1. Recognize the ekg changes of acute mi.

ACUTE MYOCARDIAL ISCHEMIA An acute ST elevation myocardial infarction (MI)

presents with a current of injury pattern characterized by elevation of the ST segment in
different leads, depending upon the location of the MI. The earliest change, which is not
frequently seen, is symmetric, hyperacute T waves (defined as amplitude more than 50
percent of the R wave in the same lead) in at least two contiguous leads, which reflects a
localized increase in plasma potassium concentration [1].
Thereafter, the ST segment elevates with the following appearance:
Initially there is elevation of the J point and the ST segment retains its concave
configuration.
Over time the ST segment elevation becomes more pronounced and the ST segment
changes its morphology, becoming more convex or rounded upward.
The ST segment may eventually become indistinguishable from the T wave; the QRS-T
complex can actually resemble a monophasic action potential.
An initial Q wave develops and there is a loss of R wave amplitude as the ST segment
becomes elevated.
An abnormal Q wave is any Q wave in leads V1 to V3 or a Q wave 30 msec in leads I, II,
aVL, aVF, or V4 to V6; the Q wave must be present in any two contiguous leads and 1 mm
in depth [1]. (See "Prior myocardial infarction" below).
Over time, there is evolution of these ECG changes: the ST segment gradually returns to the
isoelectric baseline; the R wave amplitude becomes markedly reduced; the Q wave deepens;
and the T wave becomes inverted. These changes generally occur within the first two weeks
after the event; however, in some patients they occur within a few hours of presentation.
The electrocardiographic changes that occur in patients who sustain a non-ST elevation MI
are different [1]. T wave flattening or inversion typically precedes ST segment depression. Q
waves are typically absent but can occur, and the duration of the ST and T waves changes is
variable.
The leads affected by these changes depend upon the location of the infarction:
An acute anterior wall MI presents with the changes in some or all of theprecordial chest
leads V1-V6 (show ECG 1). Reciprocal ECG changes occasionally are observed during
the initial period of the acute infarction, presenting most often as depressions of
the ST segments in the inferior leads (2, 3, and aVF).
An acute anteroseptaltransmural MI presents with the changes in leads V1-V2 (show ECG
2). Reciprocal ECG changes occasionally are observed during the initial period of the
acute infarction, presenting as depressions of the ST segments in the inferior
(2, 3, aVF) or lateral leads (1, aVL, V5, and V6).
An acute anteroapicaltransmural MI presents with the changes in leads V3 and V4 (show
ECG 3). Reciprocal ECG changes occasionally are observed during the initial period of
the acute infarction, presenting as depressions of the ST segment in the
inferior leads (2, 3, aVF).
An acute anterolateraltransmural MI presents with the changes in leads V5 and V6, often
in association with changes in leads 1 and aVL (show ECG 4). Reciprocal ECG changes
occasionally are observed during the initial period of the acute infarction,
presenting as depressions of the ST segment in the inferior leads (2, 3, aVF),
and in some cases in leads V1 and V2.
An acute lateral transmural myocardial infarction presents with the changes confined to
leads 1 and aVL (show ECG 5). Reciprocal ECG changes occasionally are observed
during the initial period of the acute infarction, presenting as ST segment depressions
in the inferior leads (2, 3 and aVF) or leads V1 and V2.
An acute inferior wall transmural myocardial infarction presents with the changes in leads 2,
3, and aVF (show ECG 6). Reciprocal ECG changes occasionally are observed during the
initial period of the acute infarction, presenting with ST segment depressions in leads
V1 to V3, 1, or aVL. The ST segment changes in the precordial leads are not reciprocal in
some cases, but represent true posterior wall involvement (which may be diagnosed by ST
elevation in leads V7 to V9) [2] or involvement of the right ventricle (which may be

diagnosed by ST elevations in right precordial chest leads). (See "Right ventricular

