TN 37 (10-26)
DI 34001.016 Cardiovascular Disorders
4.00 CARDIOVASCULAR
DISORDERS
(Effective date: 10/30/2026)
A. How
do we define cardiovascular disorders and cardiovascular
terms?
1. What do we mean by a cardiovascular
disorder?
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 disorders result from one or more of four consequences of heart
disease:
(i) Chronic heart failure (chronic HF) or ventricular dysfunction.
(ii) Discomfort or pain due to myocardial ischemia, with or without necrosis of the
heart muscle.
(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) Hypoxemia (reduced oxygen concentration in the blood) due to right-to-left shunt
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 disorders? The listings in this section describe cardiovascular disorders based on the medical
and other evidence, including response to a regimen of prescribed treatment and functional
limitations.
3. What do the following terms or phrases mean in these
listings?
a. Medical consultant is a person defined in §§ 404.1616(a) and 416.1016(a) of this chapter. 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 consultant.
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.
By “exceptions,” we mean brief periods when the required finding(s) is greatly reduced
or gone. These periods are so brief or inconsequential, the required finding(s) remains
a factor in the person's condition.
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. By “improvement
of sufficient duration,” we mean the finding is greatly reduced or not present for
long enough that the required finding(s) is no longer a factor in the person's condition.
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
review.
B.
What documentation do we need to evaluate cardiovascular
disorders?
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 disorder. 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 we already
have.
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 medical source(s). 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 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 disorder, medically equals a listing,
or we may find you disabled at a later step in the evaluation process based on a 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
we already have, a longitudinal record is still important. In instances when there
is no or insufficient longitudinal evidence, we may purchase a consultative examination(s)
to help us establish the existence, 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
attack);
(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 cardiomyopathy.
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
case.
5. Will we purchase any studies? In appropriate situations, we may purchase studies necessary to substantiate the
existence of a medically determinable impairment or to document the severity of your
impairment, generally after we have evaluated the 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 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 a catheterization are part of the existing evidence we have, we will consider them
together with the other relevant evidence. See 4.00C15a.
C.
How do we use cardiovascular test
results?
1. What is an ECG?
a. 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 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; and
(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 4.02B2, 4.04A, 4.06B, and
4.08A2. 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
person 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.
4. Do ETTs have 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.
5. How does an ETT with measurement of maximal or peak oxygen uptake
(VO2) differ from other ETTs? Occasionally, medical evidence will include the results of an ETT with VO2, which is also called a cardiopulmonary exercise test 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.)
person 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). In listings 4.02B2, 4.06B, and 4.08A2, we use the peak VO2 (oxygen uptake) measurement when evaluating the results of a cardiopulmonary exercise
test.
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 disorder 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 medical source (see §§ 404.1502 and 416.902 of this chapter) for a cardiovascular disorder, 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 not override the medical source's conclusion about the
risk of exercise testing to you. In the rare situation in which the MC does override
the medical source's conclusion, the MC must prepare a written rationale documenting
the reasons for overriding the conclusion.
d. If you do not have a medical source or we cannot obtain a statement from your medical
source, the MC is responsible for assessing the risk of 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 test?
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 mmHg);
(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 mmHg or greater;
(x) Severe arterial hypertension (systolic greater than 200 mmHg or diastolic greater
than 110 mmHg); or
(xi) Hypertrophic cardiomyopathy with a systolic gradient of 50 mmHg 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
and legs.
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
capacity.
(i) Acute myocardial infarction;
(ii) Surgical myocardial revascularization (bypass surgery);
(iii) Other open-heart surgical procedures; or
(iv) Percutaneous transluminal coronary angioplasty (PTCA) or percutaneous coronary
intervention (PCI) 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 until you are
ready and there are no medical reasons that prevent us from purchasing 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 disorder.
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
impairment.
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
or watts.
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
evidence?
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.
b. Cardiac catheterization reports commonly include an evaluation of each main coronary
artery and whether there is evidence of obstruction, as well as the grade of obstruction
(percent stenosis). Cardiac catheterization reports may include information about
the pressures of left and right side of the heart, evidence of coronary artery size
and flow patterns, and chamber size. These reports may also include evaluation of
left ventricular wall motion, left ventricular ejection fraction (left ventriculography),
fractional flow reserve (FFR) (a measure of flow access across an obstruction), and
the instantaneous wave-free ratio (iFR) (a measure of stenosis severity).
16. What details should exercise Doppler test reports
contain? 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, changes in
the person's condition during exercise (including the presence and location of leg
symptoms), and the reasons for stopping exercise if the expected level of exercise
was not attained. If the exercise Doppler test was done to evaluate peripheral vascular
disease, the report must also provide the blood pressures at the ankle and other pertinent
sites measured after exercise, and also provide 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.
D. How do we evaluate chronic heart
failure?
1. What is chronic heart failure (chronic HF)?
a. Heart failure 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 chronic HF. Ejection
fraction (EF) is the percentage of the blood in the ventricle actually pumped out
with each contraction. EF in heart failure is a continuum ranging from low EF due
to muscle dysfunction to preserved EF resulting from high intracardiac pressures.
