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 Wellens Syndrome

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john



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PostSubject: Wellens Syndrome    Wed Jun 22, 2011 9:55 am

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Wellens Syndrome

Background

Wellens
syndrome was first described by de Zwaan, Wellens, and colleagues in
the early 1980s when they recognized a subset of patients with unstable
angina who had specific precordial T-wave changes and subsequently
developed a large anterior wall myocardial infarction.[1] Wellens
syndrome refers to these specific electrocardiographic abnormalities in
the precordial T-wave segment, which are associated with critical
stenosis of the proximal left anterior descending (LAD) coronary artery.Wellens syndrome is also referred to as LAD coronary T-wave syndrome.[2] Syndrome
criteria include characteristic T-wave changes; a history of anginal
chest pain; normal or minimally elevated cardiac enzyme levels; and
finally an ECG without Q waves, without significant ST elevation, and
normal precordial R-wave progression. Recognition of this ECG
abnormality is of paramount importance because this syndrome represents a
preinfarction stage of coronary artery disease that often progresses to
a devastating anterior wall infarction. In this ECG pattern,
there is significant involvement of the T-wave, with minimal ST-segment
alteration. The ST segments themselves are usually isoelectric, but, if
abnormal, there will be less than 1 mm of elevations with a high take
off of the ST segment from the QRS complex. The characteristic changes
of this electrocardiographic syndrome occur in the T-wave and occur in 2
forms. The more common form, which occurs 76% of the time, is deep inversion of the T-wave segment in the precordial leads.[3] The
ST segment will be straight or concave, and pass into a deep negative T
wave at an angle of 60-90 degrees. The T wave is symmetric. In Wellens
syndrome, these changes generally occur in leads V1 -V4 but may also occasionally involve V5 and V6. V1 is involved in approximately 66% of patients and lead V4 nearly 75% of the time.[4] See the ECG images below.


This
ECG represents a patient who came in to the emergency department with
8/10 chest pain. The patient had old right bundle-branch block (RBBB)
and left ventricular hypertrophy (LVH), and this compared

similarly to
his previous ECGs.






Classic
Wellens syndrome T-wave changes. This ECG represents a patient who came
in to the emergency department with 8/10 chest pain after becoming pain
free secondary to medications. Notice the deep T waves in V3-V5 and
slight biphasic T wave in V6 in this chest pain– free ECG. The patient
had negative cardiac enzyme levels and later had a stent placed in the
proximal left anterior descending (LAD) artery. The less
common variant of Wellens syndrome, which occurs in 24% of patients,
consists of biphasic T waves, most commonly in leads V2 and V3 but also can include V1- V5/V6.[5] See the ECG images below.


A
57-year-old with 4/10 pressurelike chest pain. Improvement with
treatment by EMS. The patient had this ECG on arrival. Notice perhaps
the beginning of a small biphasic T wave in V2.



pain-free
ECG of a 57-year-old patient who presented wPith 4/10 pressurelike chest
pain. Notice after the patient was treated with medications and pain
subsided, the ECG shows T-wave inversion in V2 and biphasic T waves in
V3-V5. This more closely resembles the less common presentation of
Wellens syndrome with a biphasic T-wave pattern. This patient had a
cardiac catheterization that showed a subtotal occlusion of the proximal
left anterior descending (LAD) artery, which was stented, and the
patient did well. The characteristic pattern classically
presents only during chest pain–free periods and is important to notice
since it is a sign of LAD disease. This emphasizes the importance of
serial ECGs and a pain-free ECG on patients with unstable angina. More
importantly, angiography has demonstrated that 100% of patients with
this syndrome will have greater than 50% stenosis of proximal LAD. More
specifically, 83% will have the lesion proximal to the second septal
perforator.[4] Since
the LAD supplies the anterior myocardium, failure to recognize this
pattern can result in anterior wall infarction, significant left
ventricular dysfunction, and/or death.

