3. CASE
HPI:
2 hours PTA- sudden onset of squeezing,
retrosternal chest pain, radiating towards the neck,
associated with headache. (+) Vomiting x1, pain
score of 8/10, not relieved by rest, about >10
minutes. Admitted at primary hospital and managed
as essential hypertension with NSSTWCs on ECG.
Subsequently transferred to a Tertiary level for
further workup and management
4. CASEPhysical Exam
Awake, coherent, in
mild distress
Warm, good turgor
and mobility, CRT <2
seconds,
Anicteric sclerae, pink
palpebral
conjunctivae,
Equal chest
expansion, dec BS on
both lower lung fields,
with crackles
Distinct heart sounds, ,
tachycardic, regular,
no murmur
Flat, Normoactive
bowel sounds, soft, no
organomegaly
Strong peripheral
pulses, no edema
Neurologic: WNL
BP: 130/60mmHg,
HR: 118 bpm,
RR: 26 cpm,
99% O2 mp: 36.5°
Neck: No JVD, no
murmur
9. ACUTE CORONARY SYNDROME
I: Diagnosis and Management of Patients with Stable
Ischemic Heart Disease
II: Diagnosis and Management of Patients with
Non-ST Elevation Acute Coronary Syndrome
III: Diagnosis and Management of Patients with
ST Segment Elevation Myocardial Infarction
10. ACUTE CORONARY SYNDROME
What is ACS?
- refers to a spectrum of clinical presentations
ranging from those for ST-segment elevation myocardial
infarction (STEMI) to presentations found in nonâST-
segment elevation myocardial infarction (NSTEMI) or in
unstable angina
- in general reserved for ischemia precipitated by
acute coronary atherothrombosis
22. ACUTE CORONARY SYNDROME
The American
College of Cardiology (ACC) and American Heart Association (AHA)
guidelines list the following as pain descriptions uncharacteristic of
myocardial ischemia:
⢠Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory
movements or coughing)
⢠Primary or sole location of the discomfort in the middle or lower
abdominal region
⢠Pain that may be localized by the tip of one finger, particularly over
the left ventricular apex
⢠Pain reproduced with movement or palpation of the chest wall or
arms
⢠Constant pain that persists for many hours
⢠Very brief episodes of pain that last a few seconds or less
⢠Pain that radiates into the lower extremities
24. Ischemic Heart Disease
The major determinants of myocardial oxygen
demand (MVO2) are:
1) heart rate,
2) myocardial contractility, and
3) myocardial wall tension (stress)
About 75% of the total coronary resistance to flow occurs
across three sets of arteries:
(1) large epicardial arteries (Resistance 1 = R1),
(2) prearteriolar vessels (R2), and
(3) arteriolar and intramyocardial capillary vessels (R3)
25. 50% Stenosis:
there is a limitation of the ability to increase flow to
meet increased myocardial demand.
80% Stenosis:
myocardial ischemia at rest or with minimal stress
Ischemic Heart Disease
Coronary Blood Flow Limitation:
⢠spasm,
⢠arterial thrombi, and,
⢠rarely, coronary emboli
⢠as well as by ostial narrowing due to aortitis
⢠Congenital Anomalies
27. The severity and duration of the imbalance between
myocardial oxygen supply and demand determine
whether the damage is :
ďą reversible (â¤20 min for total occlusion in the absence
of collaterals) or
ďą permanent, with subsequent myocardial necrosis
(>20 min).
Ischemic Heart Disease
29. Requirements :
⢠Two sets of cardiac enzymes at 4-hr intervals should be normal
⢠ECG at the time of arrival and preexercise 12-lead ECG show no
significant abnormality
⢠Absence of rest electrocardiographic abnormalities that would preclude
accurate assessment of the exercise ECG
⢠From admission to the time that results are available from the second set
of cardiac enzymes: patient asymptomatic, lessening chest pain symptoms,
or persistent atypical symptoms
⢠Absence of ischemic chest pain at the time of exercise testing
Indications and Contraindications for Exercise
Electrocardiographic Testing in the Emergency Department
Contraindications
⢠New or evolving electrocardiographic abnormalities on the rest tracing
⢠Abnormal cardiac enzyme levels
⢠Inability to perform exercise
⢠Worsening or persistent ischemic chest pain symptoms from admission to the
time of exercise testing
⢠Clinical risk profiling indicating that imminent coronary angiography is likely
37. ISCHEMIC HEART DISEASE
ESTABLISHING DIAGNOSIS
Exercise ECG (Treadmill Exercise Test or TET)
its simplicity, lower cost and widespread availability, the
TET is the initial test of choice to identify inducible
ischemia in the majority of patients with intermediate PTP
who are able to exercise
The low sensitivity of the TET (45% to 50%) despite a high
specificity (85% to 90%) is the reason why it is not
recommended in patients with a PTP greater than 65%
In the latter case,a stress imaging study is more
appropriate.
38. ISCHEMIC HEART DISEASE
CORONARY ARTERIOGRAPHY
Coronary arteriography is indicated in:
(1) patients with chronic stable angina pectoris who are severely
symptomatic despite medical therapy and are being considered
for revascularization, i.e., a percutaneous coronary intervention
(PCI) or coronary artery bypass grafting (CABG);
(2) patients with troublesome symptoms that present diagnostic
difficulties in whom there is a need to confirm or rule out the
diagnosis of IHD;
(3) patients with known or possible angina pectoris who have
survived cardiac arrest;
(4) patients with angina or evidence of ischemia on noninvasive
testing with clinical or laboratory evidence of ventricular
dysfunction; and
(5) patients judged to be at high risk of sustaining coronary
events based on signs of severe ischemia on noninvasive testing,
regardless of the presence or severity of symptoms
40. ISCHEMIC HEART DISEASE
MANAGEMENT
Pharmacologic Therapy to Improve Prognosis
Whether or not revascularization is being considered,
receive the following medications to improve prognosis,
thereby reducing the risk for MI and death:
1. Aspirin low-dose (80 to 160 mg/day)
2. Clopidogrel in case of aspirin intolerance (75 mg/day)
3. Statins irrespective of LDL-cholesterol levels
4. Beta blockers post-MI
5. ACEIs or ARBs (especially in patients with concomitant HF,
hypertension or diabetes)
46. NSTE-ACS
Pathophysiology:
1. imbalance between oxygen supply and oxygen
demand resulting from a partially occluding
thrombus forming on a disrupted
atherothrombotic coronary plaque or on
eroded coronary artery endothelium
2. dynamic obstruction
3. severe mechanical obstruction
4. increased myocardial oxygen demand
49. NSTE-ACS
DIAGNOSIS:
Clinical :
(1) it occurs at rest (or with minimal exertion),
lasting >10 minutes;
(2) it is of relatively recent onset (i.e., within the
prior 2 weeks); and/or
(3) it occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than
previous episodes)
NSTEMI - elevated levels of biomarkers of cardiac necrosis
50. NSTE-ACS
DIAGNOSIS:
3 major noninvasive tools are used in the
evaluation of NSTEMI-ACS:
1. the electrocardiogram (ECG),
2. cardiac biomarkers, and
3. stress testing
GOALS :
(1) recognize or exclude myocardial infarction (MI) using
cardiac biomarkers, preferably cTn;
(2) detect rest ischemia (using serial or continuous ECGs);
and
(3) detect significant coronary obstruction at rest with CCTA
and myocardial ischemia using stress testing
55. MEDICAL TREATMENT
⢠Bed rest
⢠Continuous ECG monitoring
⢠Ambulation only if
No recurrence of ischemia (symptoms or ECG changes)
Does not develop an elevation of a biomarker of necrosis for
12â24 h
ANTI-ISCHEMIC ANTITHROMBOTIC
60. NSTE-ACS
ORAL ANTIPLATELETS
Aspirin Initial dose of 325 mg nonenteric formulation followed by 75â100
mg/d of an enteric or a nonenteric formulation
Clopidogrel Loading dose of 300â600 mg followed by 75 mg/d
Prasugrel Pre-PCI: Loading dose 60 mg followed by 10 mg/d
Ticagrelor Loading dose of 180 mg followed by 90 mg twice daily
Intravenous Antiplatelet Therapy
Abciximab 0.25 mg/kg bolus followed by infusion of 0.125 Îźg/ kg per min
(maximum 10 Îźg/min) for 12â24 h
Eptifibatide 180 Îźg/kg bolus followed 10 min later by second bolus of 180 Îźg
with infusion of 2.0 Îźg/kg per min for 72â96 h following first bolus
Tirofiban 5 Îźg/kg per min followed by infusion of 0.15 Îźg/kg per min for 48â
96 h
61. NSTE-ACS
HEPARINS
Unfractionated
heparin
(UFH)
Bolus 70â100 U/kg (maximum 5000 U) IV followed
by infusion of 12â15 U/kg per h (initial maximum
1000 U/h) titrated to ACT 250â300 s
Enoxaparin 1 mg/kg SC every 12 h; the first dose may be preceded
by a 30-mg IV bolus; renal adjustment to
1 mg/kg once daily if creatine clearance <30 cc/min
Fondaparinux 2.5 mg SC qd
Bivalirudin Initial IV bolus of 0.75 mg/kg and an infusion of
1.75 mg/kg per h.