myocardial infarction").
2. Compare and contrast st elevation mi and non-st elevation mi.
ST elevation MI In patients with acute ST elevation MI, the electrocardiogram evolves
through a typical sequence. (See "Electrocardiogram in the diagnosis of myocardial ischemia
and infarction" and see "ECG tutorial: Myocardial infarction").
Although not frequently seen, the earliest change in an STEMI is the development of a
hyperacute or peaked T wave that reflects localized hyperkalemia. Thereafter, the ST
segment elevates in the leads recording electrical activity of the involved region of the
myocardium; it has the following appearance:
Initially, there is elevation of the J point and the ST segment retains its concave
configuration.
Over time, the ST segment elevation becomes more pronounced and the ST segment
becomes more convex or rounded upward.
The ST segment may eventually become indistinguishable from the T wave; the QRS-T
complex can actually resemble a monophasic action potential.
The joint ESC/ACCF/AHA/WHF committee for the definition of MI established specific ECG
criteria necessary for the diagnosis of acute myocardial ischemia (show table 4) [5]. An
initial Q wave or abnormal R wave develops over a period of several hours to days.
Over time there is further evolution of these ECG changes; the ST segment gradually returns
to the isoelectric baseline, the R wave amplitude becomes markedly reduced, and the Q
wave deepens. In addition, the T wave becomes inverted. These changes generally occur
within the first two weeks after the event, but may progress more rapidly, within several
hours of presentation.
In addition to patients with ST elevation, two other groups of patients with an acute coronary
syndrome are considered to have an STEMI: those with new or presumably new left bundle
branch block and those with a true posterior MI. A separate issue, the assessment of
patients with a suspected acute MI who have known left bundle branch block or a paced
rhythm, is discussed below. (See "LBBB or paced rhythm" below and see "Electrocardiogram
in the diagnosis of myocardial ischemia and infarction", section on Posterior wall MI).
Absence of Q waves A subset of patients with an acute coronary syndrome present with
initial ST segment elevation but no Q waves. These patients are treated for an ST elevation
MI and some never develop Q waves. Such patients have a better prognosis than those who
develop Q waves because of more frequent reperfusion, a less severe infarction, and, at
follow-up, better left ventricular function and improved survival. (See "Electrocardiogram in
the prognosis of myocardial infarction or unstable angina", section on Presence or absence
of new Q waves).
Localization The ECG leads can also localize the MI [3,5]. ST elevation and/or increased T
wave positivity are seen in:
One or more of the precordial leads (V1-V6) and in leads I and aVL with acute transmural
anterior wall ischemia
Leads V1 to V3 with anteroseptalischemiaLeads II, III, and aVF with inferior wall ischemia
Leads V4 to V6 with apical or lateral ischemia
Right-sided precordial leads with right ventricular ischemia
In addition, specific combinations of findings can help predict the infarct-related artery. (See
"Electrocardiogram in the diagnosis of myocardial ischemia and infarction").
If there is evidence of inferior wall ischemia, as evidenced in leads II, III, and aVF, the rightsided leads V4R, V5R, and V6R should also be obtained. The recording of right-sided leads in
this setting was given a class I recommendation by the 2004 ACC/AHA task force [11]. No
changes to this approach were made in the 2007 focused update of the 2004 ACC/AHA
guidelines for the management of patients with ST-elevation MI [12].
Non-ST elevation ACS A non-ST elevation ACS is manifested by ST depressions and/or T
wave inversions without ST segment elevations or pathologic Q waves. These ST-T wave