Pathophysiology

Wellens
syndrome represents critical stenosis of the left anterior descending
coronary artery (LAD). The LAD arises from the left coronary artery and
travels in the interventricular groove along the anterior portion of the
heart to the apex. This groove is situated between the right and left
ventricles of the heart. The LAD gives rise to 2 main branches, the
diagonals and the septal perforators.[6] A
lesion in the LAD can have severe consequences, as evidenced by the
LAD's nickname "widow maker." The LAD supplies the anterior wall of the
heart, including both ventricles, as well as the septum. An occlusion in
this vessel can result in serious ventricular dysfunction, thus placing
the patient at serious risk of congestive heart failure and death.

Epidemiology

Frequency

United States

This
ECG pattern is relatively common in patients who have symptoms
consistent with unstable angina. In patients admitted with unstable
angina, this ECG pattern is present in 14-18%.[5, 1] Mortality/Morbidity

Wellens
syndrome represents critical LAD disease with the natural progression
leading to anterior wall infarction. This progression is so likely that
medical management alone is not enough to stop the natural process.
Evolution to an anterior wall infarction is rapid, with a mean time of
8.5 days from onset of Wellens syndrome to infarction.[1] If
anterior wall infarction occurs, there is the potential for substantial
morbidity or mortality. Thus, it is of utmost importance to recognize
this pattern early.



Wellens Syndrome Clinical Presentation




History

Wellens
syndrome represents stenosis of the left anterior descending coronary
artery (LAD), and patients typically present with symptoms or complaints
consistent with coronary artery disease. Generally, the history is most
consistent with unstable angina. Angina can have varying presentations,
but classically patients complain of the following:

  • Chest pain described as pressure, tightness, or heaviness
  • Pain classically induced by activity, relieved with rest
  • Radiation of pain to the jaw, shoulder, or neck
  • May experience multiple associated symptoms, including, but not limited to diaphoresis, nausea, vomiting, and fatigue
Elderly, diabetic, and female patients are more likely to present with atypical symptoms.

Physical


  • Physical
    examination does not provide any indicators to suspect Wellens
    syndrome. However, the patient’s examination may show evidence of
    ongoing ischemic damage (ie, congestive heart failure [CHF]).
  • In
    addition, most of the ECG changes are recognized when the patient is
    pain free, which again stresses the importance of a repeat pain-free ECG
    in the emergency department.


Causes

Wellens
syndrome is a preinfarction stage of coronary artery disease. Thus, the
causes of Wellens syndrome are similar to all of those of coronary
artery disease.

  • Atherosclerotic plaque
  • Coronary artery vasospasm (Cocaine is one possible cause.)
  • Increased cardiac demand
  • Generalized hypoxia
Risk factors include the following:

  • Smoking history
  • Diabetes mellitus (DM)
  • Hypertension
  • Increased age
  • Hypercholesterolemia
  • Hyperlipidemia
  • Metabolic syndrome
  • Strong family history of heart disease
  • Occupational stress


Wellens Syndrome Differential Diagnoses



Differentials


  • Acute Coronary Syndromes
  • Angina Pectoris
  • Atherosclerosis
  • Coronary Artery Atherosclerosis
  • Myocardial Infarction
  • Myocarditis
  • Pericarditis and Cardiac Tamponade
  • Pneumonia, Bacterial
  • Pulmonary Embolism

Laboratory Studies

The following laboratory studies are may be indicated as adjunctive tests in patients with suspected coronary artery disease, acute coronary syndrome, and Wellens syndrome:

  • Complete blood count (CBC) - To ensure anemia is not precipitant of angina RBC transfusions may be necessary.)
  • Basic metabolic profile (electrolytes, BUN, creatinine, and glucose levels)
  • Type and screen - If immediate cardiac catheterization planned
  • D-dimer, international normalized ratio (INR), partial thromboplastin time (PTT) - Only as medically necessary
  • Cardiac
    biomarkers - In Wellens syndrome, cardiac biomarkers can be falsely
    reassuring, as they are typically normal or only minimally elevated.
    Only 12% of patients with this syndrome have elevated cardiac biomarker
    levels, and these are always less than twice the upper limit of normal,
    in the absence of myocardial infarction.[5]


