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  1. 1. CHAPTER 11(Revised March 2009)Coronary Artery DiseaseEdward OnuskoOBJECTIVES Describe the impact of coronary artery disease in a primary care practice Prepare history questions that help define the risk and current problems related to coronary artery disease Explain how to use physical findings and in-office diagnostic studies to obtain objective evidence of cardiac disease Compile the pertinent components of the history, physical examination, and laboratory findings into an individual risk factor profile for coronary artery disease Recognize indications for further diagnostic studies and referral for treatment of cardiac disease Differentiate between the classes of drugs used to treat cardiac disease Explain key information about coronary artery disease and interventions that can alter cardiac risk factors using patient-appropriate termsINTRODUCTIONCoronary artery disease (CAD) [also known as coronary heart disease (CHD)] may be defined asnarrowing of the lumen of the coronary arteries secondary to the deposition of atheroscleroticplaque. CAD is associated with a wide variety of problems commonly seen in primary careoffices, including ischemic heart disease [e.g., angina, myocardial infarction (MI)], congestiveheart failure (CHF), arrhythmias, and valvular heart disease.TERMINOLOGYAcute coronary syndrome: acute MI or unstable anginaAngina pectoris: chest discomfort (i.e., pain, pressure, squeezing) caused by an ischemic myocardiumAngina, stable: a generally predictable pattern of angina pectoris that has not distinctly worsened over timeAngina, unstable: angina pectoris that is new or clearly increasing in frequency within the past 2 months, or is present at rest 1
  2. 2. Anginal equivalent: an atypical symptom (e.g., dizziness) that corresponds to myocardial ischemiaAngioplasty, balloon: a procedure involving dilation of the coronary arteries at the site of obstruction by inflation and then deflation of a balloon-tipped catheterAtherosclerosis: narrowing of large and medium-sized arteries caused by the deposition of lipids in the intima of the vessel wallAtypical chest pain: chest discomfort that does not have the typical characteristics of angina and may or may not be caused by myocardial ischemiaBody Mass Index (BMI): a measure of obesity [weight (pounds)height (inches)2 ] X 703Central obesity: pattern of truncal fat deposition more typically seen in men (apple-shaped pattern) than in womenDiastolic dysfunction: impaired filling of the left ventricle prior to contraction resulting from increased stiffness of the myocardiumDyslipidemia: abnormal blood lipids (i.e., high total cholesterol, high low-density lipoproteins (LDL), low high-density lipoproteins (HDL), or high triglycerides)Hypertension: usually quantitatively defined as elevation of the systolic blood pressure  140 mm Hg or the diastolic blood pressure  90 mm HgNSTEMI: myocardial infarction that presents without ST segment elevation on EKGPlaque, arterial: an area of lipid deposition on the inner surface of an arteryStent, arterial: a spring-like device placed in the coronary artery after angioplasty to maintain patency of the vesselSystolic dysfunction: depressed myocardial contractilitySTEMI: myocardial infarction that presents with ST segment elevation on EKGThrombosis, coronary: acute rupture of luminal plaque resulting in sudden occlusion of a coronary artery 2
  3. 3. BACKGROUNDCAD is the most common cause of morbidity and mortality for both men and women in theUnited States, affecting more than 13 million people. Along with other atherosclerotic diseases, itis one of the top 10 diagnoses seen in family practice offices. For persons aged 40 years, thelifetime incidence of CAD is 49% in men and 32% in women.PREVENTIONRisk FactorsRisk factors for CAD include: Cigarette smoking Age  than 40 years Diabetes mellitus types 1 and 2 Hypertension Dyslipidemia Obesity (i.e.,  20% over desired body weight or BMI is  29 kg/m2 ) particularly if central obesity Emotional or physical stress Sedentary lifestyle Excessive alcohol intake Related family member with cardiac disease particularly if onset in male family member was under 55 years old or in female under age 65. Male sex or postmenopausal female Elevated homocysteineNote:Multiple risk factors for CAD tend to cluster in the metabolic syndrome, defined in Chapter 12.Primary PreventionRisk factor modificationRisk factor modification is the major form of primary CAD prevention. Diet, exercise, andsmoking cessation are three key ingredients (see NONPHARMACOLOGIC THERAPY). 3
