Acute Myocardial Infarction: Questions

Acute Myocardial
Infarction
A 71-year-old man presents to the emergency
room with a sudden onset of substernal chest
pain 1 hour ago. He describes the pain as
a heavy pressure sensation that radiates down
both arms and that is 10/10 in intensity. He
states that his pain started while he was walking
around his yard and is better, but not resolved,
with rest. His past medical history is signi cant
for diabetes mellitus. He has smoked 1 pack of
cigarettes per day for the past 50 years. His
mother died of a myocardial infarction (MI) at
age 56. On heart examination, you hear an S4
gallop and on lung examination, bibasilar ne
crackles. An electrocardiogram (ECG) is
performed showing 3-mm ST-segment
elevations in leads II, III, and aVF.
QUESTIONS
1. What are the salient eatures of this patient’s
problem?
2. How do you think through his problem?
3. What are the key features, including essentials of
diagnosis and general considerations, of acute MI?
4. What are the symptoms and signs of acute MI?
5. What is the differential diagnosis of acute MI?
6. What are laboratory, imaging, and procedural
findings in acute MI?
7. What are the treatments or acute MI?
8. What are the outcomes, including follow-up,
complications, prevention, and prognosis,
of acute MI?
9. When should patients with acute MI be referred to
a specialist or admitted to the hospital?
ANSWERS
1. Salient Features
Advanced age; sudden onset of substernal chest pain
radiating to arms; pain worse with exertion; cardiac
risk actors of diabetes mellitus, smoking, and family
history; S4 gallop and crackles consistent with
pulmonary edema; ECG with ST elevations in an
inferior distribution
2. How to Think Through
Acute coronary syndrome (ACS) captures the
continuum of unstable angina, non–ST -elevation
MI (NSTEMI), and ST -elevation MI (STEMI), all
of which result from ischemia to the myocardium
due to a thrombus at a site of coronary
atherosclerosis. There are other causes
of MI, but ACS is the most common. This patient
presents with typical chest pain, meaning
substernal, pressure-like or squeezing, related to
exertion, and relieved by rest or nitroglycerin.
Radiation to both arms also correlates strongly with
cardiac chest pain. To evaluate a patient
with chest pain, we first determine the likelihood o
ACS as its cause, then stratify the patient’s
risk or mortality to ensure timely intervention in
high-risk patients. Here, the history alone
strongly suggests ACS. The patient is immediately
deemed to be high risk due to the ST elevations
on ECG. Were the ECG to show ST depressions,
would management as a high-risk patient still be
warranted? (Yes. Evidence of new heart ailure [HF]
confers high risk.)
What medications should be administered after
diagnosis? (Aspirin; P2Y12 inhibitors
[eg, prasugrel, ticagrelor, or clopidogrel]; un
ractionated heparin, enoxaparin, or fondaparinux
[if not undergoing percutaneous coronary
intervention (PCI)]; glycoprotein IIb/IIIa inhibitors
[eg, abciximab].) Should he receive a β-blocker?
(No. Evidence of new HF is a relative
contraindication.) Should he receive nitroglycerin or
morphine? (No. His inferior ST –segment elevation
MI may be affecting the right ventricle, making him
preload dependent and nitroglycerin or opiates could
result in hypotension. Right-sided ECG leads could
help with the diagnosis.) If the hospital lacks
facilities or cardiac catheterization, how should he
be managed?
(If transfer to another facility or PCI within 90
minutes of first medical contact is not
possible, and barring contraindications, fibrinolytic
therapy should be given.)