abnormalities may be present diffusely in many leads; more commonly they are localized to
the leads associated with the region of ischemic myocardium. (See "Electrocardiogram in the
diagnosis of myocardial ischemia and infarction").
The ST segment may become flattened or straightened in patients with a non-ST elevation
ACS. It is more common, however, to see ST segment depression that may be upsloping,
horizontal, or downsloping. ST depression is defined by a ST segment which is depressed >1
mm below the baseline measured at 0.08 seconds after the J point.
As noted above, the two forms of non-ST elevation ACS (UA and NSTEMI) are frequently
indistinguishable at initial evaluation. In a patient with an NSTEMI, ST segment depressions
usually evolve over the subsequent few days to result in residual ST segment depression
and T wave inversions, but not to the formation of pathologic Q waves. In a patient with UA,
ST segment and T wave changes usually resolve completely.
Non-ST elevation (non-Q wave) Patients with non-Q wave infarctions typically present
with ST segment depression and/or T wave inversion in two or more leads. As noted above,
reciprocal ST segment depression can occur during an ST elevation MI. For this reason, ST
segment elevation, which is sometimes subtle, should be sought in opposing leads
whenever ST segment depression is noted (eg, if ST depression is seen in leads V1 through
V3, leads II, III, and aVF, and the lateral/posterior chest leads should be evaluated for
concomitant ST elevation).
As noted above, the association between Q waves and transmural infarction has been
questioned and the presence or absence of Q waves may be more closely correlated with
the size of the MI than with its transmural extent [12]. (See "Formation of Q waves" above
and see "Pathogenesis and diagnosis of Q waves on the electrocardiogram").
The absence of Q waves in patients with an NSTEMI reflects a high rate of spontaneous
reperfusion or presence of a tight stenosis without initial occlusion; 60 to 85 percent do not
have occlusion of the culprit artery on arteriography performed soon after presentation. This
presumably explains the lack of benefit from thrombolytic therapy in patients with an NSTEM
3 Located the area of infarction based on EKG changes + 4. Estimate the age of an MI based
on EKG changes.
In Q-wave infarction (previously termed transmural infarction), the earliest ECG change is a
tall and spiked T wave, followed by ST-segment elevation in leads facing the infarcted region
and reciprocal ST-segment depression in the opposite leads. ST-segment elevation becomes
isoelectric within the first few days. This regression unmasks a symmetrically inverted T
wave, reflecting transmural ischemia. A few hours to a few days after the onset of STsegment elevation, a pathologic Q wave appears in the same leads, which persists for
months, years, or indefinitely and serves as an ECG sign of an old scar. Thus, the only ECG
sign of acute myocardial injury is ST-segment elevation, which along with a new Q wave,
indicates an acute Q-wave infarction (Fig. E2.3). During the first few hours of an infarction,
the ECG may be entirely normal. infarction
NonQ-wave infarction (previously termed subendocardial infarction) produces ST-segment
depression and T-wave inversion without pathologic Q waves.
In some young, healthy subjects, a normal variant of repolarization occurs (Fig. E2.4) with
ST-segment elevation, primarily in leads I, aVL, and V 4 through V6. The ST segment is
concave upward and starts from the descending limb of the R wave before it reaches the
baseline. No T-wave abnormalities are noted. This pattern may occasionally be confused for
an infarct. An elevated ST segment in myocardial injury tends to be convex upward.
5. Describe the use of cardiac enzymes for the diagnosis of MI including time
course for the presence of enzymes in the blood
Troponin: The most sensitive and specific test for myocardial damage. Troponin is released
during MI from the cytosolic pool of the myocytes. Its subsequent release is prolonged with

degradation of actin and myosin filaments. Released in 24 hours and persists for up to 7
days. Peaks in 12 hours.
CPK-MB test: Since it has a short duration, it cannot be used for late diagnosis of acute MI
but can be used to suggest infarct extension if levels rise again. This is usually back to
normal within 23 days and peaks in 10-24 hours.
Lactate dehydrogenase (LDH): Lactate dehydrogenase catalyses the conversion of pyruvate
to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found
predominately in blood serum. A high LDH-1 level to LDH-2 suggest MI. Usually back to
normal 1014 days with a peak of 72 hours.
Myoglobin (Mb): Myoglobin is used less than the other markers. It is high when muscle tissue
is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising
and falling earlier than CK-MB or troponin. Peak 2 hours.