  4. 4. ScreeningMany patients with risk factors for cardiac disease visit their family physicians for unrelatedmedical concerns. When treating a patient for a problem such as acute gastrointestinal disease,recurrent bronchitis, or depression, note all of the patient’s health risk factors. These risk factorsdo not have to be addressed thoroughly at an acute visit but should receive attention in a timelymanner. Sometimes the best approach is to ask the patient to return for a “prevention review”visit after pointing out key reasons why this type of visit is important for the patient’s long-termhealth. Because CAD is so prevalent, all adults (particularly over the age of 40) should be assessed forcardiovascular risk for the subsequent 10 years. A risk  20 percent is defined as high risk; 10-19 percent is intermediate risk; and  10 percent is low risk. Clinical prediction calculators areavailable based on epidemiological studies like the Framingham trial. Routine screening for thepresence of CAD (e.g., electrocardiogram, tomography for coronary calcium) is notrecommended in low risk individuals. (the USPSTF category D recommendation.)Note:The average woman has a risk from CAD approximately equal to that of a man 10 years herjunior. However, because women are likely to live longer than men, the number of actual deathsfrom CAD is similar in both sexes. Physical examination findings that suggest atherosclerosis (e.g., a carotid or renal bruit), othercardiac disease (e.g., a murmur or irregular heart rhythm), or the presence of cardiac risk factors(e.g., fundoscopic changes of diabetes mellitus) necessitate further evaluation for CAD. The significance of screening during a routine physical is emphasized and explored in Chapter3. In addition, see Chapters 12, 13, and 15 for recommendations on who should be screened forspecific risk factors and how often.PRIMARY PREVENTION – INTERVENTIONSDIAGNOSISThe tremendous impact of CAD in the United States dictates that it is essential for the generalpublic to be educated about the signs and symptoms of heart disease that warrant evaluation by ahealth care provider. The greatest “clot buster” drugs will not be effective if the patient withangina does not recognize the urgent need to seek medical evaluation. Delay in the diagnosis ofcardiac disease can result in significant morbidity and mortality; therefore, a healthy level ofcaution is indicated. The diagnostic information that follows is for suspected CAD, not for theurgent care of a suspected MI in progress. 4
  5. 5. PresentationPatients with symptomatic CAD may present with a large variety of complaints, including: Discomfort in the chest, arm, neck, shoulder, or abdomen Shortness of breath or exercise intolerance Dizziness or syncope “Heartburn” PalpitationsNoteWomen are less likely than men to present with classic symptoms of CAD, but more likely topresent with nonspecific complaints (e.g., fatigue).HistoryA careful history is the primary tool to explore a clinical suspicion of CAD. Physical examinationand diagnostic studies may then provide more objective evidence that can help define treatmentoptions, including the appropriate time for specialty referral.History of present illnessChest discomfort is the most common presentation for CAD in the outpatient setting. Use thefollowing mnemonic (P/PQRST) to focus history taking on this important symptom. Provocation o What brings the symptom on or makes it worse (e.g., physical exertion, emotional stress)? o What were you doing the first time (or the most recent time) you experienced the symptom? Palliation o What relieves the symptom (e.g., rest, sublingual nitroglycerin)? Quality o What words best describe the pain (e.g., pressure, tightness, crushing, squeezing, heaviness)? Radiation o Where does the pain start and, if it moves, to where does it move (e.g., over the precordium radiating to the jaw, neck, arms, or abdomen)? It is often useful to have the patient point with one finger to localize the discomfort. o What other symptoms accompany the chest discomfort (e.g., diaphoresis, nausea, palpitations, and shortness of breath)? Severity o How prominent is the symptom (rated on a scale of 1 to 10)? o What were you able to do or not able to do when the pain was present? 5
  6. 6.  Temporal o When did the pain first start? o How long does the pain last? o How often does the pain occur? o Have you ever had the pain before? o How long after the onset of exertion does the pain begin? o Does the pain occur in the early morning hours (common in acute MI)? In addition to the symptom of chest discomfort, ask the patient about risk factors for cardiacdisease (see RISK FACTORS, above.) Obtain the patient’s medication history, including: Current cardiovascular medications Medications that may impact on coagulopathies (e.g., daily aspirin) Medications that could cause or exacerbate the current symptoms (e.g., nonsteroidal anti- inflammatory drugs can increase gastrointestinal-related chest pain, herbal preparations may contain caffeine or stimulants) Prevention