The document provides details about treadmill exercise testing, including: 1) It is used to assess cardiovascular disease by estimating functional capacity and the likelihood of coronary artery disease. 2) Safety precautions and equipment are required, and protocols like the Bruce protocol are commonly used to gradually increase workload over stages. 3) Measurements of oxygen uptake, ventilation, and other cardiorespiratory parameters are obtained to evaluate functional capacity and diagnose cardiovascular impairment.

1. Department of Medicine M.L.B. Medical College, Jhansi Tread Mill Test Presenter : Dr. Awadhesh Sharma Moderator : Dr. Navneet Agarwal

4. The test is mainly used to estimate prognosis and to determine functional capacity, the likelihood and extent of coronary artery diseases (CAD), and the effects of therapy. Hemodynamic and ECG measurements combined with ancillary techniques such as metabolic gas analysis, radionuclide imaging, and echo­cardiography enhance the information content of exercise testing in selected patients. Anticipation of dynamic exercise results in an acceleration of ventricular rate due to vagal withdrawal, increase in alveolar ventilation, and increased venous return primarily as a result of sympathetic veno­constriction. In normal persons, the net effect is to increase resting cardiac output before the start of exercise. The magnitude of hemodynamic response during exercise depends on the severity of the exercise and the amount of muscle mass involved.

5. In the early phases of exercise in the upright position, cardiac output is increased by an augmentation in stroke volume mediated through the use of the Frank-Starling mechanism and heart rate; the increase in cardiac output in the latter phases of exercise is primarily due to a sympathetic-mediated increase in ventricular rate. At fixed submaximal workloads below anaerobic threshold, steady-state conditions are usually reached after the second minute of exercise, following which heart rate, cardiac output, blood pressure, and pulmonary ventilation are maintained at reason­ably constant levels. During strenuous exertion, sympathetic discharge is maximal and parasympathetic stimulation is withdrawn, resulting in vaso­constriction of most circulatory body systems, except for that in exercising muscle and in the cerebral and coronary circulations. Venous and arterial nor­epinephrine release from sympathetic postganglionic nerve endings, as well as plasma renin levels, are increased; the catecholamine release enhances ven­tricular contractility.

6. As exercise progresses, skeletal muscle blood flow is increased, oxygen extraction increases by as much as threefold, total calculated peripheral resistance decreases, and systolic blood pressure, mean arterial pressure, and pulse pressure usually increase. Diastolic blood pressure does not change significantly. The pulmonary vascular bed can accommodate as much as a sixfold increase in cardiac output with only modest increases in pulmonary artery pressure, pulmonary capillary wedge pressure, and right atrial pressure; in normal individuals, this is not a limiting determinant of peak exercise capacity. Cardiac output increases by four- to sixfold above basal levels during strenuous exertion in the upright position, depending on genetic endowment and level of train­ing. The maximum heart rate and cardiac output are decreased in older individuals, partly because of decreased beta-adrenergic responsivity.

7. Maximum heart rate can be estimated from the formula 220 - age in years, with a standard deviation of 10 to 12 beats per minute. The age-predicted maximum heart rate is a useful measure­ment for safety reasons. However, the wide standard deviation in the various regression equations used and the impact of drug therapy limit the usefulness of this param­eter in estimating the exact age-predicted maximum for an individual patient. In the postexercise phase, hemodynamics return to baseline within minutes of termi­nation of exercise. Vagal reactivation is an important cardiac deceleration mechanism after' exercise and is accelerated in well­trained athletes but blunted in patients with chronic heart failure (see also section on heart rate). Intense physical work or signif­icant cardiorespiratory impairment may interfere with achievement of a steady state, and an oxygen deficit occurs during exer­cise. The total oxygen uptake in excess of the resting oxygen uptake during the recov­ery period is the oxygen debt.

8. Patient position At rest, the cardiac output and stroke volume are higher when the person is in the supine position than when the person is in the upright position. With exercise in normal supine persons, the eleva­tion of cardiac output results almost entirely from an increase in heart rate, with little augmentation of stroke volume. In the upright posture, the increase in cardiac output in normal individuals results from a combination of elevations in stroke volume and heart rate. A change from supine to upright posture causes a decrease in venous return left ventricular end-diastolic volume and pressure, stroke volume, and cardiac index. Renin and nor­epinephrine levels are increased. End-systolic volume and ejection fraction are not significantly changed. The net effect on exercise performance is an approximate 10 percent increase in exercise time cardiac index, heart rate, and rate pressure product at peak exercise in the upright as compared with the supine position.