3. Key Features
Essentials of Diagnosis
• Sudden but not instantaneous development of
prolonged (> 30 minutes) anterior chest
discomfort (sometimes felt as “gas” or pressure)
• Sometimes painless, masquerading as acute HF,
syncope, stroke, or shock
• ECG: ST -segment elevation or new lef bundle
branch block occur with STEMI; new right
bundle branch block in STEMI is a poor prognostic
sign; ECG may show ST depressions
or no changes in NSTEMI
• Immediate reperfusion treatment is warranted in S
TEMI
— PCI within 90 minutes of first medical contact is
the goal and is superior to fibrinolytic therapy
— If PCI is unavailable within 90 minutes, fi
brinolytic therapy within 30 minutes of
hospital presentation is the goal, and reduces
mortality if given within 12 hours of
onset of symptoms; fibrinolysis is harmful in NS
EMI and unstable angina
• An early invasive strategy of reperfusion with PCI
may be indicated in NSTEMI, depending on clinical
factors
General Considerations
• Acute MI results, in most cases, from an occlusive
coronary thrombus at the site of a
preexisting (though not necessarily severe)
atherosclerotic plaque.
• More rarely, may result from prolonged
vasospasm, inadequate myocardial blood flow
(eg, hypotension), or excessive metabolic demand
• Very rarely, may be caused by embolic occlusion,
vasculitis, aortic root or coronary artery
dissection, or aortitis
• Cocaine use may cause MI and should be
considered in young individuals without risk factors
4. Symptoms and Signs

• Recent onset of angina pectoris or alteration in the
pattern of angina or chest pressure, squeezing, or
“indigestion”
• Pain characteristics
— Similar to angina in location and radiation but
more severe
— Usually occurs at rest, often in the early morning
— Builds rapidly
— Minimally responsive to sublingual nitroglycerin
or oral opioids
• Associated symptoms
— Diaphoresis
— Weakness
— Apprehensiveness
— Aversion to lying quietly
— Light-headedness
— Syncope
— Dyspnea
— Orthopnea
— Cough
— Wheezing
— Nausea and vomiting
— Abdominal bloating
• Thirty-three percent of patients do not experience
chest pain, especially older patients, women, and
patients with diabetes mellitus
• Of all deaths due to MI, ~50% occur before the
patient reaches the hospital, usually of
ventricular f brillation
• Marked bradycardia (inferior infarction) or
tachycardia (increased sympathetic activity,
low cardiac output, or arrhythmia) may occur
• Jugular venous distention indicates right atrial
hypertension, often from RV infarction or
elevated LV filling pressures.
• Soft heart sounds may indicate LV dysfunction
• S4 is common; S3 indicates significant LV dysf
unction
• Mitral regurgitation murmur usually indicates
papillary muscle dysfunction or, rarely, rupture.
• Pericardial friction rubs are uncommon in the first
24 hours but may appear later.
• Edema is usually not present.
• Cyanosis and cold temperature indicate low output
• Peripheral pulses should be noted, since later shock
or emboli may alter the examination
5. Differential Diagnosis
Unstable angina without MI
• Aortic dissection
• Pulmonary embolism
• Tension pneumothorax
• Pericarditis
• Esophageal rupture
• Stress cardiomyopathy (Tako Tsubo
cardiomyopathy or apical ballooning syndrome)
6. Laboratory, Imaging, and Procedural
Findings
Laboratory ests
• Troponin I, troponinT , and quantitative creatine
kinase (CK-MB) elevations as early as 4 to 6 hours
afer onset; almost always abnormal by 8 to 12 hours
• High-sensitivity troponin assays
— When positive, help enable myocardial infarction
to be detected earlier
— When negative, may be useful in excluding
myocardial infarction in patients with chest
pain
89
• Troponins may remain elevated for 5 to 7 days and
are therefore less useful for the
evaluation of suspected early reinfarction
Imaging Studies
• Chest radiograph: signs of HF, often lagging
behind the clinical findings
• Echocardiography: assesses global and regional
LV function, wall motion
• Doppler echocardiography: can diagnose postinf
arction mitral regurgitation or ventricular
septal defect
• Thallium-201 or technetium scintigraphy: does not
distinguish recent from old MI
Diagnostic Procedures
• ECG
— Extent of abnormalities, especially the sum of the
total amount of ST -segment deviation, is a good
indicator of extent of acute infarction and risk o
subsequent adverse events
— The classic evolution of changes is from peaked
(“hyperacute”) waves, to ST -segment
elevation, to Q wave development, to wave
inversion; this may occur over a few
hours to several days.