studies have suggested that COX-2 inhibitors (refocoxib was withdrawn from the market September 2004) and a non-steroidal anti-inflammatory (NSAID) medication naproxen may increase cardiovascular morbidity. Ask about use of these medications. Adherence for all prescribed medicationPast medical history Have you had previous evaluations for cardiac disease? Do you have diabetes, blood pressure problems, or any other major medical problems?Family historyAsk the patient about family members with: CAD Diabetes Lipid abnormalities High blood pressure Cerebrovascular disease (e.g., stroke, transient ischemic attacks) Peripheral vascular disease (e.g., surgical limb, foot, or digit loss; claudication)Social historyAsk the patient about: Use of tobacco products and alcohol Exercise and diet Current major stressors Support systems (e.g., Who lives at home? Are you involved in church activities?) Job history (e.g., significant source of stress? sedentary work duties?) 6
  7. 7. Review of SystemsAll systems need to be carefully reviewed early on to establish a baseline; Table 11–1 highlightssome important findings in selected systems that help to differentiate acute MI and CAD.TABLE 11–1. Focused Review of Systems in the Diagnosis of Coronary Artery Disease Pertinent Findings _____________________________________________________ Pertinent Positives Pertinent NegativesSystem Indicating CAD Regarding Acute MIConstitutional Sweating*, rapid weight gain Fever (fluid retention)Cardiovascular Chest discomfort (with or — without exertion*), palpitationsRespiratory Shortness of breath with or without Pain with deep exertion, PND, orthopnea, breaths, productive nonproductive cough coughGastrointestinal Abdominal or mid-epigastric pain, — nausea*Musculoskeletal Calf pain (due to claudication), Pain associated with recent neck or arm pain trauma or strain to chest, arm, neck, or calf musclesNeurologic Dizziness or lightheadedness*, Circumoral or fingertip headache (due to urgently high numbness or tingling blood pressure) (due to hyperventilation), dizziness with sensation of spinning (due to vestibular disorder)Psychologic Unusual anxiety*, panic with Multiple complaints feeling of doom* consistent with somatization disorderCAD = coronary artery disease; MI = myocardial infarction; PND = paroxysmal nocturnal dyspnea.*These findings are common in patients with acute MI. 7
  8. 8. Angina deserves special mention in the review of systems because patients with it may presentwith what first appear to be noncardiac symptoms including gastrointestinal, pulmonary,musculoskeletal, or psychogenic symptoms. When you are uncertain as to whether a stablepatient has angina, ask yourself the following questions before suggesting further work-up: How typical are this patient’s symptoms and history for angina? How likely is it that this patient’s atypical symptoms are from ischemia? What else is in the differential diagnosis? What are the patient’s risk factors? What has the physical examination revealed? What does the patient think is happening? Is an electrocardiogram (EKG) or chest radiograph necessary?NoteAll that pains the chest is not angina. A work-up without thought may needlessly waste time andmoney and produce avoidable patient and family anxiety.Physical Examination (Table 11–2)Laboratory TestsEKGThe EKG should be immediately available in any adult primary care setting. A 12-lead tracingshould be evaluated for rate, rhythm, axis, hypertrophy, signs of ischemia (i.e., ST segment, Twave, or Q wave abnormalities), and signs of metabolic abnormalities (e.g., hypokalemia).Treatment of an acute coronary syndrome should not be delayed while waiting for otherdiagnostic tests.TABLE 11–2. Physical Examination Findings in Coronary Artery DiseaseSystem FindingsVital signs Hypertension, hypotension, tachycardia, bradycardia, irregular pulse, tachypneaGeneral appearance Comfort versus distress, pallor or cyanosis, obesity, diaphoresisHEENT Signs of diabetes or hypertension on fundoscopic examinationCardiovascular Gallops, murmurs, rubs, displaced cardiac impulse (by palpation), decreased peripheral pulses, jugular venous distention, bruits 8
