TN 25 (04-21)
4.00 CARDIOVASCULAR SYSTEM (Effective date: 04/02/2021)
do we mean by a cardiovascular
a. We mean any disorder that affects the proper functioning of the heart or the circulatory
system (that is, arteries, veins, capillaries, and the lymphatic drainage). The disorder
can be congenital or acquired.
b. Cardiovascular impairment results from one or more of four consequences of heart
(i) Chronic heart failure or ventricular dysfunction.
(ii) Discomfort or pain due to myocardial ischemia, with or without necrosis of heart
(iii) Syncope, or near syncope, due to inadequate cerebral perfusion from any cardiac
cause, such as obstruction of flow or disturbance in rhythm or conduction resulting
in inadequate cardiac output.
(iv) Central cyanosis due to right-to-left shunt, reduced oxygen concentration in
the arterial blood, or pulmonary vascular disease.
c. Disorders of the veins or arteries (for example, obstruction, rupture, or aneurysm)
may cause impairments of the lower extremities (peripheral vascular disease), the
central nervous system, the eyes, the kidneys, and other organs. We will evaluate
peripheral vascular disease under 4.11 or 4.12 and impairments of another body system(s)
under the listings for that body system(s).
2. What do we consider in evaluating cardiovascular
impairments? The listings in this section describe cardiovascular impairments based on symptoms,
signs, laboratory findings, response to a regimen of prescribed treatment, and functional
3. What do the following terms or phrases mean in these listings?
a. Medical consultant is an individual defined in §§404.1616(a) and 416.1016(a). This term does not include medical sources who provide consultative examinations
for us. We use the abbreviation “MC” throughout this section to designate a medical
b. Persistent means that the longitudinal clinical record shows that, with few exceptions, the
required finding(s) has been present, or is expected to be present, for a continuous
period of at least 12 months, such that a pattern of continuing severity is established.
c. Recurrent means that the longitudinal clinical record shows that, within a consecutive 12-month
period, the finding(s) occurs at least three times, with intervening periods of improvement
of sufficient duration that it is clear that separate events are involved.
d. Appropriate medically acceptable
imaging means that the technique used is the proper one to evaluate and diagnose the impairment
and is commonly recognized as accurate for assessing the cited finding.
e. A consecutive 12-month
period means a period of 12 consecutive months, all or part of which must occur within the
period we are considering in connection with an application or continuing disability
f. Uncontrolled means the impairment does not adequately respond to standard prescribed medical treatment.
1. What basic documentation do we
need? We need sufficiently detailed reports of history, physical examinations, laboratory
studies, and any prescribed treatment and response to allow us to assess the severity
and duration of your cardiovascular impairment. A longitudinal clinical record covering
a period of not less than 3 months of observations and treatment is usually necessary,
unless we can make a determination or decision based on the current evidence.
2. Why is a longitudinal clinical record
important? We will usually need a longitudinal clinical record to assess the severity and expected
duration of your impairment(s). If you have a listing-level impairment, you probably
will have received medically prescribed treatment. Whenever there is evidence of such
treatment, your longitudinal clinical record should include a description of the ongoing
management and evaluation provided by your treating or other medical source. It should
also include your response to this medical management, as well as information about
the nature and severity of your impairment. The record will provide us with information
on your functional status over an extended period of time and show whether your ability
to function is improving, worsening, or unchanging.
3. What if you have not received ongoing medical treatment?
a. You may not have received ongoing treatment or have an ongoing relationship with
the medical community despite the existence of a severe impairment(s). In this situation,
we will base our evaluation on the current objective medical evidence and the other
evidence we have. If you do not receive treatment, you cannot show an impairment that
meets the criteria of most of these listings. However, we may find you disabled because
you have another impairment(s) that in combination with your cardiovascular impairment
medically equals the severity of a listed impairment or based on consideration of
your residual functional capacity and age, education, and work experience.
b. Unless we can decide your claim favorably on the basis of the current evidence,
a longitudinal record is still important. In rare instances where there is no or insufficient
longitudinal evidence, we may purchase a consultative examination(s) to help us establish
the severity and duration of your impairment.
4. When will we wait before we ask for more evidence?
a. We will wait when we have information showing that your impairment is not yet stable
and the expected change in your impairment might affect our determination or decision.
In these situations, we need to wait to properly evaluate the severity and duration
of your impairment during a stable period. Examples of when we might wait are:
(i) If you have had a recent acute event; for example, a myocardial infarction (heart
(ii) If you have recently had a corrective cardiac procedure; for example, coronary
artery bypass grafting.
(iii) If you have started new drug therapy and your response to this treatment has
not yet been established; for example, beta-blocker therapy for dilated congestive
b. In these situations, we will obtain more evidence 3 months following the event
before we evaluate your impairment. However, we will not wait if we have enough information
to make a determination or decision based on all of the relevant evidence in your
5. Will we purchase any
studies? In appropriate situations, we will purchase studies necessary to substantiate the
diagnosis or to document the severity of your impairment, generally after we have
evaluated the medical and other evidence we already have. We will not purchase studies
involving exercise testing if there is significant risk involved or if there is another
medical reason not to perform the test. We will follow sections 4.00C6, 4.00C7, and
4.00C8 when we decide whether to purchase exercise testing.
6. What studies will we not
purchase? We will not purchase any studies involving cardiac catheterization, such as coronary
angiography, arteriograms, or electrophysiological studies. However, if the results
of catheterization are part of the existing evidence we have, we will consider them
together with the other relevant evidence. See 4.00C15a.
Using cardiovascular test
1. What is an ECG?
stands for electrocardiograph or electrocardiogram. An electrocardiograph is a machine that records electrical impulses of your heart
on a strip of paper called an electrocardiogram or a tracing. To record the ECG, a technician positions a number of small contacts (or leads) on your arms, legs, and across your chest to connect them to the ECG machine. An
ECG may be done while you are resting or exercising.
b. The ECG tracing may indicate that you have a heart abnormality. It may indicate
that your heart muscle is not getting as much oxygen as it needs (ischemia), that
your heart rhythm is abnormal (arrhythmia), or that there are other abnormalities
of your heart, such as left ventricular enlargement.
2. How do we evaluate ECG
evidence? We consider a number of factors when we evaluate ECG evidence:
a. An original or legible copy of the 12-lead ECG obtained at rest must be appropriately
dated and labeled, with the standardization inscribed on the tracing. Alteration in
standardization of specific leads (such as to accommodate large QRS amplitudes) must
be identified on those leads.
(i) Detailed descriptions or computer-averaged signals without original or legible
copies of the ECG as described in listing 4.00C2a are not acceptable.
(ii) The effects of drugs or electrolyte abnormalities must be considered as possible
noncardiac causes of ECG abnormalities of ventricular repolarization; that is, those
involving the ST segment and T wave. If available, the predrug (especially digitalis
glycosides) ECG should be submitted.
b. ECGs obtained in conjunction with treadmill, bicycle, or arm exercise tests should
meet the following specifications:
(i) ECG reports must include the original calibrated ECG tracings or a legible copy.
(ii) A 12-lead baseline ECG must be recorded in the upright position before exercise.
(iii) A 12-lead ECG should be recorded at the end of each minute of exercise.
(iv) If ECG documentation of the effects of hyperventilation is obtained, the exercise
test should be deferred for at least 10 minutes because metabolic changes of hyperventilation
may alter the physiologic and ECG-recorded response to exercise.
(v) Post-exercise ECGs should be recorded using a generally accepted protocol consistent
with the prevailing state of medical knowledge and clinical practice.