Imaging Studies


  • Chest
    radiography: Chest radiography should be performed in order to look for
    side effects of ischemia, such as pulmonary edema. In addition, this
    test should be performed to help exclude other possible causes of chest
    pain, such as thoracic aneurysm or dissection, pneumonia, or rib
    fracture.
  • CT chest: CT scan of the chest is performed only as indicated to help rule out other causes of chest pain such as aortic dissection
    or pulmonary embolus. The value of CT angiography of the chest in
    evaluation of chest pain, coronary artery disease, and acute coronary
    syndrome is currently being investigated.


Other Tests


  • ECG:
    ECGs should be performed on any patient with complaint of chest pain if
    noncardiac causes cannot be diagnosed by other means, including
    physical examination. It may be helpful to obtain the ECG both during
    pain and then when pain is resolved. The ECG changes seen in Wellens
    syndrome typically occur when the patient is pain free but usually occur
    in the context of recent anginal chest pain.


Procedures

Patients with this syndrome have been found to have at least a 50% stenosis of the LAD on angiography.[5] Patients
with this ECG presentation should generally not undergo stress testing.
If for some reason provocative testing is determined to be necessary,
it should be performed with caution and only in close conjunction with a
cardiologist.[3, 7] Stress
testing places these patients at risk for acute anterior wall
myocardial infarction. Therefore, these patients would ideally bypass
stress testing and urgently undergo angiography to determine the extent
of disease and potentially provide information regarding the need for
percutaneous coronary intervention (PCI), coronary artery bypass graft
(CABG), or medical management.[3, 8]

Wellens Syndrome Treatment & Management


Prehospital Care

As
Wellens syndrome occurs because of stenosis of the LAD, these patients
typically complain of chest pain presenting as unstable angina. During
episodes of pain, they should be treated in the same manner as any
patient experiencing chest pain thought to be cardiac in origin, which
includes the following:

  • Immediate arrangements for transport to the nearest hospital
  • Attention to airway, breathing, and circulation
  • During transport, efforts should be made to complete the following:

    • Supplemental oxygen
    • Vital signs
    • Intravenous access
    • Aspirin
    • ECG, if available prehospital
    • If pain persists, nitroglycerin, morphine, according to local protocols
    </li>
If
Wellens syndrome is identified on an outpatient basis, then
arrangements should be made for urgent evaluation. Stress testing should be avoided.

Emergency Department Care

Patients presenting with symptoms consistent with unstable angina should generally receive medications that may help avoid myocardial infarction. Usually, this would include the following:

  • Intravenous access
  • Supplemental oxygen
  • ECG - Initially (Serial examinations and pain-free tracings may be helpful.)
  • Telemetry monitoring
  • Chest radiography
  • Laboratory studies as mentioned above (see Laboratory Studies)
  • Consideration
    should be given to providing aspirin, beta-blocker therapy,
    nitroglycerin, morphine, heparin, clopidogrel, and glycoprotein IIB/IIA
    inhibitors.
Once again, the ECG changes in Wellens
syndrome are typically only present when the patient is chest pain free.
Thus, obtaining serial ECGs on patients with unstable angina may be
helpful.Even though the ECG changes may be subtle, Wellens
syndrome should be identified because these patients can rarely undergo
stress testing safely. Because Wellens syndrome is a sign of a
pre-infarction stenosis of the left anterior descending coronary artery
(LAD), a stress test has the potential to result in acute infarction and
severe damage to the left ventricle. Therefore, these patients should
generally forgo a stress test and instead may undergo angiography to
evaluate the need for angioplasty or coronary artery bypass surgery.Even
with ideal medical management, the natural progression of Wellens
syndrome is acute anterior wall infarction. Approximately 75% of
patients with Wellens syndrome who are only medically managed and not
revascularized (either through coronary bypass surgery or angioplasty)
will go on to develop extensive anterior wall infarction within days.[9, 1] Anterior
wall infarction carries substantial morbidity/mortality, as it will
result in left ventricular dysfunction, and possibly even death. Thus,
patients generally should be medically stabilized if possible, while
arrangements are made for urgent angiography and revascularization if
appropriate.

