Screening for Cardiovascular Disease

Chapter 6

Screening for Cardiovascular Disease

The cardiovascular system consists of the heart, capillaries, veins, and lymphatics and functions in coordination with the pulmonary system to circulate oxygenated blood through the arterial system to all cells. This system then collects deoxygenated blood from the venous system and delivers it to the lungs for reoxygenation (Fig. 6-1).

Heart disease remains the leading cause of death in industrialized nations. In the United States alone, cardiovascular disease (CVD) is responsible for approximately one million deaths each year. One in three Americans has some form of cardiovascular disease. The American Heart Association (AHA) reports that about half of all deaths from heart disease are sudden and unexpected.1

Known risk factors include advancing age, hypertension, obesity, sedentary lifestyle, excessive alcohol consumption, oral contraceptive use (over age 35, combined with smoking), first-generation family history, tobacco use (including exposure to second-hand smoke), abnormal cholesterol levels, and race (e.g., African Americans, Mexican Americans, Native Americans, and Pacific Islanders are at greater risk).

Fortunately, during the last two decades cardiovascular research has greatly increased our understanding of the structure and function of the cardiovascular system in health and disease. Despite the formidable statistics regarding the prevalence of CVD, during the last 15 years a steady decline in mortality from cardiovascular disorders has been witnessed. Effective application of the increased knowledge regarding CVD and its risk factors will assist health care professionals to educate clients in achieving and maintaining cardiovascular health.

Information about heart disease is changing rapidly. Part of the therapist’s intervention includes patient/client education. The therapist can access up-to-date information at many useful websites (Box 6-1).

Box 6-1   Informational Websites

Framingham Risk Score

To calculate your Framingham risk score for heart attack in the next 10 years, go to A score of 5% to 20% suggests the need for the hsCRP test (C-reactive protein). Using the results of the CRP test, the Reynolds model will provide a more accurate assessment of risk (

Signs and Symptoms of Cardiovascular Disease

Cardinal symptoms of cardiac disease usually include chest, neck and/or arm pain or discomfort, palpitation, dyspnea, syncope (fainting), fatigue, cough, diaphoresis, and cyanosis. Edema and leg pain (claudication) are the most common symptoms of the vascular component of a cardiovascular pathologic condition. Symptoms of cardiovascular involvement should also be reviewed by system (Table 6-1).

Chest Pain or Discomfort

Chest pain or discomfort is a common presenting symptom of cardiovascular disease and must be evaluated carefully. Chest pain may be cardiac or noncardiac in origin and may radiate to the neck, jaw, upper trapezius muscle, upper back, shoulder, or arms (most commonly the left arm).

Radiating pain down the arm follows the pattern of ulnar nerve distribution. Pain of cardiac origin can be experienced in the somatic areas because the heart is supplied by the C3 to T4 spinal segments, referring visceral pain to the corresponding somatic area (see Fig. 3-3). For example, the heart and the diaphragm, supplied by the C5-6 spinal segment, can refer pain to the shoulder (see Figs. 3-4 and 3-5).

Cardiac-related chest pain may arise secondary to angina, myocardial infarction (MI), pericarditis, endocarditis, mitral valve prolapse, or dissecting aortic aneurysm. Location and description (frequency, intensity, and duration) vary according to the underlying pathologic condition (see each individual condition).

Cardiac chest pain is often accompanied by associated signs and symptoms such as nausea, vomiting, diaphoresis, dyspnea, fatigue, pallor, or syncope. These associated signs and symptoms provide the therapist with red flags to identify musculoskeletal symptoms of a systemic origin.

Cardiac chest pain or discomfort can also occur when the coronary circulation is normal, as in the case of clients with anemia, causing lack of oxygenation of the myocardium (heart muscle) during physical exertion.