6. Describe the steps in the emergency treatment of acute MI

Certain treatments are usually started right away if a heart attack is suspected, even before
the diagnosis is confirmed. These include: oxygen; aspirin to prevent further blood clotting;
nitroglycerin (glyceryl trinitrate) to reduce the workload on the heart and improve blood
flow; treatment for chest pain, commonly morphine.
Once the diagnosis of heart attack is confirmed or strongly suspected, treatments to try to
restore blood flow to the heart are started as soon as possible. Thrombolytics are used to
dissolve blood clots that are blocking the blood flow. To be most effective, these medicines
must be given within 1 hour after the start of heart attack symptoms. Beta blockers
decrease the workload on your heart and are also used to relieve chest pain or discomfort
and to help prevent additional heart attacks. ACE Inhibitors lower blood pressure and reduce
the strain on your heart. Anticoagulants thin the blood and prevent clots from forming.

Antiplatelets (such as aspirin and clopidogrel) stop platelets from clumping together and
forming unwanted clots.
If medicines cant stop a heart attack, medical procedures may be used. An angioplasty can
be used to open coronary arteries that are blocked by a blood clot. During angioplasty, a
catheter with a balloon on the end is threaded through a blood vessel to the blocked
coronary artery. Then, the balloon is inflated to push the plaque against the wall of the
artery. This widens the inside of the artery, restoring blood flow. A small mesh tube called a
stent may be put in the artery to help keep it open. Some stents are coated with medicines
that help prevent the artery from becoming blocked again.
Coronary artery bypass grafting is when arteries or veins are taken from other areas of your
body and sewn in place to bypass blocked coronary arteries. This provides a new route for
blood flow to the heart
7. List the complications of an acute MI (see question 8)
8. Describe the time line in which each complication is most likely to occur
ST-Elevation MI (STEMI) may be complicated by many life-threatening problems. If a
significant amount of myocardial necrosis has occurred, hypotension, pulmonary
vascular congestion, or cardiogenic shock may develop. A low-output state may be
present upon admission or it may develop over the first few days following presentation.
Echocardiography can be performed to evaluate the contractility of both the left and right
ventricles and the extent of myocardial damage, as well as assess for mechanical
complications such as papillary muscle rupture with resultant mitral regurgitation,
ventricular septal rupture, and left ventricular free wall rupture. If extensive
remodeling has taken place, a left ventricular aneurysm may form which can lead to
further reductions in left ventricular systolic function or rupture.
Arrhythmias are also common after STEMI, particularly early after presentation.
Ventricular fibrillation is most common in the first 4 hours after symptom onset and
remains an important cause of mortality for at least the first 24 hours. Electrolyte
abnormalities and acid-base disturbances will contribute to the development of ventricular
fibrillation. Ventricular tachycardia is also a common occurrence, usually within the first
48 hours. Most of these episodes are nonsustained (lasting less than 30 seconds). If
nonsustained episodes are seen more than 4 days after STEMI, they may represent a higher
risk of future cardiac arrest. Frequent premature ventricular contractions are not
significant and should not be treated. Supraventricular tachycardia, in particular atrial
fibrillation, occurs more commonly with large infarcts and in conjunction with other
conditions like electrolyte abnormalities, heart failure, and pericarditis. Significant
bradycardia is associated with inferior infarcts due to increased vagal tone. Heart block
may develop as well depending upon the size of infarct. Bradycardias generally manifest
early in the course of the infarct.
Hemodynamic and other complications of myocardial infarction
Heart failure
Cardiogenic shock
Postinfarction angina and infarct extension - Recurrent ischemic pain after relief of
initial MI pain really represents unstable angina. Infarct extension indicates occurrence of
another MI within 3 weeks of the preceding one.
Pericarditis - Complicates acute MI usually within the first 4 days to first few weeks
Thromboembolic complications
Left ventricular aneurysm
Right ventricular infarction
Dressler's syndrome (postmyocardial infarction syndrome) - Occurs most often 2
weeks to several months after an MI

