4.02 Chronic heart failure while on a regimen
of prescribed treatment
4.03 Hypertensive cardiovascular disease
4.04 Ischemic heart disease, with chest discomfort
associated with myocardial ischemia
4.05 Recurrent arrhythmias, not related to
4.06 Symptomatic congenital heart disease
4.07 Valvular heart disease or other stenotic
defects, or valvular regurgitation
4.09 Cardiac transplantation
4.10 Aneurysm of aorta or major branches,
due to any cause
4.11 Chronic venous insufficiency of a lower
4.12 Peripheral arterial disease
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Return to Listings
A. Introduction. The listings in this section describe impairments
resulting from cardiovascular disease based on symptoms, physical signs,
laboratory test abnormalities, and response to a regimen of therapy prescribed
by a treating source. A longitudinal clinical record covering a period of
not less than 3 months of observations and therapy is usually necessary
for the assessment of severity and expected duration of cardiovascular impairment,
unless the claim can be decided favorably on the basis of the current evidence.
All relevant evidence must be considered in assessing disability.
Many individuals, especially those who have listing-level impairments, will
have received the benefit of medically prescribed treatment. Whenever there
is evidence of such treatment, the longitudinal clinical record must include
a description of the therapy prescribed by the treating source and response,
in addition to information about the nature and severity of the impairment.
It is important to document any prescribed therapy and response because
this medical management may have improved the individual's functional status.
The longitudinal record should provide information regarding functional
recovery, if any.
Some individuals will not have received ongoing treatment or have an ongoing
relationship with the medical community despite the existence of a severe
impairment(s). Unless the claim can be decided favorably on the basis of
the current evidence, a longitudinal record is still important because it
will provide information about such things as the ongoing medical severity
of the impairment, the degree of recovery from cardiac insult, the level
of the individual's functioning, and the frequency, severity, and duration
of symptoms. Also, several listings include a requirement for continuing
signs and symptoms despite a regimen of prescribed treatment. Even though
an individual who does not receive treatment may not be able to show an
impairment that meets the criteria of these listings, the individual may
have an impairment(s) equivalent in severity to one of the listed impairments
or be disabled because of a limited residual functional capacity.
Indeed, it must be remembered that these listings are only examples of common
cardiovascular disorders that are severe enough to prevent a person from
engaging in gainful activity. Therefore, in any case in which an individual
has a medically determinable impairment that is not listed, or a combination
of impairments no one of which meets a listing, we will make a medical equivalence
determination. Individuals who have an impairment(s) with a level of severity
which does not meet or equal the criteria of the cardiovascular listings
may or may not have the residual functional capacity (RFC) which would enable
them to engage in substantial gainful activity. Evaluation of the impairment(s)
of these individuals should proceed through the final steps of the sequential
evaluation process (or, as appropriate, the steps in the medical improvement
B. Cardiovascular impairment results from one or more of four consequences
of heart disease:
1. Chronic heart failure or ventricular dysfunction.
2. Discomfort or pain due to myocardial ischemia, with or without necrosis
of heart muscle.
3. 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.
4. Central cyanosis due to right-to-left shunt, arterial desaturation, or
pulmonary vascular disease.
Impairment from diseases of arteries and veins may result from disorders
of the vasculature in the central nervous system (11.04A, B), eyes (2.02-2.04),
kidney (6.02), and other organs.
C. Documentation. Each individual's file must include sufficiently detailed
reports on history, physical examinations, laboratory studies, and any prescribed
therapy and response to allow an independent reviewer to assess the severity
and duration of the cardiovascular impairment.
a. An original or legible copy of the 12-lead electrocardiogram (ECG)
obtained at rest must be submitted, 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.
(1) Detailed descriptions or computer-averaged signals without original
or legible copies of the ECG as described in subsection 4.00Cla are not
(2) The effects of drugs or electrolyte abnormalities must be considered
as possible noncoronary causes of ECG abnormalities of ventricular repolarization,
i.e., those involving the ST segment and T wave. If available, the predrug
(especially digitalis glycoside) ECG should be submitted.
(3) The term "ischemic" is used in 4.04A to describe an abnormal
ST segment deviation. Nonspecific repolarization abnormalities should not
be confused with "ischemic" changes.
b. ECGs obtained in conjunction with treadmill, bicycle, or arm exercise
tests should meet the following specifications:
(1) ECGs must include the original calibrated ECG tracings or a legible
(2) A 12-lead baseline ECG must be recorded in the upright position before
(3) A 12-lead ECG should be recorded at the end of each minute of exercise,
including at the time the ST segment abnormalities reach or exceed the criteria
for abnormality described in 4.04A or the individual experiences chest discomfort
or other abnormalities, and also when the exercise test is terminated.