Consultations

A
cardiologist should be consulted early in the management of these
patients. If the patient remains pain free, it is appropriate to admit
to an internist on a telemetry floor, but they should be notified that
this patient is at high risk and should not have a stress test.If symptoms persist or ECG evolves into ST-segment elevations, an interventional cardiologist should be consulted immediately.


Related Topics
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The ESC Textbook of Cardiovascular Imaging
ECG-SAP III: Electrocardiography Self-Assessment Program
Echo Made Easy
How to record ECG
Basic and Bedside Electrocardiography 2011
ECGs for Nurses (Essential Clinical Skills for Nurses)

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Wellens Syndrome Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Salicylates

Class Summary

These agents have antiplatelet properties.View full drug information
Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

Odorless
white powdery substance available in 81 mg, 325 mg, and 500 mg for oral
use. When exposed to moisture, aspirin hydrolyzes into salicylic acid
and acetic acids.Stronger inhibitor of both prostaglandin
synthesis and platelet aggregation than other salicylic acid
derivatives. Acetyl group is responsible for inactivation of
cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma,
and elimination follows zero-order pharmacokinetics.Irreversibly
inhibits platelet aggregation by inhibiting platelet cyclooxygenase.
This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent
vasodilator and inhibitor of platelet activation) and thromboxane A2
(potent vasoconstrictor and platelet aggregate). Platelet inhibition
lasts for life of cell (approximately 10 d). May be used in low dose to
inhibit platelet aggregation and improve complications of venous stases
and thrombosis. Reduces likelihood of myocardial infarction. Also very
effective in reducing risk of stroke. Early administration of aspirin in
patients with acute myocardial infarction (AMI) may reduce cardiac
mortality in first month.

Antihypertensive Agents

Class Summary

These agents reduce high blood pressure.View full drug information
Metoprolol (Lopressor, Toprol XL)


Selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions.During
IV administration, carefully monitor blood pressure, heart rate, and
ECG. Goal of treatment is to reduce heart rate to 60-90 beats/min.

Antianginal Agents

Class Summary

These agents can reduce blood pressure.View full drug information
Nitroglycerin sublingual (Deponit, Nitro-Bid, Nitrol, Nitrolingual pumpspray, Nitrostat)


Causes
relaxation of the vascular smooth muscle via stimulation of
intracellular cyclic guanosine monophosphate production, causing a
decrease in blood pressure.

Antiplatelet Agents

Class Summary

These agents inhibit platelet aggregation.View full drug information
Abciximab (ReoPro)


Chimeric
human-murine monoclonal antibody approved for use in
elective/urgent/emergent percutaneous coronary intervention. Binds to
receptor with high affinity and reduces platelet aggregation by 80% for
up to 48 h following infusion. View full drug information
Clopidogrel (Plavix)


Selectively
inhibits adenosine diphosphate (ADP) binding to platelet receptor and
subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex,
thereby inhibiting platelet aggregation.May have a positive
influence on several hemorrhagic parameters and may exert protection
against atherosclerosis not only through inhibition of platelet function
but also through changes in the hemorrhagic profile.Shown to
decrease cardiovascular death, MI, and stroke in patients with acute
coronary syndrome (ie, unstable angina, non-Q-wave
MI).




Analgesics

Class Summary

Pain
control is essential to quality patient care. Analgesics ensure patient
comfort, promote pulmonary toilet, and have sedating properties, which
are beneficial for patients who experience pain. View full drug information
Morphine sulfate (Astramorph, Duramorph, MS Contin, MSIR, Oramorph)


DOC
for narcotic analgesia because of its reliable and predictable effects,
safety profile, and ease of reversibility with naloxone.Morphine sulfate administered IV may be dosed in a number of ways and commonly titrated until desired effect obtained.