(vi) All resting, exercise, and recovery ECG strips must have the standardization
inscribed on the tracing. The ECG strips should be labeled to indicate the date, the
times recorded and the relationship to the stage of the exercise protocol. The speed
and grade (treadmill test) or work rate (bicycle or arm ergometric test) should be
recorded. The highest level of exercise achieved, heart rate and blood pressure levels
during testing, and the reason(s) for terminating the test (including limiting signs
or symptoms) must be recorded.
3. What are exercise tests and what are they used for?
a. Exercise tests have you perform physical activity and record how your cardiovascular
system responds. Exercise tests usually involve walking on a treadmill, but other
forms of exercise, such as an exercise bicycle or an arm exercise machine, may be
used. Exercise testing may be done for various reasons; such as to evaluate the severity
of your coronary artery disease or peripheral vascular disease or to evaluate your
progress after a cardiac procedure or an acute event, like a myocardial infarction
(heart attack). Exercise testing is the most widely used testing for identifying the
presence of myocardial ischemia and for estimating maximal aerobic capacity (usually
expressed in METs – metabolic equivalents) if you have heart disease.
b. We include exercise tolerance test (ETT) criteria in 4.02B3 (chronic heart failure)
and 4.04A (ischemic heart disease). To meet the ETT criteria in these listings, the
ETT must be a sign- or symptom-limited test in which you exercise while connected
to an ECG until you develop a sign or symptom that indicates that you have exercised
as much as is considered safe for you.
c. In 4.12B, we also refer to exercise testing for peripheral vascular disease. In
this test, you walk on a treadmill, usually for a specified period of time, and the
individual who administers the test measures the effect of exercise on the flow of
blood in your legs, usually by using ultrasound. The test is also called an exercise
Doppler test. Even though this test is intended to evaluate peripheral vascular disease,
it will be stopped for your safety if you develop abnormal signs or symptoms because
of heart disease.
d. Each type of test is done in a certain way following specific criteria, called
a protocol. For our program, we also specify certain aspects of how any exercise test we purchase
is to be done. See 4.00C10 and 4.00C17.
limitations? An ETT provides an estimate of aerobic capacity for walking on a grade, bicycling,
or moving one’s arms in an environmentally controlled setting. Therefore, ETT results
do not correlate with the ability to perform other types of exertional activities,
such as lifting and carrying heavy loads, and do not provide an estimate of the ability
to perform activities required for work in all possible work environments or throughout
a workday. Also, certain medications (such as beta blockers) and conduction disorders
(such as left or right bundle branch blocks) can cause false-negative or false-positive
results. Therefore, we must consider the results of an ETT together with all the other
relevant evidence in your case record.
does an ETT with measurement of maximal or peak oxygen uptake
differ from other
ETTs? Occasionally, medical evidence will include the results of an ETT with VO2. While ETTs without measurement of VO2 provide only an estimate of aerobic capacity, measured maximal or peak oxygen uptake
provides an accurate measurement of aerobic capacity, which is often expressed in
METs (metabolic equivalents). The MET level may not be indicated in the report of
attained maximal or peak VO2 testing, but can be calculated as follows: 1 MET = 3.5 milliliters (ml) of oxygen
uptake per kilogram (kg) of body weight per minute. For example, a 70 kg (154 lb.)
individual who achieves a maximal or peak VO2 of 1225 ml in 1 minute has attained 5 METs (1225 ml/70 kg/1 min = 17.5 ml/kg/min.
17.5/3.5 = 5 METs).
6. When will we consider whether to purchase an exercise test?
a. We will consider whether to purchase an exercise test when:
(i) There is a question whether your cardiovascular impairment meets or medically
equals the severity of one of the listings, or there is no timely test in the evidence
we have (see 4.00C9), and we cannot find you disabled on some other basis; or
(ii) We need to assess your residual functional capacity and there is insufficient
evidence in the record to make a determination or decision.
b. We will not purchase an exercise test when we can make our determination or decision
based on the evidence we already have.
7. What must we do before purchasing an exercise test?
a. Before we purchase an exercise test, an MC, preferably one with experience in the
care of patients with cardiovascular disease, must review the pertinent history, physical
examinations, and laboratory tests that we have to determine whether the test would
present a significant risk to you or if there is some other medical reason not to
purchase the test (see 4.00C8).
b. If you are under the care of a treating source (see §§404.1502 and 416.902) for a cardiovascular impairment, this source has not performed an exercise test,
and there are no reported significant risks to testing, we will request a statement
from that source explaining why it was not done or should not be done before we decide
whether we will purchase the test.
c. The MC, in accordance with the regulations and other instructions on consultative
examinations, will generally give great weight to the treating source’s opinion about
the risk of exercise testing to you and will generally not override it. In the rare
situation in which the MC does override the treating source’s opinion, the MC must
prepare a written rationale documenting the reasons for overriding the opinion.
d. If you do not have a treating source or we cannot obtain a statement from your
treating source, the MC is responsible for assessing the risk to exercise testing
based on a review of the records we have before purchasing an exercise test for you.
e. We must also provide your records to the medical source who performs the exercise
test for review prior to conducting the test if the source does not already have them.
The medical source who performs the exercise test has the ultimate responsibility
for deciding whether you would be at risk.
8. When will we not purchase an exercise test or wait before we purchase an exercise
a. We will not purchase an exercise test when an MC finds that you have one of the
following significant risk factors:
(i) Unstable angina not previously stabilized by medical treatment.
(ii) Uncontrolled cardiac arrhythmias causing symptoms or hemodynamic compromise.
(iii) An implanted cardiac defibrillator.
(iv) Symptomatic severe aortic stenosis.
(v) Uncontrolled symptomatic heart failure.
(vi) Aortic dissection.
(vii) Severe pulmonary hypertension (pulmonary artery systolic pressure greater than
60 mm Hg).
(viii) Left main coronary stenosis of 50 percent or greater that has not been bypassed.
(ix) Moderate stenotic valvular disease with a systolic gradient across the aortic
valve of 50 mm Hg or greater.
(x) Severe arterial hypertension (systolic greater than 200 mm Hg or diastolic greater
than 110 mm Hg).
(xi) Hypertrophic cardiomyopathy with a systolic gradient of 50 mm Hg or greater.
b. We also will not purchase an exercise test when you are prevented from performing
exercise testing due to another impairment affecting your ability to use your arms
c. We will not purchase an ETT to document the presence of a cardiac arrhythmia.
d. We will wait to purchase an exercise test until 3 months after you have had one
of the following events. This will allow for maximal, attainable restoration of functional
(i) Acute myocardial infarction.
(ii) Surgical myocardial revascularization (bypass surgery).
(iii) Other open-heart surgical procedures.
(iv) Percutaneous transluminal coronary angioplasty with or without stenting.
e. If you are deconditioned after an extended period of bedrest or inactivity and
could improve with activity, or if you are in acute heart failure and are expected
to improve with treatment, we will wait an appropriate period of time for you to recuperate
before we purchase an exercise test.
9. What do we mean by a “timely” test?
a. We consider exercise test results to be timely for 12 months after the date they
are performed, provided there has been no change in your clinical status that may
alter the severity of your cardiovascular impairment.
b. However, an exercise test that is older than 12 months, especially an abnormal
one, can still provide information important to our adjudication. For example, a test
that is more than 12 months old can provide evidence of ischemic heart disease or
peripheral vascular disease, information on decreased aerobic capacity, or information
about the duration or onset of your impairment. Such tests can be an important component
of the longitudinal record.
c. When we evaluate a test that is more than 12 months old, we must consider the results
in the context of all the relevant evidence, including why the test was performed
and whether there has been an intervening event or improvement or worsening of your
d. We will purchase a new exercise test only if we cannot make a determination or
decision based on the evidence we have.