(4) 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 response to
(5) Post-exercise ECGs should be recorded using a generally accepted protocol
consistent with the prevailing state of medical knowledge and clinical practice.
(6) All resting, exercise, and recovery ECG strips must have a standardization
inscribed on the tracing. The ECG strips should be labeled to indicate 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, blood
pressure levels during testing, and the reason(s) for terminating the test
(including limiting signs or symptoms) must be recorded.
2. Purchasing Exercise Tests
a. It is well recognized by medical experts that exercise testing
is the best tool currently available for estimating maximal aerobic capacity
in individuals with cardiovascular impairments. Purchase of an exercise
test may be appropriate when there is a question whether an impairment meets
or is equivalent in severity to one of the listings, or when there is insufficient
evidence in the record to evaluate aerobic capacity, and the claim cannot
otherwise be favorably decided. Before purchasing an exercise test, a program
physician, preferably one with experience in the care of patients with cardiovascular
disease, must review the pertinent history, physical examinations, and laboratory
tests to determine whether obtaining the test would present a significant
risk to the individual (see 4.00C2c). Purchase may be indicated when there
is no significant risk to exercise testing and there is no timely test of
record. An exercise test is generally considered timely for 12 months after
the date performed, provided there has been no change in clinical status
that may alter the severity of the cardiac impairment.
(1) When an exercise test is purchased, it should be a "sign-or symptom-limited"
test characterized by a progressive multistage regimen. A purchased exercise
test 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 4.00C1b and this section. A pre-exercise posthyperventilation
tracing may be essential for the proper evaluation of an "abnormal"
test in certain circumstances, such as in women with evidence of mitral
(2) The exercise test should be paced to the capabilities of the individual
and be supervised by a physician. 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 that are used
should utilize similar workloads.
(3) Levels of exercise should be described in terms of workload and duration
of each stage, e.g., treadmill speed and grade, or bicycle ergometer work
rate in kpm/min or watts.
(4) Normally, systolic blood pressure and heart rate increase gradually
with exercise. A decrease in systolic blood pressure during exercise below
the usual resting level is often associated with ischemia-induced left ventricular
dysfunction resulting in decreased cardiac output. Some individuals (because
of deconditioning or apprehension) with increased sympathetic responses
may increase their systolic blood pressure and heart rate above their usual
resting level just before and early into exercise. This occurrence may limit
the ability to assess the significance of an early decrease in systolic
blood pressure and heart rate if exercise is discontinued shortly after
initiation. In addition, isolated systolic hypertension may be a manifestation
(5) The exercise laboratory's physical environment, staffing, and equipment
should meet the generally accepted standards for adult exercise test laboratories.
c. Risk factors in exercise testing. The following are examples of situations
in which exercise testing will not be purchased: unstable progressive angina
pectoris, a history of acute myocardial infarction within the past 3 months,
New York Heart Association (NYHA) class IV heart failure, cardiac drug toxicity,
uncontrolled serious arrhythmia (including uncontrolled atrial fibrillation,
Mobitz II, and third-degree block), Wolff-Parkinson-White syndrome, uncontrolled
severe systemic arterial hypertension, marked pulmonary hypertension, unrepaired
aortic dissection, left main stenosis of 50 percent or greater, marked aortic
stenosis, chronic or dissecting aortic aneurysm, recent pulmonary embolism,
hypertrophic cardiomyopathy, limiting neurological or musculoskeletal impairments,
or an acute illness. In addition, an exercise test should not be purchased
for individuals for whom the performance of the test is considered to constitute
a significant risk by a program physician, preferably one experienced in
the care of patients with cardiovascular disease, even in the absence of
any of the above risk factors. In defining risk, the program physician,
in accordance with the regulations and other instructions on consultative
examinations, will generally give great weight to the treating physicians'
opinions and will generally not override them. In the rare situation in
which the program physician does override the treating source's opinion,
a written rationale must be prepared documenting the reasons for overriding
d. In order to permit maximal, attainable restoration of functional capacity,
exercise testing should not be purchased until 3 months after an acute myocardial
infarction, surgical myocardial revascularization, or other open-heart surgical
procedures. Purchase of an exercise test should also be deferred for 3 months
after percutaneous transluminal coronary angioplasty because restenosis
with ischemic symptoms may occur within a few months of angioplasty (see
4.00D). Also, individuals who have had a period of bedrest or inactivity
(e.g., 2 weeks) that results in a reversible deconditioned state may do
poorly if exercise testing is performed at that time.