62. NSTE-ACS
Class I Recommendations for Use of an Early Invasive
Strategy in Patients with Non-ST-Segment Elevation
Acute Coronary Syndrome:
Class I (Level of Evidence: A) Indications
1. Recurrent angina at rest/low-level activity despite treatment
2. Elevated TnT or TnI
3. New ST-segment depression
4. CHF symptoms, rales, MR
5. EF <0.40
6. Sustained VT
7. PCI <6 months, prior CABG
8. High-risk findings from noninvasive testing
9. Hemodynamic instability
10. Mild-to-moderate renal dysfunction
11. Diabetes mellitus
12. High TIMI Risk Score (>3)b
63. NSTE-ACS
PRINZMETALâS VARIANT ANGINA
- syndrome of severe ischemic pain that usually occurs at rest and
is associated with transient ST segment elevation
- focal spasm of an epicardial coronary artery, leading to severe
transient myocardial ischemia and occasionally infarction
- may be related to hypercontractility of vascular smooth muscle
due to adrenergic vasoconstrictors, leukotrienes, or serotonin
- has decreased substantially during the past few decades
- PVA are generally younger and have fewer coronary risk factors
- The clinical diagnosis of PVA is made by the detection of
transient ST-segment elevation with rest pain
- Focal spasm is most common in the right coronary artery
64. NSTE-ACS
PRINZMETALâS VARIANT ANGINA
Diagnosis:
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
TREATMENT
Nitrates and Calcium Channel Blockers
Aspirin- may actually increase the severity of ischemic
episodes
PROGNOSIS
1. Survival at 5 years is excellent (âź90â95%)
2. Nonfatal MI occurs in up to 20% of patients by 5 years
3. There is a tendency for symptoms
4. and cardiac events to diminish over time
65. NSTE-ACS
CORONARY ANGIOGRAPHY
IS NOT RECOMMENDED in patients with
⢠extensive co-morbidities (e.g., liver or pulmonary
failure; cancer);
⢠in whom the risks of revascularization are not likely to
outweigh the benefits;
⢠in patients with acute chest pain and a low likelihood
of ACS;
⢠or in patients who will not consent to
revascularization regardless of the findings.
66. NSTE-ACS
Revascularization by PCI
PCI IS RECOMMENDED for NSTE-ACS patients with
1- to 2-vessel CAD, with or without significant proximal
left anterior descending CAD, but with a large area of
viable myocardium and high-risk criteria on
noninvasive testing.
67. NSTE-ACS
Revascularization by CABG Surgery
CABG IS RECOMMENDED for patients with
1. significant left main disease, and is the
preferred revascularization strategy for
patients with
2. multi-vessel coronary disease;
3. vessels with lesions not favorable for PCI;
4. depressed systolic function (LVEF lower than
50%); and diabetes.
68. NSTE-ACS
Drug/Medication Management
Strongly RECOMMENDED for patients with
1. aspirin indefinitely, and ticagrelor 90 mg twice daily
or clopidogrel 75 mg daily, for 12 months
2. underwent stenting, with aspirin indefinitely, plus
ticagrelor 90 mg twice daily or prasugrel 10 mg
daily or clopidogrel 75 mg daily, for 12 months in
patients with drug-eluting stents, and 6 months in
patients with bare metal stents
3. beta blockers be continued indefinitely for all NSTE-
ACS patients unless contraindicated
72. STEMI
Criteria for Acute Myocardial Infarction
⢠Detection of a rise and/or fall of cardiac biomarker values
(preferably cardiac troponin [cTn]) with at least one value
above the 99th percentile upper reference limit (URL) and
with at least one of the following:
⢠Symptoms of ischemia
⢠New or presumed new significant ST-segment T-wave (ST-T) changes or
new left bundle branch block (LBBB)
⢠Development of pathologic Q waves in the electrocardiogram (ECG)
⢠Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
⢠Identification of an intracoronary thrombus by angiography or autopsy
⢠Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB, but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker values
would be increased.
73. STEMI
Criteria for Acute Myocardial Infarction
⢠Percutaneous coronary intervention (PCI)ârelated MI is arbitrarily defined by
elevation of cTn values (>5 Ă 99th percentile URL) in patients with normal baseline
values (â¤99th percentile URL) or a rise of cTn values >20% if the baseline values are
elevated and are stable or falling. In addition, either
⢠Coronary artery bypass grafting (CABG)ârelated MI is arbitrarily defined by
elevation of cardiac biomarker values (>10 Ă 99th percentile URL) in patients with
normal baseline cTn values (â¤99th percentile URL). In addition, either
(i) symptoms suggestive of myocardial ischemia, or
(ii) new ischemic ECG changes, or
(iii) angiographic findings consistent with a procedural complication, or
(iv) imaging demonstration of new loss of viable myocardium or new regional wall motion
abnormality are required.
⢠Stent thrombosis associated with MI when detected by coronary angiography or
autopsy in the setting of myocardial ischemia and with a rise and/ or fall of cardiac
biomarker values with at least one value above the 99th percentile URL.
(i) new pathologic Q waves or new LBBB, or
(ii) angiographic documented new graft or new native coronary artery occlusion, or
(iii) imaging evidence of new loss of viable myocardium or new regional wall motion
abnormality.
74. STEMI
Classification of Myocardial Infarction
Type I: Spontaneous Myocardial Infarction
Type 2: Myocardial Infarction Secondary to an Ischemic
Imbalance
Type 3: Myocardial Infarction Resulting in Death When
Biomarker Values Are Unavailable
Type 4a: Myocardial Infarction Related to Percutaneous
Coronary Intervention (PCI)
Type 4b: Myocardial Infarction Related to Stent Thrombosis
Type 5: Myocardial Infarction Related to Coronary Artery
Bypass Grafting (CABG
76. STEMI
the goals for the management of patients with suspected
STEMI include:
1. control of cardiac discomfort,
2. rapid identification of patients who are candidates for
urgent reperfusion therapy,
3. triage of lower-risk patients to the appropriate location
in the hospital, and
4. avoidance of inappropriate discharge of patients with
STEMI
MANAGEMENT IN THE EMERGENCY DEPARTMENT
Aspirin
is essential in the management of patients with suspected STEMI and is effective across
the entire spectrum of acute coronary syndromes
OXYGEN
O2 should be administered by nasal prongs or face mask (2â4 L/min) for
the first 6â12 h after infarction
77. STEMI
1) Sublingual nitroglycerin
Up to three doses of 0.4 mg should be administered at about 5-min intervals
2) Morphine
3) Intravenous beta blockers/ Oral Beta blockers
CONTROL OF DISCOMFORT
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, or
(4) other relative contraindications to beta blockade (PR interval greater than 0.24 seconds,
second- or third-degree heart block, active asthma, or reactive airway disease).
Fifteen minutes after the last intravenous dose, an oral
regimen is initiated of 50 mg every 6 h for 48 h, followed by 100
mg every 12 h
79. STEMI
Initial ER Management
⢠Aspirin 160 to 320 mg tablet (non-enteric coated, chewed);
⢠Clopidogrel 300 to 600 mg whether or not fibrinolysis will be
given;
⢠Clopidgrel 600 mg or prasugrel 60 mg or ticagrelor 180 mg when
a patient will undergo PCI;
⢠Nitrates, either via sublingual or intravenous(IV) routes. Nitrates
are contraindicated in patients with hypotension or those who
took a phosphodiesterase 5 (PDE5) inhibitor within 24 hrs (48 hrs
for tadalafil);
⢠Morphine 2 to 4 mg IV for relief of chest pain, and;
⢠Supplemental oxygen MAY BE RECOMMENDED during the first 6
hours to patients with arterial oxygen saturation of less than 90%.
80. STEMI
In-hospital Treatment
Reperfusion therapy IS RECOMMENDED to all eligible
patients with STEMI with symptom onset within the
prior 12 hours.
Early revascularization, the goal being 12 hours, is a
primary treatment goal in patients with STEMI
82. STEMI
Fibrinolysis
15-mg bolus followed byTPA
⢠50 mg intravenously over the first 30 min,
⢠followed by 35 mg over the next 60 min
1.5 million units (MU) intravenously over 1 hStreptokinase
given as a single weight-based intravenous bolus
of 0.53 mg/kg over 10 s
Tenecteplase
(TNK)
double-bolus regimen consisting of a 10-MU
bolus given over 2â3 min, followed byReteplase (rPA)
⢠second 10-MU bolus 30 min later
85. STEMI
TIMI FLOW GRADE â The degree of perfusion in the
infarct-related artery (IRA) is typically described by the TIMI
flow grade:
âTIMI 0 refers to the absence of antegrade flow beyond a
coronary occlusion.
âTIMI 1 flow is faint antegrade coronary flow beyond the
occlusion, although filling of the distal coronary bed is
incomplete.
