Chest ACCP Member Benefits
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miller, T. D.
Right arrow Articles by Gibbons, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miller, T. D.
Right arrow Articles by Gibbons, R. J.
(Chest. 2000;117:226-232.)
© 2000 American College of Chest Physicians

Is Rest or Exercise Hypertension a Cause of a False-Positive Exercise Test?*

Todd D. Miller, MD, FCCP; Timothy F. Christian, MD; Thomas G. Allison, PhD; Ray W. Squires, PhD; David O. Hodge, MS and Raymond J. Gibbons, MD

* From the Division of Cardiovascular Diseases and Department of Internal Medicine (Drs. Miller, Christian, Allison, Squires, and Gibbons), and the Department of Biostatistics and Health Sciences Research (Mr. Hodge), Mayo Clinic, Rochester, MN.

Correspondence to: Todd D. Miller, MD, FCCP, Mayo Clinic, East 16-A, 200 First Street SW, Rochester, MN 55905; e-mail: miller.todd{at}mayo.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To determine if a history of hypertension or an exaggerated rise in exercise systolic BP is associated with a false-positive exercise ECG.

Design, setting, and patients: Retrospective analysis of the associations between exercise-induced ST-segment depression and a history of hypertension, exercise systolic BP, and several other clinical and exercise test variables. Among 20,097 patients referred for exercise tomographic thallium imaging in a nuclear cardiology laboratory at a tertiary care center, 1,873 patients met inclusion criteria for this study, which included no history of myocardial infarction or coronary artery revascularization, a normal resting ECG, and normal exercise thallium images.

Results: False-positive ST-segment depression occurred in 20% of the population. A history of hypertension was actually associated with a lower likelihood of ST-segment depression (odds ratio, 0.70; 95% confidence interval [CI], 0.55 to 0.89; p = 0.004). A higher peak exercise systolic BP was associated with a higher likelihood of ST-segment depression (odds ratio, 1.08 for each 10-mm Hg increase in systolic BP; 95% CI, 1.03 to 1.14; p < 0.001). However, the association between peak exercise systolic BP and ST-segment depression was so weak that this measurement could not be predictive in the individual patient (R2 = 0.2%). For every 20-mm Hg increase in peak exercise systolic BP, the percentage of patients with ST-segment depression increased by only 3%.

Conclusions: In patients with normal resting ECGs, we conclude the following: (1) a history of hypertension is not a cause of a false-positive exercise test, and (2) higher exercise systolic BP is a significant but weak predictor of ST-segment depression.