We consider heart failure to be chronic when the condition persists or recurs over
time despite treatment. There are two main types of chronic HF:
(i) Heart failure with reduced EF (HFrEF) or predominant systolic
dysfunction is characterized by the inability of the heart to contract normally and expel sufficient
blood due to a dilated, poorly contracting left ventricle, and
(ii) Heart failure with preserved EF (HFpEF) or predominant
diastolic dysfunction is characterized by the inability of the heart to relax and fill normally due to
a thickened ventricular muscle, poor ability of the left ventricle to distend, and
increased ventricular filling pressure.
b. Chronic HF 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. If the chronic HF is the result of primary pulmonary
hypertension secondary to disease of the lung, we evaluate your impairment under the
listings in 3.00 (for example, 3.09) or 4.00, as appropriate. For the purposes of 4.02B3, a finding of elevated B-type
natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP)
in the blood assists in differentiating chronic HF from non-heart failure symptoms.
2. What evidence of chronic HF do we need?
a. Cardiomegaly or ventricular dysfunction must be present and demonstrated by appropriate
medically acceptable imaging, such as cardiac magnetic resonance imaging (MRI), chest
x-ray, echocardiography (M-Mode, 2-dimensional, and Doppler), radionuclide studies,
or cardiac catheterization.
(i) Abnormal cardiac imaging provides objective measures of both left ventricular
function and structural abnormality in heart failure. Examples of abnormal findings
include increased left ventricular end-diastolic dimension (LVEDD), decreased EF,
increased left atrial chamber size, increased left atrial volume index (LAVI), increased
ventricular filling pressures measured at cardiac catheterization, or increased left
ventricular wall or septum thickness.
(ii) An LVEDD greater than 6.8 cm for males or 6.1 cm for females, or an EF of 30 percent or less during a period of stability (that is, not during an
episode of exacerbation of heart failure) may be associated clinically with systolic
dysfunction.
(iii) LAVI is measured in milliliters (ml) indexed to body surface area (BSA) measured
in squared meters (m2 ). Indexing is a method of standardizing measurements to different body sizes. Diastolic
dysfunction may be clinically associated with LAVI of 40 ml, BSA/m2 or greater. The imaging report will contain a measurement for the left atrium volume.
The index is calculated by dividing the left atrium volume by BSA.
(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 chronic HF may be controlled by prescribed
treatment.
(vi) Other findings on an echocardiogram report (such as an LVEDD indexed to BSA)
may be at least of medically equal significance to required findings in the listing
criteria. These findings may be evaluated under our medical equivalence policy, as
appropriate. See §§ 404.1526 and 416.926 of this chapter.
b. Your medical history and physical examination should describe characteristic symptoms
and signs of pulmonary or systemic congestion (fluid retention) 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.
People with chronic HF may also experience shortness of breath upon 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 congestion may be controlled by
prescribed treatment or may not be present at the time of evaluation.
3. Is it safe for you to have an ETT if you have chronic HF? The presence of chronic HF 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. ETT
has been used safely in people with chronic HF. Therefore, we may purchase an ETT
for evaluation under 4.02B2 if an MC, preferably one experienced in the care of patients
with cardiovascular disease, determines that the test poses no significant risk to
you. ST segment changes from digitalis use in the treatment of chronic HF do not preclude
the purchase of an ETT. (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.)
4. How do we evaluate chronic HF using 4.02?
a. We must have objective evidence, as described in 4.00D2, that you have chronic
HF.
b. To meet the required level of severity for this listing, your impairment must satisfy
the requirements of the criteria in A and B or satisfy either C or D.
c. In 4.02B1, we follow a two-part process to evaluate your impairment. Your impairment
must satisfy the requirements in the first part of this process before we will move
to the second part.
(i) Your impairment satisfies the first part if a medical source has concluded that
the performance of an ETT would present a significant risk to you. This medical source,
such as a cardiologist, may be providing your care. If your case record does not include
a conclusion from a medical source that an ETT would present a significant risk to
you, an MC as defined in 4.00A3a may make such a conclusion if evidence in your case
record supports it.
(ii) In the second part of the process, we will evaluate activities of daily living
(ADL). ADLs include, but are not limited to, such activities as doing household chores,
grooming and hygiene, shopping at a grocery store, taking public transportation, or
paying bills. We will assess whether you have persistent symptoms of chronic heart
failure (for example, easy fatigue, weakness, shortness of breath, or chest discomfort)
at rest or with activity that very seriously limit your ability to perform ADLs independently,
appropriately, effectively, and on a sustained basis. Even if you are able to perform
some ADLs, we may find your ability is very seriously limited and that your impairment
satisfies the second part of the evaluation.
d. Listing 4.02B2b requires a decrease in systolic blood pressure below the baseline
level or below any systolic pressure reading recorded during exercise. We have this
requirement 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 mmHg 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 people 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.
e. How do we evaluate chronic HF treated with a mechanical
circulatory support device? We use 4.02D1 to evaluate chronic HF treated with an implanted mechanical circulatory
support device (MCSD), such as a left ventricle assistive device (LVAD) or a right
ventricle assistive device (RVAD). Implanted MCSDs are intended for long-term circulatory
support in helping the heart pump blood. For the purposes of 4.02D1, an MCSD does
not include extracorporeal membrane oxygenation (ECMO) or devices using Impella technology.
