks encouraged to increase activity by walking about
the house and outdoors in good weather. Normal sexual activity may be
resumed during this period.
After 2 weeks - the physician must regulate the patients activity on the basis of
exercise tolerance. Most patients will be able to return to work within 2-4 weeks

SECONDARY
PREVENTION
Long-term treatment with an antiplatelet agent (usually aspirin) after
STEMI - - 25% reduction in the risk of recurrent infarction stroke or
cardiovascular mortality (36 fewer events for every 1000 patients
treated).
An alternative antiplatelet agent that may be used for secondary
prevention in patients intolerant of aspirin is clopidogrel (75 mg orally
daily).
ACE inhibitors or ARBs and in appropriate patients aldosterone
antagonists should be used indefinitely by patients with clinically evident
heart failure a moderate decrease in global ejection fraction or a
large regional wall motion abnormality to prevent late ventricular
remodeling and recurrent ischemic events.
The chronic routine use of oral beta-adrenoceptor blockers for at least 2
years after STEMI is supported by well-conducted placebo controlled
trials.

Evidence suggests that warfarin lowers the risk


of late mortality and the incidence of
reinfarction after STEMI.
Most physicians prescribe aspirin routinely for
all patients withou contraindications and add
warfarin for patients at increased risk of
embolism (see "Thromboembolism" earlier).
Several studies suggest that in patients