10. How must ETTs we purchase be performed?
a. The ETT must be a sign- or symptom-limited test characterized by a progressive
multistage regimen. It must be performed using a generally accepted protocol consistent
with the prevailing state of medical knowledge and clinical practice. A description
of the protocol that was followed must be provided, and the test must meet the requirements
of 4.00C2b and this section. A radionuclide perfusion scan may be useful for detecting
or confirming ischemia when resting ECG abnormalities, medications, or other factors
may decrease the accuracy of ECG interpretation of ischemia. (The perfusion imaging
is done at the termination of exercise, which may be at a higher MET level than that
at which ischemia first occurs. If the imaging confirms the presence of reversible
ischemia, the exercise ECG may be useful for detecting the MET level at which ischemia
initially appeared.) Exercise tests may also be performed using echocardiography to
detect stress-induced ischemia and left ventricular dysfunction (see 4.00C12 and 4.00C13).
b. The exercise test must be paced to your capabilities and be performed following
the generally accepted standards for adult exercise test laboratories. With a treadmill
test, the speed, grade (incline), and duration of exercise must be recorded for each
exercise test stage performed. Other exercise test protocols or techniques should
use similar workloads. The exercise protocol may need to be modified in individual
cases to allow for a lower initial workload with more slowly graded increments than
the standard Bruce protocol.
c. Levels of exercise must be described in terms of workload and duration of each
stage; for example, treadmill speed and grade, or bicycle ergometer work rate in kpm/min
d. The exercise laboratory's physical environment, staffing, and equipment must meet
the generally accepted standards for adult exercise test laboratories.
11. How do we evaluate ETT
results? We evaluate ETT results on the basis of the work level at which the test becomes
abnormal, as documented by onset of signs or symptoms and any ECG or imaging abnormalities.
The absence of an ischemic response on an ETT alone does not exclude the diagnosis
of ischemic heart disease. We must consider the results of an ETT in the context of
all of the other evidence in your case record.
12. When are ETTs done with
imaging? When resting ECG abnormalities preclude interpretation of ETT tracings relative to
ischemia, a radionuclide (for example, thallium-201 or technetium-99m) perfusion scan
or echocardiography in conjunction with an ETT provides better results. You may have
resting ECG abnormalities when you have a conduction defect--for example, Wolff-Parkinson-White
syndrome, left bundle branch block, left ventricular hypertrophy--or when you are
taking digitalis or other antiarrhythmic drugs, or when resting ST changes are present.
Also, these techniques can provide a reliable estimate of ejection fraction.
13. Will we purchase ETTs with
imaging? We may purchase an ETT with imaging in your case after an MC, preferably one with
experience in the care of patients with cardiovascular disease, has reviewed your
medical history and physical examination, any report(s) of appropriate medically acceptable
imaging, ECGs, and other appropriate tests. We will consider purchasing an ETT with
imaging when other information we have is not adequate for us to assess whether you
have severe ventricular dysfunction or myocardial ischemia, there is no significant
risk involved (see 4.00C8a), and we cannot make our determination or decision based
on the evidence we already have.
14. What are drug-induced stress
tests? These tests are designed primarily to provide evidence about myocardial ischemia
or prior myocardial infarction, but do not require you to exercise. These tests are
used when you cannot exercise or cannot exercise enough to achieve the desired cardiac
stress. Drug-induced stress tests can also provide evidence about heart chamber dimensions
and function; however, these tests do not provide information about your aerobic capacity
and cannot be used to help us assess your ability to function. Some of these tests
use agents, such as Persantine or adenosine, that dilate the coronary arteries and
are used in combination with nuclear agents, such as thallium or technetium (for example,
Cardiolyte or Myoview), and a myocardial scan. Other tests use agents, such as dobutamine,
that stimulate the heart to contract more forcefully and faster to simulate exercise
and are used in combination with a 2-dimensional echocardiogram. We may, when appropriate,
purchase a drug-induced stress test to confirm the presence of myocardial ischemia
after a review of the evidence in your file by an MC, preferably one with experience
in the care of patients with cardiovascular disease.
15. How do we evaluate cardiac catheterization
a. We will not purchase cardiac catheterization; however, if you have had catheterization,
we will make every reasonable effort to obtain the report and any ancillary studies.
We will consider the quality and type of data provided and its relevance to the evaluation
of your impairment. For adults, we generally see two types of catheterization reports:
Coronary arteriography and left ventriculography.
b. For coronary arteriography, the report should provide information citing the method
of assessing coronary arterial lumen diameter and the nature and location of obstructive
lesions. Drug treatment at baseline and during the procedure should be reported. Some
individuals with significant coronary atherosclerotic obstruction have collateral
vessels that supply the myocardium distal to the arterial obstruction so that there
is no evidence of myocardial damage or ischemia, even with exercise. When the results
of quantitative computer measurements and analyses are included in your case record,
we will consider them in interpreting the severity of stenotic lesions.
c. For left ventriculography, the report should describe the wall motion of the myocardium
with regard to any areas of hypokinesis (abnormally decreased motion), akinesis (lack
of motion), or dyskinesis (distortion of motion), and the overall contraction of the
ventricle as measured by the ejection fraction. Measurement of chamber volumes and
pressures may be useful. Quantitative computer analysis provides precise measurement
of segmental left ventricular wall thickness and motion. There is often a poor correlation
between left ventricular function at rest and functional capacity for physical activity.
16. What details should exercise Doppler test reports
The reports of exercise Doppler tests must describe the level of exercise; for example,
the speed and grade of the treadmill settings, the duration of exercise, symptoms
during exercise, and the reasons for stopping exercise if the expected level of exercise
was not attained. They must also include the blood pressures at the ankle and other
pertinent sites measured after exercise and the time required for the systolic blood
pressure to return toward or to the pre-exercise level. The graphic tracings, if available,
should also be included with the report. All tracings must be annotated with the standardization
used by the testing facility.
17. How must exercise Doppler tests we purchase be
performed? When we purchase an exercise Doppler test, you must exercise on a treadmill at 2
mph on a 12 percent grade for up to 5 minutes. The reports must include the information
specified in 4.00C16. Because this is an exercise test, we must evaluate whether such
testing would put you at significant risk, in accordance with the guidance found in
4.00C6, 4.00C7, and 4.00C8.
1. What is chronic heart failure (CHF)?
a. CHF is the inability of the heart to pump enough oxygenated blood to body tissues. This
syndrome is characterized by symptoms and signs of pulmonary or systemic congestion
(fluid retention) or limited cardiac output. Certain laboratory findings of cardiac
functional and structural abnormality support the diagnosis of CHF. There are two
main types of CHF:
(i) Predominant systolic
dysfunction (the inability of the heart to contract normally and expel sufficient blood), which
is characterized by a dilated, poorly contracting left ventricle and reduced ejection
fraction (abbreviated EF, it represents the percentage of the blood in the ventricle
actually pumped out with each contraction), and
(ii) Predominant diastolic
dysfunction (the inability of the heart to relax and fill normally), which is characterized by
a thickened ventricular muscle, poor ability of the left ventricle to distend, increased
ventricular filling pressure, and a normal or increased EF.
b. CHF is considered in these listings as a single category whether due to atherosclerosis
(narrowing of the arteries), cardiomyopathy, hypertension, or rheumatic, congenital,
or other heart disease. However, if the CHF is the result of primary pulmonary hypertension
secondary to disease of the lung (cor pulmonale), we will evaluate your impairment
using 3.09, in the respiratory system listings.
2. What evidence of CHF do we need?
a. Cardiomegaly or ventricular dysfunction must be present and demonstrated by appropriate
medically acceptable imaging, such as chest x-ray, echocardiography (M-Mode, 2-dimensional,
and Doppler), radionuclide studies, or cardiac catheterization.