Although these are forms of mechanical circulatory support, we do not include them
in 4.02D1 because they are intended only for short-term circulatory support (maximum
30 days), used in a setting of imminent or actual cardiac arrest.
E.
How
do we evaluate ischemic heart disease?
1. What is ischemic heart disease (IHD)? IHD is a condition in which the heart muscle does not receive enough blood to function
normally (ischemia). Ischemia can result when one or more of your coronary arteries
is narrowed or obstructed or, in rare situations, constricted due to vasospasm. 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). In the absence of coronary artery obstruction, ischemia can also occur
due to coronary microvascular dysfunction, which results in the heart muscle getting
insufficient oxygen.
2. What causes chest discomfort of myocardial
origin?
a. Chest discomfort of myocardial ischemic origin, commonly known as angina pectoris,
is usually caused by obstructive coronary artery disease (CAD). However, ischemic
discomfort may be caused by a noncoronary artery impairment, such as aortic stenosis,
hypertrophic cardiomyopathy, pulmonary hypertension, or anemia. Ischemic chest discomfort
may also be caused by microvascular coronary artery dysfunction with non-obstructive
CAD or in the absence of CAD.
b. Instead of typical angina pectoris, some people 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 atypical 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, people 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?
a. Variant 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 CAD. 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. In the absence of obstructive CAD,
the treatment of ischemia due to coronary vasospasm or microvascular dysfunction is
limited to medications such as calcium channel blockers, statins, 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. People also vary in their threshold for pain.
b. Silent ischemia occurs most often in:
(i) People 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
imaging.
(ii) People 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 person keeps while wearing
the Holter monitor.
(iii) People who have diabetes mellitus with neuropathy. People with diabetes mellitus
can have a higher threshold for pain because of the neuropathy and may not feel chest
pain or discomfort from cardiac ischemia.
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 cardiovascular disorders,
such as pericarditis. Noncardiac disorders may also produce symptoms mimicking that
of myocardial ischemia. These disorders 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 discomfort.
9. How do we evaluate IHD using 4.04?
a. We must have objective evidence, as described under 4.00C, that your symptoms are
due to myocardial ischemia.
b. In 4.04A, we need evidence, such as an ECG interpretation, from an acceptable medical
source who reviewed your ETT findings and found them positive for ischemia. These
ETT findings may include ECG tracings or systolic blood pressure measurements. If
your case record does not have such an interpretation from an acceptable medical source,
an MC, as defined in 4.00A3a, may review your ETT findings and interpret them as being
positive for ischemia if evidence in your case record supports it.
(i) ETT findings may show the classically accepted changes in ECG tracings of horizontal
or down sloping ST depression or of ST elevation. For example, ECG tracings may show
horizontal or down sloping 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
three consecutive complexes that are on a level baseline in any lead other than a
VR, and depression of at least −0.10 millivolts lasting for at least 1 minute of recovery.
Alternatively, the ECG tracings may show at least 0.10 millivolt (1 mm) ST elevation
above resting baseline in non-infarct leads during both exercise and 1 or more minutes
of recovery.
(ii) ETT findings may also show a decrease of 10 mmHg or more in systolic pressure
below the baseline systolic blood pressure or the preceding systolic pressure measured
during exercise due to left ventricular dysfunction, despite an increase in workload.
This finding is the same finding required in 4.02B2b. See 4.00D4d for full details.
c. In 4.04C, each ischemic episode must result in an unplanned hospitalization. Examples
of ischemic episodes that may result in unplanned hospitalizations include unplanned
revascularizations, myocardial infarctions, unstable angina, or dysrhythmias. Revascularization means angioplasty (with or without stent placement) or bypass surgery.
(i) How do we calculate separate ischemic episodes? 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. If you are hospitalized for documented myocardial infarction and
have a revascularization procedure during the same hospitalization, this event will
be counted as one ischemic episode.
(ii) How do we evaluate ischemic episodes not amenable to revascularizations? If your
ischemic episodes are not amenable to revascularization, we will evaluate them using
the appropriate listing (for example, 4.04D). 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.
d. We will use 4.04D 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 ETT
(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.
e. In 4.04D1, fractional flow reserve (FFR) is a measurement of the pressure differences
across an obstructive lesion, giving an estimate of the severity of stenosis. An FFR
measurement of 1.0 indicates normal blood flow. An FFR measurement equal to or less
than 0.80 indicates stenosis capable of producing serious myocardial ischemia in an
artery appropriate for revascularization. An FFR measurement that is greater than
0.80 indicates stenosis not likely to produce significant ischemia. FFR also helps
define the adequacy of collateral flow that directly affects function in ischemic
heart disease.
f. In 4.04D2, instantaneous wave-free ratio (iFR) measures the pressure ratio during
a specified period of diastole when the coronary resistance is minimized and stable.