Key Words: BP • hypertension • ST-segment depression


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Hypertension is often cited as a cause of false-positive ST-segment depression during exercise testing.1 2 3 4 5 However, studies demonstrating this relationship are few.6 7 8 9 10 ST-segment depression occurs commonly in patients with left ventricular hypertrophy, whether the etiology is hypertensive or valvular heart disease.8 9 10 11 12 Because of the high prevalence of false-positive stress tests in patients with left ventricular hypertrophy and the limited sensitivity of the resting ECG for detecting this condition,13 the value of exercise testing for diagnostic purposes in hypertensive patients with chest pain has been questioned.14 15 The American College of Cardiology/American Heart Association exercise testing guidelines indicate that there is an increase in false-positive stress studies in patients with left ventricular hypertrophy, but the guidelines do not describe such a limitation for patients with hypertension in the absence of left ventricular hypertrophy.16 Another related and unresolved issue is whether an excessive rise in exercise BP is associated with a greater likelihood of false-positive ST-segment depression. An exaggerated exercise BP response is a marker of undetected left ventricular hypertrophy.17 18 Some authors have postulated that a very high exercise rate-pressure product may cause subendocardial ischemia.2 3 19 20 The small number of studies examining exercise BP and ST-segment depression have reported conflicting results.8 21 22 The purposes of this study were to determine if false-positive ST-segment depression occurs more frequently in patients with either hypertension at rest or an exaggerated rise in systolic BP during exercise.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Group
Between October 1986 and August 1992, 20,097 patients underwent thallium exercise treadmill testing at the Mayo Clinic. The study group was selected to have no evidence of coronary artery disease and to not be predisposed to have a false-positive exercise test. Inclusion criteria therefore included the following: (1) a normal thallium image (see below); (2) no clinical history of myocardial infarction; (3) no prior percutaneous transluminal coronary angioplasty or coronary artery bypass surgery; (4) normal resting ECG; (5) no digoxin use; and (6) no evidence of clinically significant valvular heart disease or cardiomyopathy. A clinical history of hypertension was defined as either a systolic BP > 140 mm Hg or a diastolic BP > 90 mm Hg on repeated occasions, or a prior diagnosis of hypertension. A normal thallium image was used to exclude significant coronary artery disease, realizing that this criterion is not perfect. The reported sensitivity of tomographic imaging is approximately 90%.23 Since most patients with normal thallium images are not referred for coronary angiography, requiring angiography on all patients would result in a considerably smaller and more skewed study population. Patients with resting ECGs showing abnormalities of rhythm (other than sinus bradycardia), axis deviation, QRS-complex voltage, ventricular conduction, pathological Q waves, and any ST-T-segment abnormalities were excluded from the study. A normal resting ECG was required both to eliminate patients with left ventricular hypertrophy and to reduce the likelihood of exercise false-positive ST-segment depression. The presence of even nonspecific ST-segment, T wave abnormalities is associated with developing false-positive ST-segment depression.24

Exercise Testing
These techniques have been described in detail previously.25 Briefly, the patients underwent treadmill exercise using either the Bruce or Naughton protocols. Exercise duration from either protocol was converted to estimated metabolic equivalents using published nomograms. End points consisted of severe fatigue, moderate angina, >= 2.0-mm ST-segment depression, marked hypotension, or severe arrhythmia. BP was measured by cuff sphygmomanometry at rest in the standing position immediately before exercise and during the last minute of each exercise stage, including the last minute of exercise. A 12-lead ECG was performed at rest and during each minute of exercise, and three leads were monitored continuously during exercise. The exercise ECG was interpreted visually by the cardiologist or nurse supervising the exercise test. ST-segment depression was measured 0.08 s after the J point and was categorized into three groups: (1) none, any degree of upsloping, or < 1-mm horizontal or downsloping; (2) 1.0- to 1.9-mm horizontal or downsloping; and (3) >= 2.0-mm horizontal or downsloping.

Tomographic Thallium-201 Imaging
During the last minute of exercise, 3.0 to 4.0 mCi of thallium-201 were injected IV. Tomographic imaging was performed shortly after exercise and repeated 4 h later. Patients studied after January 1, 1990, underwent reinjection with 1.0-mCi thallium before delayed imaging. The images were interpreted by two experienced observers who graded thallium uptake in 14 short-axis segments on the postexercise and rest images using a 5-point scale (0 = no uptake; 1, 2, and 3 = severely, moderately, and mildly reduced uptake, respectively; and 4 = normal uptake). Only patients with completely normal images or mild fixed defects (coded 3 on both the postexercise and rest images) were included. Most mild fixed defects represent soft tissue attenuation artifacts and are not due to coronary artery disease.

Statistics
The associations between ST-segment depression and several clinical and exercise variables were tested using logistic regression. A multivariate model was then created using stepwise logistic regression analysis to determine which variables were independently associated with ST-segment depression. For all analyses, a p value < 0.05 was considered significant. The generalized coefficient of determination R2 value was used to illustrate the predictive value of the models. The R2 value is the square of the correlation coefficient and represents the amount of variability associated with a given Y variable that is explained by the potential predictor X.26


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Patient Characteristics
There were 1,873 patients in the study group. ST-segment depression developed in 378 patients (20%). Table 1 lists the characteristics of patients subgrouped by the presence or absence of ST-segment depression. A clinical history of hypertension was present in 707 patients (38%), and 780 patients (42%) were taking at least one antihypertensive medication (a small number were taking an antihypertensive medication for an indication other than hypertension). Because of the large number of patients, relatively small differences between the two groups were statistically significant. Of note is that patients with ST-segment depression were less likely to have a history of hypertension. They were also less likely to have chest pain or to be taking a ß-blocker or calcium channel blocker.