(i) Abnormal cardiac imaging showing increased left ventricular end diastolic diameter
(LVEDD), decreased EF, increased left atrial chamber size, increased ventricular filling
pressures measured at cardiac catheterization, or increased left ventricular wall
or septum thickness, provides objective measures of both left ventricular function
and structural abnormality in heart failure.
(ii) An LVEDD greater than 6.0 cm or an EF of 30 percent or less measured during a
period of stability (that is, not during an episode of acute heart failure) may be
associated clinically with systolic failure.
(iii) Left ventricular posterior wall thickness added to septal thickness totaling
2.5 cm or greater with left atrium enlarged to 4.5 cm or greater may be associated
clinically with diastolic failure.
(iv) However, these measurements alone do not reflect your functional capacity, which
we evaluate by considering all of the relevant evidence. In some situations, we may
need to purchase an ETT to help us assess your functional capacity.
(v) Other findings on appropriate medically acceptable imaging may include increased
pulmonary vascular markings, pleural effusion, and pulmonary edema. These findings
need not be present on each report, since CHF may be controlled by prescribed treatment.
b. To establish that you have chronic heart failure, your medical history and physical examination should describe characteristic
symptoms and signs of pulmonary or systemic congestion or of limited cardiac output
associated with the abnormal findings on appropriate medically acceptable imaging.
When an acute episode of heart failure is triggered by a remediable factor, such as
an arrhythmia, dietary sodium overload, or high altitude, cardiac function may be
restored and a chronic impairment may not be present.
(i) Symptoms of congestion or of limited cardiac output include easy fatigue, weakness,
shortness of breath (dyspnea), cough, or chest discomfort at rest or with activity.
Individuals with CHF may also experience shortness of breath on lying flat (orthopnea)
or episodes of shortness of breath that wake them from sleep (paroxysmal nocturnal
dyspnea). They may also experience cardiac arrhythmias resulting in palpitations,
lightheadedness, or fainting.
(ii) Signs of congestion may include hepatomegaly, ascites, increased jugular venous
distention or pressure, rales, peripheral edema, or rapid weight gain. However, these
signs need not be found on all examinations because fluid retention may be controlled
by prescribed treatment.
3. Is it safe for you to have an ETT, if you have
CHF? The presence of CHF is not necessarily a contraindication to an ETT, unless you are
having an acute episode of heart failure. Measures of cardiac performance are valuable
in helping us evaluate your ability to do work-related activities. Exercise testing
has been safely used in individuals with CHF; therefore, we may purchase an ETT for
evaluation under 4.02B3 if an MC, preferably one experienced in the care of patients
with cardiovascular disease, determines that there is no significant risk to you.
(See 4.00C6 for when we will consider the purchase of an ETT. See 4.00C7- 4.00C8 for
what we must do before we purchase an ETT and when we will not purchase one.) ST segment
changes from digitalis use in the treatment of CHF do not preclude the purchase of
4. How do we evaluate CHF using
a. We must have objective evidence, as described in 4.00D2, that you have chronic
b. To meet the required level of severity for this listing, your impairment must satisfy
the requirements of one of the criteria in A and one of the criteria in B.
c. In 4.02B2, the phrase periods of stabilization means that, for at least 2 weeks between episodes of acute heart failure, there must
be objective evidence of clearing of the pulmonary edema or pleural effusions and
evidence that you returned to, or you were medically considered able to return to,
your prior level of activity.
d. Listing 4.02B3c requires a decrease in systolic blood pressure below the baseline
level (taken in the standing position immediately prior to exercise) or below any
systolic pressure reading recorded during exercise. This is because, normally, systolic
blood pressure and heart rate increase gradually with exercise. Decreases in systolic
blood pressure below the baseline level that occur during exercise are often associated
with ischemia-induced left ventricular dysfunction resulting in decreased cardiac
output. However, a blunted response (that is, failure of the systolic blood pressure
to rise 10 mm Hg or more), particularly in the first 3 minutes of exercise, may be
drug-related and is not necessarily associated with left ventricular dysfunction.
Also, some individuals with increased sympathetic responses because of deconditioning
or apprehension may increase their systolic blood pressure and heart rate above their
baseline level just before and early into exercise. This can be associated with a
drop in systolic pressure in early exercise that is not due to left ventricular dysfunction.
Therefore, an early decrease in systolic blood pressure must be interpreted within
the total context of the test; that is, the presence or absence of symptoms such as
lightheadedness, ischemic changes, or arrhythmias on the ECG.
1. What is ischemic heart disease (IHD)?
IHD results when one or more of your coronary arteries is narrowed or obstructed or,
in rare situations, constricted due to vasospasm, interfering with the normal flow
of blood to your heart muscle (ischemia). The obstruction may be the result of an
embolus, a thrombus, or plaque. When heart muscle tissue dies as a result of the reduced
blood supply, it is called a myocardial infarction (heart attack).
2. What causes chest discomfort of myocardial origin?
a. Chest discomfort of myocardial ischemic origin, commonly known as angina pectoris,
is usually caused by coronary artery disease (often abbreviated CAD). However, ischemic
discomfort may be caused by a noncoronary artery impairment, such as aortic stenosis,
hypertrophic cardiomyopathy, pulmonary hypertension, or anemia.
b. Instead of typical angina pectoris, some individuals with IHD experience atypical
angina, anginal equivalent, variant angina, or silent ischemia, all of which we may
evaluate using 4.04. We discuss the various manifestations of ischemia in 4.00E3-4.00E7.
3. What are the characteristics of typical angina
pectoris? Discomfort of myocardial ischemic origin (angina pectoris) is discomfort that is
precipitated by effort or emotion and promptly relieved by rest, sublingual nitroglycerin
(that is, nitroglycerin tablets that are placed under the tongue), or other rapidly
acting nitrates. Typically, the discomfort is located in the chest (usually substernal)
and described as pressing, crushing, squeezing, burning, aching, or oppressive. Sharp,
sticking, or cramping discomfort is less common. Discomfort occurring with activity
or emotion should be described specifically as to timing and usual inciting factors
(type and intensity), character, location, radiation, duration, and response to nitrate
treatment or rest.
4. What is
angina? Atypical angina describes discomfort or pain from myocardial ischemia that is felt
in places other than the chest. The common sites of cardiac pain are the inner aspect
of the left arm, neck, jaw(s), upper abdomen, and back, but the discomfort or pain
can be elsewhere. When pain of cardiac ischemic origin presents in an atypical site
in the absence of chest discomfort, the source of the pain may be difficult to diagnose.
To represent atypical angina, your discomfort or pain should have precipitating and
relieving factors similar to those of typical chest discomfort, and we must have objective
medical evidence of myocardial ischemia; for example, ECG or ETT evidence or appropriate
medically acceptable imaging.
5. What is anginal
equivalent? Often, individuals with IHD will complain of shortness of breath (dyspnea) on exertion
without chest pain or discomfort. In a minority of such situations, the shortness
of breath is due to myocardial ischemia; this is called anginal
equivalent. To represent anginal equivalent, your shortness of breath should have precipitating
and relieving factors similar to those of typical chest discomfort, and we must have
objective medical evidence of myocardial ischemia; for example, ECG or ETT evidence
or appropriate medically acceptable imaging. In these situations, it is essential
to establish objective evidence of myocardial ischemia to ensure that you do not have
effort dyspnea due to non-ischemic or non-cardiac causes.