Noncardiac chest pain can be caused by an extensive list of disorders requiring screening for medical disease. For example, cervical disk disease and arthritic changes can mimic atypical chest pain. Chest pain that is attributed to anxiety, trigger points, cocaine use, and other noncardiac causes is discussed in Chapter 17.


Palpitation, the presence of an irregular heartbeat, may also be referred to as arrhythmia or dysrhythmia, which may be caused by a relatively benign condition (e.g., mitral valve prolapse, “athlete’s heart,” caffeine, anxiety, exercise) or a severe condition (e.g., coronary artery disease, cardiomyopathy, complete heart block, ventricular aneurysm, atrioventricular valve disease, mitral or aortic stenosis).

The sensation of palpitations has been described as a bump, pound, jump, flop, flutter, or racing sensation of the heart. Associated symptoms may include lightheadedness or syncope. Palpated pulse may feel rapid or irregular, as if the heart “skipped” a beat.

Occasionally, a client will report “fluttering” sensations in the neck. Generally, unless accompanied by other symptoms, these sensations in the neck are caused by anxiety, random muscle fasciculation, or minor muscle strain or overuse.

Palpitations can be considered physiologic (i.e., when less than six occur per minute, this may be considered within normal function of the heart). However, palpitation lasting for hours or occurring in association with pain, shortness of breath, fainting, or severe lightheadedness requires medical evaluation. Palpitation in any person with a history of unexplained sudden death in the family requires medical referral.

Clients describing “palpitations” or similar phenomena may not be experiencing symptoms of heart disease. Palpitations may occur as a result of an overactive thyroid, secondary to caffeine sensitivity, as a side effect of some medications, and with the use of drugs such as cocaine. Encourage the client to report any such symptoms to the physician if this information has not already been brought to the physician’s attention.


Dyspnea, also referred to as breathlessness or shortness of breath, can be cardiovascular in origin, but it may also occur secondary to a pulmonary pathologic condition (see also Chapter 7), fever, certain medications, allergies, poor physical conditioning, or obesity. Early onset of dyspnea may be described as having to breathe too much or as an uncomfortable feeling during breathing after exercise or exertion.

Shortness of breath with mild exertion (dyspnea on exertion [DOE]), when caused by an impaired left ventricle that is unable to contract completely, results in the lung’s inability to empty itself of blood. Pulmonary congestion and shortness of breath then occur. With severe compromise of the cardiovascular or pulmonary systems, dyspnea may occur at rest.

The severity of dyspnea is determined by the extent of disease. Thus the more severe the heart disease is, the easier it is to bring on dyspnea. Extreme dyspnea includes paroxysmal nocturnal dyspnea (PND) and orthopnea (breathlessness that is relieved by sitting upright with pillows used to prop the trunk and head).

PND and sudden, unexplained episodes of shortness of breath frequently accompany congestive heart failure (CHF). During the day the effects of gravity in the upright position and the shunting of excessive fluid to the lower extremities permit more effective ventilation and perfusion of the lungs, keeping the lungs relatively fluid free, depending on the degree of CHF. PND awakens the person sleeping in the recumbent position because the amount of blood returning to the heart and lungs from the lower extremities increases in this position.

Anyone who cannot climb a single flight of stairs without feeling moderately to severely winded or who awakens at night or experiences shortness of breath when lying down should be evaluated by a physician. Anyone with known cardiac involvement who develops progressively worse dyspnea must also notify the physician of these changes.

Dyspnea relieved by specific breathing patterns (e.g., pursed-lip breathing) or by specific body position (e.g., leaning forward on the arms to lock the shoulder girdle) is more likely to be pulmonary than cardiac in origin. Because breathlessness can be a terrifying experience for many persons, any activity that provokes the sensation is avoided, thus quickly reducing functional activities.

Cardiac Syncope

Cardiac syncope (fainting) or more mild lightheadedness can be caused by reduced oxygen delivery to the brain. Cardiac conditions resulting in syncope include arrhythmias, orthostatic hypotension, poor ventricular function, coronary artery disease, and vertebral artery insufficiency.