View this table:
[in this window]
[in a new window]

  		Table 1.. Clinical Characteristics*

 
Exercise Test Results
These results are listed in Table 2 . Patients with ST-segment depression had slightly higher systolic BP both at rest and at peak exercise. They also exercised longer and attained a higher peak exercise heart rate and rate-pressure product.


View this table:
[in this window]
[in a new window]

  		Table 2.. Exercise Test Variables*

 
Association Between ST-Segment Depression and Exercise Systolic BP
For the entire study population (Fig 1 ), there was a statistically significant (p < 0.001) but very weak association (R2 = 0.2%) between ST-segment depression and exercise systolic BP. The percentage of patients with ST-segment depression increased modestly but progressively from 18% with exercise systolic BP < 180 mm Hg to 27% for those with exercise systolic BP >= 220 mm Hg. Attributable risk was calculated using exercise systolic BP cut-points >= 200 mm Hg and >= 220 mm Hg. For the cut-point >= 200 mm Hg, 28% of the excess occurrence of ST-segment depression was attributable to the elevated exercise systolic BP. The attributable risk increased to 39% using the cut-point >= 220 mm Hg.



View larger version (28K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1.. Percentages of patients with ST-segment depression for categories of peak exercise systolic BP (SBP) for the entire study population. The numbers within the bars indicate the percentages of patients with 1.0- to 1.9-mm and >= 2-mm ST-segment depression. The numbers at the bottom of the graph indicate the numbers of patients in each subgroup.

 
The results were analyzed with patients being categorized as with or without a history of hypertension (Fig 2 ), and as taking or not taking either a ß-blocker or calcium channel blocker (Fig 3 ). The same effect of a modest increase in the percentage of patients with ST-segment depression by increasing exercise systolic BP was present for each of these subgroups. The increase in percentage of patients with ST-segment depression was progressive with increasing BP for all subgroups except those taking a ß-blocker or calcium channel blocker, where a decrease in the percentage occurred between the third and fourth categories of BP. The magnitude of the association between ST-segment depression and exercise BP was greater in patients without a history of hypertension and in those not taking a ß-blocker or calcium channel blocker.



View larger version (33K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2.. Patients with hypertension (top, A) and without hypertension (bottom, B). See Figure 1 legend.

 


View larger version (32K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3.. Patients taking a ß-blocker or calcium channel blocker (top, A) and not taking these medications (bottom, B). See Figure 1 legend.

 
There was a small but significant gender difference: 22% of men and 18% of women had ST-segment depression. The increase in percentage of men with ST-segment depression was progressive with increasing BP, but women demonstrated a decrease between the third and fourth categories (Fig 4 ). Men were more likely than women to have ST-segment depression in three of the four categories of systolic BP, but not for the category from 200 to 219 mm Hg.



View larger version (32K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 4.. Study subjects classified by gender: men (top, A) and women (bottom, B). See Figure 1 legend.

 
An inspection of Figures 1 2 3 4 reveals that the increase in the percentage of patients with ST-segment depression associated with increasing exercise systolic BP was due to more patients with severe (>= 2 mm) ST-segment depression for all subgroups. This association was greater for patients without hypertension, for patients not taking a ß-blocker or calcium channel blocker, and for men. An additional analysis revealed that 22% of men without hypertension and not taking a ß-blocker or calcium channel blocker whose exercise systolic BP was >= 220 mm Hg had >= 2-mm ST-segment depression (Fig 5 ). Note that there were only 23 men in this subgroup. There was no consistent association between exercise systolic BP and modest (1.0 to 1.9 mm) ST-segment depression for the entire study population or any of the subgroups analyzed.