(1) Exercise testing is evaluated on the basis of the work level at which
the test becomes abnormal, as documented by onset of signs or symptoms and
any ECG abnormalities listed in 4.04A. The ability or inability to complete
an exercise test is not, by itself, evidence that a person is free from
ischemic heart disease. The results of an exercise test must be considered
in the context of all of the other evidence in the individual's case record.
If the individual is under the care of a treating physician for a cardiac
impairment, and this physician has not performed an exercise test and there
are no reported significant risks to testing (see 4.00C2c), a statement
should be requested from the treating physician explaining why it was not
done or should not be done before deciding whether an exercise test should
be purchased. In those rare situations in which the treating source's opinion
is overridden, follow 4.00C2c. If there is no treating physician, the program
physician will be responsible for assessing the risk to exercise testing.
(2) Limitations to exercise test interpretation include the presence of
noncoronary or nonischemic factors that may influence the hemodynamic and
ECG response to exercise, such as hypokalemia or other electrolyte abnormality,
hyperventilation, vasoregulatory deconditioning, prolonged periods of physical
inactivity (e.g., 2 weeks of bedrest), significant anemia, left bundle branch
block pattern on the ECG (and other conduction abnormalities that do not
preclude the purchase of exercise testing), and other heart diseases or
abnormalities (particularly valvular heart disease). Digitalis glycosides
may cause ST segment abnormalities at rest, during, and after exercise.
Digitalis or other drug-related ST segment displacement, present at rest,
may become accentuated with exercise and make ECG interpretation difficult,
but such drugs do not invalidate an otherwise normal exercise test. Diuretic-induced
hypokalemia and left ventricular hypertrophy may also be associated with
repolarization changes and behave similarly. Finally, treatment with beta
blockers slows the heart rate more at near-maximal exertion than at rest;
this limits apparent chronotropic capacity.
3. Other Studies
Information from two-dimensional and Doppler echocardiographic studies
of ventricular size and function as well as radionuclide (thallium sub201
) myocardial "perfusion" or radionuclide (technetium 99m) ventriculograms
(RVG or MUGA) may be useful. These techniques can provide a reliable estimate
of ejection fraction. In selected cases, these tests may be purchased after
a medical history and physical examination, report of chest x-rays, ECGs,
and other appropriate tests have been evaluated, preferably by a program
physician with experience in the care of patients with cardiovascular disease.
Purchase should be considered when other information available is not adequate
to assess whether the individual may have severe ventricular dysfunction
or myocardial ischemia and there is no significant risk involved (follow
4.00C2a guides), and the claim cannot be favorably decided on any other
Exercise testing with measurement of maximal oxygen uptake (VO sub2 ) provides
an accurate determination of aerobic capacity. An exercise test without
measurement of oxygen uptake provides an estimate of aerobic capacity. When
the results of tests with measurement of oxygen uptake are available, every
reasonable effort should be made to obtain them.
The recording of properly calibrated ambulatory ECGs for analysis of ST
segment signals with a concomitantly recorded symptom and treatment log
may permit more adequate evaluation of chest discomfort during activities
of daily living, but the significance of these data for disability evaluation
has not been established in the absence of symptoms (e.g., silent ischemia).
This information (including selected segments of both the ECG recording
and summary report of the patient diary) may be submitted for the record.
4. Cardiac catheterization will not be purchased by the Social Security
a. Coronary arteriography. If results of such testing are available, the
report should be obtained and considered as to the quality and type of data
provided and its relevance to the evaluation of the impairment. A copy of
the report of the cardiac catheterization and ancillary studies should also
be obtained. 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. Coronary artery spasm induced by intracoronary catheterization
is not to be considered evidence of ischemic disease. 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
available, quantitative computer measurements and analyses should be considered
in the interpretation of severity of stenotic lesions.
b. Left ventriculography (by angiography). The report should describe the
wall motion of the myocardium with regard to any areas of hypokinesis, akinesis,
or dyskinesis, and the overall contraction of the ventricle as measured
by the ejection fraction. Measurement of chamber volumes and pressures may
be useful. When available, 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.
D. Treatment and relationship to functional status.
1. In general, conclusions about the severity of a cardiovascular impairment
cannot be made on the basis of type of treatment rendered or anticipated.
The overall clinical and laboratory evidence, including the treatment plan(s)
or results, should be persuasive that a listing-level impairment exists.
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, impairment evaluation may need
to be deferred for a period of up to 3 months from the date of treatment
to permit consideration of treatment effects. Evaluation should not be deferred
if the claim can be favorably decided based upon the available evidence.
2. The usual time after myocardial infarction, valvular and/or revascularization
surgery for adequate assessment of the results of treatment is considered
to be 3 months. If an exercise test is performed by a treating source within
a week or two after angioplasty, and there is no significant change in clinical
status during the 3-month period after the angioplasty that would invalidate
the implications of the exercise test results, the exercise test results
may be used to reflect functional capacity during the period in question.
However, if the test was done immediately following an acute myocardial
infarction or during a period of protracted inactivity, the results should
not be projected to 3 months even if there is no change in clinical status.
3. An individual who has undergone cardiac transplantation will be considered
under a disability for 1 year following the surgery because, during the
first year, there is a greater likelihood of rejection of the organ and
recurrent infection. After the first year posttransplantation, continuing
disability evaluation will be based upon residual impairment as shown by
symptoms, signs, and laboratory findings. Absence of symptoms, signs, and
laboratory findings indicative of cardiac dysfunction will be included in
the consideration of whether medical improvement (as defined in §§
404.1579(b)(1) and (c)(1), 404.1594(b)(1) and (c)(1), or 416.994(b)(1)(i)
and (b)(2)(i), as appropriate) has occurred.
E. Clinical syndromes.
1. Chronic heart failure (ventricular dysfunction) is considered in these
listings as one category whatever its etiology, i.e., atherosclerotic, hypertensive,
rheumatic, pulmonary, congenital or other organic heart disease. Chronic
heart failure may manifest itself by:
a. Pulmonary or systemic congestion, or both; or
b. Symptoms of limited cardiac output, such as weakness, fatigue, or intolerance
of physical activity.
For the purpose of 4.02A, pulmonary and systemic congestion are not considered
to have been established unless there is or has been evidence of fluid retention,
such as hepatomegaly or ascites, or peripheral or pulmonary edema of cardiac
origin. The findings of fluid retention need not be present at the time
of adjudication because congestion may be controlled with medication. Chronic
heart failure due to limited cardiac output is not considered to have been
established for the purpose of 4.02B unless symptoms occur with ordinary
daily activities, i.e., activity restriction as manifested by a need to
decrease activity or pace, or to rest intermittently, and are associated
with one or more physical signs or abnormal laboratory studies listed in
4.02B. These studies include exercise testing with ECG and blood pressure
recording and/or appropriate imaging techniques, such as two-dimensional
echocardiography or radionuclide or contrast ventriculography. The exercise
criteria are outlined in 4.02B1. In addition, other abnormal symptoms, signs,
or laboratory test results that lend credence to the impression of ventricular
dysfunction should be considered.
2. For the purposes of 4.03, hypertensive cardiovascular disease is evaluated
by reference to the specific organ system involved (heart, brain, kidneys,
or eyes). The presence of organic impairment must be established by appropriate
physical signs and laboratory test abnormalities as specified in 4.02 or
4.04, or for the body system involved.
3. Ischemic (coronary) heart disease may result in an impairment due to
myocardial ischemia and/or ventricular dysfunction or infarction. For the
purposes of 4.04, the clinical determination that discomfort of myocardial
ischemic origin (angina pectoris) is present must be supported by objective
evidence as described under 4.00C l, 2, 3, or 4.
a. Discomfort of myocardial ischemic origin (angina pectoris) is discomfort
that is precipitated by effort and/or emotion and promptly relieved by sublingual
nitroglycerin, other rapidly acting nitrates, or rest. Typically the discomfort
is located in the chest (usually substernal) and described as crushing,
squeezing, burning, aching, or oppressive. Sharp, sticking, or cramping
discomfort is considered less common or atypical. 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 therapy or rest.
b. So-called anginal equivalent may be localized to the neck, jaw(s), or
hand(s) and has the same precipitating and relieving factors as typical
chest discomfort. Isolated shortness of breath (dyspnea) is not considered
an anginal equivalent for purposes of adjudication.