  9. 9. TABLE 11–2. (Continued)System FindingsRespiratory Abnormal breath sounds (e.g., rales, wheezes, rhonchi), increased respiratory effortGastrointestinal OrganomegalyMusculoskeletal Peripheral edemaBloodCardiac enzymes [e.g., troponin-T or troponin-I; total creatine phosphokinase (CPK) and CPK-MB band; and/or myoglobin] are evaluated if acute MI is suspected. This evaluation is usuallydone in the emergency department or inpatient care setting. A complete blood count, fasting lipidprofile, renal profile, glucose, and clotting studies (prothrombin time and partial thromboplastintime) are also performed.UrineA urinalysis may reveal proteinuria (indicating renal disease) or glucosuria (indicating diabetes).Imaging StudiesPosteroanterior and lateral chest films may be obtained.Chest radiographs are helpful in assessing cardiac enlargement, pulmonary vascular congestion,and pulmonary pathology (e.g., pneumonia) that may be causing symptoms or affecting cardiacstatus.Additional studiesOximetryOxygen saturation by pulse oximetry may demonstrate possible respiratory compromise..Cardiac stress testsCardiac stress tests can be very useful in the nonurgent diagnosis of CAD. These tests consist oftwo parts:1. A mechanism to stress the cardiovascular system. Exercise (e.g., treadmill, bicycle, arm ergometer) or the administration of pharmacologic agents (e.g., adenosine, 9
  10. 10. dobutamine, dipyridamole) can result in increased myocardial oxygen requirements or alteration of cardiac perfusion.2. A means to measure the heart’s response to stress. When inadequate coronary blood supply is unable to provide sufficient perfusion to the stressed heart, ischemia may be evidenced by:  A drop in ST segments on the EKG  Abnormal distribution of radioisotope (thallium, sestamibi) perfusion to the myocardium  Ventricular wall motion abnormalities seen on echocardiography (dobutamine stress echocardiography)The individual patient needs to be matched with the appropriate type of stress test (Table 11–3). 10
  11. 11. TABLE 11–3. (Continued)Test Description Indications ContraindicationsExercise EKG Most commonly done on a treadmill; For men or postmenopausal women Not for patients with unstable continuous EKG tracing is monitored for with a intermediate pretest probability angina, critical aortic stenosis, ST segment depression; least expensive of CAD based on age, gender, and left ventricular outflow tract stress test; less helpful if baseline ST symptoms (or for risk stratification obstruction, a recent thrombotic segment abnormalities are present at in patients considered high risk) event, or cerebral ischemia, rest (e.g., LBBB, ventricular pacemaker, or for those who have had digitalis effect) a large MI within the past 3 daysExercise EKG Same as exercise EKG, but a See indications for exercise EKG, except See contraindications for exercisewith radiolabeled radiopharmaceutical is this test is better for patients with EKGtracer (thallium, injected immediately postexercise and baseline ST abnormalities on EKGsestamibi, boroxime its distribution by the cardiacor tetrofosmin) circulation is imaged; may demonstrate fixed (suggesting previous MI) or reversible (suggesting compromised circulation worsened by stress) areas of myocardial ischemiaPharmacologic Administration of adenosine or For patients who are unable to do Not for patients with activestress EKG dipyridamole results in alteration exercise because of physical bronchospasm, high-grade heart of coronary artery blood flow; effect limitations (e.g., severe emphysema, block without pacemaker, or may then be assessed by thallium morbid obesity) or who have a high hypotension, or for those who are studies probability of a false–positive result taking theophylline or caffeine (e.g., valvular disease, left ventricular hypertrophy).Stress Exercise or IV dobutamine is the stressor; an For patients who are unable to tolerate Not for patients with symptomaticechocardiogram echocardiogram detects the degree of physical exertion or other nuclear aortic aneurysm, those with wall motion abnormalities and measures perfusion isotopes, or if information uncontrolled ventricular tachycardia, the response; stress echocardiograms on ventricular wall thickness or and those who are difficult to image may have superior specificity and valvular structure and function is with echocardiography (e.g., because sensitivity to other forms of stress testing also needed of morbid obesity, severe lung disease)CAD = coronary artery disease; EKG = electrocardiogram; IV = intravenous; LBBB = left bundle branch block; MI = myocardial infarction. 11
  12. 12. EchocardiographyAn echocardiogram may be useful in assessing systolic heart failure (poor contractility may besecondary to ischemia), diastolic dysfunction, valvular heart disease, and ejection fraction.However, an echocardiogram may not be helpful for CAD that is not associated with these otherpathologies, except to rule them out. Echocardiography has the advantages of being noninvasive(as opposed to cardiac catheterization), nonprovocative (as opposed to a stress test), andrelatively inexpensive.Cardiac catheterizationCardiac catheterization is invasive and more expensive than stress testing but gives a definitivepicture of the coronary artery anatomy. It has the added advantage of allowing for immediateinterventional therapy (e.g., angioplasty).NoteElectronic beam computed tomography (CT) scanning and magnetic resonance angiography ofthe coronary