6. What is variant angina?
angina (Prinzmetal’s angina, vasospastic angina) refers to the occurrence of anginal episodes
at rest, especially at night, accompanied by transitory ST segment elevation (or,
at times, ST depression) on an ECG. It is due to severe spasm of a coronary artery,
causing ischemia of the heart wall, and is often accompanied by major ventricular
arrhythmias, such as ventricular tachycardia. We will consider variant angina under
4.04 only if you have spasm of a coronary artery in relation to an obstructive lesion
of the vessel. If you have an arrhythmia as a result of variant angina, we may consider
your impairment under 4.05.
b. Variant angina may also occur in the absence of obstructive coronary disease. In
this situation, an ETT will not demonstrate ischemia. The diagnosis will be established
by showing the typical transitory ST segment changes during attacks of pain, and the
absence of obstructive lesions shown by catheterization. Treatment in cases where
there is no obstructive coronary disease is limited to medications that reduce coronary
vasospasm, such as calcium channel blockers and nitrates. In such situations, we will
consider the frequency of anginal episodes despite prescribed treatment when evaluating
your residual functional capacity.
c. Vasospasm that is catheter-induced during coronary angiography is not variant angina.
7. What is silent ischemia?
a. Myocardial ischemia, and even myocardial infarction, can occur without perception
of pain or any other symptoms; when this happens, we call it silent
ischemia. Pain sensitivity may be altered by a variety of diseases, most notably diabetes
mellitus and other neuropathic disorders. Individuals also vary in their threshold
b. Silent ischemia occurs most often in:
(i) Individuals with documented past myocardial infarction or established angina without
prior infarction who do not have chest pain on ETT, but have a positive test with
ischemic abnormality on ECG, perfusion scan, or other appropriate medically acceptable
(ii) Individuals with documented past myocardial infarction or angina who have ST
segment changes on ambulatory monitoring (Holter monitoring) that are similar to those
that occur during episodes of angina. ST depression shown on the ambulatory recording
should not be interpreted as positive for ischemia unless similar depression is also
seen during chest pain episodes annotated in the diary that the individual keeps while
wearing the Holter monitor.
c. ST depression can result from a variety of factors, such as postural changes and
variations in cardiac sympathetic tone. In addition, there are differences in how
different Holter monitors record the electrical responses. Therefore, we do not consider
the Holter monitor reliable for the diagnosis of silent ischemia except in the situation
described in 4.00E7b(ii).
8. What other sources of chest discomfort are
there? Chest discomfort of nonischemic origin may result from other cardiac impairments,
such as pericarditis. Noncardiac impairments may also produce symptoms mimicking that
of myocardial ischemia. These impairments include acute anxiety or panic attacks,
gastrointestinal tract disorders, such as esophageal spasm, esophagitis, hiatal hernia,
biliary tract disease, gastritis, peptic ulcer, and pancreatitis, and musculoskeletal
syndromes, such as chest wall muscle spasm, chest wall syndrome (especially after
coronary bypass surgery), costochondritis, and cervical or dorsal spine arthritis.
Hyperventilation may also mimic ischemic discomfort. Thus, in the absence of documented
myocardial ischemia, such disorders should be considered as possible causes of chest
9. How do we evaluate IHD using
a. We must have objective evidence, as described under 4.00C, that your symptoms are
due to myocardial ischemia.
b. Listing-level changes on the ECG in 4.04A1 are the classically accepted changes
of horizontal or downsloping ST depression occurring both during exercise and recovery.
Although we recognize that ischemic changes may at times occur only during exercise
or recovery, and may at times be upsloping with only junctional ST depression, such
changes can be false positive; that is, occur in the absence of ischemia. Diagnosis
of ischemia in this situation requires radionuclide or echocardiogram confirmation.
See 4.00C12 and 4.00C13.
c. Also in 4.04A1, we require that the depression of the ST segment last for at least
1 minute of recovery because ST depression that occurs during exercise but that rapidly
normalizes in recovery is a common false-positive response.
d. In 4.04A2, we specify that the ST elevation must be in non-infarct leads during
both exercise and recovery. This is because, in the absence of ECG signs of prior
infarction, ST elevation during exercise denotes ischemia, usually severe, requiring
immediate termination of exercise. However, if there is baseline ST elevation in association
with a prior infarction or ventricular aneurysm, further ST elevation during exercise
does not necessarily denote ischemia and could be a false-positive ECG response. Diagnosis
of ischemia in this situation requires radionuclide or echocardiogram confirmation.
See 4.00C12 and 4.00C13.
e. Listing 4.04A3 requires a decrease in systolic blood pressure below the baseline
level (taken in the standing position immediately prior to exercise) or below any
systolic pressure reading recorded during exercise. This is the same finding required
in 4.02B3c. See 4.00D4d for full details.
f. In 4.04B, each of the three ischemic episodes must require revascularization or
be not amenable to treatment. Revascularization means angioplasty (with or without stent placement) or bypass surgery. However, reocclusion
that occurs after a revascularization procedure but during the same hospitalization
and that requires a second procedure during the same hospitalization will not be counted
as another ischemic episode. Not amenable means that the revascularization procedure
could not be done because of another medical impairment or because the vessel was
not suitable for revascularization.
g. We will use 4.04C only when you have symptoms due to myocardial ischemia as described
in 4.00E3-4.00E7 while on a regimen of prescribed treatment, you are at risk for exercise
testing (see 4.00C8), and we do not have a timely ETT or a timely normal drug-induced
stress test for you. See 4.00C9 for what we mean by a timely test.
h. In 4.04C1 the term nonbypassed means that the blockage is in a vessel that is potentially bypassable; that is, large
enough to be bypassed and considered to be a cause of your ischemia. These vessels
are usually major arteries or one of a major artery’s major branches. A vessel that
has become obstructed again after angioplasty or stent placement and has remained
obstructed or is not amenable to another revascularization is considered a nonbypassed
vessel for purposes of this listing. When you have had revascularization, we will
not use the pre-operative findings to assess the current severity of your coronary
artery disease under 4.04C, although we will consider the severity and duration of
your impairment prior to your surgery in making our determination or decision.
1. What is an
arrhythmia? An arrhythmia is a change in the regular beat of the heart. Your heart may seem to
skip a beat or beat irregularly, very quickly (tachycardia), or very slowly (bradycardia).
2. What are the different types of arrhythmias?
a. There are many types of arrhythmias. Arrhythmias are identified by where they occur
in the heart (atria or ventricles) and by what happens to the heart's rhythm when
b. Arrhythmias arising in the cardiac atria (upper chambers of the heart) are called
atrial or supraventricular arrhythmias. Ventricular arrhythmias begin in the ventricles
(lower chambers). In general, ventricular arrhythmias caused by heart disease are
the most serious.
3. How do we evaluate arrhythmias using 4.05?
a. We will use 4.05 when you have arrhythmias that are not fully controlled by medication,
an implanted pacemaker, or an implanted cardiac defibrillator and you have uncontrolled
recurrent episodes of syncope or near syncope. If your arrhythmias are controlled,
we will evaluate your underlying heart disease using the appropriate listing. For
other considerations when we evaluate arrhythmias in the presence of an implanted
cardiac defibrillator, see 4.00F4.
b. We consider near syncope to be a period of altered consciousness, since syncope
is a loss of consciousness or a faint. It is not merely a feeling of light-headedness,
momentary weakness, or dizziness.
c. For purposes of 4.05, there must be a documented association between the syncope
or near syncope and the recurrent arrhythmia. The recurrent arrhythmia, not some other
cardiac or non-cardiac disorder, must be established as the cause of the associated
symptom. This documentation of the association between the symptoms and the arrhythmia
may come from the usual diagnostic methods, including Holter monitoring (also called
ambulatory electrocardiography) and tilt-table testing with a concurrent ECG. Although
an arrhythmia may be a coincidental finding on an ETT, we will not purchase an ETT
to document the presence of a cardiac arrhythmia.