An iFR value equal to or less than 0.89 indicates a hemodynamically significant stenosis
that is appropriately treated with percutaneous coronary intervention.
g. In 4.04D3 and 4.04D4, 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 the listings. When you have had
revascularization, we will not use the pre-operative findings to assess the current
severity of your coronary artery disease under 4.04D, although we will consider the
severity and duration of your impairment before your surgery in making our determination
or decision.
F.
How do we evaluate
arrhythmias?
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). Although
we use the term arrhythmia in the listings, the term “dysrhythmia” may also be used in the medical evidence
to describe this condition.
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
they occur.
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 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 do 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 people
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 people
with cardiomyopathy (ischemic or non-ischemic) and reduced ventricular function. However,
life-threatening ventricular arrhythmias can also occur in people with little or no
ventricular dysfunction. The shock from the implanted cardiac defibrillator rescues
a person from what may have been cardiac arrest. However, as a consequence of the
shock(s), similar to the effects of treatments for other cardiovascular disease, a
person may experience psychological distress, which we may evaluate under the listings
in 12.00.
b. Most implantable cardiac defibrillators have rhythm-correcting and pacemaker capabilities.
In some people, 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 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 people 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.
G.
How
do we evaluate peripheral vascular
disease?
1. What is peripheral vascular disease (PVD)? Generally, PVD is any impairment that affects either the arteries (peripheral artery 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 artery disease, you may have
pain in your leg after walking a distance that goes away when you rest (intermittent
claudication); at more advanced stages, you may have pain in your leg or foot at rest
or you may develop ulceration or gangrene. Neuropathy may mask these typical symptoms.
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
and Doppler studies or other appropriate diagnostic techniques. However, if the PVD
has resulted in amputation, we will evaluate any limitations related to the amputation
under the listings in 1.00.
3. What is brawny edema? Brawny 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 do 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. Symptoms
of lymphedema include but are not limited to swelling in an extremity, changes in
skin, and pain or sensory changes in the affected area. The symptoms may limit movement
in affected joints.
b. Lymphedema does not meet the requirements of 4.11, although it may medically equal
the listing. We evaluate lymphedema by considering whether the underlying cause meets
or medically equals any listing, or whether the lymphedema medically equals a cardiovascular
disorders listing such as 4.11 or a listing in 1.00 or 14.00. If no listing is met or medically equaled, we 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
artery disease (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 index 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 index. (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 or
air 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 evaluation tool that compares waveforms
in normal and compromised peripheral blood flow. Qualitative analysis of the Doppler
waveforms and plethysmographic tracings is helpful in the overall assessment of the
severity of the occlusive disease. Tracings help 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. When there is evidence of medial calcification of the ankle arteries
or the ankle-brachial index is 0.50 or greater, other appropriate tests for PAD include
magnetic resonance angiography, computed tomography angiography, contrast angiography,
and graded treadmill tests.
7. How do we evaluate PAD under 4.12?
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 index 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. The
criterion in 4.12A is met when your resting ankle-brachial index is less than 0.50.
If your resting ankle-brachial index 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 indices
(determined the same way as the ankle-brachial index, 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 people 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 measured? 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 or
stenting? 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
artery impairment. However, if you have had peripheral grafting or stenting 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.
H.
How
do we evaluate congenital heart disease?
1. What is congenital heart disease? Congenital heart disease is any abnormality of the heart or the major blood vessels
that is present at birth. Congenital heart disease includes abnormal structure of
the individual heart chambers, valves, and blood vessels, and abnormal relative relationship
of the chambers to each other that alters the normal pattern of blood flow. Surgery
in childhood is the usual treatment, and with improving surgical techniques and medical
management, more children with congenital heart disease are surviving into adulthood.
Rarely, a person with congenital heart disease may not have received the usual surgery
in childhood, and later, as an adult, they are no longer a surgical candidate, as
for example, in Eisenmenger syndrome.
2. What is Eisenmenger syndrome? Eisenmenger syndrome refers to any surgically untreated congenital heart defect with
intracardiac communication that over time leads to pulmonary hypertension, reversal
of blood flow, and hypoxemia.
a. Lesions in Eisenmenger syndrome, such as large septal defects, are characterized
by elevated pulmonary pressures or a high pulmonary flow rate. In response, the pulmonary
blood vessels pathologically change, leading eventually to pulmonary hypertension.
Development of Eisenmenger syndrome represents a point at which pulmonary hypertension
is irreversible and the cardiac lesion is likely inoperable.
b. Examples of congenital heart disease that if untreated may cause pulmonary vascular
disease leading to Eisenmenger syndrome include atrial septal defect (ASD), ventricular
septal defect (VSD), and large patent ductus arteriosus (PDA).
3. What is single ventricle? The term “single ventricle” (also known as “single ventricle physiology” or “functional
single ventricle”) describes a diverse group of congenital cardiac anomalies sharing
the common feature that only one of the two heart ventricles is adequately developed.
At birth, one ventricle must functionally do the work of two, pumping blood for both
the body (systemic) and the lungs (pulmonary). Because of this feature, the ultimate
plan for cardiac reconstruction is similar for most of these anomalies. People with
single ventricle will generally undergo staged reconstructive “Fontan procedures,”
ultimately resulting in a “Fontan circulation.” Fontan circulation describes the hemodynamic
state in which virtually all systemic venous return-blood passively flows directly
into the pulmonary arteries via surgical or catheter-placed shunts, without the blood
passing through a ventricle. The Fontan circulation results in difficulties augmenting,
and sometimes maintaining, cardiac output. Some of the anomalies described as single
ventricle include the following:
(a) Hypoplastic left heart syndrome;
(b) Hypoplastic right ventricle;
(c) Tricuspid valve atresia;
(d) Pulmonary atresia with intact ventricular septum;
(e) Double inlet left ventricle; and
(f) Some variations of double outlet right ventricle.
4. How do we evaluate conditions associated with congenital heart
disease?
a. We evaluate congenital heart disease that results in chronic heart failure with
evidence of ventricular dysfunction or in recurrent arrhythmias under 4.02 or 4.05,
respectively. Otherwise, we evaluate your impairment under 4.06.
b. We evaluate pulmonary hypertension due to congenital heart disease under 4.06B
or 4.06C. We evaluate pulmonary hypertension not due to congenital heart disease under
the listings in 3.00 (for example, 3.09).
c. We need pulse oximetry measurements documented by medical sources using methods
consistent with the prevailing state of medical knowledge and clinical practice to
evaluate chronic hypoxemia in congenital heart disease under 4.06A3. These pulse oximetry
measurements also must be consistent with the other evidence in the case record.
d. We evaluate single ventricle physiology under 4.06D and will consider you disabled
if your medical evidence documents that you have any congenital heart disorder that
results in single ventricle physiology (functional single ventricle). In addition
to the above congenital heart disorders, examples of palliative surgical procedures
that indicate single ventricle physiology include the Glenn, Fontan, and Norwood procedures.
I.
How
do we evaluate other cardiovascular
disorders?
1. How do we evaluate hypertension? Hypertension (high blood pressure) over time may significantly raise the pressures in the heart
to the point of ineffective heart muscle function known generally as hypertensive
heart disease that we can evaluate under 4.02. Other body systems, such as the brain,
kidneys, or eyes may also be affected. We evaluate these impairments by reference
to the specific body system(s) that is affected. We will also consider any limitations
imposed by your hypertension when we assess your residual functional capacity.
2. What is cardiomyopathy and how do 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).
a. 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, but is not limited to several types:
dilated, hypertrophic, restrictive, and arrhythmogenic. Cardiomyopathy includes hypertrophic
cardiomyopathy, endomyocardial fibrosis, or cardiac amyloidosis AL (light-chain) type.
b. We evaluate cardiomyopathy under 4.08. Depending on the underlying cause of the
cardiomyopathy or its effects on you, we may also evaluate your cardiomyopathy under
4.02, 4.04, or 4.05. If your cardiomyopathy results in vascular insult to the brain,
we may also evaluate it under 11.04.
c. Under 4.08A1a, we need a conclusion from a medical source that the performance
of an exercise test would present a significant risk to you. If your case record does
not have a conclusion from a medical source that an exercise test would present a
significant risk to you, an MC as defined in 4.00A3a may make such a conclusion if
evidence in your case record supports it.
3. How do we evaluate valvular heart disease? We evaluate aortic valvular disease under 4.07. We may also evaluate aortic valvular
disease, as well as other forms of valvular disease, under 4.02, 4.04, 4.05, 4.06,
or a listing in 11.00, depending on its effects on you.
4. What do we consider when we evaluate heart transplant
recipients?
a. After your heart transplant, we will consider you disabled under 4.09 for 1 year
following the surgery because there is a greater likelihood of rejection of the organ
and infection during the first year. If you develop cardiac allograft vasculopathy
after your transplant, we will evaluate this impairment under 4.16.
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
as permitted.
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 the evidence in your case
record, including any side effects of medication. We will consider all evidence indicative
of cardiac dysfunction in deciding whether medical improvement (as defined in §§ 404.1594 and 416.994 of this chapter) has occurred.
5. What is cardiac allograft vasculopathy and how do we evaluate
it? Cardiac allograft vasculopathy (CAV) may affect a person who has received a heart transplant and involves thickening
in the walls of the coronary arteries that may progress quickly into serious vascular
stenosis and heart dysfunction. Stenosis in CAV is caused by a pathological process
different from classic atherosclerosis and treatment often is only palliative. We
evaluate CAV under 4.16.
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 do 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 you.
8. What is Marfan syndrome and how do we evaluate
it?
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 people 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 cardiovascular manifestations of your Marfan syndrome under the
appropriate criteria, such as 4.10, or, if necessary, consider the functional limitations
imposed by your impairment.
c. Other genetic connective tissue disorders, such as Loeys-Dietz syndrome or Ehlers-Danlos
syndrome, may have abnormalities associated with the heart and blood vessels. We will
evaluate the cardiovascular manifestations of your genetic connective tissue disorder
under the appropriate criteria, such as 4.10, or, if necessary, consider the functional
limitations imposed by your impairment.
J. How do we evaluate other
issues that affect the cardiovascular system?
1. How do we consider the effects of obesity when we evaluate your
cardiovascular disorder? Obesity is a medically determinable impairment that may be associated with cardiovascular
disorders. The additional body mass may make it harder for the chest and lungs to
expand or may cause the heart to work harder to pump blood to carry oxygen to the
body. The combined effects of obesity with a cardiovascular disorder can be greater
than the effects of each of the impairments considered separately. We consider the
additional and cumulative effects of obesity when we determine whether you have a
severe cardiovascular disorder, a listing-level cardiovascular disorder, 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 disorder cannot be
made on the basis of the 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 consider hospitalizations? When we evaluate hospitalizations for chronic heart failure (4.02B3), ischemic heart
disease (4.04E), congenital heart disease (4.06E), and cardiomyopathy (4.08D), the
hospitalizations do not all have to be for the same cardiovascular disorder(s). They
may be for three different exacerbations or complications resulting from your cardiovascular
disorder. The hospitalizations must be at least 30 days apart, and each one must last
at least 48 hours, including hours in a hospital emergency department immediately
before the hospitalization.
K. How do we evaluate
cardiovascular disorders that do not meet one of these
listings?
1. These listings are only examples of common cardiovascular disorders that we consider
severe enough to prevent you from doing any gainful activity. If your 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
system.
2. If you have a severe medically determinable impairment(s) that does not meet a
listing, we will determine whether your impairment(s) medically equals a listing.
See §§ 404.1526 and 416.926 of this chapter. If your impairment(s) does not meet or medically equal a listing,
you may or may not have the residual functional capacity to engage in substantial
gainful activity. We will proceed to the fourth step and, if necessary, the fifth
step of the sequential evaluation process in §§ 404.1520 and 416.920 of this chapter. We will use the rules in §§ 404.1594 or 416.994 of this chapter, as appropriate, when we decide whether you continue to be disabled.
4.01 Category of Impairments, Cardiovascular
Disorders
4.02 Chronic heart failure (see 4.00D) 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
are satisfied by A and B; or C alone; or D alone.
A. Medically documented presence of one of the following:
1. Heart failure with reduced ejection fraction documented by appropriate medically
acceptable imaging during a period of stability (not during an episode of exacerbation
of heart failure), with either a. or b.
a. Left ventricular end diastolic dimension greater than 6.8 cm for males or 6.1 cm
for females during a period of stability (not during an episode of exacerbation of
heart failure); or
b. Ejection fraction of 30 percent or less during a period of stability (not during
an episode of exacerbation of heart failure); OR
2. Heart failure with preserved ejection fraction documented by appropriate medically
acceptable imaging during a period of stability (not during an episode of exacerbation
of heart failure), with either a. or b.
a. Left ventricular posterior wall plus septal thickness totaling 2.5 cm or greater,
with an enlarged left atrium greater than or equal to 4.5 cm, or
b. Left atrial volume index (LAVI) greater than or equal to 40 ml, BSA/m2 (milliliters to body surface area in squared meters).
AND
B. Resulting in one of the following:
1. Recurrent (see 4.00A3c) symptoms of heart failure, resulting in both a and b:
a. A medical source (see 4.00D4c(i)) has concluded that the performance of an exercise
test would present a significant risk to the person; and
b. Very serious limitation in the ability to perform activities of daily living independently,
appropriately, effectively, and on a sustained basis; or
2. Inability to perform on an exercise tolerance test at a workload equivalent to
5 METs or less if using a standard treadmill (or bicycle) test without gas exchange,
or at 15 ml/kg/min peak VO2 (oxygen consumption) on a cardiopulmonary exercise test, due to either a or b.
a. Dyspnea, fatigue, palpitations, or chest discomfort; or
b. Decrease of 10 mmHg 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
3. Exacerbations or complications of chronic heart failure (see 4.00D1b) requiring
three hospitalizations within a consecutive 12-month period (see 4.00A3e) and at least
30 days apart. Each hospitalization must last at least 48 hours, including hours in
a hospital emergency department immediately before the hospitalization (see 4.00J3);
OR
C. Heart failure with left ventricular ejection fraction of 20 percent or less while
on a regimen of prescribed therapy, on two evaluations at least 90 days apart within
a consecutive 12-month period (see 4.00A3e) during a period of stability (not during
an episode of exacerbation of heart failure);
OR
D. One of the following while hospitalized, at home, or both:
1. An implanted mechanical circulatory support device except extracorporeal membrane
oxygenation (ECMO) (see 4.00D4e). Consider under a disability for 1 year from the
date of implantation; after that, evaluate any residual impairment(s) under the criteria
for the affected body system.
2. Continuous intravenous administration of inotropic medication (for example, milrinone)
for at least 30 consecutive days. Consider under a disability for 1 year from the
date of initiation of the treatment; after that, evaluate any residual impairment(s)
under the criteria for the affected body system.