arteries are in development as noninvasive screening tools but are not currentlyrecommended screening procedures.DIFFERENTIAL DIAGNOSIS (Table 11–4)THERAPYNonpharmacologic TherapyExercise prescriptions Exercise is an important aspect of the patient treatment plan to achieve the goals of weightloss, blood pressure control, improved cardiovascular fitness, and correction of dyslipidemias.NoteA stress test may be needed before undertaking an exercise program to evaluate the safety ofstressing the heart and to determine what level of exercise the patient should be prescribed. Askyour preceptor before prescribing exercise for any patient with CAD. Thirty minutes of aerobic activity daily (at least three times a week) is usually recommended.Shorter, more frequent exercise (e.g., taking the stairs instead of the elevator, parking at the farcorner of the lot and walking) is also beneficial. 12
  13. 13. TABLE 11–4. Differential Diagnosis of Chest PainDifferential Diagnosis Description of Chest PainAortic dissection Associated with severe hypertensionEsophageal rupture Worse with emesis or swallowingGastroesophageal reflux Worse when lying down; radiates to the backMusculoskeletal pain Worse with cough, deep breathing, palpation, or movementPancreatitis Radiates to the back and is coincident with abdominal painPanic attack Coincident with palpitations, severe anxiety, a feeling of doom, hyperventilation symptomsPericarditis Worse with cough, deep breathing, or when lying down; radiates to the neck, shoulder, or backPneumomediastinum Worse with cough, deep breathing, emesis, or swallowing; radiates to the jaw or neckPneumonia Coincident with dyspnea and cough; worse with cough or deep breathingPneumothorax Coincident with dyspnea; radiates to the back or shoulderPulmonary embolus Coincident with dyspnea; worse with cough or deep breathingNoteChoosing an activity that is enjoyable to the patient is important in ensuring adherence to theexercise regimen. Any activity, as long as it is not too strenuous for the patient’s heart, is betterthan none at all.Dietary recommendationsDietary specifics suggested by most authorities include salt restriction for control of bloodpressure and CHF, saturated fat restriction for dyslipidemias, plenty of fresh fruits andvegetables, and caloric restriction for obesity. Intake of fish has been associated with a reducedrisk of CAD, though pregnant/child-bearing potential women need to avoid fish with a relativelyhigh mercury content (e.g., shark, swordfish, king mackerel, and tile fish). 13
  14. 14. NoteAs little as 10 pounds of weight loss may have a significant cardiovascular benefit.Moderate alcohol use (i.e., 1 oz of ethanol per day for men and 0.5 oz for women) has beenshown to be associated with a decreased risk of CAD. Recommendations for regular alcohol useshould be made with caution, however. Alcohol is an addictive substance that may have adverseeffects on hypertension, obesity, diabetes mellitus, triglycerides, liver, and the uppergastrointestinal tract when consumed in excess.Smoking cessationEfforts by physicians have been shown to significantly impact on a patient’s ability to quitsmoking. See Chapter 24 for a discussion of smoking cessation.Stress reductionRelaxation techniques and lifestyle modifications that decrease psychological stress have beenshown to lower anxiety and depression in patients with CAD, but have not been shown todecrease mortality or the need for revascularization procedures.PharmacotherapyCholesterol plaque–induced fixed narrowing of the coronary arteries usually causes exercise-sensitive stable angina. Pharmaceuticals for stable angina are generally targeted at decreasingischemia, providing anticoagulation, and modifying risk factors.IschemiaIschemia can be decreased with -blockers, nitrates, or calcium channel blockers. -Blockersand calcium channel blockers appear to have similar clinical outcomes; however, -blockers arepreferred because they appear to have fewer adverse effects when treating stable angina. Recentstudies have suggested that -blockers may be better for anginal symptoms. Thus far, trialscomparing nitrates to -blockers and calcium channel blockers for antianginal treatment havebeen inconclusive.NoteThe American College of Cardiology and the American Heart Association recommend -blockers as the first-line agents for chronic, stable angina unless there is some contraindicationto their use.AnticoagulationProphylaxis with 81 mg of aspirin a day is usually indicated for its antithrombotic (i.e.,antiplatelet) effect. Aspirin prophylaxis should be considered for high-risk, asymptomatic 14
  15. 15. patients. Because of long-term risk of aspirin use (i.e., gastrointestinal bleeding and hemorrhagicstroke), chronic aspirin prophylaxis for CAD should probably not be used in either low-riskasymptomatic patients or patients with uncontrolled hypertension. Clopidogrel may be used inpatients intolerant of aspirin.Risk factor modificationLow dose 81 mg Aspirin daily has been shown to decrease the risk of first MI by 32%. The useof low dose aspirin is recommended by the USPSTF and the AHA for patients with Framinghamrisk scores of >6^ and 10% respectedly. Risk factors can be altered with antihypertensives,lipid-lowering agents, and smoking cessation. Postmenopausal hormone replacement therapyis no longer recommended for primary or secondary prevention of CAD. See Chapters 3, 15, and24 for more information.ProceduresThe decision about whether to suggest coronary artery bypass grafting (CABG), angioplasty, ormanagement with antianginal medications alone is often preceded by defining the coronary arteryanatomy with a cardiac catheterization. At times the catheterization can proceed to includecorrection of certain structural abnormalities (e.g., coronary artery stenosis, valvular stenosis)using balloon angioplasty, stent placement in the coronary arteries, or laser or mechanicalablation (to minimize obstructing plaques). CABG is an effective therapy for the treatment of CAD and may provide more effectivesymptomatic relief than medical management. It improves survival rates in patients with leftmain artery disease, three-vessel disease, or significant CAD with left ventricular dysfunction.URGENCIES & EMERGENCIES—ACUTE CORONARY SYNDROMESUnstable angina and acute MI are likely to be sudden, thrombotic, platelet-mediated eventscaused by acute rupture of plaque in the endothelium of the coronary arteries. The patient and theclinician must be able to quickly recognize the presentation of an acute coronary syndrome andact accordingly. Individuals with chest pain and ST segment elevation on their EKG (STEMI)usually have a reddish, fibrin-rich clot with a high degree of occlusion in the infarct-relatedcoronary artery and therefore benefit from therapy with thrombolytics. Patients with an acutecoronary syndrome without ST segment elevation (NSTEMI or unstable angina) usually havegrayish-white, platelet-rich, nonoccluding clot in the coronary artery and should receiveantiplatelet therapy but NOT thombolytics. Actively instruct patients with known CAD in themanagement of patterns of unstable angina. 15
  16. 16. NoteWhen treating a patient with the acute onset pain consistent with a MI or unstable angina,follow the mantra, “Time is Muscle.” The sooner an acute coronary occlusion is treated withtherapies such as thrombolytics, the greater the benefit to the endangered myocardium.Goals for acute treatment inlude: within 10 minutes: rapid triage, EKG, oxygen, aspirin, nitroglycerin, morphine, establish IV within 30 minutes: administer thrombolytic if indicated, or within 90 minutes: angioplasty if indicated Many therapies for unstable angina and acute MI (Table 11–5) can be administered in theoutpatient setting. These therapies may decrease clot formation, ischemia, and pain as well asimprove outcomes. Life-threatening delays in therapy may result from waiting for nonessentiallaboratory tests to return, trying to contact other health care providers, or misdiagnosingnontypical complaints as being noncardiac in origin.TABLE 11–5. Urgent Outpatient Therapy for a Suspected Myocardial Infarction  Administer CPR if needed.  Call 911 or your local emergency system activation number.  Administer oxygen.  Administer nitroglycerin sublingually for chest pain.  Administer aspirin for antiplatelet therapy.  Use a cardiac monitor to assess for arrhythmias. Also consider…..  Morphine for pain and sedation The mnemonic “MONA” (morphine, oxygen, nitrates, aspirin) has been used for treatment of acute ischemia. CPR = cardiopulmonary resuscitation.NoteBecause thrombolytics or urgent angioplasty may be a highly effective treatment alternatives inacute coronary syndromes, patients should get to the hospital as soon as possible. Clot formation can be decreased with aspirin, heparin and glycoprotein IIb/IIIainhibitors. Aspirin’s antiplatelet effects have been shown to be highly efficacious in acutecoronary syndromes. Heparin anticoagulation has been a mainstay of therapy. Newer alternativesto unfractionated heparin that modify the coagulation pathway include low molecular weightheparin (a more purified heparin preparation that requires less blood monitoring of anticoagulanteffect). Clopidogrel and glycoprotein IIb/IIIa inhibitors are also used for their antiplatelet activityin this setting. Ischemia and pain can be reduced with oxygen, nitroglycerin, and morphine. Oxygenshould be administered by nasal cannula. Patients with chronic obstructive pulmonary disease 16