4. What will we consider when you have an implanted cardiac defibrillator and you do
not have arrhythmias that meet the requirements of 4.05?
a. Implanted cardiac defibrillators are used to prevent sudden cardiac death in individuals
who have had, or are at high risk for, cardiac arrest from life-threatening ventricular
arrhythmias. The largest group at risk for sudden cardiac death consists of individuals
with cardiomyopathy (ischemic or non-ischemic) and reduced ventricular function. However,
life-threatening ventricular arrhythmias can also occur in individuals with little
or no ventricular dysfunction. The shock from the implanted cardiac defibrillator
is a unique form of treatment; it rescues an individual from what may have been cardiac
arrest. However, as a consequence of the shock(s), individuals may experience psychological
distress, which we may evaluate under the mental disorders listings in 12.00.
b. Most implantable cardiac defibrillators have rhythm-correcting and pacemaker capabilities.
In some individuals, these functions may result in the termination of ventricular
arrhythmias without an otherwise painful shock. (The shock is like being kicked in
the chest.) Implanted cardiac defibrillators may deliver inappropriate shocks, often
repeatedly, in response to benign arrhythmias or electrical malfunction. Also, exposure
to strong electrical or magnetic fields, such as from MRI (magnetic resonance imaging),
can trigger or reprogram an implanted cardiac defibrillator, resulting in inappropriate
shocks. We must consider the frequency of, and the reason(s) for, the shocks when
evaluating the severity and duration of your impairment.
c. In general, the exercise limitations imposed on individuals with an implanted cardiac
defibrillator are those dictated by the underlying heart impairment. However, the
exercise limitations may be greater when the implanted cardiac defibrillator delivers
an inappropriate shock in response to the increase in heart rate with exercise, or
when there is exercise-induced ventricular arrhythmia.
1. What is peripheral vascular disease
(PVD)? Generally, PVD is any impairment that affects either the arteries (peripheral arterial disease)
or the veins (venous insufficiency) in the extremities, particularly the lower extremities.
The usual effect is blockage of the flow of blood either from the heart (arterial)
or back to the heart (venous). If you have peripheral arterial disease, you may have
pain in your calf after walking a distance that goes away when you rest (intermittent
claudication); at more advanced stages, you may have pain in your calf at rest or
you may develop ulceration or gangrene. If you have venous insufficiency, you may
have swelling, varicose veins, skin pigmentation changes, or skin ulceration.
2. How do we assess limitations resulting from PVD? We will assess your limitations based on your symptoms together with physical findings,
Doppler studies, other appropriate non-invasive studies, or angiographic findings.
However, if the PVD has resulted in amputation, we will evaluate any limitations related
to the amputation under the musculoskeletal listings, 1.00.
3. What is brawny edema?
edema (4.11A) is swelling that is usually dense and feels firm due to the presence of increased
connective tissue; it is also associated with characteristic skin pigmentation changes.
It is not the same thing as pitting edema. Brawny edema generally does not pit (indent
on pressure), and the terms are not interchangeable. Pitting edema does not satisfy
the requirements of 4.11A.
4. What is lymphedema and how will we evaluate it?
a. Lymphedema is edema of the extremities due to a disorder of the lymphatic circulation; at its
worst, it is called elephantiasis. Primary lymphedema is caused by abnormal development
of lymph vessels and may be present at birth (congenital lymphedema), but more often
develops during the teens (lymphedema praecox). It may also appear later, usually
after age 35 (lymphedema tarda). Secondary lymphedema is due to obstruction or destruction
of normal lymphatic channels due to tumor, surgery, repeated infections, or parasitic
infection such as filariasis. Lymphedema most commonly affects one extremity.
b. Lymphedema does not meet the requirements of 4.11, although it may medically equal
the severity of that listing. We will evaluate lymphedema by considering whether the
underlying cause meets or medically equals any listing or whether the lymphedema medically
equals a cardiovascular listing, such as 4.11, or a musculoskeletal disorders listing,
such as 1.18. If no listing is met or medically equaled, we will evaluate any functional limitations
imposed by your lymphedema when we assess your residual functional capacity.
5. When will we purchase exercise Doppler studies for evaluating peripheral arterial
(PAD)? If we need additional evidence of your PAD, we will generally purchase exercise Doppler
studies (see 4.00C16 and 4.00C17) when your resting ankle/brachial systolic blood
pressure ratio is at least 0.50 but less than 0.80, and only rarely when it is 0.80
or above. We will not purchase exercise Doppler testing if you have a disease that
results in abnormal arterial calcification or small vessel disease, but will use your
resting toe systolic blood pressure or resting toe/brachial systolic blood pressure
ratio. (See 4.00G7c and 4.00G8.) There are no current medical standards for evaluating
exercise toe pressures. Because any exercise test stresses your entire cardiovascular
system, we will purchase exercise Doppler studies only after an MC, preferably one
with experience in the care of patients with cardiovascular disease, has determined
that the test would not present a significant risk to you and that there is no other
medical reason not to purchase the test (see 4.00C6, 4.00C7, and 4.00C8).
6. Are there any other studies that are helpful in evaluating
PAD? Doppler studies done using a recording ultrasonic Doppler unit and strain-gauge plethysmography
are other useful tools for evaluating PAD. A recording Doppler, which prints a tracing
of the arterial pulse wave in the femoral, popliteal, dorsalis pedis, and posterior
tibial arteries, is an excellent evaluation tool to compare wave forms in normal and
compromised peripheral blood flow. Qualitative analysis of the pulse wave is very
helpful in the overall assessment of the severity of the occlusive disease. Tracings
are especially helpful in assessing severity if you have small vessel disease related
to diabetes mellitus or other diseases with similar vascular changes, or diseases
causing medial calcifications when ankle pressure is either normal or falsely high.
7. How do we evaluate PAD under
a. The ankle blood pressure referred to in 4.12A and B is the higher of the pressures
recorded from the posterior tibial and dorsalis pedis arteries in the affected leg.
The higher pressure recorded from the two sites is the more significant measurement
in assessing the extent of arterial insufficiency. Techniques for obtaining ankle
systolic blood pressures include Doppler (See 4.00C16 and 4.00C17), plethysmographic
studies, or other techniques. We will request any available tracings generated by
these studies so that we can review them.
b. In 4.12A, the ankle/brachial systolic blood pressure ratio is the ratio of the
systolic blood pressure at the ankle to the systolic blood pressure at the brachial
artery; both taken at the same time while you are lying on your back. We do not require
that the ankle and brachial pressures be taken on the same side of your body. This
is because, as with the ankle pressure, we will use the higher brachial systolic pressure
measured. Listing 4.12A is met when your resting ankle/brachial systolic blood pressure
ratio is less than 0.50. If your resting ankle/brachial systolic blood pressure ratio
is 0.50 or above, we will use 4.12B to evaluate the severity of your PAD, unless you
also have a disease causing abnormal arterial calcification or small vessel disease,
such as diabetes mellitus. See 4.00G7c and 4.00G8.
c. We will use resting toe systolic blood pressures or resting toe/brachial systolic
blood pressure ratios (determined the same way as ankle/brachial ratios, see 4.00G7b)
when you have intermittent claudication and a disease that results in abnormal arterial
calcification (for example, Monckeberg’s sclerosis or diabetes mellitus) or small
vessel disease (for example, diabetes mellitus). These diseases may result in misleadingly
high blood pressure readings at the ankle. However, high blood pressures due to vascular
changes related to these diseases seldom occur at the toe level. While the criteria
in 4.12C and 4.12D are intended primarily for individuals who have a disease causing
abnormal arterial calcification or small vessel disease, we may also use them for
evaluating anyone with PAD.
8. How are toe pressures
Toe pressures are measured routinely in most vascular laboratories through one of
three methods: most frequently, photoplethysmography; less frequently, plethysmography
using strain gauge cuffs; and Doppler ultrasound. Toe pressure can also be measured
by using any blood pressure cuff that fits snugly around the big toe and is neither
too tight nor too loose. A neonatal cuff or a cuff designed for use on fingers or
toes can be used in the measurement of toe pressure.