c. Variant angina of the Prinzmetal type, i.e., rest angina with transitory
ST segment elevation on ECG, may have the same significance as typical angina,
described in 4.00E3a.
d. If there is documented evidence of silent ischemia or restricted activity
to prevent chest discomfort, this information must be considered along with
all available evidence to determine if an equivalence decision is appropriate.
e. Chest discomfort of myocardial ischemic origin is usually caused by coronary
artery disease. However, ischemic discomfort may be caused by noncoronary
artery conditions, such as critical aortic stenosis, hypertrophic cardiomyopathy,
pulmonary hypertension, or anemia. These conditions should be distinguished
from coronary artery disease, because the evaluation criteria, management,
and prognosis (duration) may differ from that of coronary artery disease.
f. Chest discomfort of nonischemic origin may result from other cardiac
conditions such as pericarditis and mitral valve prolapse. Noncardiac conditions
may also produce symptoms mimicking that of myocardial ischemia. These conditions
include 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 arthritis. Hyperventilation may also mimic ischemic discomfort.
Such disorders should be considered before concluding that chest discomfort
is of myocardial ischemic origin.
4.01 Category of Impairments, Cardiovascular System
4.02 Chronic heart failure while on a regimen of prescribed treatment
(see 4.00A if there is no regimen of prescribed treatment). With one of
A. Documented cardiac enlargement by appropriate imaging techniques (e.g.,
a cardiothoracic ratio of greater than 0.50 on a PA chest x-ray with good
inspiratory effort or left ventricular diastolic diameter of greater than
5.5 cm on two-dimensional echocardiography), resulting in inability to carry
on any physical activity, and with symptoms of inadequate cardiac output,
pulmonary congestion, systemic congestion, or anginal syndrome at rest (e.g.,
recurrent or persistent fatigue, dyspnea, orthopnea, anginal discomfort);
B. Documented cardiac enlargement by appropriate imaging techniques (see
4.02A) or ventricular dysfunction manifested by S3, abnormal wall motion,
or left ventricular ejection fraction of 30 percent or less by appropriate
imaging techniques; and
1. Inability to perform on an exercise test at a workload equivalent to
5 METs or less due to symptoms of chronic heart failure, or, in rare instances,
a need to stop exercise testing at less than this level of work because
a. Three or more consecutive ventricular premature beats or three or more
multiform beats; or
b. Failure to increase systolic blood pressure by 10 mmHg, or decrease in
systolic pressure below the usual resting level (see 4.00C2b); or
c. Signs attributable to inadequate cerebral perfusion, such as ataxic gait
or mental confusion; and
2. Resulting in marked limitation of physical activity, as demonstrated
by fatigue, palpitation, dyspnea, or anginal discomfort on ordinary physical
activity, even though the individual is comfortable at rest;
C. Cor pulmonale fulfilling the criteria in 4.02A or B.
4.03 Hypertensive cardiovascular disease. Evaluate under 4.02 or 4.04, or
under the criteria for the affected body system (2.02 through 2.04, 6.02,
or 11.04A or B).