4.03 [Reserved]
4.04 Ischemic heart disease (see 4.00E), with symptoms due to myocardial ischemia, while on a regimen of prescribed
treatment (see 4.00B3 if there is no regimen of prescribed treatment), with A, B,
C, D, or E:
A. Inability to perform on an exercise tolerance test at a workload equivalent to 5
METs or less with findings interpreted by an acceptable medical source as positive
for ischemia (see 4.00E9b).
OR
B. Ischemic response with exercise or pharmacological (drug-induced) stress testing
(see 4.00C14) on medically appropriate imaging, with either 1 or 2:
1. At least two reversible or fixed regional myocardial perfusion defects and either
a or b:
a. Transient ischemic dilatation; or
b. Resting left ventricular ejection fraction of less than 50 percent; or
2. At least two reversible or fixed regional wall motion abnormalities and either
a or b:
a. Decrease in left ventricular ejection fraction during testing; or
b. Resting left ventricular ejection fraction of less than 50 percent.
OR
C. Documentation of three separate ischemic episodes (see 4.00E9c) requiring unplanned
hospitalization (inpatient or observation status) within a consecutive 12-month period
(see 4.00A3e).
OR
D. Coronary artery disease, documented by coronary angiography (obtained independently
of Social Security disability evaluation) with 1, 2, 3 or 4:
1. Fractional flow reserve (FFR) (see 4.00E9e) measurement of equal to or less than
0.80 of a proximal segment or mid segment coronary artery not amenable to revascularization
(see 4.00E9c(ii)).
2. Instantaneous wave-free ratio (iFR) (see 4.00E9f) measurement of equal to or less
than 0.89 of a proximal segment or mid segment coronary artery not amenable to revascularization
(see 4.00E9c(ii)).
3. History of coronary artery bypass graft surgery with manifestations of 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 a, b, c, or d:
a. 50 percent or more stenosis of a nonbypassed left main coronary artery; or
b. 70 percent or more stenosis in the proximal segment or mid segment of another nonbypassed
coronary artery; or
c. 50 percent or more stenosis in the proximal segment or mid segment of at least
two nonbypassed coronary arteries; or
d. 70 percent or more stenosis of a bypass graft vessel.
4. Resting left ventricular ejection fraction of less than 50 percent while medically
stable (see 4.00B4) with manifestations of 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 a, b, or c:
a. 50 percent or more stenosis of a nonbypassed left main coronary artery; or
b. 70 percent stenosis in the proximal segment or mid segment of another nonbypassed
coronary artery; or
c. 50 percent or more stenosis in the proximal segment or mid segment of at least
two nonbypassed coronary arteries.
OR
E. Exacerbations or complications of ischemic heart disease (see 4.00E2-4.00E7) requiring
three hospitalizations within a consecutive 12-month period (see 4.00A3e) and at least
30 days apart. Each hospitalization must last at least 48 hours, including hours in
a hospital emergency department immediately before the hospitalization (see 4.00J3).
4.05 Recurrent arrhythmias (see 4.00F), not related to reversible causes such as electrolyte abnormalities or
digitalis glycoside or antiarrhythmic drug toxicity, while on a regimen of prescribed
treatment (see 4.00B3 if there is no prescribed treatment), demonstrated by both A
and B:
A. Coincident with recurrent (see 4.00A3c) episodes of cardiac syncope or near syncope
(see 4.00F3b).
AND
B. Documented by either 1 or 2:
1. Resting or ambulatory (Holter) electrocardiography; or
2. Other appropriate medically acceptable testing.
4.06 Congenital heart disease (see 4.00H), documented by appropriate medically acceptable imaging (see 4.00A3d)
or cardiac catheterization, with A, B, C, D, or E:
A. Chronic hypoxemia, and 1, 2, or 3:
1. Hematocrit of 55 percent or greater on two evaluations at least 90 days apart within
a consecutive 12-month period (see 4.00A3e); or
2. Arterial blood gas test measurement obtained at rest while breathing room air,
as described in either a or b:
a. SaO2 (arterial oxygen saturation) less than or equal to 89 percent; or
b. PO2 or PaO2 (partial pressure of oxygen) less than or equal to 60 mmHg; or
3. SpO2 (percentage of oxygen saturation of blood hemoglobin) measured by pulse oximetry
either at rest, during a 6-minute walk test (6MWT), or after a 6MWT, while breathing
room air, less than or equal to 87 percent on three evaluations at least 30 days apart
within a consecutive 12-month period (see 4.00A3e).
OR
B. Intermittent right-to-left shunting (for example, Eisenmenger syndrome; see 4.00H2)
during cardiopulmonary exercise testing while breathing room air, resulting in oxygen
desaturation on exertion at a workload equivalent to 5 METs or less, or peak VO2 (oxygen uptake) of 15.0 ml/kg/min or less, and arterial blood gas test measurement, with either 1 or 2:
1. SaO2 less than or equal to 89 percent; or
2. PO2 or PaO2 less than or equal to 60 mmHg.
OR
C. Pulmonary hypertension documented by cardiac catheterization while medically stable,
as described in 1, 2, or 3:
1. Pulmonary arterial systolic pressure elevated to at least 70 percent of the systemic
arterial systolic pressure; or
2. Pulmonary arterial systolic pressure equal to or greater than 70 mmHg; or
3. Mean pulmonary artery pressure equal to or greater than 40 mmHg.
OR
D. Single ventricle (with or without Fontan procedures) (see 4.00H3).
OR
E. Exacerbations or complications of congenital heart disease (see 4.00J3) requiring
three hospitalizations within a consecutive 12-month period (see 4.00A3e) and at least
30 days apart. Each hospitalization must last at least 48 hours, including hours in
a hospital emergency department immediately before the hospitalization (see 4.00J3).
4.07 Aortic valvular disease
(see 4.00I3), with symptoms due to stenosis, determined by appropriate test or tests
showing an aortic valve area of less than 1.0 cm2.
4.08 Cardiomyopathy (see 4.00I2) while on a regimen of prescribed treatment, with A, B, C, or D:
A. Hypertrophic cardiomyopathy documented by appropriate medically acceptable imaging,
with left ventricular or septal wall thickness equal to or greater than 20 mm in the
absence of other causes of left ventricular hypertrophy (for example, hypertension
or aortic valvular disease) and either 1 or 2:
1. Recurrent (see 4.00A3c) symptoms of cardiomyopathy, resulting in both a and b:
a. A medical source (see 4.00I2c) has concluded that the performance of an exercise
tolerance test would present a significant risk to the person; and
b. Very serious limitation in the ability to perform activities of daily living independently,
appropriately, effectively, and on a sustained basis; or
2. Inability to perform on an exercise tolerance test at a workload equivalent to
5 METs or less if using a standard treadmill (or bicycle) test without gas exchange,
or at 15 ml/kg/min peak VO2 (oxygen consumption) on a cardiopulmonary exercise test.
OR
B. Endomyocardial fibrosis documented by appropriate medically acceptable imaging, with
1, 2, and 3:
1. Loss of chamber volume due to fibrosis of the endocardium of at least one ventricle;
and
2. Right or left atrial dilatation (chamber enlargement); and
3. Regurgitant (backward) blood flow through the mitral or tricuspid valve.
OR
C. Cardiac amyloidosis AL (light-chain) type documented by biopsy.
OR
D. Exacerbations or complications of cardiomyopathy requiring three hospitalizations
within a consecutive 12-month period (see 4.00A3e) and at least 30 days apart. Each
hospitalization must last at least 48 hours, including hours in a hospital emergency
department immediately before the hospitalization (see 4.00J3).
4.09 Heart transplantation
(see 4.00I4). Consider under a disability for 1 year from the date of the transplant;
after that, evaluate the residual impairment(s).
4.10 Dissecting aneurysm of the aorta or major
branches (see 4.00I6), due to any cause (for example, atherosclerosis, cystic medial necrosis,
Marfan syndrome, or trauma), with A and B:
A. Documented by appropriate medically acceptable imaging.
AND
B. Dissection not controlled by prescribed treatment.
4.11 Chronic venous insufficiency (see 4.00G) of a lower extremity with reflux or obstruction of the venous system
documented by duplex ultrasound or other appropriate diagnostic technique, with A
or B:
A. Extensive trophic changes of skin (for example, hyperpigmentation, lipodermatosclerosis,
brawny edema) involving at least two-thirds of the leg below the knee, on two evaluations
at least 90 days apart within a consecutive 12-month period (see 4.00A3e), with both
1 and 2:
1. Consistent with chronic venous insufficiency; and
2. Unresponsive to compression therapy.
OR
B. Two or more episodes of ulceration that have not healed following at least 6 months
of prescribed treatment.
4.12 Peripheral artery disease (see 4.00G7) while on a regimen of prescribed treatment resulting in intermittent
claudication or leg pain that interferes with mobility (see 4.00G1), with A, B, C,
or D, as determined by an appropriate test(s) (see 4.00G5-4.00G6):
A. Resting ankle-brachial index of less than 0.50 (see 4.00G7b).
OR
B. Decrease in systolic blood pressure at the ankle on exercise test (see 4.00G7a) of
50 percent or more of the pre-exercise level and requiring 10 minutes or more to return
to pre-exercise level.
OR
C. Resting toe systolic pressure of less than 30 mmHg (see 4.00G7c and 4.00G8).
OR
D. Resting toe-brachial index of less than 0.40 (see 4.00G7c).
4.13-4.15 [Reserved]
4.16 Cardiac allograft vasculopathy (see 4.00I5), documented by appropriate medically acceptable imaging (for example,
intravascular ultrasonography or coronary angiography) (see 4.00A3d), with A, B, C,
or D:
A. Cardiac index (CI) or cardiac output (CO) less than 2 l/min/m2.
OR
B. Left ventricular ejection fraction equal to or less than 45 percent.
OR
C. Right atrial pressure (RAP) greater than 12 mmHg.
OR
D. Pulmonary capillary wedge pressure (PCWP) greater than 15 mmHg.