Low Molecular Weight Heparins

Class Summary

These agents inhibit thrombogenesis.View full drug information
Enoxaparin (Lovenox)


Produced
by partial chemical or enzymatic depolymerization of unfractionated
heparin (UFH). LMWH differs from UFH by having a higher ratio of
antifactor Xa to antifactor IIa compared with UFH. Binds to antithrombin
III, enhancing its therapeutic effect. The heparin-antithrombin III
complex binds to and inactivates activated factor X (Xa) and factor II
(thrombin). Does not actively lyse but is able to inhibit further
thrombogenesis. Prevents reaccumulation of clot after spontaneous
fibrinolysis.Advantages include intermittent dosing and decreased
requirement for monitoring. Heparin anti–factor Xa levels may be
obtained if needed to establish adequate dosing. No utility in checking
aPTT (drug has wide therapeutic window and aPTT does not correlate with
anticoagulant effect). Maximum antifactor Xa and antithrombin activities
occur 3-5 h postadministration.Indicated for treatment of acute
ST-segment elevation myocardial infarction (STEMI) managed medically or
with subsequent percutaneous coronary intervention (PCI). Also indicated
as prophylaxis of ischemic complications caused by unstable angina and
non-Q-wave MI.

Antiarrhythmic Agents

Class Summary

These agents reduce episodes of chest pain and clinical cardiac events.View full drug information
Esmolol (Brevibloc)


Ultra–short-acting
agent that selectively blocks beta1-receptors with little or no effect
on beta2-receptor types. Particularly useful in patients with elevated
arterial pressure, especially if surgery is planned. Shown to reduce
episodes of chest pain and clinical cardiac events compared with
placebo. Can be discontinued abruptly if necessary.Useful in
patients at risk for experiencing complications from beta-blockade;
particularly those with reactive airway disease, mild-moderate LV
dysfunction, and/or peripheral vascular disease. Short half-life of 8
min allows for titration to desired effect and quick discontinuation if
needed.

Anticoagulants

Class Summary

These agents are used for anticoagulation in unstable angina.View full drug information
Lepirudin (Refludan)




When
compared with unfractionated heparin in unstable angina trials, hirudin
demonstrated a modest short-term reduction in the composite end point
of death or nonfatal MI. Risk of bleeding is increased modestly.
Currently, hirudin is indicated only in patients unable to receive
heparin because of heparin-induced thrombocytopenia. View full drug information
Bivalirudin (Angiomax)


Synthetic
analogue of recombinant hirudin. Inhibits thrombin. Used for
anticoagulation in unstable angina undergoing PTCA. With provisional use
of glycoprotein IIb/IIIa inhibitor (GPIIb/IIIa inhibitor) indicated for
use as anticoagulant in patients undergoing PCI. Potential advantages
over conventional heparin therapy include more predictable and precise
levels of anticoagulation, activity against clot-bound thrombin, absence
of natural inhibitors (eg, platelet factor 4, heparinase), and
continued efficacy following clearance from plasma (because of binding
to thrombin).

Further Inpatient Care

Further inpatient care for patients with Wellens syndrome includes the following:

  • Attempts should be made to keep the patient pain free.
  • Provide telemetry bed to monitor the patient.
  • Consult a cardiologist.


Transfer


  • Transfer of these patients to institutions with cardiac catheterization capabilities is generally appropriate.


Related Topics
ECG VIDEOS PACKAGE the Best untill Now
The ESC Textbook of Cardiovascular Imaging
ECG-SAP III: Electrocardiography Self-Assessment Program
Echo Made Easy
How to record ECG
Basic and Bedside Electrocardiography 2011
ECGs for Nurses (Essential Clinical Skills for Nurses)




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