9. Cardiopulmonary Exercise Testing Cardiopulmonary exercise testing involves measurements of respiratory oxygen uptake (VO 2 ), carbon dioxide production (VCO 2 ), and ventilatory parameters during a symptom-limited exercise test. VO 2 max is the product of maximal arterial-venous oxygen difference and cardiac output and represents the largest amount of oxygen a person can use while performing dynamic exercise involving a large part of total muscle mass. The VO 2 max decreases with age, is usually less in women than in men, and can vary among individuals as a result of genetic factors. VO 2 max is diminished by degree of cardio­vascular impairment and by physical inactivity. Peak exercise capacity is decreased when the ratio of measured to predicted VO2 max is less than 85 to 90 percent.

12. At high exercise levels, carbon dioxide pro­duction exceeds VO 2 , and a respiratory exchange ratio greater than 1.1 often indicates that the subject has performed at maximal effort. METABOLIC EQUIVALENT In current use, the term metabolic equivalent (MET) refers to a unit of oxygen uptake in a sitting, resting person; 1 MET is equivalent to 3.5 ml 02/kg/min of body weight. Measured VO 2 in ml 02/min/kg divided by 3.5 ml 02/kg/min determines the number of METs associated with activity. Work activities can be calculated in multiples of METs; this measurement is useful to determine exercise prescriptions, assess disability, and standardize the reporting of submaximal and peak exercise workloads when different protocols are used.

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25. Exercise Protocols The main types of exercise are isotonic or dynamic exercise, isometric or static exercise, and resistive (combined isometric and isotonic) exercise. Dynamic protocols most frequently are used to assess cardiovascular reserve, and those suitable for clinical testing should include a low intensity warm-up phase. In general, 6 to 12 minutes of con­tinuous progressive exercise during which the myocardial oxygen demand is elevated to the patient's maximal level is optimal for diagnostic and prognostic purposes. The protocol should include a suitable recovery or cool-down period. If the protocol is too strenuous for an individual patient, the test must be terminated early, and there is no opportunity to observe clinically important responses. If the exercise protocol is too easy for an individual patient, the prolonged procedure tests endurance and not aerobic capacity.

26. Thus, exercise protocols should be individualized to accommodate a patient’s limitations. Protocols may be set up at a fixed duration of exercise for a certain intensity to meet minimal qualifications for certain industrial tasks or sports programs. TREADMILL PROTOCOL The treadmill protocol should be consistent with the patient’s physical capacity and the purpose of the test. In healthy individuals, the standard Bruce protocol is popular, and a large diagnostic and prognostic data base has been published using this protocol. The Bruce multistage maximal treadmill protocol has 3-minute periods to allow achievement of a steady state before work­load is increased. In older individuals or those whose exercise capacity is limited by cardiac disease, the protocol can be modified by two 3-minute warm ­up stages at 1.7 mph and 0 percent grade and 1.7 mph and 5 percent grade.

27. A limitation of the Bruce protocol is the rela­tively large increase in VO 2 between stages and the additional energy cost of running as compared with walking at stages in excess of Bruce’s stage III. It is important to encourage patients not to grasp the handrails of the treadmill during exercise, particularly the front handrails. Functional capacity can be overestimated by as much as 20 percent in tests in which handrail support is permitted, and VO 2 is decreased. Because the degree of handrail support is difficult to quantify from one test to another, more consistent results can be obtained during serial testing when handrail support is not permitted. The 6-Minute Walk Test The 6-minute walk test can be used for patients who have marked left ventricular dysfunc­tion or peripheral arterial occlusive disease and who cannot perform bicycle or treadmill exercise.

28. Patients are instructed to walk down a 100-foot corridor at their own pace, attempt­ing to cover as much ground as possible in 6 minutes. At the end of the 6-minute interval, the total distance walked is determined and the symptoms experienced by the patient are recorded. The 6-minute walk test as a clinical measure of ambulatory function requires highly skilled personnel fol­lowing a rigid protocol to elicit reproducible and reliable results. The coefficient of variation for distance walked during two 6-minute walk tests was 10 percent in one series of patients with peripheral arterial occlusive disease.

