Prognostic Significance of Systolic Blood Pressure Increases in Men During Exercise Stress Testing

The American Journal of Cardiology
Volume 100, Issue 11, 1 December 2007, Pages 1609-1613
doi:10.1016/j.amjcard.2007.06.070

Prognostic Significance of Systolic Blood Pressure Increases in Men
During Exercise Stress Testing

Manish Prakash Gupta MDa, , , Sotir Polena MDa, Neil Coplan MDa,
Georgia Panagopoulos PhDa, Charu Dhingra MDb, Jonathan Myers PhDb and
Victor Froelicher MDb
aLenox Hill Hospital, New York, New York
bPAVAHCS/Stanford University, Palo Alto, California.
Received 17 April 2007; revised 22 June 2007; accepted 22 June
2007. Available online 23 October 2007.

Abstract

Our aim was to investigate whether exercise-induced increase in
systolic blood pressure (BP) measured during exercise stress testing
(EST) adds prognostic information to cardiovascular (CV) mortality.
EST is ideally suited to evaluate the prognostic power of systolic BP;
it not only measures systolic BP response to exercise but also
provides information about exercise capacity and other EST variables,
which may affect the peak systolic BP. The study population consisted
of 6,145 consecutive patients who underwent symptom-limited EST. Using
the median value of change in systolic BP from baseline, patients were
grouped according to exercise-induced increases in systolic BP ≤43 mm
Hg (group A, n = 3,062) and ≥ 44 mm Hg (group B, n = 3,083).
Multivariate analysis was used to adjust for baseline differences
between the 2 groups with CV mortality as the end point for follow-up.
Six thousand one hundred forty-five men underwent EST with a mean
follow-up of 6.6 years. During follow-up, 676 patients died of CV
causes with an average annual CV mortality of 1.6%. CV mortality was
significantly higher in group A than in group B (13.7% vs 8.2%, p
<0.001). After adjusting for baseline differences in the 2 groups
using multivariate analysis, an increase in systolic BP of ≤44 mm Hg
was a significant predictor of mortality (hazard ratio 1.2, 95%
confidence interval 1.02 to 1.44, p <0.05). In conclusion, systolic BP
response to maximal EST adds prognostic information to CV mortality
independent of age, ST-segment abnormalities, and exercise capacity.
In our study an increment in systolic BP of ≥44 mm Hg during EST was
associated with a 23% improvement in survival over a mean follow-up of
6 years.

Article

Most epidemiologic studies assessing the relation between hypertension
and increased cardiovascular (CV) morbidity and mortality have
obtained random blood pressure (BP) readings. Other modalities such as
BP measurement during basal conditions, ambulation, or exercise may be
better risk indicators.[1] and [2] Fagard et al3 reported no
additional prognostic information from exercise systolic BP readings
in 143 hypertensive patients with 11 years of follow-up when age and
BP at rest were taken into account. However, in a 17-year follow-up
study that included 4,907 healthy patients without CV disease,
Filipovsky et al4 found that an exercise-induced increase in systolic
BP was a risk factor for death from CV and non-CV causes independent
of age, BP at rest, and other risk factors. Similarly, Mundal et al5
evaluated an exercise-induced BP increase >200 mm Hg in 1,999 healthy
middle-aged men and concluded that an early increase in systolic BP
added prognostic information to CV mortality.

Our aim was to investigate whether exercise-induced increases in
systolic BP measured during a treadmill exercise test adds prognostic
information to CV mortality beyond that provided by casual BP readings
independent of other CV risk factors as previously reported.6 The
present study is unique because it evaluated the systolic BP response
to exercise and CV mortality with long-term follow-up based on a
clinically referred population for exercise testing.