— The evolution of new Q waves (> 30 milliseconds
in duration and 25% of the R wave
amplitude) is diagnostic, but Q waves do not occur
in 30% to 50% o acute infarctions
(non-Q wave infarctions)
• Cardiac catheterization and coronary angiography
can demonstrate coronary artery occlusions and
allow PCI.
• Echocardiography or left ventriculography can
demonstrate akinesis or dyskinesis and measure
ejection fraction
• Swan-Ganz hemodynamic measurements can be
invaluable in managing suspected cardiogenic shock
7. Treatments
Medications
• Aspirin
— All patients with definite or suspected acute MI
should receive aspirin at a dose of
162 mg or 325 mg at once, regardless of whether
fibrinolytic therapy is being considered or the patient
has been taking aspirin.
— Chewable aspirin provides more rapid blood
levels
• Statin
— Atorvastatin 80 mg orally should be given
initially and continued once daily, based on
the benefits seen in the PROVE I - IMI 22 and
MIRACL trials
• P2Y12 inhibitor (eg, prasugrel, ticagrelor, or
clopidogrel)
— Given to patients with a definite aspirin allergy
— P2Y12 inhibitors, in combination with aspirin,
have been shown to be beneficial to
patients with acute STEMI
— Guidelines call for a P2Y12 inhibitor to be added
to aspirin to all patients with STEMI,
regardless of whether reperfusion is given, and
continued for at least 14 days, and
generally for 1 year
— Prasugrel and ticagrelor are preferred; both have
shown superior outcomes compared to clopidogrel
— All patients who receive a coronary stent should
be discharged with both aspirin and a P2Y12 inhibitor
• Prasugrel
— Dose is 60 mg orally on day 1, then 10 mg daily
— In the TRITON study, prasugrel was shown to be
of greater benefit than clopidogrel in reducing
thrombotic events in the subgroup of patients with
STEMI, including a 50% reduction in stent
thrombosis
— Contraindicated in patients with history of stroke
or who are older than age 75 years
Ticagrelor
— Dose is 150 mg orally on day 1, then 90 mg twice
daily
— In the PLATO trial, ticagrelor was shown to be of
greater benefit than clopidogrel in reducing
cardiovascular death, myocardial infarction, and
stroke as well as in reducing stent thrombosis
• Clopidogrel
— Loading dose of 600 mg orally (or 300 mg)
results in faster onset of action than standard
75 mg maintenance dose
• Nitroglycerin
— Agent of choice for continued or recurrent
ischemic pain and is useful in lowering BP
or relieving pulmonary congestion.
• Morphine sulfate, 4 to 8 mg intravenously, or
meperidine, 50 to 75 mg intravenously, if
nitroglycerin alone does not relieve pain
• Enoxaparin reduced death and MI at day 30
(compared with unfractionated heparin) at
the expense of a modest increase in bleeding
— Give as a 30-mg intravenous bolus and 1 mg/kg
every 12 hours or patients under age 75 years
— Give with no bolus and 0.75 mg/kg intravenously
every 12 hours or patients age ≥ 75 years
• Fondaparinux reduced death and reinfarction
(compared with unfractionated heparin
when indicated, otherwise placebo) with less
bleeding.
— Dose: 2.5 mg once daily subcutaneously
— Not recommended as sole anticoagulant during
PCI due to risk of catheter thrombosis
• Fibrinolytic therapy
— Reduces mortality and limits infarct size in
patients with acute MI associated with
ST -segment elevation (defined as ≥ 0.1 mV in two
inferior or lateral leads or two contiguous precordial
leads), or with left bundle branch block
— Greatest benefit occurs if initiated within the first
3 hours, when up to a 50% reduction in mortality
rate can be achieved.
— The magnitude of benefit declines rapidly
thereafter, but a 10% relative mortality reduction
can be achieved up to 12 hours after the onset of
chest pain
—Fibrinolytic therapy should not be used in
NSTEMI or unstable angina
Fibrinolytic therapy for acute myocardial infarction.
1.Alteplase; Tissue Plasminogen Activator (t-PA)
DOSE..100 mg
Initial bolus of 15 mg, followed by 50 mg infused over
the next 30 min and 35 mg over the following 60 min.
2. Reteplase
3.Tenecteplase (TNK-t-PA)
4. Streptokinasea
DOSE. 1.5 million units
750,000 units over 20 min followed by
750,000 units over 40 min
91
• Glycoprotein IIb/IIIa inhibitors, specifically
abciximab, have been shown to reduce major
thrombotic events, and possibly mortality, or
patients undergoing primary PCI.
Therapeutic Procedures
• ST elevation connotes an acute total coronary
occlusion with transmural ischemia and
infarction and thus warrants immediate reperfusion
therapy
• NSTEMI connotes subendocardial ischemia and in
farction and may be treated with an early
conservative or early invasive approach with cardiac
catheterization and PCI.
• In patients with cardiogenic shock, early
catheterization and percutaneous or surgical
revascularization are the preferred management and
have been shown to reduce mortality
• For patients who have received f brinolytic therapy
but will undergo angiography in the
first day or two, the early benefits of a P2Y12
inhibitor need to be weighed against the necessary
delay in bypass surgery or approximately 5 days or
those patients found to require surgical
revascularization
• Patients with continued circulatory compromise
after revascularization may need ventricular support
8. Outcomes
Follow-Up
• For nonhypotensive patients with low ejection
ractions, large infarctions, or clinical evidence of
HF, start angiotensin-converting enzyme (ACE)
inhibitor on first postinfarction day; titrate and
continue long term.
• Patients with recurrent ischemic pain prior to
discharge should undergo catheterization
and, if indicated, revascularization
Complications
• Myocardial dysfunction, HF, hypotension,
cardiogenic shock
• Postinfarction ischemia
• Sinus bradycardia, sinus tachycardia
• Supraventricular premature beats
• Atrial fibrillation, ventricular fibrillation
• Ventricular premature beats
• Ventricular tachycardia
• Accelerated idioventricular rhythm
• Right bundle branch block (RBBB) or left bundle
branch block (LBBB) or fascicular blocks
• Second- or third-degree AV block
• Rupture of a papillary muscle, interventricular
septum, or LV free wall
• LV aneurysm
• Pericarditis, Dressler syndrome
• Mural thrombi
Prevention
• Smoking cessation
• reat hyperlipidemia
• Control HBP
• β-blockers
• Antiplatelet agents
• Exercise training and cardiac rehabilitation
programs
Prognosis
• Killip classification classifies HF in patients with
acute MI and has powerful prognostic
value
— Class I is absence of rales and S3
— Class II is rales that do not clear with coughing
over one-third or less of the lung fields
or presence of an S3
— Class III is rales that do not clear with coughing
over more than one-third of the lung fields
— Class IV is cardiogenic shock (rales, hypotension,
and signs of hypoper usion)
9. When to Refer and When to Admit
When to Refer
• Following an acute MI, all patients should be ref
erred to a cardiologist
When to Admit
• All patients with possible acute MI should be
admitted to the Coronary Care Unit hospital?
Secondary prevention
1. Control of cardiac risk factors is even more important once the
presence of coronary artery disease has been established. It
should be a routine part of the management.
2. Dietary advice for weight and lipid reduction may be indicated.
Lipid-lowering drug treatment with a statin should be introduced
for all patients who can tolerate it.
3. Patients should be encouraged to take part in a cardiac
rehabilitation program, if this is available, where advice about
safe exercise, weight reduction and changes to dietary
and smoking habits can be dicouraged.

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4. Symptoms and Signs

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