Recurrent fever, chest pain, pericardial friction rub, leukocytosis, and bloody pericardial
and/or pleural fluid.
Mechanical complications of myocardial infarction
Ventricular septal rupture with VSD - usually in the first week after infarction.
Sudden, loud pansystolic murmur Lower Left Sternal Border.
Severe CHF and/or cardiogenic shock
Acute MR
Rupture of LV free wall - Most patients die suddenly
Arrhythmic complications of myocardial infarction
Sinus bradycardia
Atrial tachycardia, atrial fibrillation
Premature ventricular complexes
Ventricular tachycardia, ventricular fibrillation - Primary within the first 48 hours of
MI, usually do not recur
Secondary ventricular tachycardia and fibrillation (later than 48 hours after MI) is recurrent,
poor prognosis
AV blocks
Acute stroke is usually embolic in nature. Risk of stroke is highest within the first month
after the infarct and remains elevated for the first year.
9. List the relative and absolute contraindications of thrombolytic therapy.
Absolute contraindications Absolute contraindications to fibrinolytic therapy include
previous intracerebral hemorrhage, known structural cerebral vascular lesion, known
malignant intracranial neoplasm, ischemic stroke within three months, suspected aortic
dissection, active bleeding or bleeding diathesis, or significant closed-head or facial trauma
within three months. Patients older than 75 years may get less overall benefit than younger
patients but advanced age is no longer considered a major contraindication for lytic therapy.
Relative contraindications
Poorly controlled or chronic sustained hypertension (systolic >180 mmHg)
Ischemic stroke more than three months previously
Dementia or other intracranial pathology (except as above)
Traumatic or prolonged cardiopulmonary resuscitation (>10 minutes) or major
surgery (within <3 weeks)
Recent (within two to four weeks) internal bleeding
Noncompressible vascular puncture
For streptokinase or anistreplase: prior exposure (more than five days previously) or
prior allergic reaction to these agents
Pregnancy
Active peptic ulcer
Current use of anticoagulants: the higher the INR, the higher the risk of bleeding
Special Case - Diabetes Mellitus - DM is a risk factor for coronary disease and is
associated with increased MIs. While fibinolytic therapy does have a benefit in those with
DM, there is an increased mortality for DM patients at the 30 day mark post treatment.
While diabetic retinopathy is classified as a contraindication for thrombolytic therapyl, the
risk of hemorrhage is extremely low and thrombolytic agents can be used in an acute MI.
10. Discuss the evidence supporting the role of coronary angiogram in acute MI.
Although coronary angiography may be performed during or after MI solely for
diagnostic purposes, the vast majority of studies are done to evaluate the patient for a

percutaneous or surgical revascularization procedure. Therefore, the appropriateness of