Methods
The study population consisted of 6,213 consecutive men referred for
exercise stress testing (EST) for clinical reasons beginning in 1987.
A thorough clinical history, current medications, and risk factors
were recorded prospectively on computerized forms at the time of the
exercise tests.[7] and [8] After providing written informed consent,
subjects underwent symptom-limited treadmill testing according to
standardized graded or individualized ramp-treadmill protocols.9
Before testing, subjects were given a questionnaire that was used to
estimate their exercise capacity; the use of this estimate allowed
most subjects to reach maximal exercise capacity within the
recommended range of 8 to 12 minutes.10 We previously observed that
this protocol results in the closest relation between measured and
estimated exercise capacities.11

BP at rest was measured standing before exercise. Subjects were
discouraged from using handrails for support. Target heart rates were
not used as predetermined end points. Subjects were placed in a supine
position as soon as possible after exercise.12 Medications were not
changed or discontinued before testing.

ST-segment depression was measured visually. Abnormal ST-segment
response to exercise was ≥1 mm of ST-segment depression compared with
baseline. Ventricular tachycardia was defined as a run of ≥3
consecutive premature ventricular contractions. If premature
ventricular contractions occurred in ≥10% of all ventricular
contractions, the subject was considered to have frequent premature
ventricular contractions.13 Exercise capacity (in METs) was estimated
on the basis of the speed and grade of the treadmill. BP before,
during, and after exercise was measured manually. Subjects with a
decrease of 10 mm Hg in systolic BP after an initial increase with
exercise or a decrease below the value measured while standing before
testing were considered to have exertion hypotension.14 Left
ventricular hypertrophy was defined using standard criteria on
electrocardiogram.

No test results were classified as indeterminate.15 EST was performed,
analyzed, and reported according to a standardized protocol using a
computerized data base.16 Normal standards for predicted energy
expenditure were derived from regression equations developed on the
basis of results in veterans who were referred for EST and the
predicted peak exercise capacity was calculated as 18.0 - (0.15 × age).
17 Percentage of normal exercise capacity achieved was defined as
([achieved exercise capacity/predicted energy expenditure] × 100).

The Social Security Death Index was used to match all subjects to
their records according to name and Social Security number. Vital
status was determined as of July 2000. Information about CV mortality
was obtained from death certificates. Patients were followed for >12
years using CV mortality as the end point.

Differences between systolic BP values at rest and peak exercise were
calculated and the median value of the total group (44 mm Hg) was
chosen as the cutoff to create 2 groups (A and B) representing low
versus normal increase in systolic BP, respectively. The 2 groups were
analyzed univariately for clinical and exercise test variables.
Variables that were significantly different between groups were
analyzed for outcomes using a Cox regression model. Significant
predictors of CV death were selected using multivariate analysis to
adjust for baseline differences between the 2 groups. Predictors of
higher systolic BP response were analyzed in a similar fashion using
logistic regression analysis to adjust for baseline differences.

SPSS 14.0 (SPSS, Inc., Chicago, Illinois) was used for statistical
analyses where hazard ratios and 95% confidence intervals were
obtained. Cox proportional hazard regression model was used to
evaluate the association among demographic, clinical, and exercise
variables with CV mortality. Independent sample t tests were used to
analyze normally distributed variables and chi-square tests and Mann-
Whitney U tests were used for categorical variables. CV mortality
using Kaplan-Meier curves was assessed in patients with and without a
history of hypertension at rest and quartiles of systolic BP response
to exercise. Cumulative event rates were calculated for the 2 groups
using Kaplan-Meier curves; differences between groups were assessed
using log-rank test.

Results
A total of 6,145 men underwent exercise testing with a mean follow-up
of 6.6 ± 3.7 years. During follow-up, 676 patients died of CV causes.
The average annual CV mortality was 1.6% over the follow-up period.
Using the median value of change in systolic BP from baseline, the
following 2 groups were formed: patients with an exercise-induced
increase in systolic BP ≤43 mm Hg (group A, n = 3,062) and patients
with an exercise-induced increase in systolic BP ≥44 mm Hg (group B, n
= 3,083). Total CV mortality was significantly higher in group A than
in group B (13.7% vs 8.2%, p <0.001).

Patients in group A were significantly older, had a slightly lower
body mass index, and had more CV interventions; risk factors as
presented in Table 1. There was a significantly higher use of β
blockers in group A, although there were no significant differences in
the use of calcium channel blockers or other antihypertensive
medications between the 2 groups. Electrocardiographic signs of left
ventricular hypertrophy were also significantly higher in group A.