View larger version (32K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 5.. Men without hypertension and not taking a ß-blocker or calcium channel blocker. See Figure 1 legend.

 
The results of the multivariate analysis testing the association between ST-segment depression and several clinical and exercise variables are shown in Table 3 . These variables were all independent but weak predictors of ST-segment depression. Peak ex-ercise systolic BP was of borderline significance (p = 0.046). The R2 value for the multivariate model was 5.3%.


View this table:
[in this window]
[in a new window]

  		Table 3.. Variables Independently Predictive of ST-Segment Depression*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
This study demonstrates that an exaggerated exercise systolic BP was associated with a slightly increased likelihood of false-positive ST-segment depression in patients without evidence of coronary artery disease by tomographic thallium scintigraphy. However, the association was so weak that it could not be highly predictive in the individual patient. For every 20-mm Hg increment in exercise systolic BP, the increase in the percentage of patients with false-positive ST-segment depression was only 3%. This association was most evident for men without a history of hypertension who developed >= 2-mm ST-segment depression. In contrast to exercise BP, a history of hypertension was actually associated with a slightly lower likelihood of false-positive ST-segment depression.

Exercise BP and ST-Segment Depression
Potential mechanisms by which an exaggerated rise in exercise BP could cause exercise-induced ST-segment depression include the following: (1) An excessive rate-pressure product could result in global subendocardial ischemia due to a mismatch between myocardial oxygen supply and demand.2 3 19 20 The potential for abnormal loading conditions to cause false-positive ST-segment depression is supported by the finding that healthy young adults can develop ST-segment depression and abnormal left ventricular contractility by performing sudden vigorous exercise.27 (2) As noted earlier, exercise-induced ST-segment depression occurs commonly in patients with left ventricular hypertrophy.8 9 10 11 12 The ECG has limited sensitivity for detecting left ventricular hypertrophy.13 An exaggerated systolic BP response has been proposed as a marker of left ventricular hypertrophy.17 18 Coronary vasodilator reserve is reduced in patients with left ventricular hypertrophy.28 The net result could be global subendocardial ischemia causing ST-segment depression but no focal thallium defect. (3) Even in the absence of left ventricular hypertrophy, myocardial ischemia can occur in hypertensive patients due to abnormally elevated resistance at the coronary microvascular level.29 Conceivably, the same mechanism could occur in patients who are normotensive at rest but hypertensive during exercise. (4) PR-segment depression can result in ST-segment depression during exercise.30 A greater rise in exercise BP could have a greater impact on atrial repolarization.31

Comparison to Other Studies
The data supporting hypertension as a cause of false-positive ST-segment depression are scanty. Some studies have been limited by small numbers of patients6 7 or lack of confirmatory evidence that patients who did develop ST-segment depression did not in fact have coronary disease since no additional evaluation was pursued.6 7 8 9 Other studies have reported that the hypertensive patients who developed ST-segment depression were those with left ventricular hypertrophy on the resting ECG.9 10 Even fewer studies have investigated exercise BP. Both Chaing et al8 and Ellestad et al21 reported that exercise BP was significantly associated with ST-segment depression. In a more recent study, however, Lauer and colleagues22 found that there was no increase in false-positive ST-segment depression in subjects with exercise hypertension.

Study Limitations
BP was measured indirectly by cuff sphygmomanometer rather than directly. Indirect BP measurement during exercise is reasonably accurate32 but can be difficult in occasional patients. Given the large size of the study group, occasional inaccurate readings are unlikely to have significantly impacted on the study results. Indirect measurement is standard clinical practice. As already discussed, a normal thallium image rather than coronary angiography was used to exclude coronary artery disease. One would assume that the small percentage of patients with coronary disease that thallium failed to detect more likely had ST-segment depression. Excluding these patients from the study population would only further weaken the associations that were detected and would not change the message of this article. Finally, although the study group was large, the number of patients with an excessively elevated exercise BP was relatively small (131 patients >= 220 mm Hg and 21 patients >= 240 mm Hg). It is possible that patients with an excessively elevated exercise BP may have a greater likelihood of developing ST-segment depression that we failed to show, but from a practical standpoint, these patients are uncommonly encountered in clinical practice.