29. Estimated oxygen cost of bicycle ergometer and selected treadmill protocols. The standard Bruce protocol starts at 1.7 mph and 10 percent grade (5 METs), with a larger increment between stages than protocols such as the Naughton, ACIP, and Weber, which start at less than 2 METs at 2mph and increase by 1- to 1.5-MET increments between stages. The Bruce protocol can be modified by two 3-minute warm-up stages at 1.7mph and 0 percent grade and 1.7mph and 5 percent grade. METs = metabolic equivalents. (Adapted from Fletcher GF, Balady G, Amsterdam EA, et al: Exercise Standards for Testing and Training. A statement for healthcare professionals from the American Heart Association. Circulation 104:1694, 2001.

30. Electrocardiographic Measurements LEAD SYSTEMS. The Mason-Likar modification of the standard 12-lead ECG requires that the extremity electrodes be moved to the torso to reduce motion artifact. The arm elec­trodes should be located in the most lateral aspects of the infraclavicular fossae, and the leg electrodes should be in a stable position above the anterior iliac crest and below the rib cage. The Mason-Likar modification results in a right-axis shift and increased voltage in the inferior leads and may produce a loss of inferior Q waves and the development of new Q waves in lead aV 1 . Thus, the body torso limb lead posi­tions cannot be used to interpret a diagnostic resting 12-1ead ECG. The more cephalad the leg electrodes are placed, the greater is the degree of change and the greater is the aug­mentation of R wave amplitude.

32. Types of ST Segment Displacement In normal persons, the PR, QRS, and QT intervals shorten as heart rate increases. P amplitude increases, and the PR segment becomes progressively more downsloping in the inferior leads. J point, or junctional, depression is a normal finding during exercise.

33. J point depression of 2 to 3 mm in leads V 4 to V 6 with rapid upsloping ST segments depressed approximately 1mm 80msec after the J point. The ST segment slope in leads V 4 and V 5 is 3.0mV/sec. This response should not be considered abnormal.

34. In patients with myocar­dial ischemia, however, the ST segment usually becomes more horizontal (flattens) as the severity of the ischemic response worsens. With progressive exercise, the depth of ST segment depression may increase, involving more ECG leads, and the patient may develop angina. In the immediate post re­covery phase, the ST segment displacement may persist, with downsloping ST segments and T wave inversion, gradually returning to baseline after 5 to 10 minutes.

35. Bruce protocol. lead V 4 , the exercise electrocardiographic (ECG) result is abnormal early in the test, reaching 0.3mV (3mm) of horizontal ST segment depression at the end of exercise. The ischemic changes persist for at least 1 minute and 30 seconds into the recovery phase. The right panel provides a continuous plot of the J point, ST slope, and ST segment displacement at 80msec after the J point (ST level) during exercise and in the recovery phase. Exercise ends at the vertical line at 4.5 minutes (red arrow). The computer trends permit a more precise identification of initial onset and offset of ischemic ST segment depression. This type of ECG pattern, with early onset of ischemic ST segment depression, reaching more than 3mm of horizontal ST segment displacement and persisting several minutes into the recovery phase, is consistent with a severe ischemic response.

36. Bruce protocol. In this type of ischemic pattern, the J point at peak exertion is depressed 2.5mm, the ST segment slope is 1.5mV/sec, and the ST segment level at 80msec after the J point is depressed 1.6mm. This “ slow upsloping” ST segment at peak exercise indicates an ischemic pattern in patients with a high pretest prevalence of coronary disease. A typical ischemic pattern is seen at 3 minutes of the recovery phase when the ST segment is horizontal and 5 minutes after exertion when the ST segment is downsloping. Exercise is discontinued at the vertical line in the right panels at 7.5 minutes.

37. Ischemic ST segment displacement may be seen only during exercise, emphasizing the importance of adequate skin preparation and electrode placement to capture high~ quality recordings during maximum exertion. In about 10 percent of patients, the ischemic response may appear only in the recovery phase. This is a relevant finding, and the prevalence of reversible perfusion defects by single­photon emission computed tomography criteria are compa­rable to those observed when the ischemic ST segment response occurs both during and after exercise. Patients should not leave the exercise laboratory area until the post­exercise ECG has returned to baseline.

38. Bruce protocol. The exercise electrocardiographic (ECG) result is not yet abnormal at 8:50 minutes but becomes abnormal at 9:30 minutes (horizontal arrows, right ) of a 12-minute exercise test and resolves in the immediate recovery phase. This ECG pattern in which the ST segment becomes abnormal only at high exercise workloads and returns to baseline in the immediate recovery phase may indicate a false-positive result in an asymptomatic individual without atherosclerotic risk factors. Exercise myocardial imaging would provide more diagnostic and prognostic information if this were an older person with several atherosclerotic risk factors. Vertical arrow indicates termination of exercise.