performing coronary angiography after MI is, by necessity, linked to the efficacy of these
revascularization procedures as measured by improved outcome for the patient. Guidelines
covering PTCA, coronary artery bypass graft surgery, and management of acute MI have
been published by the ACC/AHA Task Force on the Assessment of Diagnostic and Therapeutic
Procedures within the past 5 years and include recommendations relevant to the use of
coronary angiography.
In practical terms, the use of coronary angiography in patients with acute MI is
considered during 3 separate time periods. The first is related to the use of coronary
angiography during recognition and treatment of MI in the emergency department. It is only
applicable to patients who present with an acute evolving MI within a time frame when
reperfusion therapy will likely be beneficial. It is useful to stratify these patients by the
presence or absence of ST-segment elevation on the ECG. Because clinical outcomes,
especially with thrombolysis, are similar, the committee included in the group with STsegment elevation patients with typical ischemic chest pain and a new or presumed new left
bundle-branch block (BBB) obscuring the ECG diagnosis of MI. In the presence of ongoing
ischemic chest pain and ST-segment elevation (or left BBB), the clinician must quickly weigh
the risks and benefits of reperfusion therapy and determine whether to use thrombolysis or
mechanical techniques. Patients with ongoing ischemic chest pain but without ST-segment
elevation are a distinct group with different indications for coronary angiography compared
with those with ST-segment elevation.
The second time period relates to the use of coronary angiography during the
hospital-management phase, after completion of reperfusion therapy, if used, or
immediately if reperfusion therapy is not used. Throughout the remainder of the hospitalmanagement phase, the clinician is mainly concerned with treatment of various
complications, such as arrhythmia, heart failure, or recurrent ischemia that may develop.
The final time period is defined not by a specific time but rather by evaluations to
determine the risk of future morbid events and the need for additional therapies. In these
guidelines, the risk stratification phase refers to testing specifically performed in the patient
with MI to determine if high-risk indicators are present.
11. Discuss indications for stenting in acute MI.
Percutaneous coronary intervention often involves performing angioplasty. This procedure
entails maneuvering a small balloon to the site of significant stenosis within the coronary
artery. The balloon P.162 is then inflated creating a dissection plane within the vessel. This
will allow for increased blood flow. By itself, this procedure has historically been associated
with restenosis rates of greater than 40%. Within the last 10 to 15 years, coronary stents
have been introduced. These are small, wire, meshlike devices comprised of stainless steel,
titanium, or cobalt that are mounted on a balloon. The stent is delivered to the area of
significant plaque and deployed under high pressures. As a result, it will become embedded
in the wall of the vessel, thereby increasing the luminal diameter. With stents, restenosis
rates were initially reduced to 15% to 30%. The most recent innovation involves stents
coated with immunomodulating agents such as sirolimus and paclitaxel, which prevent the
growth of excess tissue within the stents. This has reduced restenosis rates to less than 5%.
The metal stent that has been embedded in the arterial wall is thrombogenic, not only
because it is a foreign body, but also because stent deployment leads to endothelial
damage, which can set off a cascade leading to formation of a thrombus. Therefore, the
patient should be maintained on antiplatelet therapy including aspirin and clopidogrel. These
drugs will help maintain stent patency until the endothelium grows over the exposed metal
stent, thereby eliminating any thrombogenic potential.
As people age, the normal flow of blood through the arteries can be affected by the buildup
of plaque inside the arteries. Over time, plaque continues to grow on arterial walls as
cholesterol circulates in the blood; as the plaques enlarge, the arteries become narrow and
stiffened. This process is called atherosclerosis, commonly known as hardening of the
arteries, because the plaque buildup thickens the walls of the arteries and narrows the