  17. 17. should be monitored carefully because they may retain carbon dioxide. Nitroglycerin should begiven sublingually, topically, or intravenously to decrease vasoconstriction and pain. Morphinemay be given intravenously for sedation, to enhance vasodilation, and to decrease pain notrelieved by nitrates. Outcomes may improve with -blockers, angiotensin-converting enzyme (ACE) andstatins inhibitors. -Blockers improve outcome when used in acute MI and chronically in thepostinfarct patient and are probably underused for these indications. ACE inhibitors may enhancethe remodeling process that begins soon after ischemic injury of the myocardium.SPECIAL POPULATIONSChildrenCardiac disease in children is usually not secondary to CAD. Some forms of vasculitis (e.g.,Kawasaki’s disease) may result in nonatherosclerotic aneurysmal abnormalities of the coronaryarteries, with a risk of sudden death. Because cardiac risk factors are well defined in the adult population and effective treatment ofthese factors (e.g., hypertension, dyslipidemia) has been demonstrated to decrease morbidity andmortality, it is tempting to define certain children as being at high risk for CAD. Is the firstgrader with the highest cholesterol in his class at risk for heart disease? Is the tenth grader on thebasketball team with blood pressure in the 95th percentile at higher risk of experiencing an MI onthe court? Or are these children normal? Whether such definitions of risk are appropriate and whether treatment of the risk factor doesmore harm than good is the subject of continued debate and research. However, it is known thateducation of school-aged children about the health effects of tobacco use, exercise, diet, andother aspects of a healthy lifestyle is beneficial.SeniorsNormal physiologic changes associated with aging may complicate or worsen cardiac diseaseprocesses. These changes include:  Blunting of heart rate response to exercise (secondary to diminished -adrenergic receptor responsiveness)  Decreased compliance of the arteries (results in hypertension and increased cardiac workload)  Decreased compliance of the ventricles (results in increased end-diastolic pressures) For example, seniors are more dependent on atrial contraction to adequately fill the relativelystiff ventricles, thus making atrial fibrillation a more symptomatic problem than it might be in ayounger person. In addition, -blocker therapy for hypertension is less effective in seniorsbecause of decreased baseline -adrenergic receptor responsiveness. 17
  18. 18. Because CAD is usually a lifelong, progressive process, the prevalence increases withadvancing age and is very common in the elderly. Frequent comorbidities, increased propensityfor adverse drug reactions, and adherence problems all complicate the evaluation and treatmentof cardiac risk factors, management of adverse cardiac events, and postevent monitoring andtreatment in the elderly patient.PregnancyNormal pregnancy is a hyperdynamic cardiovascular state. Heart rate, cardiac output, and bloodvolume are increased. Normal women have enough cardiac reserves to respond to the increaseddemands without problems. However, women with significant baseline cardiac disease may findpregnancy to be a stressor that compromises their cardiovascular well-being. These women mustbe followed carefully during pregnancy, labor, and delivery.COMPLEMENTARY/ALTERNATIVE MEDICINEThe following therapies have limited scientific acceptance:  Vitamin E has known antioxidant effects that are postulated to help prevent the endothelial damage that occurs with the atherosclerotic process. Primary and secondary prevention trials have not demonstrated a significant reduction in cardiovascular events, however. There is some concern that Vitamin E supplements might actually increase mortality in people with chronic diseases taking high doses. Doses higher than 400 iu/day are not recommended.  Chelation therapy has been advocated as a means of reversing plaque buildup, but it is not accepted by mainstream cardiologists and should not be recommended.  Garlic has purported benefits in the treatment of CAD, but proof of efficacy from controlled trials is lacking.  Fish oil and other omega-3 fatty acid supplements may be effective treatments for hyperlipidemia with possible benefit of decreased mortality.  Adjunctive therapies (e.g., hypnotherapy, acupuncture, guided imagery, yoga, biofeedback) may aid traditional treatment of cardiac risk factors (e.g., cigarette smoking, hypertension).REFERRALSSpecialty consultation is indicated for highly technical diagnostic evaluation (e.g., cardiaccatheterization) or when therapies are needed that are beyond the usual scope of the familyphysician. As with all diagnoses, your preceptor may refer sooner or later than one of hiscolleagues because of variable comfort levels with the evaluation and treatment of CAD. 18
  19. 19. REFERENCESwww.guideline.govwww.americanheart.orgwww.acc.orgRevised3/09 19