39. Illustration of eight typical exercise electrocardiographic (ECG) patterns at rest and at peak exertion. The computer-processed incrementally averaged beat corresponds with the raw data taken at the same time point during exercise and is illustrated in the last column. The patterns represent worsening ECG responses during exercise. In the column of computer-averaged beats, ST 80 displacement (top number) indicates the magnitude of ST segment displacement 80 msec after the J point relative to the PQ junction or E point. ST segment slope measurement (bottom number) indicates the ST segment slope at a fixed time point after the J point to the ST 80 measurement. At least three noncomputer average complexes with a stable baseline should meet criteria for abnormality before the exercise ECG result can be considered abnormal (see Fig. 10-9). The normal and rapid upsloping ST segment responses are normal responses to exercise. J point depression with rapid upsloping ST segments is a common response in an older, apparently healthy population. Minor ST depression can occur occasionally at submaximal workloads in patients with coronary disease; in this illustration, the ST segment is depressed 0.09mV (0.9mm) 80msec after the J point. The slow upsloping ST segment pattern often demonstrates an ischemic response in patients with known coronary disease or those with a high pretest clinical risk of coronary disease. Criteria for slow upsloping ST segment depression include J point and ST 80 depression of 0.15mV or more and ST segment slope of more than 1.0mV/sec. Classic criteria for myocardial ischemia include horizontal ST segment depression observed when both the J point and ST 80 depression are 0.1mV or more and ST segment slope is within the range of 1.0mV/sec. Downsloping ST segment depression occurs when the J point and ST 80 depression are 0.1mV and ST segment slope is − 1.0mV/sec. ST segment elevation in a non-Q wave noninfarct lead occurs when the J point and ST 60 are 1.0mV or greater and represents a severe ischemic response. ST segment elevation in an infarct territory (Q wave lead) indicates a severe wall motion abnormality and in most cases is not considered an ischemic response.

40. Measurement of ST Segment Displacement For purposes of interpretation, the PQ junction is usually chosen as the isoelectric point. The TP segment represents a true isoelectric point but is an impractical choice for most routine clinical measurements. The development of 0.10 mV (1 mm) or greater of J point depression measured from the PQ junction, with a relatively flat ST segment slope (e.g., <0.7 to 1 mV/sec), depressed 0.10 mV or more 80 msec after the J point (ST 80) in three consecutive beats with a stable base­line is considered to be an abnormal response. When the ST 80 measurement is difficult to determine at rapid heart rates (e.g., >130 beats/min), the ST 60 measure­ment should be used. The ST segment at rest may occasion­ally be depressed. When this occurs, the J point and ST 60 or ST 80 measurements should be depressed an additional 0.10 mV or greater to be considered abnormal.

41. Magnified ischemic exercise– induced electrocardiographic pattern. Three consecutive complexes with a relatively stable baseline are selected. The PQ junction (1) and J point (2) are determined; the ST 80 (3) is determined at 80 msec after the J point. In this example, average J point displacement is 0.2mV (2mm) and ST 80 is 0.24mV (24mm). The average slope measurement from the J point to ST 80 is −1.1 mV/sec.

42. When the degree of resting ST segment depression is 0.1 mV or greater, the exercise ECG becomes less specific, and myocardial imaging modalities should be considered. In patients with early repolarization and resting ST segment elevation, return to the PQ junction is normal. Therefore, the magnitude of exercise-induced ST segment depression in a patient with early repolarization should be determined from the PQ junction and not from the elevated position of the J point before exercise. Exercise-induced ST segment depres­sion does not localize the site of myocardial ischemia, nor does it provide a clue about which coronary artery is involved. For example, it is not unusual for patients with isolated right CAD to exhibit exercise-induced ST segment depression only in leads V 4 to V 6 , nor is it unusual for patients with disease of the left anterior descending coronary artery to exhibit exercise-induced ST segment displacements in leads II, III, and aVf,

43. Exercise-induced ST segment elevation is relatively specific for the territory of myocardial ischemia and the coronary artery involved. UPSLOPING ST SEGMENTS. Junctional or J point depression is a normal finding during maximal exercise, and a rapid upsloping ST segment (>1 mV/sec) depressed less than 0.15 mV (1.5 mm) after the J point should be considered to be normal. Occasionally, however, the ST segment is depressed 0.15 mV (1.5 mm) or greater at 80 msec after the J point. This type of slow upsloping ST segment may be the only ECG finding in patients with well-defined obstructive CAD and may depend on the lead set used. In patient subsets with a high CAD prevalence, a slow upsloping ST segment depressed 0.15 mV or greater at 80 msec after the J point should be considered abnormal. The importance of this finding in asymptomatic individuals or those with a low CAD prevalence is less certain.

44. Increasing the degree of ST segment depression at 80 msec after the J point to 0.20 mV (2.0 mm) or greater in patients with a slow upsloping ST segment increases speci­ficity but decreases sensitivity. ST SEGMENT ELEVATION. Exercise-induced ST seg­ment elevation may occur in an infarct territory where Q waves are present or in a noninfarct territory. The develop­ment of 0.10 mV (1 mm) or greater of J point elevation, per­sistently elevated greater than 0.10 mV at 60 msec after the J point in three consecutive beats with a stable baseline, is con­sidered an abnormal response. This finding occurs in approximately 30 percent of patients with anterior myocardial infarctions and 15 percent of those with inferior ones tested early (within 2 weeks) after the index event and decreases in frequency by 6 weeks.

45. As a group, postinfarct patients with exercise-induced ST segment elevation have a lower ejection fraction than those without, a greater severity of resting wall motion abnormalities, and a worse prognosis. Exercise-induced ST segment elevation in leads with abnor­mal Q waves is not a marker of more extensive CAD and rarely indicates myocardial ischemia. Exercise-induced ST segment elevation may occasionally occur in a patient who has regenerated embryonic R waves after an acute myocardial infarction; the clinical significance of this finding is similar to that observed when Q waves are present. When ST segment elevation develops during exercise in a non-Q wave lead in a patient without a previous myocardial infarction, the finding should be considered as likely evi­dence of transmural myocardial ischemia caused by coronary vasospasm or a high-grade coronary narrowing. This finding is relatively uncommon, occurring in approxi­mately 1 percent of patients with obstructive CAD.

46. The ECG site of ST segment elevation is relatively specific for the coro­nary artery involved, and myocardial perfusion scintigraphy usually reveals a defect in the territory involved.

47. A 48-year-old man with several atherosclerotic risk factors and a normal resting electrocardiographic (ECG) result developed marked ST segment elevation (4 mm [arrows]) in leads V 2 and V 3 with lesser degrees of ST segment elevation in leads V 1 and V 4 and J point depression with upsloping ST segments in lead II, associated with angina. This type of ECG pattern is usually associated with a full-thickness, reversible myocardial perfusion defect in the corresponding left ventricular myocardial segments and high-grade intraluminal narrowing at coronary angiography. Rarely, coronary vasospasm produces this result in the absence of significant intraluminal atherosclerotic narrowing. HR = heart rate; METs = metabolic equivalents; SBP = systolic blood pressure.

48. T WAVE CHANGES. The morphology of the T wave is influenced by body position, respiration, hyperventilation, drug therapy, and myocardial ischemia/necrosis. In patient populations with a low CAD prevalence, pseudonormaliza­tion of T waves (inverted at rest and becoming upright with exercise) is a nondiagnostic finding. In rare instances, this finding may be a marker for myocardial ischemia in a patient with documented CAD, although it would need to be substantiated by an ancillary technique, such as the concomitant finding of a reversible myocardial perfusion defect.

49. Pseudonormalization of T waves in a 49-year-old man referred for exercise testing. The patient had previously been seen for typical angina. The resting electrocardiogram in this patient with coronary artery disease shows inferior and anterolateral T wave inversion, an adverse long-term prognosticator. The patient exercised to 8 METs, reaching a peak heart rate of 142 beats/min and a peak systolic blood pressure of 248 mm Hg. At that point, the test was stopped because of hypertension. During exercise, pseudonormalization of T waves occurs, and it returns to baseline (inverted T wave) in the postexercise phase. The patient denied chest discomfort, and no arrhythmia or ST segment displacement was noted. Transient conversion of a negative T wave at rest to a positive T wave during exercise is a nonspecific finding in patients without prior myocardial infarction and does not enhance the diagnostic or prognostic content of the test; however, the ability to exercise to 8 METs without ischemic changes in the ST segment places this patient into a subset of lower risk. HR = heart rate; METs = metabolic equivalents; SBP = systolic blood pressure.

50. OTHER ELECTROCARDIOGRAPHIC MARKERS. Changes in R wave amplitude during exercise are relatively nonspecific and are related to the level of exercise performed. When the R wave amplitude meets voltage criteria for left ventricular hypertrophy, the ST segment response cannot be used reliably to diagnose CAD, even in the absence of a left ventricular strain pattern. U wave inversion can occasionally be seen in the precordial leads at heart rates of 120 beats/min. Although this finding is relatively specific for CAD, it is relatively insensitive. COMPUTER-ASSISTED ANALYSIS When the raw ECG data are of high quality, the computer can filter and average or select median complexes from which the degree of J point displacement, ST segment slope, and ST displacement 60 to 80 msec after the J point (ST 60 to 80) can be measured. The selection of ST 60 or ST 80 depends on the heart rate response.

51. At ventricular rates greater than 130 beats/min, the ST 80 measurement may fall on the upslope of the T wave, and the ST 60 measurement should be used instead. In some computerized systems, the PQ junction or isoelectric interval is detected by scanning before the R wave for the 10-msec inter­val with the least slope. J point, ST slope, and ST levels are determined; the ST integral can be calculated from the area below the isoelectric line from the J point to ST 60 or ST 80. ST/HEART RATE SLOPE MEASUREMENTS. Heart rate adjustment of ST segment depression appears to improve the sensitivity of the exer­cise test, particularly the prediction of multivessel CAD. The ST/heart rate slope depends on the type of exercise performed, number and loca­tion of monitoring electrodes, method of measuring ST segment depres­sion, and clinical characteristics of the study population.

52. Calculation of maximal 5ST/heart rate slope in mV/beats/min is performed by linear regression analysis relating the measured amount of ST segment depres­sion in individual leads to the heart rate at the end of each stage of exercise, starting at the end of exercise. An ST/heart rate slope of 2.4 mV/beats/min is considered abnormal, and values that exceed 6 mV/beats/min are suggestive evidence of three-vessel CAD. The use of this measurement requires modification of the exercise protocol such that increments in heart rate are gradual, as in the Cornell protocol, as opposed to more abrupt increases in heart rate between stages, as in the Bruce or Ellestad protocols, which limit the ability to calculate statistically valid ST segment heart rate slopes. The measurement is not accurate in the early postinfarction phase. A modification of the ST segment/heart rate slope method is the ST segment/heart rate index calculation, which represents the average change of ST segment depres­sion with heart rate throughout the course of the exercise test.

53. The ST/heart rate index measurements are less than the ST/heart rate slope measurements, and a ST/heart rate index of 1.6 is defined as abnormal. Mechanism of ST Segment Displacement PATHOPHYSIOLOGY OF THE MYOCARDIAL ISCHE­MIC RESPONSE. Myocardial oxygen consumption (MO 2 ) is determined by heart rate, systolic blood pressure, left ven­tricular end-diastolic volume, wall thickness, and contractility. The rate-pressure or double product (heart rate × systolic blood pressure) increases progressively with increasing work and can be used to estimate the myo­cardial perfusion requirement in normal persons and in many patients with coronary artery disease. The heart is an aerobic organ with little capacity to generate energy through anaerobic metabolism. Oxygen extraction in the coronary circulation is nearly maximal at rest.

54. The only significant mechanism available to the heart to increase oxygen con­sumption is to increase perfusion, and there is a direct linear relationship between MO 2 and coronary blood flow in normal individuals. The principal mechanism for increasing coronary blood flow during exercise is to decrease resistance at the coronary arteriolar level. In patients with progressive ath­erosclerotic narrowing of the epicardial vessels, an ischemic threshold occurs, and exercise beyond this threshold can produce abnormalities in diastolic and systolic ventricular function, ECG changes, and chest pain. The subendocardium is more susceptible to myocardial ischemia than the subepi­cardium because of increased wall tension; causing a relative increase in myocardial oxygen demand in the subendo­cardium.

55. Dynamic changes in coronary artery tone at the site of an atherosclerotic plaque may result in diminished coronary flow during static or dynamic exercise instead of the expected increase that normally occurs from coronary vasodilation in a normal vessel; that is, perfusion pressure distal to the stenotic plaque actually falls as during exercise, resulting in reduced subendocardial blood flow. Thus, regional left ventricular myocardial ischemia may result not only from an increase in myocardial oxygen demand during exercise but also from a limitation of coronary flow as a result of coronary vasoconstriction, or inability of vessels to suffi­ciently vasodilate at or near the site of an atherosclerotic plaque. Increased myocardial oxygen demand associated with a­ failure to increase or an actual decrease in regional coronary blood flow usually causes ST segment depression; ST segment elevation may occasionally occur in patients with more severe coronary flow reduction.