4.04 Ischemic heart disease, with chest discomfort associated with myocardial
ischemia, as described in 4.00E3, while on a regimen of prescribed treatment
(see 4.00A if there is no regimen of prescribed treatment). With one of
A. Sign- or symptom-limited exercise 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
therapy and/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 that have a typical ischemic time course
of development and resolution (progression of horizontal or downsloping
ST depression with exercise, and persistence of depression of at least -0.10
millivolts for at least 1 minute of recovery); or
2. An upsloping ST junction depression, in the absence of digitalis glycoside
therapy and/or hypokalemia, in any lead (except aVR) of at least -0.2 millivolts
or more for at least 0.08 seconds after the J junction and persisting for
at least 1 minute of recovery; or
3. At least 0.1 millivolt (1 mm) ST elevation above resting baseline during
both exercise and 3 or more minutes of recovery in ECG leads with low R
and T waves in the leads demonstrating the ST segment displacement; or
4. Failure to increase systolic pressure by 10 mmHg, or decrease in systolic
pressure below usual clinical resting level (see 4.00C2b); or
5. Documented reversible radionuclide "perfusion" (thallium201)
defect at an exercise level equivalent to 5 METs or less;
B. Impaired myocardial function, documented by evidence (as outlined under
4.00C3 or 4.00C4b) of hypokinetic, akinetic, or dyskinetic myocardial free
wall or septal wall motion with left ventricular ejection fraction of 30
percent or less, and an evaluating program physician, preferably one experienced
in the care of patients with cardiovascular disease, has concluded that
performance of exercise testing would present a significant risk to the
individual, and resulting in marked limitation of physical activity, as
demonstrated by fatigue, palpitation, dyspnea, or anginal discomfort on
ordinary physical activity, even though the individual is comfortable at
C. Coronary artery disease, demonstrated by angiography (obtained independent
of Social Security disability evaluation), and an evaluating program physician,
preferably one experienced in the care of patients with cardiovascular disease,
has concluded that performance of exercise testing would present a significant
risk to the individual, with both 1 and 2:
1. Angiographic evidence revealing:
a. 50 percent or more narrowing of a nonbypassed left main coronary artery;
b. 70 percent or more narrowing of another nonbypassed coronary artery;
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 2 nonbypassed coronary arteries;
e. Total obstruction of a bypass graft vessel; and
2. Resulting in marked limitation of physical activity, as demonstrated
by fatigue, palpitation, dyspnea, or anginal discomfort on ordinary physical
activity, even though the individual is comfortable at rest.
4.05 Recurrent arrhythmias, not related to reversible causes such as electrolyte
abnormalities or digitalis glycoside or antiarrhythmic drug toxicity, resulting
in uncontrolled repeated episodes of cardiac syncope or near syncope and
arrhythmia despite prescribed treatment (see 4.00A if there is no prescribed
treatment), documented by resting or ambulatory (Holter) electrocardiography
coincident with the occurrence of syncope or near syncope.
4.06 Symptomatic congenital heart disease (cyanotic or acyanotic), documented
by appropriate imaging techniques (as outlined under 4.00C3) or cardiac
catheterization. With one of the following:
A. Cyanosis at rest, and:
1. Hematocrit of 55 percent or greater, or
2. Arterial O sub2 saturation of less than 90 percent in room air, or resting
arterial PO sub2 of 60 Torr or less;
B. Intermittent right-to-left shunting resulting in cyanosis on exertion
(e.g., Eisenmenger's physiology) and with arterial PO sub2 of 60 Torr or
less at a workload equivalent to 5 METs or less;
C. Chronic heart failure with evidence of ventricular dysfunction, as described
D. Recurrent arrhythmias as described in 4.05;
E. Secondary pulmonary vascular obstructive disease with a mean pulmonary
arterial pressure elevated to at least 70 percent of the mean systemic arterial
4.07 Valvular heart disease or other stenotic defects, or valvular regurgitation,
documented by appropriate imaging techniques or cardiac catheterization.
Evaluate under the criteria in 4.02, 4.04, 4.05, or 11.04.
4.08 Cardiomyopathies, documented by appropriate imaging techniques or cardiac
catheterization. Evaluate under the criteria in 4.02, 4.04, 4.05, or 11.04.
4.09 Cardiac transplantation. Consider under a disability for 1 year following
surgery; thereafter, reevaluate residual impairment under 4.02 to 4.08.
4.10 Aneurysm of aorta or major branches, due to any cause (e.g., atherosclerosis,
cystic medial necrosis, Marfan syndrome, trauma), demonstrated by an appropriate
imaging technique. With one of the following:
A. Acute or chronic dissection not controlled by prescribed medical or surgical
B. Chronic heart failure as described under 4.02;
C. Renal failure as described under 6.02;
D. Neurological complications as described under 11.04.
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;
B. Superficial varicosities, stasis dermatitis, and recurrent or persistent
ulceration which has not healed following at least 3 months of prescribed
medical or surgical therapy.
4.12 Peripheral arterial disease. With one of the following:
A. Intermittent claudication with failure to visualize (on arteriogram obtained
independent of Social Security disability evaluation) the common femoral
or deep femoral artery in one extremity;
B. Intermittent claudication with marked impairment of peripheral arterial
circulation as determined by Doppler studies showing:
1. Resting ankle/brachial systolic blood pressure ratio of less than 0.50;
2. Decrease in systolic blood pressure at the ankle on exercise (see 4.00E4)
of 50 percent or more of pre-exercise level at the ankle, and requiring
10 minutes or more to return to pre-exercise level;
C. Amputation at or above the tarsal region due to peripheral vascular disease.