âTIMI 2 flow is delayed or sluggish antegrade flow with
complete filling of the distal territory.
âTIMI 3 flow is normal flow which fills the distal coronary
bed completely.
TIMI
86. STEMI
Primary Percutaneous Coronary
Intervention (PCI)
1. RECOMMENDED in patients with STEMI and ischemic
symptoms of less than 12 hoursâ duration
2. RECOMMENDED in patients with STEMI and ischemic
symptoms of less than 12 hoursâ duration who have
contraindications to fibrinolytic therapy, irrespective of
the time delay from first medical contact.
3. RECOMMENDED in patients with STEMI and cardiogenic
shock or acute severe heart failure (HF), irrespective of
time delay from MI onset
4. MAY BE RECOMMENDED in patients with STEMI if there is
clinical and/or ECG evidence of ongoing ischemia between
12 and 24 hours after symptom onset
87. STEMI
Coronary Artery Bypass Grafting (CABG)
1. IS RECOMMENDED in failed PCI with persistent pain or
hemodynamic instability in patients with coronary anatomy
suitable for surgery
2. IS RECOMMENDED in persistent or recurrent ischemia
refractory to medical therapy in patients who have coronary
anatomy suitable for surgery, and are not candidates for PCI
or fibronolytic therapy
3. RECOMMENDED in patients with STEMI at the time of
operative repair of mechanical defects.
88. STEMI
Antiplatelets and Antithrombotics
1. It IS RECOMMENDED that aspirin should be used
indefinitely in all patients with STEMI with a dosage of 80 to
100 mg/day.
2. It IS RECOMMENDED that clopidogrel 75 mg per day orally
should be added to aspirin in patients with STEMI and
maintained for at least 14 days
3. It IS RECOMMENDED that patients who are truly intolerant
to aspirin can instead receive clopidogrel 75 mg per day as
long-term secondary prevention
89. STEMI
Duration of Dual Antiplatelet Therapy and Antithrombotic
Combination Therapies after STEMI
1. Combination Therapies after STEMI DAPT by combining
aspirin and an ADP-receptor blocker (clopidogrel, prasugrel
or ticagrelor) IS RECOMMENDED in patients with STEMI
who are undergoing primary PCI (for up to 12 months) or
(clopidogrel) fibrinolysis (for up to 12 months, although the
data available pertain only to one month of DAPT), and in
those who have not undergone reperfusion therapy (for at
least 1 month and up to 12 months).
90. STEMI
Lipid Lowering Agents
1. High-dose statins are RECOMMENDED in all patients during
the first 24 hours of admission for STEMI, irrespective of the
patientâs cholesterol concentration, in the absence of
contraindications (allergy, active liver disease).
2. Atorvastatin or Rosuvastatin are recommended during the
early phase of therapy up to at least four weeks.
3. It IS RECOMMENDED to give high-dose rosuvastatin (20 to
40 mg) or atorvastatin (40 to 80 mg) therapy before
emergency percutaneous coronary intervention to
1. reduce periprocedural inflammatory response,
2. to reduce myocardial dysfunction, and
3. to prevent contrast-induced nephropathy
the term acute coronary syndrome, which encompasses
unstable angina, NSTEMI, and STEMI, is in general reserved for
ischemia precipitated by acute coronary atherothrombosis
the term acute coronary syndrome, which encompasses
unstable angina, NSTEMI, and STEMI, is in general reserved for
ischemia precipitated by acute coronary atherothrombosis.
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in nonâST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. It is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery.
the term acute coronary syndrome, which encompasses
unstable angina, NSTEMI, and STEMI, is in general reserved for
ischemia precipitated by acute coronary atherothrombosis
The classic manifestation of ischemia is angina, which is usually described as a heavy chest pressure or squeezing, a burning feeling, or difficulty breathing (see Chapter 11).
The discomfort often radiates to the left shoulder, neck, or arm. It typically builds in intensity over a period of a few minutes.
The pain may begin with exercise or psychological stress, but ACS most commonly occurs without obvious precipitating factors.
Myocardial ischemia causing chest discomfort, termed angina pectoris, is a primary clinical concern in patients presenting with chest symptoms.
Myocardial ischemia is precipitated by an imbalance between myocardial oxygen requirements and myocardial oxygen supply, resulting in insufficient delivery of oxygen to meet the heartâs metabolic demands.
Myocardial oxygen consumption may be elevated by
increases in heart rate, ventricular wall stress, and myocardial contractility,
whereas myocardial oxygen supply is determined by coronary
This picture shows the main symptoms of a heart attack. People who are having a heart attack often have only some of these symptoms. The pain, pressure, and discomfort caused by a heart attack mostly affect the left side of the body (shown in darker red) but can also affect the right. If you think you are having a heart attack, call 9-1-1 for an ambulance. Do not try to get yourself to the hospital.
Figure 12.9 Coronary Circulation
The coronary arteries supply arterial blood to the muscular wall of the heart.
The pressure gradient for flow through the arteries is affected by tissue pressure in the wall of
the heart during systole, particularly in the left coronary circulation.
Thus, while flow through both right and left coronary arteries is related to aortic pressure, these compressive forces reduce left coronary flow during
systole.
During diastole, flow is greatly enhanced in the left coronary circulation by the actions of vasodilator metabolites that build up during systole.
The metabolite adenosine is believed to be particularly important in this enhancement of coronary flow.
Figure 12.9 Coronary Circulation
The coronary arteries supply arterial blood to the muscular wall of the heart.
The pressure gradient for flow through the arteries is affected by tissue pressure in the wall of
the heart during systole, particularly in the left coronary circulation.
Thus, while flow through both right and left coronary arteries is related to aortic pressure, these compressive forces reduce left coronary flow during
systole.
During diastole, flow is greatly enhanced in the left coronary circulation by the actions of vasodilator metabolites that build up during systole.
The metabolite adenosine is believed to be particularly important in this enhancement of coronary flow.
Figure 12.9 Coronary Circulation
The coronary arteries supply arterial blood to the muscular wall of the heart.
The pressure gradient for flow through the arteries is affected by tissue pressure in the wall of
the heart during systole, particularly in the left coronary circulation.
Thus, while flow through both right and left coronary arteries is related to aortic pressure, these compressive forces reduce left coronary flow during
systole.
During diastole, flow is greatly enhanced in the left coronary circulation by the actions of vasodilator metabolites that build up during systole.
The metabolite adenosine is believed to be particularly important in this enhancement of coronary flow.
Criteria for Acute Myocardial Infarction
The term acute myocardial infarction (MI) should be used when there is evidence
of myocardial necrosis in a clinical setting consistent with acute myocardial
ischemia. Under these conditions, any one of the following criteria
meets the diagnosis for MI:
⢠Detection of a rise and/or fall of cardiac biomarker values (preferably
cardiac troponin [cTn]) with at least one value above the 99th percentile
upper reference limit (URL) and with at least one of the following:
⢠Symptoms of ischemia
⢠New or presumed new significant ST-segment T-wave (ST-T) changes or
new left bundle branch block (LBBB)
⢠Development of pathologic Q waves in the electrocardiogram (ECG)
⢠Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
⢠Identification of an intracoronary thrombus by angiography or autopsy
⢠Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB, but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased.
⢠Percutaneous coronary intervention (PCI)ârelated MI is arbitrarily defined
by elevation of cTn values (>5 Ă 99th percentile URL) in patients with normal
baseline values (â¤99th percentile URL) or a rise of cTn values >20% if
the baseline values are elevated and are stable or falling. In addition, either
(i) symptoms suggestive of myocardial ischemia, or (ii) new ischemic ECG
changes, or (iii) angiographic findings consistent with a procedural complication,
or (iv) imaging demonstration of new loss of viable myocardium or
new regional wall motion abnormality are required.
⢠Stent thrombosis associated with MI when detected by coronary angiography
or autopsy in the setting of myocardial ischemia and with a rise and/
or fall of cardiac biomarker values with at least one value above the 99th
percentile URL.
⢠Coronary artery bypass grafting (CABG)ârelated MI is arbitrarily defined
by elevation of cardiac biomarker values (>10 Ă 99th percentile URL) in
patients with normal baseline cTn values (â¤99th percentile URL). In addition,
either (i) new pathologic Q waves or new LBBB, or (ii) angiographic
documented new graft or new native coronary artery occlusion, or (iii)
imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
The American
College of Cardiology (ACC) and American Heart Association (AHA)
guidelines list the following as pain descriptions uncharacteristic of
myocardial ischemia7:
⢠Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory
movements or coughing)
⢠Primary or sole location of the discomfort in the middle or lower
abdominal region
⢠Pain that may be localized by the tip of one finger, particularly over
the left ventricular apex
⢠Pain reproduced with movement or palpation of the chest wall or
arms
⢠Constant pain that persists for many hours
⢠Very brief episodes of pain that last a few seconds or less
⢠Pain that radiates into the lower extremities
The major determinants of myocardial oxygen demand
(MVO2) are heart rate, myocardial contractility, and myocardial wall
tension (stress).