space through which the blood flows. When this happens, it reduces the circulation of blood
through the area of the body that gets its blood from the artery.
Angioplasty is a procedure during which a physician inflates a small balloon inside a blood
vessel to eliminate or reduce areas of narrowing. The goal of angioplasty is the restoration of
adequate blood flow (revascularization) through the affected part of the body. This is
accomplished by enlarging the blood vessel from within.
Stenting is a procedure in which a physician inserts a tiny, slender, expandable metal-mesh
tube (stent) that fits inside an artery once the artery has been widened by angioplasty. The
goal of stenting is to prevent the artery from collapsing or being closed by plaque again.
When Are Angioplasty and Stenting Indicated?
Atherosclerosis can cause a variety of diseases or conditions depending on the location of
the plaque within the body. Some of these include:
Coronary heart disease
Carotid artery disease
Aortoiliac occlusive disease
Leg artery disease
Arm artery disease
Visceral artery conditions
Renovascular conditions
In less advanced cases of atherosclerosis, medication is the first line of treatment; when
atherosclerosis is advanced or does not respond to medication, angioplasty and stenting are
recommended. In many cases, angioplasty is an alternative to bypass surgery.
Conditions that can affect the flow of blood through the venous system, such as deep
venous thrombosis and portal hypertension, are sometimes treated with forms of
angioplasty. Angioplasty may be used to treat blocked surgical bypasses when they occur.
12. Discuss post-stenting care and follow-up.
Complications of angioplasty are relatively infrequent, but they do exist. The most common
complications include discomfort and bleeding at the puncture site where the catheter was
inserted. Occasionally, angioplasty creates a small tear (dissection) of an internal layer in
the coronary artery. Usually, the tear is small and heals by itself. In some cases the tear is
corrected with a stent. If the tear is severe, causing a blockage in blood flow in the artery or
loss of blood into the pericardial sac, immediate treatment is needed. This usually includes a
repeat angioplasty and insertion of another stent. Rarely, a person will need urgent bypass
surgery.
Approximately 10 percent of patients develop chest pain within 48 hours of their procedure.
In some cases this pain is caused by ischemia that occurs when a dissection develops or
pieces of the plaque material travel downstream (embolization). Many patients have
evidence of a very small amount of heart damage after angioplasty, based upon blood
testing. However, less than one percent of patients have a heart attack large enough to
cause a substantial amount of damage.
Although angioplasty restores blood flow and relieves symptoms in over 90 percent of
patients, there is a risk of recurrent symptoms within six months, often due to recurrent
narrowing (restenosis) of the artery. Restenosis that is severe enough to cause bothersome
or life-threatening symptoms occurs in:

Approximately 30 percent of people who have balloon angioplasty without stent

placement.
Approximately 15 percent of people who have a bare metal stent.

Less than 10 percent of people who have a drug-coated stent.

Some coronary artery sites are more prone to renarrowing than others. In addition, some
conditions increase the risk of narrowing, potentially requiring a repeat catheterization and
reopening or bypass of the narrowed artery:
Diabetes
Continued cigarette smoking
High blood pressure
Arteries that are narrow
High level of bad (LDL) cholesterol
Narrowing in a major blood vessel that is at or near the beginning of a side branch
Recurrent symptoms can develop as a result of other vessels that become narrowed. Some
vessels that are very small, have long-standing total blockages, or have a very calcified
lesion cannot be adequately opened.
Following the angioplasty procedure, the catheter is removed from the artery and pressure is
applied to the area. In some cases, a pressure device is used to limit bleeding from the site.
In other cases the artery is sealed closed at the time the catheter is removed.
The patient must lie flat and remain still for several hours to reduce the risk of bleeding.
During this time, the patient will remain in a recovery area where his or her blood pressure,
heart rate, oxygen level, temperature, and puncture site can be monitored frequently. As the
sedative medication begins to wear off, pain medication may be given if needed.
Most patients will remain in the hospital overnight after angioplasty. A friend or family
member must be available to drive the patient home. Most patients are able to walk on the
day after the angioplasty and can resume their normal activities, including returning to work,
within a week. Driving and heavy lifting and pushing or pulling is not allowed for a few days.
Specific activity restrictions should be discussed with the patient.
One of the most serious complications that can develop after stent placement is the
development of a blood clot (thrombosis) inside the stent. This can potentially block blood
flow to the heart, causing a heart attack or even death. Stent thrombosis can occur within
24 hours, 30 days, or as late as one year or more after stent placement. Stent thromboses
that occur later are slightly more common with use of drug-coated stents.
Fortunately, stent thrombosis is relatively uncommon because two medications, aspirin and
clopidogrel (Plavix), are given before and after stent placement to reduce the risk of clot
formation. Aspirin is usually continued indefinitely to prevent heart attacks. Clopidogrel is
often continued for a year or more.
Researchers recommendations concerning anticoagulant therapy (UpToDate):
After placement of a BMS (Bare Metal Stent), aspirin should be given at a dose of 162 to 325
mg/day and clopidogrel at a dose of 75 mg/day. The dose of aspirin can be reduced to 75 to
162 mg/day after at least one month.
Among patients with DES (Drug Eluding Stent), we recommend as MINIMUM therapy,
uninterrupted dual antiplatelet therapy with aspirin and clopidogrel for one year. After
placement of a DES, aspirin should be given initially at a dose of 162 to 325 mg/day and
clopidogrel at a dose of 75 mg/day. The dose of aspirin should be 162 to 325 mg/day for
three and six months for SES and PES, respectively, and, after six months, may be reduced
to 75 to 162 mg/day. For patients receiving zotarolimus or everolimus-eluting stents, aspirin
should be given at a dose of 162 to 325 mg/day and clopidogrel at a dose of 75 mg/day. The
dose of aspirin should be 162 to 325 mg/day for six months and then may be reduced to 75
to 162 mg/day. For patients at higher than average risk of bleeding while on dual antiplatelet
therapy, such as those who are also taking warfarin, physicians and patients may reasonably
choose to lower the dose of aspirin sooner than we suggest here.
We recommend that aspirin at a dose of 75 to 162 mg/day be continued indefinitely in all
stented patients. We suggest continuing dual antiplatelet therapy indefinitely after DES in
some patients, particularly when the antithrombotic benefit appears to exceed the risk for