Implications
Patients who have hypertension and a normal resting ECG are not more likely than those without hypertension to develop false-positive ST-segment depression. Standard exercise testing should remain a useful diagnostic modality when evaluating these patients for myocardial ischemia. Although a high systolic BP during exercise is associated with a slightly greater likelihood of false-positive ST-segment depression, the strength of this association is so weak that this finding cannot be predictive in an individual patient. Patients with a positive exercise ECG and a high exercise systolic BP should not be assumed to have a false-positive study.


   Acknowledgements
 
We thank Lisa VanDeWalker for secretarial preparation of the manuscript.

Received for publication March 30, 1999. Accepted for publication August 20, 1999.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. The Committee on Exercise. Exercise testing and training of individuals with heart disease or at high risk for its development: a handbook for physicians. Dallas, TX: American Heart Association, 1975
  2. Erickssen, J, Myhre, E (1984) False positive exercise ECG: a misnomer? Int J Cardiol 6,263-268[CrossRef][Medline]
  3. Detrano, R, Froelicher, VF (1988) Exercise testing: uses and limitations considering recent studies. Prog Cardiovasc Dis 31,173-204[CrossRef][ISI][Medline]
  4. Fletcher, GF, Balady, G, Froelicher, VF, et al (1995) Exercise standards: a statement for healthcare professionals from the American Heart Association. Circulation 91,580-615[Free Full Text]
  5. Ellestad, MH (1996) Stress testing principles and practice 4th ed. ,333-334 FA Davis Company Philadelphia, PA.
  6. Lepeschkin, E, Surawicz, B (1958) Characteristics of true-positive and false-positive electrocardiographic Master two-step exercise tests. N Engl J Med 258,511-520
  7. Bellet, S, Roman, L (1967) Exercise test in hypertensive subjects studies by radioelectrocardiography. Am J Med Sci 254,398-405[CrossRef][ISI][Medline]
  8. Chaing, BN, Alexander, R, Bruce, RA, et al (1969) Factors related to ST-segment depression after exercise in middle-aged Chinese men. Circulation 40,315-325[Abstract/Free Full Text]
  9. Wong, HO, Kasser, IS, Bruce, RA (1969) Impaired maximal exercise performance with hypertensive cardiovascular disease. Circulation 39,633-638[Abstract/Free Full Text]
  10. Massie, BM, Szlachcic, Y, Tuban, JF, et al (1993) Scintographic and electrocardiographic evidence of silent coronary artery disease in asymptomatic hypertension: a case-control study. J Am Coll Cardiol 22,1598-1606[Abstract]
  11. Harris, CN, Aronow, WS, Parker, DP, et al (1973) Treadmill stress test in left ventricular hypertrophy. Chest 63,353-357[Abstract/Free Full Text]
  12. Wroblewski, EM, Pearl, FJ, Hammer, WJ, et al (1982) False positive stress tests due to undetected left ventricular hypertrophy. Am J Epidemiol 115,412-417[Abstract/Free Full Text]
  13. Carr, AA, Prisant, LM, Watkins, LO (1985) Detection of hypertensive left ventricular hypertrophy. Hypertension 7,948-954[Abstract/Free Full Text]
  14. Prisant, LM, Frank, MJ, Carr, AA, et al (1987) Can we diagnose coronary heart disease in hypertensive patients? Hypertension 10,467-472[Abstract/Free Full Text]
  15. Frohlich, ED, Apstein, C, Chobanian, AV, et al (1992) The heart in hypertension. N Engl J Med 327,998-1008[ISI][Medline]
  16. Gibbons, RJ, Balady, GJ, Beasley, JW, et al (1997) ACC/AHA guidelines for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). J Am Coll Cardiol 30,260-315[CrossRef][ISI][Medline]