9. How do we use listing 4.12 if you have had a peripheral
graft? Peripheral grafting serves the same purpose as coronary grafting; that is, to bypass
a narrow or obstructed arterial segment. If intermittent claudication recurs or persists
after peripheral grafting, we may purchase Doppler studies to assess the flow of blood
through the bypassed vessel and to establish the current severity of the peripheral
arterial impairment. However, if you have had peripheral grafting done for your PAD,
we will not use the findings from before the surgery to assess the current severity
of your impairment, although we will consider the severity and duration of your impairment
prior to your surgery in making our determination or decision.
1. How will we evaluate
hypertension? Because hypertension (high blood pressure) generally causes disability through its
effects on other body systems, we will evaluate it by reference to the specific body
system(s) affected (heart, brain, kidneys, or eyes) when we consider its effects under
the listings. We will also consider any limitations imposed by your hypertension when
we assess your residual functional capacity.
2. How will we evaluate symptomatic congenital heart disease? Congenital heart disease is any abnormality of the heart or the major blood vessels
that is present at birth. Because of improved treatment methods, more children with
congenital heart disease are living to adulthood. Although some types of congenital
heart disease may be corrected by surgery, many individuals with treated congenital
heart disease continue to have problems throughout their lives (symptomatic congenital
heart disease). If you have congenital heart disease that results in chronic heart
failure with evidence of ventricular dysfunction or in recurrent arrhythmias, we will
evaluate your impairment under 4.02 or 4.05. Otherwise, we will evaluate your impairment
3. What is cardiomyopathy and how will we evaluate it? Cardiomyopathy is a disease of the heart muscle. The heart loses its ability to pump
blood (heart failure), and in some instances, heart rhythm is disturbed, leading to
irregular heartbeats (arrhythmias). Usually, the exact cause of the muscle damage
is never found (idiopathic cardiomyopathy). There are various types of cardiomyopathy,
which fall into two major categories: Ischemic and nonischemic cardiomyopathy. Ischemic
cardiomyopathy typically refers to heart muscle damage that results from coronary
artery disease, including heart attacks. Nonischemic cardiomyopathy includes several
types: Dilated, hypertrophic, and restrictive. We will evaluate cardiomyopathy under
4.02, 4.04, 4.05, or 11.04, depending on its effects on you.
4. How will we evaluate valvular heart disease? We will evaluate valvular heart disease under the listing appropriate for its effect
on you. Thus, we may use 4.02, 4.04, 4.05, 4.06, or an appropriate neurological listing
5. What do we consider when we evaluate heart transplant recipients?
a. After your heart transplant, we will consider you disabled for 1 year following
the surgery because there is a greater likelihood of rejection of the organ and infection
during the first year.
b. However, heart transplant patients generally meet our definition of disability
before they undergo transplantation. We will determine the onset of your disability
based on the facts in your case.
c. We will not assume that you became disabled when your name was placed on a transplant
waiting list. This is because you may be placed on a waiting list soon after diagnosis
of the cardiac disorder that may eventually require a transplant. Physicians recognize
that candidates for transplantation often have to wait months or even years before
a suitable donor heart is found, so they place their patients on the list as soon
d. When we do a continuing disability review to determine whether you are still disabled,
we will evaluate your residual impairment(s), as shown by symptoms, signs, and laboratory
findings, including any side effects of medication. We will consider any remaining
symptoms, signs, and laboratory findings indicative of cardiac dysfunction in deciding
whether medical improvement (as defined in §§ 404.1594 and 416.994) has occurred.
6. When does an aneurysm have “dissection not controlled by prescribed
treatment,” as required under 4.10? An aneurysm (or bulge in the aorta or one of its major branches)
is dissecting when the inner lining of the artery begins to separate from the arterial wall. We
consider the dissection not controlled when you have persistence of chest pain due
to progression of the dissection, an increase in the size of the aneurysm, or compression
of one or more branches of the aorta supplying the heart, kidneys, brain, or other
organs. An aneurysm with dissection can cause heart failure, renal (kidney) failure,
or neurological complications. If you have an aneurysm that does not meet the requirements
of 4.10 and you have one or more of these associated conditions, we will evaluate
the condition(s) using the appropriate listing.
7. What is hyperlipidemia and how will we evaluate it? Hyperlipidemia is the general term for an elevation of any or all of the lipids (fats
or cholesterol) in the blood; for example, hypertriglyceridemia, hypercholesterolemia,
and hyperlipoproteinemia. These disorders of lipoprotein metabolism and transport
can cause defects throughout the body. The effects most likely to interfere with function
are those produced by atherosclerosis (narrowing of the arteries) and coronary artery
disease. We will evaluate your lipoprotein disorder by considering its effects on
8. What is Marfan syndrome and how will we evaluate
a. Marfan syndrome is a genetic connective tissue disorder that affects multiple body
systems, including the skeleton, eyes, heart, blood vessels, nervous system, skin,
and lungs. There is no specific laboratory test to diagnose Marfan syndrome. The diagnosis
is generally made by medical history, including family history, physical examination,
including an evaluation of the ratio of arm/leg size to trunk size, a slit lamp eye
examination, and a heart test(s), such as an echocardiogram. In some cases, a genetic
analysis may be useful, but such analyses may not provide any additional helpful information.
b. The effects of Marfan syndrome can range from mild to severe. In most cases, the
disorder progresses as you age. Most individuals with Marfan syndrome have abnormalities
associated with the heart and blood vessels. Your heart’s mitral valve may leak, causing
a heart murmur. Small leaks may not cause symptoms, but larger ones may cause shortness
of breath, fatigue, and palpitations. Another effect is that the wall of the aorta
may be weakened and abnormally stretch (aortic dilation). This aortic dilation may
tear, dissect, or rupture, causing serious heart problems or sometimes sudden death.
We will evaluate the manifestations of your Marfan syndrome under the appropriate
body system criteria, such as 4.10, or if necessary, consider the functional limitations
imposed by your impairment.
1. What effect does obesity have on the cardiovascular system and how will we evaluate
it? Obesity is a medically determinable impairment that is often associated with disorders
of the cardiovascular system. Disturbance of this system can be a major cause of disability
if you have obesity. Obesity may affect the cardiovascular system because of the increased
workload the additional body mass places on the heart. Obesity may make it harder
for the chest and lungs to expand. This can mean that the respiratory system must
work harder to provide needed oxygen. This in turn would make the heart work harder
to pump blood to carry oxygen to the body. Because the body would be working harder
at rest, its ability to perform additional work would be less than would otherwise
be expected. Thus, the combined effects of obesity with cardiovascular impairments
can be greater than the effects of each of the impairments considered separately.
We must consider any additional and cumulative effects of obesity when we determine
whether you have a severe cardiovascular impairment or a listing-level cardiovascular
impairment (or a combination of impairments that medically equals the severity of
a listed impairment), and when we assess your residual functional capacity.
2. How do we relate treatment to functional
status? In general, conclusions about the severity of a cardiovascular impairment cannot
be made on the basis of type of treatment rendered or anticipated. The amount of function
restored and the time required for improvement after treatment (medical, surgical,
or a prescribed program of progressive physical activity) vary with the nature and
extent of the disorder, the type of treatment, and other factors. Depending upon the
timing of this treatment in relation to the alleged onset date of disability, we may
need to defer evaluation of the impairment for a period of up to 3 months from the
date treatment began to permit consideration of treatment effects, unless we can make
a determination or decision using the evidence we have. See 4.00B4.
3. How do we evaluate impairments that do not meet one of the cardiovascular listings?
a. These listings are only examples of common cardiovascular impairments that we consider
severe enough to prevent you from doing any gainful activity. If your severe impairment(s)
does not meet the criteria of any of these listings, we must also consider whether
you have an impairment(s) that satisfies the criteria of a listing in another body
b. If you have a severe medically determinable impairment(s) that does not meet a
listing, we will determine whether your impairments(s) medically equals a listing.
(See §§404.1526 and 416.926.) If you have a severe impairment(s) that does not meet or medically equal the criteria
of a listing, you may or may not have the residual functional capacity to engage in
substantial gainful activity. Therefore, we proceed to the fourth and, if necessary,
the fifth steps of the sequential evaluation process in §§404.1520 and 416.920. If you are an adult, we use the rules in §§404.1594 or 416.994, as appropriate, when we decide whether you continue to be disabled.
Category of Impairments, Cardiovascular
4.02 Chronic heart
failure while on a regimen of prescribed treatment, with symptoms and signs described in
4.00D2. The required level of severity for this impairment is met when the requirements
in both A and B are satisfied.
A. Medically documented presence of one of the following:
1. Systolic failure (see 4.00D1a(i)), with left ventricular end diastolic dimensions
greater than 6.0 cm or ejection fraction of 30 percent or less during a period of
stability (not during an episode of acute heart failure); or
2. Diastolic failure (see 4.00D1a(ii)), with left ventricular posterior wall plus
septal thickness totaling 2.5 cm or greater on imaging, with an enlarged left atrium
greater than or equal to 4.5 cm, with normal or elevated ejection fraction during
a period of stability (not during an episode of acute heart failure);
B. Resulting in one of the following:
1. Persistent symptoms of heart failure which very seriously limit the ability to
independently initiate, sustain, or complete activities of daily living in an individual
for whom an MC, preferably one experienced in the care of patients with cardiovascular
disease, has concluded that the performance of an exercise test would present a significant
risk to the individual; or
2. Three or more separate episodes of acute congestive heart failure within a consecutive
12-month period (see 4.00A3e), with evidence of fluid retention (see 4.00D2b(ii))
from clinical and imaging assessments at the time of the episodes, requiring acute
extended physician intervention such as hospitalization or emergency room treatment
for 12 hours or more, separated by periods of stabilization (see 4.00D4c); or
3. Inability to perform on an exercise tolerance test at a workload equivalent to
5 METs or less due to:
a. Dyspnea, fatigue, palpitations, or chest discomfort; or
b. Three or more consecutive premature ventricular contractions (ventricular tachycardia),
or increasing frequency of ventricular ectopy with at least 6 premature ventricular
contractions per minute; or
c. Decrease of 10 mm Hg or more in systolic pressure below the baseline systolic blood
pressure or the preceding systolic pressure measured during exercise (see 4.00D4d)
due to left ventricular dysfunction, despite an increase in workload; or
d. Signs attributable to inadequate cerebral perfusion, such as ataxic gait or mental
disease, with symptoms due to myocardial ischemia, as described in 4.00E3-4.00E7, while on
a regimen of prescribed treatment (see 4.00B3 if there is no regimen of prescribed
treatment), with one of the following:
A. Sign- or symptom-limited exercise tolerance test demonstrating at least one of
the following manifestations at a workload equivalent to 5 METs or less:
1. Horizontal or downsloping depression, in the absence of digitalis glycoside treatment
or hypokalemia, of the ST segment of at least -0.10 millivolts (-1.0 mm) in at least
3 consecutive complexes that are on a level baseline in any lead other than aVR, and
depression of at least -0.10 millivolts lasting for at least 1 minute of recovery;
2. At least 0.1 millivolt (1 mm) ST elevation above resting baseline in non-infarct
leads during both exercise and 1 or more minutes of recovery; or
3. Decrease of 10 mm Hg or more in systolic pressure below the baseline blood pressure
or the preceding systolic pressure measured during exercise (see 4.00E9e) due to left
ventricular dysfunction, despite an increase in workload; or
4. Documented ischemia at an exercise level equivalent to 5 METs or less on appropriate
medically acceptable imaging, such as radionuclide perfusion scans or stress echocardiography.
B. Three separate ischemic episodes, each requiring revascularization or not amenable
to revascularization (see 4.00E9f), within a consecutive 12-month period (see 4.00A3e).
C. Coronary artery disease, demonstrated by angiography (obtained independent of Social
Security disability evaluation) or other appropriate medically acceptable imaging,
and in the absence of a timely exercise tolerance test or a timely normal drug-induced
stress test, an MC, preferably one experienced in the care of patients with cardiovascular
disease, has concluded that performance of exercise tolerance testing would present
a significant risk to the individual, with both 1 and 2:
1. Angiographic evidence showing:
a. 50 percent or more narrowing of a nonbypassed left main coronary artery; or
b. 70 percent or more narrowing of another nonbypassed coronary artery; or
c. 50 percent or more narrowing involving a long (greater than 1 cm) segment of a
nonbypassed coronary artery; or
d. 50 percent or more narrowing of at least two nonbypassed coronary arteries; or
e. 70 percent or more narrowing of a bypass graft vessel; and
2. Resulting in very serious limitations in the ability to independently initiate,
sustain, or complete activities of daily living.
arrhythmias, not related to reversible causes, such as electrolyte abnormalities or digitalis
glycoside or antiarrhythmic drug toxicity, resulting in uncontrolled (see 4.00A3f),
recurrent (see 4.00A3c) episodes of cardiac syncope or near syncope (see 4.00F3b),
despite prescribed treatment (see 4.00B3 if there is no prescribed treatment), and
documented by resting or ambulatory (Holter) electrocardiography, or by other appropriate
medically acceptable testing, coincident with the occurrence of syncope or near syncope
disease (cyanotic or acyanotic), documented by appropriate medically acceptable imaging (see
4.00A3d) or cardiac catheterization, with one of the following:
A. Cyanosis at rest, and:
1. Hematocrit of 55 percent or greater; or
2. Arterial O2 saturation of less than 90 percent in room air, or resting arterial PO2 of 60 Torr or less.
B. Intermittent right-to-left shunting resulting in cyanosis on exertion (e.g., Eisenmenger's
physiology) and with arterial PO2 of 60 Torr or less at a workload equivalent to 5 METs or less.
C. Secondary pulmonary vascular obstructive disease with pulmonary arterial systolic
pressure elevated to at least 70 percent of the systemic arterial systolic pressure.
transplant. Consider under a disability for 1 year following surgery; thereafter, evaluate residual
impairment under the appropriate listing.
of aorta or major
branches, due to any cause (e.g., atherosclerosis, cystic medial necrosis, Marfan syndrome,
trauma), demonstrated by appropriate medically acceptable imaging, with dissection
not controlled by prescribed treatment (see 4.00H6).
4.11 Chronic venous
insufficiency of a lower extremity with incompetency or obstruction of the deep venous system and
one of the following:
A. Extensive brawny edema (see 4.00G3) involving at least two-thirds of the leg between
the ankle and knee or the distal one-third of the lower extremity between the ankle
B. Superficial varicosities, stasis dermatitis, and either recurrent ulceration or
persistent ulceration that has not healed following at least 3 months of prescribed
disease, as determined by appropriate medically acceptable imaging (see 4.00A3d, 4.00G2,
4.00G5, and 4.00G6), causing intermittent claudication (see 4.00G1) and one of the
A. Resting ankle/brachial systolic blood pressure ratio of less than 0.50.
B. Decrease in systolic blood pressure at the ankle on exercise (see 4.00G7a and 4.00C16-4.00C17)
of 50 percent or more of pre-exercise level and requiring 10 minutes or more to return
to pre-exercise level.
C. Resting toe systolic pressure of less than 30 mm Hg (see 4.00G7c and 4.00G8).
D. Resting toe/brachial systolic blood pressure ratio of less than 0.40 (see 4.00G7c).