67. Indications of TMT Clearly indicated Diagnosis of CAD in men with atypical symptoms . Patient has known CAD; assess prognosis and functional capacity Symptomatic, recurrent, exercise-induced arrhythmias Patient has experienced an uncomplicated myocardial infarction; evaluate prognosis and functional capacity Patient has undergone coronary artery revascularization; evaluation recommended Possibly indicated Diagnosis of CAD in woman with typical or atypical angina Diagnosis of CAD in patient taking digitalis Diagnosis of CAD in patient with complete right bundle branch block

68. Patient has CAD or heart failure; evaluate functional capacity and response to therapy Patient has variant angina; evaluation recommended . Patient has known CAD; serial evaluation recommended Asymptomatic man who is older than 40 yr and in a high-risk occupation, who has-two or more risk factors for CAD, or who is sedentary and plans to begin a vigoi'ous exercise program; evaluation recommended Asymptomatic patient after coronary revascularization; annual evaluation recommended Selected patients with valvular heart disease; evaluate functional capacity Probably not indicated Asymptomatic patient with isolated ventricular ectopy; evaluation recommended

69. Patient is enrolled in a cardiac rehabilitation program; serial evaluation recommended Diagnosis of CAD in patient with left bundle branch block or ventricular preexcitation (Wolff­ Parkinson-White) syndrome on resting electrocardiography Asymptomatic man or woman; evaluation recommended Man or woman with chest pain of noncardiac etiology; evaluation recommended Diagnostic Use of Exercise Testing Approximately 75 to 80 percent of the diagnostic information on exercise-induced ST segment depression in patients with a normal resting ECG is contained in leads V 4 to V 6 Exercise ECG is less specific when patients in whom false-positive results are more common are included, such as those with valvular heart disease, left ventricular hypertrophy, marked resting ST segment depression, or digitalis therapy.

70. Exercise Testing in Determining Prognosis Exercise testing provides not only diagnostic information but also, more importantly, prognostic data. The value of exercise testing to estimate prognosis must be considered in light of what is already known about a patient’s risk status. Left ventricular dysfunction, CAD extent, electrical instability, and noncoronary comorbid conditions must be taken into consideration when estimating long-term outcome. ASYMPTOMATIC POPULATION. The prevalence of an abnormal exercise ECG result in middle-aged asymptomatic men ranges from 5 to 12 percent. The future risk of cardiac events is greatest if the test result is strongly pos­itive or if an asymptomatic subject has atherosclerotic risk factors such as diabetes, hypertension, hypercholesterolemia, smoking history, or familial history of premature coronary disease.

71. Serial change of a negative exercise ECG result to a positive one in an asymptomatic person carries the same prognostic importance as an initially abnormal test result. However, when an asymptomatic indi­vidual with an initially abnormal test result has significant worsening of the ECG abnormalities at lower exercise work­loads, this finding may indicate significant CAD progression and warrants a more aggressive diagnostic work-up. In general , the prognostic value of an ST segment shift in women is less than in men. SYMPTOMATIC PATIENTS. Exercise testing should be routinely performed (unless this is not feasible or unless there are contraindications) before coronary angiography in patients with chronic ischemic heart disease. Patients who have excellent exercise tolerance (e.g., >10 METs) usually have an excellent prognosis regardless of the anatomical extent of CAD.

72. Mark and colleagues developed a treadmill score based on 2842 consecutive patients with chest pain in the Duke data bank; these patients underwent treadmill testing using the Bruce protocol and cardiac catheterization. Patients with left bundle branch block (LBBB) or those with exercise ­induced ST elevation in a Q wave lead were excluded. The treadmill (TM) score is calculated as follows: TM score = exercise time - (5 × ST deviation) ­- (4 × treadmill angina index) Angina index was assigned a value of 0 if angina was absent, 1 if typical angina occurred during exercise, and 2 if angina was the reason the patient stopped exercising. ST deviation was defined as the largest net ST displacement in any lead.