  17. Ren, JF, Hakki, AH, Kotler, MN, et al (1985) Exercise systolic blood pressure: a powerful determinant of increased left ventricular mass in patients with hypertension. J Am Coll Cardiol 5,1224-1231[Abstract]
  18. Gottdiener, JS, Brown, J, Zoltick, J, et al (1990) Left ventricular hypertrophy in men with normal blood pressure: relation to exaggerated blood pressure response to exercise. Ann Intern Med 112,161-166
  19. Wolthuis, RA, Froelicher, VF, Jr, Fischer, J, et al (1977) The response of healthy men to treadmill exercise. Circulation 55,153-157[Abstract/Free Full Text]
  20. Froelicher VF, Myers KJ, Follansbee WP, et al. Interpretation of ECG responses. In: Manning S. ed. Exercise and the heart. St. Louis, MO: Mosby Year Book, 1993; 119
  21. Ellestad, MH, Savitz, S, Bergdall, D, et al (1977) The false positive stress test: multivariate analysis of 215 subjects with hemodynamic, angiographic and clinical data. Am J Cardiol 40,681-685[CrossRef][ISI][Medline]
  22. Lauer, MS, Pashkow, FJ, Harvey, SA, et al (1995) Angiographic and prognostic implications of an exaggerated exercise systolic blood pressure response and rest systolic blood pressure in adults undergoing evaluation for suspected coronary artery disease. J Am Coll Cardiol 26,1630-1636[Abstract]
  23. Kotler, TS, Diamond, GA (1990) Exercise thallium-201 scintigraphy in the diagnosis and prognosis of coronary artery disease. Ann Intern Med 113,684-702
  24. Weiner, DL, Ryan, TJ, McCabe, CH, et al (1979) Exercise stress testing: correlations among history of angina, ST-segment response and prevalence of coronary artery disease in the Coronary Artery Surgery Study (CASS). N Engl J Med 301,230-235[Abstract]
  25. Christian, TF, Miller, TD, Bailey, KR, et al (1992) Noninvasive identification of severe coronary artery disease using exercise tomographic thallium-201 imaging. Am J Cardiol 70,14-20[CrossRef][ISI][Medline]
  26. Neter, J, Wasserman, W, Kutner, MH (1985) Applied linear statistical models 2nd ed. ,96 Irwin Homewood, IL.
  27. Barnard, RJ, MacAlpin, R, Kattus, AA, et al (1973) Ischemic response to sudden strenuous exercise in healthy men. Circulation 48,936-942[Abstract/Free Full Text]
  28. Houghton, JL, Frank, MJ, Carr, AA, et al (1990) Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease. J Am Coll Cardiol 15,43-51[Abstract]
  29. Brush, JE, Cannon, RO, III, Schenke, WH, et al (1988) Angina due to microvascular disease in hypertensive patients without left ventricular hypertrophy. N Engl J Med 319,1302-1307[Abstract]
  30. Riff, DP, Carleton, RA (1971) Effect of exercise on the atrial recovery wave. Am Heart J 82,759-763[CrossRef][ISI][Medline]
  31. Naimark, BJ, Tate, RB, Manfreda, J, et al (1990) The association between exercise blood pressure and the prevalence of ECG abnormalities. Can J Cardiol 6,267-273[ISI][Medline]
  32. Rasmussen, PH, Staats, BA, Driscoll, DJ, et al (1985) Direct and indirect blood pressure during exercise. Chest 87,743-748[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 J Am Coll CardiolHome page
J.-W. Ha, E. M. Juracan, D. W. Mahoney, J. K. Oh, C. Shub, J. B. Seward, and P. A. Pellikka
Hypertensive response to exercise: a potential cause for new wall motion abnormality in the absence of coronary artery disease
J. Am. Coll. Cardiol., January 16, 2002; 39(2): 323 - 327.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miller, T. D.
Right arrow Articles by Gibbons, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miller, T. D.
Right arrow Articles by Gibbons, R. J.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS