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 www.youtube.com and type in “Gans video vertebral artery test.”

Fatigue

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.

Cough

Cough (see also Chapter 7) is usually associated with pulmonary conditions, but it may occur as a pulmonary complication of a cardiovascular pathologic complex. Left ventricular dysfunction, including mitral valve dysfunction resulting from pulmonary edema or left ventricular CHF, may result in a cough when aggravated by exercise, metabolic stress, supine position, or PND. The cough is often hacking and may produce large amounts of frothy, blood-tinged sputum. In the case of CHF, cough develops because a large amount of fluid is trapped in the pulmonary tree, irritating the lung mucosa.

Cyanosis

Cyanosis is a bluish discoloration of the lips and nail beds of the fingers and toes that accompanies inadequate blood oxygen levels (reduced amounts of hemoglobin). Although cyanosis can accompany hematologic or central nervous system disorders, most often, visible cyanosis accompanies cardiac and pulmonary problems.

Edema

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

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:

1. Get-up-and-go test: 17 seconds (within normal limits [WNL])

2. Functional reach test: 8 inches (WNL)

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).

TABLE 6-2

Cardiac Diseases

Conditions Affecting the Heart Muscle

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

1. Obstruction or restriction

2. Inflammation

3. Dilation or distention

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

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.^13–15

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

Age

Constant, bilateral myalgic pain unchanged by position or motion

Recent dosage change in medication

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.

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.

• Age over 80 (women more than men)

• Small body frame or frail

• Kidney or liver disease

• Drinks excessive grapefruit juice daily (more than 1 quart/day)

• Use of other medications (e.g., cyclosporine, some antibiotics, verapamil, human immunodeficiency virus [HIV] protease inhibitors, some antidepressants)²³

• Alcohol abuse (independently predisposes to myopathy)

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

Clinical Signs and Symptoms

Statin-Induced Side Effects

• Symptomatic myopathy (muscle soreness, pain, weakness, dyspnea); myositis (elevated CK level); look for weakness in several muscle groups

• Unexplained fever

• Nausea, vomiting

• Signs and symptoms of liver impairment:

• Dark urine

• Asterixis (liver flap)

• Bilateral carpal tunnel syndrome

• Palmar erythema (liver palms)

• Spider angiomas

• Nail bed changes, skin color changes

• Ascites

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).

Fig. 6-2 Hardening of the arteries. Atherosclerosis begins with an injury to the endothelial lining of the artery (intimal layer) that makes the vessel permeable to circulating lipoproteins. Penetration of lipoproteins into the smooth muscle cells of the intima produces “fatty streaks.” A fibrous plaque large enough to decrease blood flow through the artery develops. Calcification with rupture or hemorrhage of the fibrous plaque is the final advanced stage. Thrombosis (stationary blood clot) may occur, further occluding the lumen of the blood vessel.

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.

Fig. 6-3 Updated model of atherosclerosis. New technology using intravascular ultrasound shows the whole atherosclerotic plaque and has changed the way we view things. The traditional model held that an atherosclerotic plaque in the blood vessel, particularly a coronary blood vessel, kept growing inward and obstructing flow until it closed off and caused a heart attack. This is not entirely correct. It is more accurate to say that in the normal vessel (A), penetration of lipoproteins into the smooth muscle cells of the intima produces fatty streaks (B) and the start of a coronary lesion forms. C and D, The coronary lesion grows outward first in a compensatory manner to maintain the open lumen. This is called positive remodeling, as the blood vessel tries to maintain an open lumen until it can do so no more. E, Only then does the plaque (atheroma) begin to build up, gradually pressing inward into the lumen with obstruction of blood flow and possible rupture and thrombosis, potentially leading to myocardial infarction (MI) or stroke. F, Vascular disease today is considered a disease of the wall. Some researchers like to say the disease is in the donut, not the hole of a donut, and that is a new concept.¹⁰²

Thrombus: When plaque builds up on the artery walls, the blood flow is slowed and a clot (thrombus) may form on the plaque. When a vessel becomes blocked with a clot, it is called thrombosis. Coronary thrombosis refers to the formation of a clot in one of the coronary arteries, usually causing a heart attack.

Spasm: Sudden constriction of a coronary artery is called a spasm; blood flow to that part of the heart is cut off or decreased. A brief spasm may cause mild symptoms that never return. A prolonged spasm may cause heart damage such as an infarct. This process can occur in healthy persons who have no cardiac history, as well as in those who have known atherosclerosis. Chemicals like nicotine and cocaine may lead to coronary artery spasm; other possible factors include anxiety and cold air.

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).

TABLE 6-3

Risk Factors for Coronary Artery Disease

AHA Scientific Statements on Prevention of Coronary Heart Disease and Stroke, 2010. Available on-line at www.heart.org (Risk Factors and Coronary Heart Disease). Accessed Sept. 1, 2010.

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:

1. Exposure to bacteria such as Chlamydia pneumoniae, Porphyromonas gingivalis, and Cytomegalovirus organisms 31–33

2. Excess levels of homocysteine, an amino acid by-product of food rich in proteins

3. High levels of α-lipoprotein, a close cousin of LDL that transports fat throughout the body

4. High levels of fibrinogen, a protein that binds together platelet cells in blood clots ³⁴

5. Large amounts of C-reactive protein (CRP), a specialized protein necessary for repair of tissue injury.35,36

6. The presence of troponin T, a regulatory protein that helps heart muscle contract ³⁷

7. The presence of diagonal earlobe creases (under continued investigation)38–42

8. Past history of cancer treatment (cardiotoxic chemotherapeutic agents, trunk radiation)⁴³

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 http://hin.nhlbi.nih.gov/atpiii/calculator.asp?usertype=prof.

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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