73. The 13 percent of patients with a treadmill score of -11 or less had a 5-year survival rate of 72 percent, as compared with a 97 percent survival rate among the 34 percent of patients at low risk with a treadmill score of +5 or greater. The score worked equally well in men and women, although women had a lower overall risk than men for similar scores. SILENT MYOCARDIAL ISCHEMIA In patients with documented CAD, the presence of exercise­induced ischemic ST segment depression confers increased risk of subsequent cardiac events regardless of whether angina occurs during the test. ACUTE CORONARY SYNDROMES The prognostic risk assess­ment after an acute coronary syndrome should incorporate findings from the history, physical examination, resting 12-lead ECG, and level of serum markers to optimize mortality and morbidity estimates and to categorize patients into low- intermediate, and high-risk groups.

74. Exercise testing should be considered in the outpatient evaluation of low-risk patients with unstable angina (biomarker negative) who are free of active ischemic symptoms for a minimum of 8 to 12 hours, and in hospitalized low- to intermediate-risk ambulatory patients who are free of angina or heart failure symptoms for at least 48 hours. In many intermediate or high-risk patients, coronary angiography will have been performed during the acute phase of the illness; coronary disease extent, left ven­tricular function, and degree of coronary revascularization, if performed, should then be incorporated with the exercise test data to determine the overall predischarge prognostic risk estimate.

75. MYOCARDIAL INFARCTION Exercise testing after myocardial infarction (both non-ST and ST eleva­tion) is useful to determine (1) risk stratification and assessment of prog­nosis, (2) functional capacity for activity prescription after hospital discharge, and (3) assessment of adequacy of medical therapy and need to use supplemental diagnostic or treatment options. A low-level exercise test (achievement of 5 to 6 METs or 70 to 80 percent of age-predicted maximum) is frequently per­formed before hospital discharge to establish the hemodynamic response and functional capacity. The ability to complete 5 to 6 METs of exer­cise or 70 to 80 percent of age-predicted maximum in the absence of abnormal ECG or blood pressure is associated with a I-year mortality rate of 1 to 2 percent and may help guide the timing of early hospital discharge.

76. Parameters associated with increased risk include inability to perform or complete the low-level predischarge exercise test, poor exercise capacity, inability to increase or a decrease in exercise systolic blood pressure, and angina or exercise-induced ST segment depression at low workloads. Many postinfarct patients referred for exercise testing have been prescribed beta-adrenergic blocking agents and angiotensin­converting enzyme inhibitors. Although beta-adrenergic blocking drugs may attenuate the ischemic response, they do not interfere with poor functional capacity as a marker of adverse prognosis and should be con­tinued in patients referred for testing. The relative prognostic value of a 3- to 6-week postdischarge exercise test is minimal once clinical variables and the results of the low-level predischarge test are adjusted for.

77. For this reason, the timing of the exercise test after the infarct event favors pre­discharge exercise testing to allow implementation of a definitive treat­ment plan in patients in whom coronary anatomy is known as well as risk stratification of patients in whom coronary anatomy has not yet been determined. There is a trend toward early predischarge exercise testing (within 3 to 5 days) in uncomplicated cases after acute myocardial infarc­tion. A 3 to 6-week test is useful in clearing patients to return to work in occupations involving physical labor in which the MET expenditure is likely to be greater than that performed on a predischarge test. In patients with negative T waves after infarction, stress-induced normalization of the T waves may also indicate higher coronary flow reserve than in patients unable to normalize their T waves.

78. Nomogram of prognostic relations using the Duke treadmill score, which incorporates duration of exercise (in minutes) – (5 × maximal ST segment deviation during or after exercise) (in mm)–(4 × treadmill angina index). Treadmill angina index is 0 for no angina, 1 for nonlimiting angina, and 2 for exercise-limiting angina. The nomogram can be used to assess the prognosis of ambulatory outpatients referred for exercise testing. In this example, the observed amount of exercise-induced ST segment deviation (minus resting changes) is marked on the line for ST segment deviation during exercise (1). The degree of angina during exercise is plotted (2), and the points are connected. The point of intersection on the ischemic reading line is noted (3). The number of METs (or minutes of exercise if the Bruce protocol is used) is marked on the exercise duration line (4). The marks on the ischemia reading line and duration of exercise line are connected, and the intersection on the prognosis line determines 5-year survival rate and average annual mortality for patients with these selected specific variables. In this example, the 5-year prognosis is estimated at 78 percent in this patient with exercise-induced 2-mm ST depression, nonlimiting exercise angina, and peak exercise workload of 5 METs. MET = metabolic equivalent.

79. Thank You