Blood flows through the coronary arteries in
a phasic fashion, with the majority occurring during diastole. About
75% of the total coronary resistance to flow occurs across three sets
of arteries: (1) large epicardial arteries (Resistance 1 = R1), (2) prearteriolar
vessels (R2), and (3) arteriolar and intramyocardial capillary
vessels (R3). In the absence of significant flow-limiting atherosclerotic obstructions, R1 is trivial; the major determinant of coronary resistance
is found in R2 and R3.
Coronary blood flow also can be limited by spasm (see Prinzmetalâs
angina in Chap. 294), arterial thrombi, and, rarely, coronary emboli
as well as by ostial narrowing due to aortitis.
Congenital abnormalities such as the origin of the left anterior descending coronary artery from
the pulmonary artery may cause myocardial ischemia and infarction in
infancy, but this cause is very rare in adults.
When a stenosis reduces the diameter of an epicardial artery by 50%, there is a limitation of the ability to increase flow to
meet increased myocardial demand.
When the diameter is reduced by âź80%, blood flow at rest may be reduced, and further minor decreases
in the stenotic orifice area can reduce coronary flow dramatically to cause myocardial ischemia at rest or with minimal stress.
Cascade of mechanisms and manifestations of ischemia.
The severity and duration of
the imbalance between myocardial oxygen supply and demand determine
whether the damage is reversible (â¤20 min for total occlusion in
the absence of collaterals) or permanent, with subsequent myocardial
necrosis (>20 min).
Figure 293-2 Evaluation of the patient with known or suspected ischemic heart disease.
On the left of the figure is an algorithm for
identifying patients who should be referred for stress testing and the decision pathway for determining whether a standard treadmill exercise
with electrocardiogram (ECG) monitoring alone is adequate. A specialized imaging study is necessary if the patient cannot exercise adequately
(pharmacologic challenge is given) or if there are confounding features on the resting ECG (symptom-limited treadmill exercise may
be used to stress the coronary circulation). Panels BâE, continued on the next page, are examples of the data obtained with ECG monitoring
and specialized imaging procedures. CMR, cardiac magnetic resonance; EBCT, electron beam computed tomography; ECHO, echocardiography;
IHD, ischemic heart disease; MIBI, methoxyisobutyl isonitrite; MR, magnetic resonance; PET, positron emission tomography. A. Lead
V4 at rest (top panel) and after 4.5 min of exercise (bottom panel). There is 3 mm (0.3 mV) of horizontal ST-segment depression, indicating a positive
test for ischemia. (Modified from BR Chaitman, in E Braunwald et al [eds]: Heart Disease, 8th ed, Philadelphia, Saunders, 2008.) B. A 45-year-old avid
jogger who began experiencing classic substernal chest pressure underwent an exercise echo study. With exercise the patientâs heart rate
increased from 52 to 153 beats/min. The left ventricular chamber dilated with exercise, and the septal and apical portions became akinetic
to dyskinetic (red arrow). These findings are strongly suggestive of a significant flow-limiting stenosis in the proximal left anterior descending
artery, which was confirmed at coronary angiography. (Modified from SD Solomon, in E. Braunwald et al [eds]: Primary Cardiology, 2nd ed,
Philadelphia, Saunders, 2003.) C. Stress and rest myocardial perfusion single-photon emission computed tomography images obtained with
99m-technetium sestamibi in a patient with chest pain and dyspnea on exertion. The images demonstrate a medium-size and severe stress
perfusion defect involving the inferolateral and basal inferior walls, showing nearly complete reversibility, consistent with moderate ischemia
in the right coronary artery territory (red arrows). (Images provided by Dr. Marcello Di Carli, Nuclear Medicine Division, Brigham and Womenâs
Hospital, Boston, MA.) D. A patient with a prior myocardial infarction presented with recurrent chest discomfort. On cardiac magnetic resonance
(CMR) cine imaging, a large area of anterior akinesia was noted (marked by the arrows in the top left and right images, systolic frame only). This
area of akinesia was matched by a larger extent of late gadolinium-DTPA enhancements consistent with a large transmural myocardial infarction
(marked by arrows in the middle left and right images). Resting (bottom left) and adenosine vasodilating stress (bottom right) first-pass perfusion
images revealed reversible perfusion abnormality that extended to the inferior septum. This patient was found to have an occluded proximal
left anterior descending coronary artery with extensive collateral formation. This case illustrates the utility of different modalities in a CMR
examination in characterizing ischemic and infarcted myocardium. DTPA, diethylenetriamine penta-acetic acid. (Images provided by Dr. Raymond
Kwong, Cardiovascular Division, Brigham and Womenâs Hospital, Boston, MA.) E. Stress and rest myocardial perfusion PET images obtained with
rubidium-82 in a patient with chest pain on exertion. The images demonstrate a large and severe stress perfusion defect involving the mid
and apical anterior, anterolateral, and anteroseptal walls and the left ventricular apex, showing complete reversibility,
consistent with extensive and severe ischemia in the mid-left anterior descending coronary artery territory (red arrows). (Images provided by
Dr. Marcello Di Carli, Nuclear Medicine Division, Brigham and Womenâs Hospital, Boston, MA.)
TABLE 50-7 Indications and Contraindications for Exercise Electrocardiographic Testing in the Emergency Department
Requirements before exercise electrocardiographic testing that should be considered in the ED setting:
⢠Two sets of cardiac enzymes at 4-hr intervals should be normal
⢠ECG at the time of arrival and preexercise 12-lead ECG show no significant abnormality
⢠Absence of rest electrocardiographic abnormalities that would preclude accurate assessment of the exercise ECG
⢠From admission to the time that results are available from the second set of cardiac enzymes: patient asymptomatic, lessening chest pain symptoms, or persistent atypical symptoms
⢠Absence of ischemic chest pain at the time of exercise testing
Contraindications to exercise electrocardiographic testing in the ED setting:
⢠New or evolving electrocardiographic abnormalities on the rest tracing
⢠Abnormal cardiac enzyme levels
⢠Inability to perform exercise
⢠Worsening or persistent ischemic chest pain symptoms from admission to the time of exercise testing
⢠Clinical risk profiling indicating that imminent coronary angiography is likely
Laboratory Tests
It IS RECOMMENDED that the following initial laboratory tests be
performed to establish CV risk factors, identify possible causes of
ischemia and determine prognosis:
1. Fasting lipid profile (total cholesterol, high density lipoprotein
[HDL] cholesterol, low density lipoprotein [LDL] cholesterol and
triglyceride levels);
2. Fasting glucose and/or glycated hemoglobin (HbA1c) level if
available; additional oral glucose tolerance test (OGTT) if both
are inconclusive;
3. Complete blood count (CBC);
4. Creatinine level with estimation of glomerular filtration rate (GFR);
5. Biochemical markers of myocardial injury (Troponin T or I) if
clinical evaluation suggests an Acute Coronary Syndrome (ACS);
6. Thyroid hormone levels if with clinical suspicion of thyroid
disorder, and;
7. Liver function tests early after beginning statin therapy.
High: > 90% pre-test probability
Intermediate: between 10% and 90% pre-test probability
Low: between 5% and 10% pre-test probability
Very low: < 5% pre-test probability
Adapted from Diamond GA, Forrester JS. (1982). Probability of CAD.8
A stress imaging study IS RECOMMENDED as the initial diagnostic
and prognostic test, if facilities, resources and local expertise permit,
in patients within the higher range of PTP; patients with LVEF less than
50% without typical angina; patients with resting ECG abnormalities
and especially symptomatic patients with prior revascularization
(percutaneous coronary intervention [PCI] or coronary artery bypass
grafting [CABG]). Exercise testing rather than pharmacological testing
is recommended whenever possible.
An exercise ECG (TET) IS RECOMMENDED as the initial diagnostic
and prognostic test, if resources and local expertise for a stress imaging
study are not available, in patients with intermediate PTP who have
normal resting ECGs and are able to exercise.
30
Because of its simplicity, lower cost and widespread availability, the TET is
the initial test of choice to identify inducible ischemia in the majority of patients
with intermediate PTP who are able to exercise. The low sensitivity of the TET
(45% to 50%) despite a high specificity (85% to 90%) is the reason why it is
not recommended in patients with a PTP greater than 65%. In the latter case,
a stress imaging study is more appropriate.
Examples of other indications for coronary arteriography include
the following:
1. Patients with chest discomfort suggestive of angina pectoris but a
negative or nondiagnostic stress test who require a definitive diagnosis
for guiding medical management, alleviating psychological
stress, career or family planning, or insurance purposes.
2. Patients who have been admitted repeatedly to the hospital for a
suspected acute coronary syndrome (Chaps. 294 and 295), but
in whom this diagnosis has not been established and in whom the
presence or absence of CAD should be determined.
3. Patients with careers that involve the safety of others (e.g., pilots,
firefighters, police) who have questionable symptoms or suspicious
or positive noninvasive tests and in whom there are reasonable
doubts about the state of the coronary arteries.
4. Patients with aortic stenosis or hypertrophic cardiomyopathy and
angina in whom the chest pain could be due to IHD.
5. Male patients >45 years and females >55 years who are to undergo a
cardiac operation such as valve replacement or repair and who may
or may not have clinical evidence of myocardial ischemia.
6. Patients after myocardial infarction, especially those who are at
high risk after myocardial infarction because of the recurrence of
angina or the presence of heart failure, frequent ventricular premature
contractions, or signs of ischemia on the stress test.
7. Patients with angina pectoris, regardless of severity, in whom
noninvasive testing indicates a high risk of coronary events (poor
exercise performance or severe ischemia).
8. Patients in whom coronary spasm or another nonatherosclerotic
cause of myocardial ischemia (e.g., coronary artery anomaly,
Kawasaki disease) is suspected.
1. Increase polyunsaturated fatty acid consumption, mainly from oily fish:
2 to 3 servings of oily fish per week may help prevent CV disease
(CVD);
2. Saturated fatty acids must comprise less than 10% of the total energy
intake; protein sources that are low in saturated fats should replace
those high in these harmful fats;
3. Limit salt intake to less than 5 grams per day; added salt should be
limited;
4. Consume 30 to 45 grams of fiber per day (wholegrain products, fruits
and vegetables); simple carbohydrates that have a high glycemic load
should be avoided in favor of carbohydrate sources that are high in
fiber;
5. Consume 200 grams of vegetables per day (2 to 3 servings or 1 to 4
cups per day);
6. Eat 200 grams of fruits per day (2 to 3 servings or 1 to 2.5 cups per
day), and;
7. Limit consumption of alcoholic beverages to two glasses per day (20
grams) for men, and one glass per day (10 grams) for women
An exercise ECG (TET) IS RECOMMENDED as the initial diagnostic
and prognostic test, if resources and local expertise for a stress imaging
study are not available, in patients with intermediate PTP who have
normal resting ECGs and are able to exercise.
30
Because of its simplicity, lower cost and widespread availability, the TET is
the initial test of choice to identify inducible ischemia in the majority of patients
with intermediate PTP who are able to exercise. The low sensitivity of the TET
(45% to 50%) despite a high specificity (85% to 90%) is the reason why it is
not recommended in patients with a PTP greater than 65%. In the latter case,
a stress imaging study is more appropriate.
Patients considered high risk for mortality are those with high-risk coronary
anatomy and those with moderate or severe LV dysfunction. High-risk
coronary anatomy includes: at least 50% stenosis of the left main coronary
artery and/or significant (at least 70% stenosis) 3-vessel CAD; significant
proximal LAD stenosis; and a Synergy between PCI with Taxus and Cardiac
Surgery (SYNTAX) score of 33 or higher. Moderate or severe LV dysfunction
is defined as LVEF of less than 45% and 35%, respectively. These subset of
patients have a better prognosis with CABG than with medical treatment.
PATHOPHYSIOLOGY
NSTE-ACS is most commonly caused by an imbalance between oxygen
supply and oxygen demand resulting from a partially occluding
thrombus forming on a disrupted atherothrombotic coronary plaque or on eroded coronary artery endothelium.
Severe ischemia or myocardial
necrosis may occur consequent to the reduction of coronary
blood flow caused by the thrombus and by downstream embolization
of platelet aggregates and/or atherosclerotic debris. Other causes of
NSTE-ACS include:
(1) dynamic obstruction (e.g., coronary spasm,
as in Prinzmetalâs variant angina [see âPrinzmetalâs Variant Anginaâ
later]);
(2) severe mechanical obstruction due to progressive coronary
atherosclerosis; and
(3) increased myocardial oxygen demand produced
by conditions such as fever, tachycardia, and thyrotoxicosis in
the presence of fixed epicardial coronary obstruction.
More than one
of these processes may be involved.
Figure 294-1 Trends of incidence of ST-segment elevation
myocardial infarction (STEMI) and non-ST-segment elevation
myocardial infarction (NSTEMI) and of frequency of use of troponin
assay to diagnose acute myocardial infarction. NRMI, National Registry
of Myocardial Infarction.
294-3 Algorithm for evaluation and management of patients with suspected acute coronary syndrome (ACS). Follow-up studies
refer to ST deviations and elevation of troponin levels. cTn, cardiac troponin; ECG, electrocardiogram; LV, left ventricular. (Modified from
JL Anderson et al: J Am Coll Cardiol 61:e179, 2013.)
The diagnosis of NSTE-ACS is based largely on the clinical
presentation. Typically, 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 (i.e., within the prior 2
weeks); and/or (3) it occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than previous episodes).
The diagnosis of NSTEMI is established if a patient with these clinical features
develops evidence of myocardial necrosis, as reflected in abnormally
elevated levels of biomarkers of cardiac necrosis (see below).
DIAGNOSTIC EVALUATION
In addition to the clinical examination, three major noninvasive tools
are used in the evaluation of NSTEMI-ACS: the electrocardiogram
(ECG), cardiac biomarkers, and stress testing. CCTA is an additional
emerging option (Fig. 294-2).
The goals are to: (1) recognize or exclude
myocardial infarction (MI) using cardiac biomarkers, preferably cTn;
(2) detect rest ischemia (using serial or continuous ECGs); and (3)
detect significant coronary obstruction at rest with CCTA and myocardial
ischemia using stress testing (Chap 270e
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 12â24 h. Medical therapy involves simultaneous
anti-ischemic and antithrombotic
Drugs Commonly Used in Intensive Medical Management of Patients with Unstable Angina and Non-ST-Segment Elevation
Myocardial Infarction
In 1959 Prinzmetal et al. described a syndrome of severe ischemic pain
that usually occurs at rest and is associated with transient ST-segment
elevation.
Prinzmetalâs variant angina (PVA) is caused by focal spasm
of an epicardial coronary artery, leading to severe transient myocardial
ischemia and occasionally infarction.
The 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.
For reasons that are not clear, the prevalence of PVA has decreased substantially during the past few decades.
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.
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 (âź90â95%).
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.
Coronary angiography IS NOT RECOMMENDED in patients with
extensive co-morbidities (e.g., liver or pulmonary failure; cancer);
in whom the risks of revascularization are not likely to outweigh the
benefits; in patients with acute chest pain and a low likelihood of ACS;
or in patients who will not consent to revascularization regardless of
the findings.
The benefits of coronary angiography should be balanced by its risks. The
benefits of coronary angiography are highest among high risk patients. It is
not recommended for patients whose risks may outweigh the benefits, such
as in those with extensive comorbidities, or those with a low probability of
ACS. In these patients, invasive evaluation can be delayed without increased
risk. Non-invasive assessments of inducible ischemia may be performed
before hospital discharge.
Statement 20: Revascularization by PCI
PCI IS RECOMMENDED for NSTE-ACS patients with 1- to 2-vessel
CAD, with or without significant proximal left anterior descending CAD,
but with a large area of viable myocardium and high-risk criteria on noinvasive
testing.
If lesions are difficult to assess, fractional flow reserve measurements may
be used in order to decide on the treatment strategy.
Statement 21: Revascularization by CABG Surgery
CABG IS RECOMMENDED for patients with significant left main
disease, and is the preferred revascularization strategy for patients with
multi-vessel coronary disease; vessels with lesions not favorable for
PCI; depressed systolic function (LVEF lower than 50%); and diabetes.
The general consensus in other guidelines is that CABG is most beneficial
in patients with disease of the left main coronary artery; involvement of
multiple vessels; and other high-risk patients such as those with ventricular
dysfunction or diabetes.38
STATEMENT 24: Drug/Medication Management
It IS STRONGLY RECOMMENDED to maintain patients who were
treated medically with aspirin indefinitely, and ticagrelor 90 mg twice
daily or clopidogrel 75 mg daily, for 12 months.
It IS STRONGLY RECOMMENDED to maintain patients who
underwent stenting, with aspirin indefinitely, plus ticagrelor 90 mg twice
daily or prasugrel 10 mg daily or clopidogrel 75 mg daily, for 12 months
in patients with drug-eluting stents, and 6 months in patients with bare
metal stents.
It IS STRONGLY RECOMMENDED that beta blockers be continued
indefinitely for all NSTE-ACS patients unless contraindicated. In those
with moderate or severe systolic dysfunction, the dosing regimen must
be titrated slowly.
Figure 295-3 Major components of time delay between onset of symptoms from ST-segment elevation myocardial infarction and
restoration of flow in the infarct-related artery. Plotted sequentially from left to right are the times for patients to recognize symptoms and
seek medical attention, transportation to the hospital, in-hospital decision making, implementation of reperfusion strategy, and restoration of
flow once the reperfusion strategy has been initiated. The time to initiate fibrinolytic therapy is the âdoor-to-needleâ (D-N) time; this is followed
by the period of time required for pharmacologic restoration of flow. More time is required to move the patient to the catheterization laboratory
for a percutaneous coronary interventional (PCI) procedure, referred to as the âdoor-to-balloonâ (D-B) time, but restoration of flow in the
epicardial infarctârelated artery occurs promptly after PCI. At the bottom is a variety of methods for speeding the time to reperfusion along with
the goals for the time intervals for the various components of the time delay. (Adapted from CP Cannon et al: J Thromb Thrombol 1:27, 1994.)
Definition of Myocardial Infarction
Criteria for Acute Myocardial Infarction
The term acute myocardial infarction (MI) should be used when there is evidence
of myocardial necrosis in a clinical setting consistent with acute myocardial
ischemia. Under these conditions, any one of the following criteria
meets the diagnosis for MI:
⢠Detection of a rise and/or fall of cardiac biomarker values (preferably
cardiac troponin [cTn]) with at least one value above the 99th percentile
upper reference limit (URL) and with at least one of the following:
⢠Symptoms of ischemia
⢠New or presumed new significant ST-segment T-wave (ST-T) changes or
new left bundle branch block (LBBB)
⢠Development of pathologic Q waves in the electrocardiogram (ECG)
⢠Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
⢠Identification of an intracoronary thrombus by angiography or autopsy
⢠Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB, but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased.
⢠Percutaneous coronary intervention (PCI)ârelated MI is arbitrarily defined
by elevation of cTn values (>5 Ă 99th percentile URL) in patients with normal
baseline values (â¤99th percentile URL) or a rise of cTn values >20% if
the baseline values are elevated and are stable or falling. In addition, either
(i) symptoms suggestive of myocardial ischemia, or (ii) new ischemic ECG
changes, or (iii) angiographic findings consistent with a procedural complication,
or (iv) imaging demonstration of new loss of viable myocardium or
new regional wall motion abnormality are required.
⢠Stent thrombosis associated with MI when detected by coronary angiography
or autopsy in the setting of myocardial ischemia and with a rise and/
or fall of cardiac biomarker values with at least one value above the 99th
percentile URL.
⢠Coronary artery bypass grafting (CABG)ârelated MI is arbitrarily defined
by elevation of cardiac biomarker values (>10 Ă 99th percentile URL) in
patients with normal baseline cTn values (â¤99th percentile URL). In addition,
either (i) new pathologic Q waves or new LBBB, or (ii) angiographic
documented new graft or new native coronary artery occlusion, or (iii)
imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality.
Criteria for Prior Myocardial Infarction
Any one of the following criteria meets the diagnosis for prior MI:
⢠Pathologic Q waves with or without symptoms in the absence of nonischemic
causes.
⢠Imaging evidence of a region of loss of viable myocardium that is thinned
and fails to contract, in the absence of a nonischemic cause.
⢠Pathologic findings of a prior M
Definition of Myocardial Infarction
Criteria for Acute Myocardial Infarction
The term acute myocardial infarction (MI) should be used when there is evidence
of myocardial necrosis in a clinical setting consistent with acute myocardial
ischemia. Under these conditions, any one of the following criteria
meets the diagnosis for MI:
⢠Detection of a rise and/or fall of cardiac biomarker values (preferably
cardiac troponin [cTn]) with at least one value above the 99th percentile
upper reference limit (URL) and with at least one of the following:
⢠Symptoms of ischemia
⢠New or presumed new significant ST-segment T-wave (ST-T) changes or
new left bundle branch block (LBBB)
⢠Development of pathologic Q waves in the electrocardiogram (ECG)
⢠Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
⢠Identification of an intracoronary thrombus by angiography or autopsy
⢠Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB, but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased.
⢠Percutaneous coronary intervention (PCI)ârelated MI is arbitrarily defined
by elevation of cTn values (>5 Ă 99th percentile URL) in patients with normal
baseline values (â¤99th percentile URL) or a rise of cTn values >20% if
the baseline values are elevated and are stable or falling. In addition, either
(i) symptoms suggestive of myocardial ischemia, or (ii) new ischemic ECG
changes, or (iii) angiographic findings consistent with a procedural complication,
or (iv) imaging demonstration of new loss of viable myocardium or
new regional wall motion abnormality are required.
⢠Stent thrombosis associated with MI when detected by coronary angiography
or autopsy in the setting of myocardial ischemia and with a rise and/
or fall of cardiac biomarker values with at least one value above the 99th
percentile URL.
⢠Coronary artery bypass grafting (CABG)ârelated MI is arbitrarily defined
by elevation of cardiac biomarker values (>10 Ă 99th percentile URL) in
patients with normal baseline cTn values (â¤99th percentile URL). In addition,
either (i) new pathologic Q waves or new LBBB, or (ii) angiographic
documented new graft or new native coronary artery occlusion, or (iii)
imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality.
Criteria for Prior Myocardial Infarction
Any one of the following criteria meets the diagnosis for prior MI:
⢠Pathologic Q waves with or without symptoms in the absence of nonischemic
causes.
⢠Imaging evidence of a region of loss of viable myocardium that is thinned
and fails to contract, in the absence of a nonischemic cause.
⢠Pathologic findings of a prior M
Type I: Spontaneous Myocardial Infarction
Spontaneous myocardial infarction related to atherosclerotic plaque rupture,
ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus
in one or more of the coronary arteries leading to decreased myocardial
blood flow or distal platelet emboli with ensuing myocyte necrosis. The
patient may have underlying severe coronary artery disease (CAD) but on
occasion nonobstructive or no CAD.
Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance
In instances of myocardial injury with necrosis where a condition other than
CAD contributes to an imbalance between myocardial oxygen supply and/
or demand, e.g., coronary endothelial dysfunction, coronary artery spasm,
coronary embolism, tachy-brady-arrhythmias, anemia, respiratory failure,
hypotension, and hypertension with or without left ventricular hypertrophy.
Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable
Cardiac death with symptoms suggestive of myocardial ischemia and presumed
new ischemic electrocardiogram (ECG) changes or new left bundle
branch block (LBBB), but death occurring before blood samples could be
obtained or before cardiac biomarker could rise, or in rare cases, cardiac biomarkers
were not collected.
Type 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention (PCI)
Myocardial infarction associated with PCI is arbitrarily defined by elevation
of cardiac troponin (cTn) values >5 Ă 99th percentile upper reference limit
(URL) in patients with normal baseline values (â¤99th percentile URL) or a rise
of cTn values >20% if the baseline values are elevated and are stable or falling.
In addition, either (i) symptoms suggestive of myocardial ischemia, or (ii)
new ischemic ECG changes or new LBBB, or (iii) angiographic loss of patency
of a major coronary artery or a side branch or persistent slow or no flow or
embolization, or (iv) imaging demonstration of new loss of viable myocardium
or new regional wall motion abnormality is required.
Type 4b: Myocardial Infarction Related to Stent Thrombosis
Myocardial infarction associated with stent thrombosis is detected by coronary
angiography or autopsy in the setting of myocardial ischemia and with
a rise and/or fall of cardiac biomarker values with at least one value above
the 99th percentile URL.
Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting (CABG)
Myocardial infarction associated with CABG is arbitrarily defined by elevation
of cardiac biomarker values >10 Ă 99th percentile URL in patients with
normal baseline cTn values (â¤99th percentile URL). In addition, either (i) new
pathologic Q waves or new LBBB, or (ii) angiographic documented new graft
or new native coronary artery occlusion, or (iii) imaging evidence of new loss
of viable myocardium or new regional wall motion abnormality.
In the Emergency Department, the goals for the management of
patients with suspected STEMI include control of cardiac discomfort,
rapid identification of patients who are candidates for urgent reperfusion
therapy, triage of lower-risk patients to the appropriate location
in the hospital, and avoidance of inappropriate discharge of patients
with STEMI.
Many aspects of the treatment of STEMI are initiated in
the Emergency Department and then continued during the in-hospital
phase of management (Fig. 295-4). 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 (Fig. 295-4).
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 160â325-mg tablet in the Emergency
Department. This measure should be followed by daily oral administration
of aspirin in a dose of 75â162 mg.
In patients whose arterial O2 saturation is normal, supplemental O2
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 (2â4 L/min) for the first 6â12 h after infarction;
the patient should then be reassessed
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. In addition to diminishing or abolishing chest discomfort,
nitroglycerin 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
nitroglycerin is followed by the return of chest discomfort, particularly
if accompanied by other evidence of ongoing ischemia such as further
ST-segment or T-wave shifts, the use of intravenous nitroglycerin
should be considered. Therapy with nitrates should be avoided in
patients who present with low systolic arterial pressure (<90 mmHg)
or in whom there is clinical suspicion of RV infarction (inferior infarction
on ECG, elevated jugular venous pressure, clear lungs, and hypotension).
Nitrates should not be administered to patients who have
taken a phosphodiesterase-5 inhibitor for erectile dysfunction within
the preceding 24 h, because it may potentiate the 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. However, 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.
Morphine also has a 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).
Morphine is routinely administered by repetitive (every
5 min) intravenous injection of small doses (2â4 mg), rather than by
the subcutaneous administration of a larger quantity, because absorption
may be unpredictable by the latter route.
Intravenous beta blockers are also useful in the control of the pain
of STEMI. These drugs control pain effectively in some patients, presumably
by diminishing myocardial O2 demand and hence ischemia.
More important, there is evidence that intravenous beta blockers
reduce the risks of reinfarction and ventricular fibrillation (see âBeta-
Adrenoceptor Blockersâ below).
However, patient selection is important
when considering beta blockers for STEMI.
Oral beta blocker
therapy should be initiated in the first 24 h for patients who do not
have any of the following:
signs of heart failure,
(2) evidence of a
low-output state,
(3) increased risk for cardiogenic shock, or
(4) other relative contraindications to beta blockade (PR interval greater than
0.24 seconds, second- or third-degree heart block, active asthma, or
reactive airway disease).
A commonly employed regimen is metoprolol,
5 mg every 2â5 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 100 mg
every 12 h.
Unlike beta blockers, calcium antagonists are of little value in the
acute setting, and there is evidence that short-acting dihydropyridines
may be associated with an increased mortality risk.
Figure 295-4 Reperfusion therapy for patients with ST-segment elevation myocardial infarction (STEMI). The bold arrows and boxes are
the preferred strategies. Performance of percutaneous coronary intervention (PCI) is dictated by an anatomically appropriate culprit stenosis.
*Patients with cardiogenic shock or severe heart failure initially seen at a nonâPCI-capable hospital should be transferred for cardiac catheterization
and revascularization as soon as possible, irrespective of time delay from myocardial infarction (MI) onset (Class I, LOE: B). â Angiography and
revascularization should not be performed within the first 2 to 3 hours after administration of fibrinolytic therapy. CABG, coronary artery bypass
graft; DIDO, door-inâdoor-out; FMC, first medical contact; LOE, level of evidence; STEMI, ST-elevation myocardial infarction. (Adapted with permission
from P OâGara et al: Circulation 127:e362, 2013.)
Statement 5: Initial ER Management
Unless contraindicated, it IS RECOMMENDED that the following
routine treatment measures be administered in STEMI patients upon
arrival at the ER:
⢠Aspirin 160 to 320 mg tablet (non-enteric coated, chewed);
⢠Clopidogrel 300 to 600 mg whether or not fibrinolysis will be
given;
⢠Clopidgrel 600 mg or prasugrel 60 mg or ticagrelor 180 mg when
a patient will undergo PCI;
⢠Nitrates, either via sublingual or intravenous(IV) routes. Nitrates
are contraindicated in patients with hypotension or those who
took a phosphodiesterase 5 (PDE5) inhibitor within 24 hrs (48 hrs
for tadalafil);
⢠Morphine 2 to 4 mg IV for relief of chest pain, and;
⢠Supplemental oxygen MAY BE RECOMMENDED during the first 6
hours to patients with arterial oxygen saturation of less than 90%.
Statement 6: In-hospital Treatment
Reperfusion therapy IS RECOMMENDED to all eligible patients with
STEMI with symptom onset within the prior 12 hours.
Early revascularization, the goal being 12 hours, is a primary treatment
goal in patients with STEMI.
2 Delayed reperfusion is associated with poorer
myocardial salvage and outcomes
Figure 295-4 Reperfusion therapy for patients with ST-segment elevation myocardial infarction (STEMI). The bold arrows and boxes are
the preferred strategies. Performance of percutaneous coronary intervention (PCI) is dictated by an anatomically appropriate culprit stenosis.
*Patients with cardiogenic shock or severe heart failure initially seen at a nonâPCI-capable hospital should be transferred for cardiac catheterization
and revascularization as soon as possible, irrespective of time delay from myocardial infarction (MI) onset (Class I, LOE: B). â Angiography and
revascularization should not be performed within the first 2 to 3 hours after administration of fibrinolytic therapy. CABG, coronary artery bypass
graft; DIDO, door-inâdoor-out; FMC, first medical contact; LOE, level of evidence; STEMI, ST-elevation myocardial infarction. (Adapted with permission
from P OâGara et al: Circulation 127:e362, 2013.)
Fibrinolysis
If no contraindications are present (see below), fibrinolytic therapy
should ideally be initiated within 30 min of presentation (i.e., doorto-
needle time â¤30 min). The principal goal of fibrinolysis is prompt
restoration of full coronary arterial patency. The fibrinolytic agents
tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK),
and reteplase (rPA) have been approved by the U.S. Food and Drug
Administration for intravenous use in patients with STEMI. These
drugs all act by promoting the conversion of plasminogen to plasmin,
which subsequently lyses fibrin thrombi. Although considerable
emphasis was first placed on a distinction between more fibrin-specific
agents, such as tPA, and non-fibrin-specific agents, such as streptokinase,
it is now recognized that these differences are only relative, as
some degree of systemic fibrinolysis occurs with the former agents.
TNK and rPA are referred to as bolus fibrinolytics since their administration
does not require a prolonged intravenous infusion.
Allergic reactions to streptokinase occur in âź2% of patients who
receive it. While a minor degree of hypotension occurs in 4â10% of
patients given this agent, marked hypotension occurs, although rarely,
in association with severe allergic reactions.
Hemorrhage is the most frequent and potentially the most serious
complication. Because bleeding episodes that require transfusion are
more common when patients require invasive procedures, unnecessary
venous or arterial interventions should be avoided in patients
receiving fibrinolytic agents. Hemorrhagic stroke is the most serious
complication and occurs in âź0.5â0.9% of patients being treated with
these agents. This rate increases with advancing age, with patients >70
years experiencing roughly twice the rate of intracranial hemorrhage
as those <65 years. Large-scale trials have suggested that the rate of
intracranial hemorrhage with tPA or rPA is slightly higher than with
streptokinase.
When assessed angiographically, flow in the culprit coronary artery
is described by a simple qualitative scale called the Thrombolysis in
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; and grade 3
indicates full perfusion of the infarct vessel with normal flow.
The latter is the goal of reperfusion therapy, because full perfusion of the
infarct-related coronary artery yields far better results in terms of limiting
infarct size, maintenance of LV function, and reduction of both
short- and long-term mortality rates.
Additional methods of angiographic
assessment of the efficacy of fibrinolysis include counting the
number of frames on the cine film required for dye to flow from the
origin of the infarct-related artery to a landmark in the distal vascular
bed (TIMI frame count) and determining the rate of entry and exit
of contrast dye from the microvasculature in the myocardial infarct
zone (TIMI myocardial perfusion grade). These methods have an even
tighter correlation with outcomes after STEMI than the more commonly
employed TIMI flow grade
Primary Percutaneous Coronary Intervention (PCI)
Primary PCI IS RECOMMENDED in patients with STEMI and ischemic
symptoms of less than 12 hoursâ duration.
Primary PCI IS RECOMMENDED in patients with STEMI and ischemic
symptoms of less than 12 hoursâ duration who have contraindications
to fibrinolytic therapy, irrespective of the time delay from first medical
contact.
Primary PCI IS RECOMMENDED in patients with STEMI and
cardiogenic shock or acute severe heart failure (HF), irrespective of time
delay from MI onset.
It MAY BE RECOMMENDED in patients with STEMI if there is clinical
and/or ECG evidence of ongoing ischemia between 12 and 24 hours
after symptom onset.
Primary PCI is the recommended method of reperfusion when it can be
performed in a timely fashion by experienced operators within 90 minutes.
Based on the 2-year report of the PHA ACS registry, the median door-toballoon
time was 120 minutes, which was 30 minutes longer than what is
being recommended by international guidelines.4 Two of the primary reasons
that caused delays were financial constraints and delay in securing consent.
Proposals or new approaches to address these two reasons could be adopted
by hospitals to ultimately improve door-to-balloon time.
Statement 12: Coronary Artery Bypass Grafting (CABG)
CABG IS RECOMMENDED in failed PCI with persistent pain or
hemodynamic instability in patients with coronary anatomy suitable
for surgery. It IS RECOMMENDED in persistent or recurrent ischemia
refractory to medical therapy in patients who have coronary anatomy
suitable for surgery, and are not candidates for PCI or fibronolytic
therapy. It IS RECOMMENDED in patients with STEMI at the time of
operative repair of mechanical defects.
Emergency CABG within 6 hours of symptom onset MAY BE
RECOMMENDED in patients with STEMI who do not have cardiogenic
shock and are not candidates for PCI or fibrinolytic therapy.
The use of mechanical circulatory support MAY BE RECOMMENDED
in patients with STEMI who are hemodynamically stable and require
urgent CABG.
Antiplatelets and Antithrombotics
It IS RECOMMENDED that aspirin should be used indefinitely in all
patients with STEMI with a dosage of 80 to 100 mg/day.
It IS RECOMMENDED that clopidogrel 75 mg per day orally should
be added to aspirin in patients with STEMI and maintained for at least
14 days.
It IS RECOMMENDED that patients who are truly intolerant to aspirin
can instead receive clopidogrel 75 mg per day as long-term secondary
prevention.
Antiplatelets can interfere with a number of platelet functions, including
aggregation and platelet-mediated vascular constriction, thus giving benefit to
patients with ACS. Aspirin block the enzyme cyclooxygenase that mediates
the first step in the biosynthesis of prostaglandins and thromboxanes from
arachidonic acid, which are potent stimulators of platelet aggregation. The
platelet P2Y12 receptor blockers (clopidogrel, ticagrelor, prasugrel) block the
binding of ADP to a specific platelet P2Y12, thereby inhibiting activation of the
glycoprotein IIb/IIIa complex and platelet aggregation.
Duration of Dual Antiplatelet Therapy and Antithrombotic
Combination Therapies after STEMI
DAPT by combining aspirin and an ADP-receptor blocker (clopidogrel,
prasugrel or ticagrelor) IS RECOMMENDED in patients with STEMI
who are undergoing primary PCI (for up to 12 months) or (clopidogrel)
fibrinolysis (for up to 12 months, although the data available pertain
only to one month of DAPT), and in those who have not undergone
reperfusion therapy (for at least 1 month and up to 12 months).
DAPT treatment for 12 months after stenting and following STEMI has
104 PHA Clinical Practice Guidelines for the Management of Coronary Artery Disease
traditionally been recommended by consensus in Western guidelines.2,3 It is
important to inform patients and their primary physicians about the need to
avoid premature discontinuation of DAPT
Lipid Lowering Agents
High-dose statins are RECOMMENDED in all patients during the first
24 hours of admission for STEMI, irrespective of the patientâs cholesterol
concentration, in the absence of contraindications (allergy, active liver
disease). Atorvastatin or rosuvastatin are recommended during the
early phase of therapy up to at least four weeks.
It IS RECOMMENDED to give high-dose rosuvastatin (20 to 40 mg)
or atorvastatin (40 to 80 mg) therapy before emergency percutaneous
coronary intervention to reduce periprocedural inflammatory response,
to reduce myocardial dysfunction, and to prevent contrast-induced
nephropathy.
Figure 295-5 Algorithm for assessment of need for implantation
of a cardioverter-defibrillator. The appropriate management
is selected based on measurement of left ventricular ejection fraction
and assessment of the New York Heart Association (NYHA) functional
class. Patients with depressed left ventricular function at least 40 days
after ST-segment elevation myocardial infarction (STEMI) are referred
for insertion of an implantable cardioverter-defibrillator (ICD) if the left
ventricular ejection fraction (LVEF) is <30â40% and they are in NYHA
class IIâIII or if the LVEF is <30â35% and they are in NYHA class I functional
status. Patients with preserved left ventricular function (LVEF
>40%) do not receive an ICD regardless of NYHA functional class. All
patients are treated with medical therapy after STEMI. VF, ventricular
fibrillation; VT, ventricular tachycardia. (Adapted from data contained in
DP Zipes et al: ACC/AHA/ESC 2006 guidelines for management of patients
with ventricular arrhythmias and the prevention of sudden cardiac
death; a report of the American College of Cardiology/American Heart
Association Task Force and the European Society of Cardiology Committee
for Practice Guidelines [Writing Committee to Develop Guidelines for
Management of Patients with Ventricular Arrhythmias and the Prevention
There are several reasons why echocardiography should be performed in
all patients with a first presentation of suspected SIHD. First of all, disorders
such as aortic stenosis or hypertrophic obstructive cardiomyopathy can be
ruled out as alternative causes of angina. Secondly, regional wall motion
abnormalities may be detected, which increase the likelihood of CAD.
The segmental wall motion abnormalities seen with ischemia or infarction
correspond closely with the coronary artery blood supply to the myocardium.
Resting two-dimensional and Doppler transthoracic echocardiography also
provide information on global ventricular function, an important prognostic
parameter in patients with SIHD. Estimation of LV systolic function is important
in all patients for risk stratification as stated in current foreign guidelines (ESC
and ACC/AHA).2,
Ischemia also causes characteristic changes in the electrocardiogram
(ECG) such as repolarization abnormalities, as evidenced by
inversion of T waves and, when more severe, displacement of ST segments
(Chap. 268). Transient T-wave inversion probably reflects nontransmural,
intramyocardial ischemia; transient ST-segment depression
often reflects patchy subendocardial ischemia; and ST-segment
elevation is thought to be caused by more severe transmural ischemia.
Another important consequence of myocardial ischemia is electrical
instability, which may lead to isolated ventricular premature beats
or even ventricular tachycardia or ventricular fibrillation (Chap.
277). Most patients who die suddenly from IHD do so as a result of
ischemia-induced ventricular tachyarrhythmias (
Criteria for Acute Myocardial Infarction
The term acute myocardial infarction (MI) should be used when there is evidence
of myocardial necrosis in a clinical setting consistent with acute myocardial
ischemia. Under these conditions, any one of the following criteria
meets the diagnosis for MI:
⢠Detection of a rise and/or fall of cardiac biomarker values (preferably
cardiac troponin [cTn]) with at least one value above the 99th percentile
upper reference limit (URL) and with at least one of the following:
⢠Symptoms of ischemia
⢠New or presumed new significant ST-segment T-wave (ST-T) changes or
new left bundle branch block (LBBB)
⢠Development of pathologic Q waves in the electrocardiogram (ECG)
⢠Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
⢠Identification of an intracoronary thrombus by angiography or autopsy
⢠Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB, but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased.
⢠Percutaneous coronary intervention (PCI)ârelated MI is arbitrarily defined
by elevation of cTn values (>5 Ă 99th percentile URL) in patients with normal
baseline values (â¤99th percentile URL) or a rise of cTn values >20% if
the baseline values are elevated and are stable or falling. In addition, either
(i) symptoms suggestive of myocardial ischemia, or (ii) new ischemic ECG
changes, or (iii) angiographic findings consistent with a procedural complication,
or (iv) imaging demonstration of new loss of viable myocardium or
new regional wall motion abnormality are required.
⢠Stent thrombosis associated with MI when detected by coronary angiography
or autopsy in the setting of myocardial ischemia and with a rise and/
or fall of cardiac biomarker values with at least one value above the 99th
percentile URL.
⢠Coronary artery bypass grafting (CABG)ârelated MI is arbitrarily defined
by elevation of cardiac biomarker values (>10 Ă 99th percentile URL) in
patients with normal baseline cTn values (â¤99th percentile URL). In addition,
either (i) new pathologic Q waves or new LBBB, or (ii) angiographic
documented new graft or new native coronary artery occlusion, or (iii)
imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
TABLE 295-2 Classification of Myocardial Infarction
Type I: Spontaneous Myocardial Infarction
Spontaneous myocardial infarction related to atherosclerotic plaque rupture,
ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus
in one or more of the coronary arteries leading to decreased myocardial
blood flow or distal platelet emboli with ensuing myocyte necrosis. The
patient may have underlying severe coronary artery disease (CAD) but on
occasion nonobstructive or no CAD.
Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance
In instances of myocardial injury with necrosis where a condition other than
CAD contributes to an imbalance between myocardial oxygen supply and/
or demand, e.g., coronary endothelial dysfunction, coronary artery spasm,
coronary embolism, tachy-brady-arrhythmias, anemia, respiratory failure,
hypotension, and hypertension with or without left ventricular hypertrophy.
Type 3: Myocardial Infarction Resulting in Death When Biomarker
Values Are Unavailable
Cardiac death with symptoms suggestive of myocardial ischemia and presumed
new ischemic electrocardiogram (ECG) changes or new left bundle
branch block (LBBB), but death occurring before blood samples could be
obtained or before cardiac biomarker could rise, or in rare cases, cardiac biomarkers
were not collected.
Type 4a: Myocardial Infarction Related to Percutaneous Coronary
Intervention (PCI)
Myocardial infarction associated with PCI is arbitrarily defined by elevation
of cardiac troponin (cTn) values >5 Ă 99th percentile upper reference limit
(URL) in patients with normal baseline values (â¤99th percentile URL) or a rise
of cTn values >20% if the baseline values are elevated and are stable or falling.
In addition, either (i) symptoms suggestive of myocardial ischemia, or (ii)
new ischemic ECG changes or new LBBB, or (iii) angiographic loss of patency
of a major coronary artery or a side branch or persistent slow or no flow or
embolization, or (iv) imaging demonstration of new loss of viable myocardium
or new regional wall motion abnormality is required.
Type 4b: Myocardial Infarction Related to Stent Thrombosis
Myocardial infarction associated with stent thrombosis is detected by coronary
angiography or autopsy in the setting of myocardial ischemia and with
a rise and/or fall of cardiac biomarker values with at least one value above
the 99th percentile URL.
Type 5: Myocardial Infarction Related to Coronary Artery Bypass
Grafting (CABG)
Myocardial infarction associated with CABG is arbitrarily defined by elevation
of cardiac biomarker values >10 Ă 99th percentile URL in patients with
normal baseline cTn values (â¤99th percentile URL). In addition, either (i) new
pathologic Q waves or new LBBB, or (ii) angiographic documented new graft
or new native coronary artery occlusion, or (iii) imaging evidence of new loss
of viable myocardium or new regional wall motion abnormality.