Lightheadedness that results from orthostatic hypotension (sudden drop in blood pressure [BP]) may occur with any quick change in a prolonged position (e.g., going from a supine position to an upright posture or standing up from a sitting position) or physical exertion involving increased abdominal pressure (e.g., straining with a bowel movement, lifting). Any client with aortic stenosis is likely to experience lightheadedness as a result of these activities.

Noncardiac conditions, such as anxiety and emotional stress, can cause hyperventilation and subsequent lightheadedness (vasovagal syncope). Side effects, such as orthostatic hypotension, may also occur during the period of initiation and regulation of cardiac medications (e.g., vasodilators).

Syncope that occurs without any warning period of lightheadedness, dizziness, or nausea may be a sign of heart valve or arrhythmia problems. Since sudden death can thus occur, medical referral is recommended for any unexplained syncope, especially in the presence of heart or circulatory problems or if the client has any risk factors for heart attack or stroke.

Examination of the cervical spine may include vertebral artery tests for compression of the vertebral arteries.2-5 If signs of eye nystagmus, changes in pupil size, or visual disturbances and symptoms of dizziness or lightheadedness occur, care must be taken concerning any treatment that follows. It has been suggested, however, that other factors, such as individual sensitivity to extreme head positions, age, and vestibular responsiveness, could affect the results of these tests.6

The test may be contraindicated in individuals with cervical spine fusion, Down syndrome (due to cervical hypermobility and/or instability), or other cervical spine instabilities. Although there is controversy and uncertainty about the safety and accuracy of vertebral artery tests, long-term complications have not been reported as a result of administering these tests.7,8 For a video of how to perform this test, go to and type in “Gans video vertebral artery test.”


Fatigue provoked by minimal exertion indicates a lack of energy, which may be cardiac in origin (e.g., coronary artery disease, aortic valve dysfunction, cardiomyopathy, or myocarditis) or may occur secondary to a neurologic, muscular, metabolic, or pulmonary pathologic condition. Often, fatigue of a cardiac nature is accompanied by associated symptoms such as dyspnea, chest pain, palpitations, or headache.

Fatigue that goes beyond expectations during or after exercise, especially in a client with a known cardiac condition, must be closely monitored. It should be remembered that beta-blockers prescribed for cardiac problems can also cause unusual fatigue symptoms.

For the client experiencing fatigue without a prior diagnosis of heart disease, monitoring vital signs may indicate a failure of the BP to rise with increasing workloads. Such a situation may indicate cardiac output that is inadequate in meeting the demands of exercise. However, poor exercise tolerance is often the result of deconditioning, especially in the older adult population. Further testing (e.g., exercise treadmill test) may be helpful in determining whether fatigue is cardiac-induced.


Edema in the form of a 3-pound or greater weight gain or a gradual, continuous gain over several days that results in swelling of the ankles, abdomen, and hands combined with shortness of breath, fatigue, and dizziness may be red-flag symptoms of CHF.

Other accompanying symptoms may include jugular vein distention (JVD; see Fig. 4-44) and cyanosis (of lips and appendages). Right upper quadrant pain described as a constant aching or sharp pain may occur secondary to an enlarged liver in this condition.

Right heart failure and subsequent edema can also occur secondary to cardiac surgery, venous valve incompetence or obstruction, cardiac valve stenosis, coronary artery disease, or mitral valve dysfunction.

Noncardiac causes of edema may include pulmonary hypertension, kidney dysfunction, cirrhosis, burns, infection, lymphatic obstruction, use of nonsteroidal antiinflammatory drugs (NSAIDs), or allergic reaction.

When edema and other accompanying symptoms persist despite rest, medical referral is required. Edema of a cardiac origin may require electrocardiogram (ECG) monitoring during exercise or activity (the physician may not want the client stressed when extensive ECG changes are present), whereas edema of peripheral origin requires treatment of the underlying etiologic complex.


Claudication or leg pain occurs with peripheral vascular disease (PVD; arterial or venous), often occurring simultaneously with coronary artery disease. Claudication can be more functionally debilitating than other associated symptoms, such as angina or dyspnea, and may occur in addition to these other symptoms. The presence of pitting edema along with leg pain is usually associated with vascular disease.

Other noncardiac causes of leg pain (e.g., sciatica, pseudoclaudication, anterior compartment syndrome, gout, peripheral neuropathy) must be differentiated from pain associated with peripheral vascular disease. Low back pain associated with pseudoclaudication often indicates spinal stenosis. The discomfort associated with pseudoclaudication is frequently bilateral and improves with rest or flexion of the lumbar spine (see also Chapter 14).

Vascular claudication may occur in the absence of physical findings but is usually accompanied by skin discoloration and trophic changes (e.g., thin, dry, hairless skin) in the presence of vascular disease. Core temperature, peripheral pulses, and skin temperature should be assessed. Cool skin is more indicative of vascular obstruction; warm to hot skin may indicate inflammation or infection. Abrupt onset of ischemic rest pain or sudden worsening of intermittent claudication may be due to thromboembolism and must be reported to the physician immediately.

If people with intermittent claudication have normal-appearing skin at rest, exercising the extremity to the point of claudication usually produces marked pallor in the skin over the distal third of the extremity. This postexercise cutaneous ischemia occurs in both upper and lower extremities and is due to selective shunting of the available blood to the exercised muscle and away from the more distal parts of the extremity.

Vital Signs

The therapist may see signs of cardiac dysfunction as abnormal responses of heart rate and BP during exercise. The therapist must remain alert to a heart rate that is either too high or too low during exercise, an irregular pulse rate, a systolic BP that does not rise progressively as the work level increases, a systolic BP that falls during exercise, or a change in diastolic pressure greater than 15 to 20 mm Hg (Case Example 6-1).

Case Example 6-1

Cardiac Impairment Affecting Balance

Chief Complaint: An 84-year-old woman was referred to outpatient physical therapy for gait training with a diagnosis of ataxia and “at risk” status for falls. The client’s goal is to walk without staggering.

Social History: Retired, lives alone in a two-story house.

Past Medical History: Atrial fibrillation, hypertension, arthritis in both hands, visual impairment (right eye), allergies to Novocain and antibiotics, transient ischemic attacks (TIAs), recurrent pneumonia.

Current Medications: Diltiazem (calcium channel blocker), Toprol (antihypertensive, beta blocker), aspirin (nonsteroidal antiinflammatory), Os-Cal (antacid, calcium supplement)

Clinical Presentation: Client is independent with activities of daily living but slow to complete tasks. She goes up and down one flight of steep stairs 3 to 4 times a day, using a handrail. She is an independent community ambulator but admits to frequently “staggering” (ataxia) with several falls. Baseline testing:

Presence of other symptoms includes numbness along both feet that does not change with position. Shortness of breath with activity (short distance walking, ascending and descending 6 steps); recovers after a short rest. Thoracic kyphosis. Mild strength losses in hips, knees, and ankles. Reports of being “dizzy” and “lightheaded,” feeling like she is going to “fall out.”

Vital signs:

Blood pressure (before activity): 136/79 mm Hg (arm and position not recorded)
Blood pressure (after 10 minutes of activity): 132/69
Pulse (before activity): 82 bpm
Pulse (after activity): 73 bpm

Assessment: This 84-year-old client with a diagnosis of ataxia and risk of falls presented with fairly good bilateral lower extremity strength but had deficits in sensation and vision, increasing her risk for falling. She was quite resistant to using a cane for increased safety.

The client experienced an abnormal response to exercise in which the pulse rate and BP decreased. She required several rest breaks during the exercise session due to “fading.”

The therapist referred the client to her cardiologist for evaluation to determine medical stability before further intervention.

Result: Nuclear stress testing revealed blockage of two major coronary arteries requiring cardiac catheterization with balloon angioplasty and placement of a stent. The cardiologist confirmed the therapist’s suspicions that the client’s balance deficits from neuropathy and decreased vision were made worse by shortness of breath and lightheadedness from cardiac impairment.

Monitoring vital signs before and during exercise was a simple way to screen for underlying cardiovascular impairment.

From Goff T: Case report presented in partial fulfillment of DPT 910. Principles of differential diagnosis, Institute for Physical Therapy Education, Chester, Pennsylvania, 2005, Widener University. Used with permission.

Monitor vital signs in anyone with known heart disease. Some BP lowering medications can keep a client’s heart rate from exceeding 90 bpm. For these individuals the therapist can monitor heart rate, but use perceived rate of exertion (PRE) as a gauge of exercise intensity. See Chapter 4 for more specific information about vital sign assessment.

Cardiac Pathophysiology

Three components of cardiac disease are discussed, including diseases affecting the heart muscle, diseases affecting heart valves, and defects of the cardiac nervous system (Table 6-2).

Conditions Affecting the Heart Muscle

In most cases, a cardiopulmonary pathologic condition can be traced to at least one of three processes:

Any combination of these can cause chest, neck, back, and/or shoulder pain. Frequently, these conditions occur sequentially. For example, an underlying obstruction, such as pulmonary embolus, leads to congestion, and subsequent dilation of the vessels blocked by the embolus.

The most common cardiovascular conditions to mimic musculoskeletal dysfunction are angina, MI, pericarditis, and dissecting aortic aneurysm. Other cardiovascular diseases are not included in this text because they are rare or because they do not mimic musculoskeletal symptoms.

Degenerative heart disease refers to the changes in the heart and blood supply to the heart and major blood vessels that occur with aging. As the population ages, degenerative heart disease becomes the most prevalent form of cardiovascular disease. Degenerative heart disease is also called atherosclerotic cardiovascular disease, arteriosclerotic cardiovascular disease, coronary heart disease (CHD), and coronary artery disease (CAD).


Hyperlipidemia refers to a group of metabolic abnormalities resulting in combinations of elevated serum total cholesterol (hypercholesterolemia), elevated low-density lipoproteins, elevated triglycerides (hypertriglyceridemia) and decreased high-density lipoproteins. These abnormalities are the primary risk factors for atherosclerosis and coronary artery disease.9-11

Statin medications (e.g., Zocor, Lipitor, Crestor, Lescol, Mevacor, Pravachol) are used to reduce low-density lipoprotein (LDL) cholesterol. While statins are generally well tolerated, there is a wide body of medical literature that associates the adverse reaction of myalgia and the more serious reaction of rhabdomyolysis with statin medications.11,12 If detected early, statin-related symptoms can be reversible with reduction of dose, selection of another statin, or cessation of statin use.1315

Screening for Side Effects of Statins: Myalgia and myopathy (including respiratory myopathy) are the most common myotoxic event associated with statins; joint pain is also reported.16,17 The incidence of myotoxic events appears to be dose-dependent. Rates of adverse events from statins vary in the literature from 5% up to 18%18 but with an increasing number of people taking these medications, physical therapists can expect to see a rise in the prevalence of this condition among the older age group.19,20

Monitoring for elevated serum liver enzymes and creatine kinase are significant laboratory indicators of muscle and liver impairment.21 Symptoms of mild myalgia (muscle ache or weakness without increased creatine kinase [CK] levels), myositis (muscle symptoms with increased CK levels), or frank rhabdomyolysis (muscle symptoms with marked CK elevation; more than 10 times the normal upper limit) range from 1% to 7%.11

Muscle soreness after exercise that is caused by statin use may go undetected even by the therapist. Awareness of potential risk factors and monitoring in anyone taking statins and any of these additional risk factors is advised. Muscular symptoms are more common in older individuals (Case Example 6-2).11,22 Other risk factors include23:

Case Example 6-2

Statins and Myalgia

Referral: The client was a 53-year-old woman who complained of right-sided knee pain and stiffness and constant, bilateral thigh pain. She was referred by her orthopedic surgeon for physical therapy with a musculoskeletal diagnosis of osteoarthritis (OA) of both knees.

Medications: Lipitor (antilipemic for high cholesterol), Lopressor (antihypertensive, beta blocker), Ambien (sedative for insomnia), Naprosyn (antiinflammatory). Dosage of the Lipitor was increased from 20 mg to 40 mg at the last physician visit.

Past Medical History: Hypertension, hypercholesterolemia, insomnia.

Clinical Presentation: Pain pattern—Client reported constant but variable pain in the right knee, ranging from 2/10 at rest and 5/10 during and after weightbearing activities. Morning stiffness was prominent, and the client described difficulty transitioning from prolonged sitting to standing. The client reported increased pain in the right knee after weightbearing for approximately 5 minutes.

In addition to the right-sided knee pain, the client also complained of a constant anterior thigh pain. This pain was described as a “flushing” sensation and was unchanged by position or motion. The intensity of the bilateral constant thigh pain was rated 3-4/10.

Complete physical examination of integument and gait inspection, muscle strength, and joint range of motion (ROM) was conducted, and results were recorded (on file). Findings from the lower quarter screen (LQS) were unremarkable. Lumbar ROM was within normal limits (WNL).

Neurologic screening exam—WNL

Review of Systems (ROS): Unremarkable; no other associated signs or symptoms reported.

What are the red flags in this scenario?

Red Flags

Is it safe to treat this client?

Physical therapy intervention can be implemented despite complaints of pain from an unknown origin. In the past 10 weeks prior to the initial physical therapy examination, this client had been evaluated by a physician four times. The most recent evaluation was by an orthopedic surgeon one week prior to her initial evaluation.

Additionally, the client appeared to be otherwise in good health, her ROS was unremarkable. The presence of three red flags warrants careful observation of response to intervention, progression of current symptoms, or onset of any new symptoms.

Symptoms related to OA were expected to improve, while symptoms from a non-musculoskeletal origin were not expected to improve. The plan of care was explained to the client, and it was mutually agreed that if the constant thigh pain did not significantly improve within 4 weeks, the client would be referred back to her physician.

Result: Four weeks after the initial physical therapy visit, symptoms of constant thigh pain had not resolved. The client had a follow-up appointment with her orthopedic surgeon at which time she presented documentation of the physical therapy intervention to date and the therapist’s concerns about the thigh pain.

The orthopedic surgeon reiterated his belief that the origin of her symptoms was due to OA. The client was instructed to continue physical therapy and to take Naprosyn as prescribed.

The client was discharged after receiving 8 weeks of physical therapy intervention. At this juncture, the therapist believed that the client’s right-sided knee symptoms were sufficiently improved and that the client could maintain or improve upon her current status by following her discharge instructions.

Furthermore, the myalgic thigh symptoms had not improved in the last 8 weeks and the therapist did not feel the bilateral thigh myalgia would be improved by further physical therapy interventions.

The client was instructed to contact her primary care physician regarding her myalgic symptoms. Three days later, the client called the physical therapy clinic. She had called her orthopedic surgeon rather than the primary care physician.

According to the client, the orthopedic surgeon dismissed the association between the thigh myalgia and the increased dosage of atorvastatin calcium (Lipitor). The client was again instructed to contact her primary care physician regarding the possibility of an adverse myalgic reaction to atorvastatin calcium (Lipitor). The client was also asked to contact the physical therapy clinic after being evaluated by her primary care physician.

Two weeks later, the client called and indicated her primary care physician evaluated her two days following our telephone conversation. The primary care physician discontinued the atorvastatin calcium (Lipitor). The client reported approximately a 50% reduction in the constant bilateral thigh myalgia after discontinuing the atorvastatin calcium (Lipitor).

The client was asked to contact the therapist in 2 or 3 weeks to provide an update of her status. Three weeks passed without hearing from the client. The therapist contacted the client by telephone. The client indicated that approximately 4 weeks following the discontinuation of the atorvastatin calcium (Lipitor) her myalgic thigh complaints were fully resolved.

She stated that she would remain off the atorvastatin calcium (Lipitor) for a total of 12 weeks and then would receive clinical laboratory testing to evaluate serum cholesterol levels. The primary care physician would consider prescribing a different statin to control her hypercholesterolemia based on future cholesterol levels.

Summary: Medication used in many situations may have a significant effect on the health of the client and may alter the clinical presentation or course of the individual’s symptoms. It is important to ask if the client is taking any new medication (over the counter or by prescription), nutraceutical supplements, and if there have been any recent changes in the dosages of current medications.

There is a wide body of medical literature that associates the adverse reaction of myalgia and the more serious reaction of rhabdomyolysis with statin medications. Therapists must perform good pharmacovigilance.

From Trumbore DJ: Case report presented in partial fulfillment of DPT 910. Principles of differential diagnosis, Institute for Physical Therapy Education, Chester, Pennsylvania, 2005, Widener University. Used with permission.

Muscle aches and pain, unexplained fever, nausea, vomiting and dark urine can potentially be signs of myositis and should be referred to a physician immediately. Risk for statin-induced myositis is highest in people with liver disease, acute infection, and hypothyroidism. Severe statin-induced myopathy can lead to rhabdomyolysis (enzyme leakage, muscle cell destruction, and elevated CK levels). Rhabdomyolysis is associated with impaired renal and liver function. Screening for liver impairment (see Chapter 9) in people taking statins is an important part of assessing for rhabdomyolysis (see further discussion of rhabdomyolysis in Chapter 9).24

The therapist will need to perform clinical tests and measures to differentiate exercise-related muscle fatigue and soreness from statin-induced symptoms. For example, exercise-induced muscle fatigue and soreness should be limited to the muscles exercised and resolve within 24 to 48 hours. Statin-related weakness may involve muscles not recently exercised and may progress or fail to show signs of improvement even after several days of rest.25 Dynamometer testing can be used as a valid and reliable indicator of change in muscle strength.26,27

Strength testing, combined with client history, risk factors, and performance on the Stair-Climbing Test and Six-Minute Walk test, may prove to be an adequate means of assessment to detect meaningful declines in functional status; baseline measures are important.25

Coronary Artery Disease

The heart muscle must have an adequate blood supply to contract properly. As mentioned, the coronary arteries carry oxygen and blood to the myocardium. When a coronary artery becomes narrowed or blocked, the area of the heart muscle supplied by that artery becomes ischemic and injured, and infarction may result.

The major disorders caused by insufficient blood supply to the myocardium are angina pectoris and MI. These disorders are collectively known as coronary artery disease (CAD), also called coronary heart disease or ischemic heart disease. CAD includes atherosclerosis (fatty buildup), thrombus (blood clot), and spasm (intermittent constriction).

CAD results from a person’s complex genetic makeup and interactions with the environment, including nutrition, activity levels, and history of smoking. Susceptibility to CVD may be explained by genetic factors, and it is likely that an “atherosclerosis gene” or “heart attack gene” will be identified.28 The therapeutic use of drugs that act by modifying gene transcription is a well-established practice in the treatment of CAD and essential hypertension.29,30

Atherosclerosis: Atherosclerosis is the disease process often called arteriosclerosis or hardening of the arteries. It is a progressive process that begins in childhood. It can occur in any artery in the body, but it is most common in medium-sized arteries such as those of the heart, brain, kidneys, and legs. Starting in childhood, the arteries begin to fill with a fatty substance, or lipids such as triglycerides and cholesterol, which then calcify or harden (Fig. 6-2).

This filler, called plaque, is made up of fats, calcium, and fibrous scar tissue, and lines the usually supple arterial walls, progressively narrowing the arteries. These arteries carry blood rich in oxygen to the myocardium (middle layer of the heart consisting of the heart muscle), but the atherosclerotic process leads to ischemia and to necrosis of the heart muscle. Necrotic tissue gradually forms a scar, but before scar formation, the weakened area is susceptible to aneurysm development.

When fully developed, plaque can cause bleeding, clot formation, and distortion or rupture of a blood vessel (Fig. 6-3). Heart attacks and strokes are the most sudden and often fatal signs of the disease.

Risk Factors: In 1948 the United States government decided to investigate the etiology, incidence, and pathology of CAD by studying the residents of Framingham, Massachusetts, a typical small town in the United States. Over the next multiple decades, various aspects of lifestyle, health, and disease were studied.

The research revealed important modifiable and nonmodifiable risk factors associated with death caused by CAD. Since that time, an additional category, contributing factors, has been added (Table 6-3). The AHA has also developed a validated health-risk appraisal instrument to assess individual risk of heart attack, stroke, and diabetes (see Box 6-1).

More recent research has identified other possible risk factors for and predictors of cardiac events, especially for those persons who have already had a heart attack. These additional risk factors include:

Therapists can assist clients in assessing their 10-year risk for heart attack using a risk assessment tool from the National Cholesterol Education program available at

Women and Heart Disease: Many women know about the risk of breast cancer, but in truth, they are 10 times more likely to die of cardiovascular disease. While 1 in 30 deaths is from breast cancer, 1 in 2.5 deaths are from heart disease.44

Women do not seem to do as well as men after taking medications to dissolve blood clots or after undergoing heart-related medical procedures. Of the women who survive a heart attack, 46% will be disabled by heart failure within 6 years.45

In general, the rate of CAD is rising among women and falling among men. Men develop CAD at a younger age than women, but women make up for it after menopause. African-American women have a 70% higher death rate from CAD than white women. So whenever screening chest pain, keep in mind the demographics: older men and women, menopausal women, and black women are at greatest risk.

Diabetes alone poses a greater risk than any other factor in predicting cardiovascular problems in women. Women with diabetes are seven times more likely to have cardiovascular complications and about half of them will die of CAD.46

Studies have shown that women and men actually differ in the symptoms of CAD and in the manner in which acute MI can present. Women experience symptoms of CAD, which are more subtle and are “atypical” compared to the traditional symptoms such as angina and chest pain.

One of the most important primary signs of CAD in women is unexplained, severe episodic fatigue and weakness associated with decreased ability to carry out normal activities of daily living (ADLs). Because fatigue, weakness, and trouble sleeping are general types of symptoms, they are not as easily associated with cardiovascular events and are many times missed by health care providers in screening for heart disease.47

Symptoms of weakness, fatigue and sleeping difficulty, and nausea have been reported as a common occurrence as much as a month prior to the development of acute MI in women (see Table 6-4). The classic pain of CAD is usually substernal chest pain characterized by a crushing, heavy, squeezing sensation commonly occurring during emotion or exertion. The pain of CAD in women, however, may vary greatly from that in men (see further discussion on MI in this chapter).

Risk reduction in women focuses on lifestyle changes such as smoking cessation; low fat, low cholesterol diet; increased intake of omega-3 fatty acids; increased fruit, vegetable, whole grain intake; salt and alcohol limitation; and increased exercise and weight loss. If the woman has diabetes, strict glucose control is extremely important.48

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Mar 20, 2017 | Posted by in MANUAL THERAPIST | Comments Off on Screening for Cardiovascular Disease
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