Table 1.

Demographic, clinical, and exercise test responses in group A, group
B, and total sample Characteristics Group A (SBP ≤43 mm Hg) (n =
3,062) Group B (SBP ≥44 mm Hg) (n = 3,083) Total (n = 6,145) p Value
Age (yrs) 61 ± 11 57 ± 11 59 ± 12 <0.001
Age >65 yrs 1,201 (39.2%) 870 (28.3%) 2,071 (33.7%) <0.001
β Blockers 780 (25.5%) 377 (12.2%) 1,157 (18.8%) <0.001
Nitrate 70 (24.2%) 745 (24.2%) 1,485 (24.2%) NS
Antihypertensive agent 740 (12.0%) 745 (21.1%) 1,485 (24.2%) NS
Previous MI 855 (28.8%) 487 (15.8%) 1,368 (22.3%) <0.001
Previous CHF 324 (10.6%) 192 (6.2%) 516 (8.4%) <0.001
Previous coronary artery bypass 356 (11.6%) 217 (7%) 573 (9.3%)
<0.001
Previous angioplasty 235 (7.7%) 145 (4.7%) 380 (6.2%) <0.001
Smoker 876 (28.6%) 1,007 (32.7%) 1,883 (30.6%) <0.001
Hyperlipidemia (total cholesterol >200 mg/dl) 871 (28.4%) 957 (31%)
1,828 (29.7%) 0.03
Diabetes mellitus 338 (11%) 305 (9.9%) 643 (10.5%) 0.14
Family history 644 (21%) 708 (23%) 1,352 (22%) 0.07
Hypertension 1,548 (50.6%) 1,405 (45.6%) 2,953 (48.1%) <0.001
Obesity (BMI >30 kg/m2) 1,543 (50.4%) 1,648 (53.5%) 3,191 (51.9%)
0.02
Heart rate at rest (beats/min) 76 ± 15 78 ± 15 77 ± 15 <0.001
SBP at rest (mm Hg) 137 ± 22 130 ± 19 133 ± 21 <0.001
Diastolic BP at rest (mm Hg) 82 ± 12 82 ± 12 82 ± 12 NS
Left ventricular hypertrophy on ECG 193 (6.3%) 129 (4.2%) 322 (5.2%)
<0.001
Angina pectoris (TMAP) 636 (20.8%) 397 (12.9%) 1,033 (16.8%) <0.001
ST abnormality 927 (30.3%) 600 (19.5%) 1,527 (24.8%) <0.001
Silent myocardial ischemia 587 (19.2%) 430 (13.9%) 1,017 (16.6%)
<0.001
Peak exercise heart rate (beats/min) 128 ± 25 145 ± 22 137 ± 25
<0.001
Peak exercise SBP (mm Hg) 161 ± 25 195 ± 23 178 ± 30 <0.001
Peak exercise diastolic BP (mm Hg) 83 ± 15 88 ± 15 86 ± 5 <0.001
Exercise capacity (METs) 6.9 ± 3.3 9.4 ± 3.6 8.1 ± 3.6 <0.001
Heart rate achieved 79 ± 15 88 ± 12 84 ± 14 <0.001
CV death 419 (6.8%) 252 (8.2%) 671 (10.9%) <0.001


Values are means ± SDs or numbers of patients (percentages).

BMI = body mass index; CHF = congestive heart failure; ECG =
electrocardiogram; MI = myocardial infarction; SBP = systolic BP; TMAP
= angina during or after exercise testing.



No major complications occurred during exercise testing. Average
hemodynamic values at rest differed significantly in the 2 groups. ST
abnormalities and angina during or after exercise testing occurred
more frequently in group A (p <0.001). Peak heart rate, peak systolic
BP, and exercise capacity were significantly higher in group B.
Failure to reach 85% age-predicted heart rate target was significantly
higher in group A.

Kaplan-Meier survival curves for the 2 groups are shown in Figure 1.
Patients with an increase in systolic BP ≥44 mm Hg from baseline had
lower mortality than patients with a systolic BP increase ≤43 mm Hg
(log rank 53.3, p <0.001). Clinical and exercise test predictors of CV
survival from the Cox proportional hazards are presented in Table 2.
After adjustment for age, exercise capacity, ST abnormalities, history
of myocardial infarction or congestive heart failure, history of
hypertension, and use of a β blocker, a difference in systolic BP ≥44
mm Hg was associated with improved survival (hazard ratio 1.2, 95%
confidence interval 1.02 to 1.44, p <0.05).



Figure 1. Kaplan-Meier survival curve. SBP = systolic BP.


Table 2.
Multivariate predictors of cardiovascular survival
Variables HR 95% CI p Value

Age 0.96 1.032-1.05 0.001
ST abnormalities 0.76 0.642-0.89 0.001
Exercise capacity 1.41 0.491-0.701 0.001
Difference in systolic BP >44 mm Hg 1.21 1.022-1.443 0.028
Previous MI 0.54 0.459-0.637 0.001
Previous CHF 0.43 0.356-0.524 0.001
Hypertension 0.71 0.602-0.839 0.001
β-Blocker use 1 1.022-1.443 0.94
Heart rate response 0.68 0.996-1.441 0.86
Hyperlipidemia 1.05 0.881-1.262 0.56

CI = confidence interval; HR = hazard ratio; other abbreviations as in
Table 1.


Figure 2 shows Kaplan-Meier survival curves for quartiles of systolic
BP increase. There was an incremental benefit in survival with a
greater increase in systolic BP response to exercise. Subjects in the
highest quartile of increased systolic BP had a significantly lower CV
mortality compared with subjects in the lowest quartile (7.3% vs
16.7%, log rank 94.7, p <0.001).

Figure 2. Kaplan-Meier survival curves for quartiles of systolic BP
response. Diff = difference; other abbreviation as in Figure 1.

History of hypertension had an independent and statistically
significant association with a higher systolic BP response to exercise
(odds ratio 1.5, p <0.001). Other factors that were significantly
associated with a higher systolic BP response to exercise are listed
in Table 3. Patients with a history of hypertension had a higher CV
mortality compared with normotensive patients (13.2% vs 9%, p <0.001).
Kaplan-Meier survival curves for groups with and without a history of
hypertension are shown in Figure 3 and Figure 4. An exercise-induced
increase in systolic BP ≤44 mm Hg was a significant predictor of
mortality in patients with and without a history of hypertension.

Table 3.

Multivariate predictors of higher systolic blood pressure response to
exercise

Variables Odds Ratio 95% CI p Value
Hypertension 1.5 1.32-1.68 0.001
Exercise capacity 1.23 1.2-1.25 0.001
Age 1.01 1.004-1.016 0.001
Diabetes 1.2 0.99-1.43 0.059
ST abnormalities with exercise 0.792 0.694-0.903 0.001
History of MI 0.6 0.53-0.69 0.001
History of CHF 0.84 0.68-1.03 0.102
β Blockers 0.44 0.38-0.51 0.001
Systolic BP at rest 0.98 0.98-0.98 0.001

Abbreviations as in Table 1 and Table 2.



Figure 3. Kaplan-Meier survival curves for patients with no history of
hypertension. Abbreviation as in Figure 1.


Figure 4. Kaplan-Meier survival curves for patients with a history of
hypertension. Abbreviation as in Figure 1.

Discussion
The major aim of the present study was to evaluate the prognostic
significance of an increased systolic BP with exercise and with other
EST variables. This study demonstrates that an increase in systolic BP
with EST predicts CV mortality independent of age, exercise capacity,
and ST-segment abnormalities. An increase in systolic BP ≥44 mm Hg
from baseline was associated with better survival, and this response
was associated with survival even in patients with a history of
hypertension.

In our study, we found that a greater increase in systolic BP at peak
exercise was associated with improved survival over long-term follow-
up. Although Kaplan-Meier survival curves showed improved survival
with an increase in systolic BP, these findings should be interpreted
with caution for very high systolic BP response. In an exaggerated
systolic BP response as described by Kurl et al,18 a systolic BP
increase >19.7 mm Hg for every minute of exercise was associated with
an increased incidence of stroke. Our systolic BP cutoff was 44 mm Hg,
much lower that that used by Kurl et al.18 The ideal cutoff for peak
systolic BP seems to vary among different investigators but most would
agree that a value ≥220 mm Hg requires closer follow-up.

The second end point previously reported has been an increase of
systolic BP recovery time or persistence of an increased systolic BP
even after 4 minutes of recovery. These findings have been associated
with an increased incidence of future hypertension.19 Mean BP is a
product of cardiac output and peripheral vascular resistance. Cardiac
output is determined by stroke volume and heart rate. Given the wealth
of prognostic information regarding heart rate recovery in recent
years, findings of delayed systolic BP recovery time seem to be
consistent.[20] and [21] We did not have the recovery BP data to
validate these findings in our study.

Patients in group B had a significantly higher exercise capacity
compared with group A. METs achieved was a statistically significant
predictor of a higher BP response (odds ratio 1.22, p <0.001). Because
greater exercise capacity reflects better physical fitness, these
results are in general agreement with previous studies examining the
role of physical training on maximal BP during exercise. Ekbolm et
al22 and Stratton et al23 reported that 16 to 24 weeks of endurance
training increased maximal systolic BP in trained versus untrained
subjects. In the Coronary Artery Risk Development in Young Adults
(CARDIA) study, after adjusting for confounding factors, it was
concluded that an exaggerated systolic BP response was associated with
an increase in systolic BP but not with new-onset hypertension over
the 5-year follow-up.24 These findings are similar to our previous
study evaluating exercise capacity and mortality in patients with a
history of hypertension, in which an exercise capacity <5 METs had a
relative risk of death of 1.7 to 2.3 compared with patients with an
exercise capacity >8 METs.10 In the present study, a greater systolic
BP response was a significant predictor of survival after adjusting
for METs achieved.

Prospective longitudinal studies have reported that increased systolic
BP levels during exercise are predictive of future hypertension and
higher CV events.[25] and [26] These studies did not incorporate other
exercise test data or clinical information. Because better trained
subjects exhibit a higher systolic BP response to exercise, it appears
that systolic BP response is not a valid prognostic test in physically
fit subjects. In our study we had the ability to adjust for this and
other confounding factors, and an exaggerated systolic BP response
remained a significant predictor of improved survival.

There is a significant association between systolic BP at rest and
left ventricular mass, but the association between left ventricular
hypertrophy and exercise BP is more uncertain.[27] and [28] Consistent
with some previous studies left ventricular hypertrophy was also a
significant predictor of CV mortality in our study.29

Our findings are applicable only to men because exercise test results
have been shown to differ in men and women.30 A limitation of this
study was the lack of data on clinical events during the follow-up
period. These data would have helped us clarify the association
between increased systolic BP response and development of future
hypertension.

References
1 D. Perloff, M. Sokolow and R. Cowan, The prognostic value of
ambulatory blood pressure, JAMA 249 (1983), pp. 2792-2798. View Record
in Scopus | Cited By in Scopus (392)

2 D. Perloff, M. Sokolow, R.M. Cowan and R.P. Juster, Prognostic value
of ambulatory blood pressure measurements: further analysis, J
Hypertens 7 (suppl 3) (1989), pp. S3-S10. View Record in Scopus |
Cited By in Scopus (178)

3 R. Fagard, J. Staessenm, L. Thijs and A. Amery, Prognostic
significance of exercise versus resting blood pressure in hypertensive
men, Hypertension 17 (1991), pp. 574-578. View Record in Scopus |
Cited By in Scopus (38)

4 J. Filipovsky, P. Ducimetiere and M.E. Safar, Prognostic
significance of exercise blood pressure and heart rate in middle-aged
men, Hypertension 20 (1992), pp. 337-339.

5 R. Mundal, S.E. Kjeldsen, L. Sandvik, G. Erikssen, E. Thaulow and J.
Erikssen, Exercise blood pressure predicts mortality from myocardial
infarction, Hypertension 27 (1996), pp. 324-329. View Record in Scopus
| Cited By in Scopus (47)

6 J. Myers, M. Prakash, V. Froelicher, D. Do, S. Partington and J.E.
Atwood, Exercise capacity and mortality among men referred for
exercise testing, N Engl J Med 346 (2002), pp. 793-801. View Record in
Scopus | Cited By in Scopus (415)

7 V.F. Froelicher and J. Myers, Research as part of clinical practice:
use of Windows-based relational data bases, Veterans Health Syst J 3
(1998), pp. 53-57.

8 V.F. Froelicher and P. Shiu, Exercise test interpretation system,
Phys Comput 14 (1996), pp. 40-44.

9 R.A. Wolthuis, V.F. Froelicher Jr, J. Fischer, I. Noguera, A.J.
Stewart and J.H. Triebwasser, New practical treadmill protocol for
clinical use, Am J Cardiol 39 (1977), pp. 697-700. Abstract | PDF (379
K) | View Record in Scopus | Cited By in Scopus (27)

10 J. Myers, D. Do, W. Herbert, P. Ribisl and V.F. Froelicher, A
nomogram to predict exercise capacity from a specific activity
questionnaire and clinical data, Am J Cardiol 73 (1994), pp. 591-596.
Abstract | Full Text + Links | PDF (631 K) | View Record in Scopus |
Cited By in Scopus (62)

11 J. Myers, N. Buchanan, D. Walsh, M. Kraemer, P. McAuley, M.
Hamilton-Wessler and V.F. Froelicher, Comparison of the ramp versus
standard exercise protocols, J Am Coll Cardiol 17 (1991), pp. 1334-
1342. View Record in Scopus | Cited By in Scopus (138)

12 B. Lachterman, K.G. Lehmann, D. Abrahamson and V.F. Froelicher,
"Recovery only" ST-segment depression and the predictive accuracy of
the exercise test, Ann Intern Med 112 (1990), pp. 11-16. View Record
in Scopus | Cited By in Scopus (30)

13 J.C. Yang, R.C. Wesley Jr and V.F. Froelicher, Ventricular
tachycardia during routine treadmill testing: risk and prognosis, Arch
Intern Med 151 (1991), pp. 349-353. View Record in Scopus | Cited By
in Scopus (22)

14 K. Morrow, C.K. Morris, V.F. Froelicher, A. Hideg, D. Hunter, E.
Johnson, T. Kawaguchi, K. Lehmann, P.M. Ribisl and R. Thomas et al.,
Prediction of cardiovascular death in men undergoing noninvasive
evaluation for coronary artery disease, Ann Intern Med 118 (1993), pp.
689-695. View Record in Scopus | Cited By in Scopus (72)

15 M.C. Reid, M.S. Lachs and A.R. Feinstein, Use of methodological
standards in diagnostic test research: getting better but still not
good, JAMA 274 (1995), pp. 645-651. View Record in Scopus | Cited By
in Scopus (386)

16 P. Shue and V.F. Froelicher, EXTRA: an expert system for exercise
test reporting, J Noninvasive Test II-4 (suppl) (1998), pp. 21-27.

17 C.K. Morris, J. Myers, V.F. Froelicher, T. Kawaguchi, K. Ueshima
and A. Hideg, Nomogram based on metabolic equivalents and age for
assessing aerobic exercise capacity in men, J Am Coll Cardiol 22
(1993), pp. 175-182. View Record in Scopus | Cited By in Scopus (43)

18 S. Kurl, J.A. Laukkanen, R. Rauramaa, T.A. Lakka, J. Sivenius and
J.T. Salonen, Systolic blood pressure response to exercise stress test
and risk of stroke, Stroke 32 (2001), pp. 2036-2041. View Record in
Scopus | Cited By in Scopus (28)

19 J.P. Singh, M.G. Larson, T.A. Manolio, C.J. O'Donnell, M. Lauer,
J.C. Evans and D. Levy, Blood pressure response during treadmill
testing as a risk factor for new-onset hypertension The Framingham
Heart Study, Circulation 99 (1999), pp. 1831-1836. View Record in
Scopus | Cited By in Scopus (82)

20 M.S. Lauer and V. Froelicher, Abnormal heart-rate recovery after
exercise, Lancet 360 (2002), pp. 1176-1177. Abstract | Full Text +
Links | PDF (58 K) | View Record in Scopus | Cited By in Scopus (8)

21 K. Shetler, R. Marcus, V.F. Froelicher, S. Vora, D. Kalisetti, M.
Prakash, D. Do and J. Myers, Heart rate recovery: validation and
methodologic issues, J Am Coll Cardiol 38 (2001), pp. 1980-1987.
SummaryPlus | Full Text + Links | PDF (132 K) | View Record in Scopus
| Cited By in Scopus (72)

22 B. Ekbolm, P.O. Astrand, B. Saltin, J. Stenberg and B. Wallstrom,
Effect of training on circulatory response to exercise, J Appl Physiol
24 (1968), pp. 518-528.

23 J.R. Stratton, W.C. Levy, M.D. Cerqueria, R.S. Schwartz and I.B.
Abrass, Cardiovascular response to exercise: effects of aging and
exercise training in healthy men, Circulation 89 (1994), pp. 1648-
1655. View Record in Scopus | Cited By in Scopus (103)

24 T.A. Manolio, G.L. Burke, S. Savage PJ Sidney, J.M. Gardin and A.
Oberman, Exercise BP response and 5-year risk of elevates BP in a
cohort of young adults: the CARDIA study, Am J Hypertens 99 (1994),
pp. 1831-1836.

25 N.V. Wilson and B.M. Meyer, Early prediction of hypertension using
exercise blood pressure, Prev Med 10 (1981), pp. 62-68. Abstract |
Full Text + Links | PDF (492 K) | View Record in Scopus | Cited By in
Scopus (42)

26 M. Jette, F. Landry and K. Sidney, Exaggerated blood pressure
response to exercise in the detection of hypertension, J Cardiopulm
Rehabil 8 (1988), pp. 171-177. View Record in Scopus | Cited By in
Scopus (7)

27 D. Levy, R.J. Garrison, D.D. Savage, W.B. Kannel and W.P. Castelli,
Prognostic implications of echocardiographically determined left
ventricular mass in Framingham heart study, N Eng J Med 322 (1990),
pp. 1561-1566. View Record in Scopus | Cited By in Scopus (2109)

28 D.B. Rowlands, D.R. Glover, M.A. Ireland, R.A. McLeay, T.J.
Stallard, R.D. Watson and W.A. Littler, Assessment of left-ventricular
mass and its response to antihypertensive treatment, Lancet 1 (1982),
pp. 467-470. Abstract | Full Text + Links | PDF (527 K) | View Record
in Scopus | Cited By in Scopus (54)

29 J.S. Gottdiener, J. Brown, J. Zoltick and R.D. Fletcher, Left
ventricular hypertrophy in men with normal blood pressure: relation to
exaggerated blood pressure response to exercise, Ann Intern Med 112
(1990), pp. 161-166. View Record in Scopus | Cited By in Scopus (73)

30 D.A. Weiner, T.J. Ryen, L. Parsons, L.D. Fisher, B.R. Chaitman,
L.T. Sheffield and F.E. Tristani, Long term prognostic value of
exercise testing in men and women from Coronary Artery Surgery Study
(CASS) registry, Am J Cardiol 75 (1995), pp. 865-870. Abstract | PDF
(657 K) | View Record in Scopus | Cited By in Scopus (65)

Corresponding author: Tel: 212-434-2551; fax: 212-434-2111.

The American Journal of Cardiology
Volume 100, Issue 11, 1 December 2007, Pages 1609-1613

* * *
Just for fun, see how many errors you can catch in this article.

Marilyn
.