bleeding, until data are available defining the optimal duration of clopidogrel therapy in this
setting. We suggest the routine administration of a proton pump inhibitor to only those
patients on long term dual antiplatelet therapy who are at high risk for gastrointestinal
bleeding due to the presence of a history of ulcer complication, history of ulcer disease (nonbleeding), gastrointestinal bleeding, concomitant anticoagulant therapy. PPI prophylaxis may
also be considered in patients with additional risk factors such as age older than 60 years,
corticosteroid use or dyspepsia/gastroesophageal reflux disease symptoms, especially when
several risk factors are present; discussion of the risks and benefits with the patient may
help guide clinical decisions.
More research is needed to determine which PPIs interfere with clopidogrel and which people
benefit from PPIs. Until more is known, people who require PPIs and clopidogrel should speak
to their healthcare provider about the potential risks and benefits of PPIs.
As stated earlier, it is extremely important for the patient to continue taking the aspirin and
clopidogrel for at least one year unless a serious bleeding-related problem develops.
Stopping one or both medications could allow a clot to form in the stent, which can have
very serious consequences, including a heart attack or even death. Patients should notify
their healthcare provider if either medication needs to be stopped for any reason.
Allergic-type reaction Uncommonly, clopidogrel can cause an allergic-type reaction.
The reaction usually begins within the first week of starting the medication.
Symptoms can include a red, raised, itchy rash that begins on the face, chest, or
abdomen. The rash may spread to include the arms and legs, or even the entire body.
Bleeding People who take antiplatelet medications, such as aspirin and clopidogrel,
have an increased risk of bleeding. Excessing bleeding can occur after an injury or if
an ulcer develops in the stomach. To reduce the risk of developing an ulcer, some
people are advised to take an acid-reducing medication called a proton pump
inhibitor (PPI). However, there is concern that some PPIs will interfere with
clopidogrel, increasing the risk of developing a blood clot in the stent, having a heart
attack, or even dying.
Patient should seek help if any of the following occur:
Chest pain develops and is not relieved with one dose of sublingual nitroglycerin
The puncture site becomes very painful, swollen, warm, bleeds more than a few
drops, or drains pus.
A fever higher than 100.4 F (38 C) develops
OTHER MEASURES TO SLOW OR REVERSE HEART DISEASE In all patients with coronary
artery disease, it is important to follow guidelines to reduce the risk of worsening heart
disease. These guidelines include the following:
Treat high blood pressure
Treat high cholesterol
Quit smoking
Lose excess weight
Reduce stress
Exercise regularly
Avoid or minimize activities that provoke angina, such as exercising during cold weather
or exercising vigorously, particularly after a meal
Learn to use nitroglycerin preventively