Usefulness of Paradoxical Systolic Blood Pressure Increase After Exercise as a Predictor of Cardiovascular Mortality

Article Outline

• Abstract
• Methods
• Results
• Discussion
• Acknowledgment
• References
• Copyright

Exercise treadmill testing (ETT) is a well-accepted examination for patients with suspected coronary artery disease (CAD), and exercise induced ST-segment deviation is commonly used for CAD detection. However, recent evidence shows that systolic blood pressure (SBP) changes during and after exercise were associated with CAD severity, risk of acute myocardial infarction and stroke, new-onset hypertension, and even cardiovascular mortality. We retrospectively assessed 3,054 patients referred for ETT in 1996. Blood pressure and heart rate were recorded at rest, during peak exercise, and 1 and 3 min after exercise. SBP at 3 min of recovery equal to or higher than that at 1-min of recovery was defined as paradoxical SBP increase. These patients were categorized into 4 groups according to ETT ST-segment change and postexercise SBP change. After 10 years of follow-up, 346 patients (11%) died, with 129 (4%) dying from cardiovascular disease (CVD). Among the 4 groups, patients with ischemic ST-segment change and paradoxical SBP increase were associated with a higher risk for mortality, with odds ratios of 1.86 (95% confidence interval 1.31 to 2.65) for all-cause mortality and 3.18 (95% confidence interval 1.94 to 5.20) for CVD mortality, respectively. Patients with isolated paradoxical SBP increase still had a higher risk of CVD mortality (odds ratio 1.80, 95% confidence interval 1.70 to 3.04), even after controlling other cardiovascular risk factors. In subgroup analysis of 346 mortality subjects, patients with ischemic ST-segment change and paradoxical SBP increase would be more likely to die from CVD. In conclusion, compared with ischemic ST-segment change, paradoxical SBP increase after exercise is an important and significant predictor of CVD mortality.

Increased systolic blood pressure (SBP) is a major risk factor for cardiovascular disease (CVD) morbidity and mortality.¹ SBP changes during exercise also gain much attention. An exercise-induced increase in SBP has been found to be a predictor of future hypertension,², ³, ⁴, ⁵ left ventricular hypertrophy,⁶, ⁷, ⁸ stroke,⁹ and CVD mortality¹⁰, ¹¹, ¹² in apparently healthy subjects. Previous studies have reported that a blunted decrease in SBP and increased SBP after exercise were also associated with an increased risk of coronary heart disease,¹³, ¹⁴ stroke,⁹ and hypertension.⁵ Exercise treadmill testing (ETT) is recommended as an initial evaluation for patients with suspected coronary artery disease (CAD). Our previous study confirmed that paradoxical SBP increase during recovery after graded exercise correlates with severity of CAD.¹⁵ However, the association between postexercise SBP change and mortality has not been well established. The purpose of this study was to investigate whether paradoxical SBP increase during ETT adds additional prognostic information on all-cause and cardiovascular mortalities in addition to ischemic ST-segment change.

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Methods 

We retrospectively studied patients who underwent symptom-limited ETT at National Taiwan University Hospital in 1996. Patients <20 years old, with pre-excitation syndrome, and/or with left bundle branch block on electrocardiogram at rest were excluded. After ruling out CAD, known CAD and preoperative evaluation in patients during follow-up were the most common indications for exercise testing. We obtained clinical disease history and cardiovascular risk factors from detailed chart review.

Subjects with SBP >140 mm Hg and/or diastolic BP >90 mm Hg or receiving antihypertension agents were considered to be hypertensive. Prevalent diabetes mellitus was defined as fasting glucose level ≥6.99 mmol/L (126 mg/dl) and/or a history of diabetes mellitus with management. Cholesterol levels ≥5.17 mmol/L (200 mg/dl), low-density lipoprotein cholesterol levels ≥3.36 mmol/L (130 mg/dl), or use of lipid-lowering agents was defined as hyperlipidemia. Mortality data were obtained by matching all study subjects with mortality certificate data file (2005 edition) from the department of health, Executive Yuan, Republic of China (Taiwan). All-cause mortality and cardiovascular mortality were defined according to codes in the International Classification of Diseases, Ninth Revision. Mortality data of codes 390 to 459 were coded as CVD in the analyses.

Electrocardiograms were recorded using an exercise system (CASE Marquette 16, Marquette Electronics, Inc., Milwaukee, Wisconsin). The modified Bruce protocol was used for symptom-limited ETT. Heart rate, BP, and 12-lead electrocardiogram with a shift of ST segment were recorded during the standing pre-exercise period, 60 seconds before the end of each stage, during peak exercise, and after 1 minute and 3 and 5 minutes of recovery. Total exercise time was also recorded. Target heart rate was defined as 85% of maximal achievable heart rate (220 beats/min minus age in years). The Tango exercise BP monitor (SunTech Medical, Morrisville, North Carolina) was used to automatically measure and display a patient's SBP and diastolic BP in addition to heart rate. ST-segment level 60 ms after the J point was measured in each lead using a computer-assisted system. An ischemic or positive ST-segment change was defined as ≥1 mm horizontal or downsloping ST-segment depression and ≥2 mm upsloping ST-segment depression. Percent maximal heart rate achievable was defined as the ratio of maximal heart rate achieved to maximal heart rate predicted. Paradoxical SBP increase, a phenomenon of abnormal postexercise SBP change, was defined as SBP at 3 min of recovery equal to or higher than SBP at 1 min of recovery during ETT (SBP_{3 min}/SBP_{1 min} ≥1).

In the data analysis, demographic and cardiovascular risk factors of study subjects were first compared among the 4 groups. Continuous variables were expressed as mean ± 1 SD. One-way analysis of variance was used to compare continuous variables among the 4 groups. For categorical data, chi-square test was used to test the significance level among the 4 groups. Multiple logistic regression analysis was applied to estimate the hazard risk of all-cause and CVD mortalities with paradoxical SBP increase, ischemic ST-segment change, and various risk factors. Adjusted variables included age, gender, hypertension, diabetes mellitus, smoking habits, hyperlipidemia, and exercise time. The person-year method was used to calculate incidence rates of all-cause and CVD mortalities, and survival curves were estimated according to ETT ST-segment change and postexercise SBP change results using the Kaplan-Meier procedure. All analyses were performed using SAS 8.2 (SAS Institute, Cary, North Carolina), and a p value <0.05 was considered statistically significant.

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Results 

This study population consisted of 3,054 patients (1,898 men and 1,156 women) with a mean age of 57 years. According to ETT ST-segment change and postexercise SBP change, these patients were categorized into 4 groups. Patients in group 1 had positive ST-segment change and positive paradoxical SBP increase, those in group 2 had negative ST-segment change and positive paradoxical SBP increase, those in group 3 had positive ST-segment change and negative paradoxical SBP increase, and those in group 4 had negative ST-segment change and negative paradoxical SBP increase.

Baseline characteristics of the 4 groups are listed in Table 1. Patients with ischemic ST-segment change and paradoxical SBP increase (group 1) tended to be older and predominantly men and to have a lower baseline heart rate and shorter exercise time. They were much more likely to have hypertension, hyperlipidemia, and diabetes mellitus. Patients with ischemic ST-segment change tended to be older and have higher pretest SBPs.

Table 1. Comparison of baseline characteristics in the four groups of patients

Variable	Groups⁎				p Value
	1	2	3	4
	(n = 279)	(n = 436)	(n = 776)	(n = 1,563)
Age (yrs)	58.62 ± 11.29	56.02 ± 13.15	58.11 ± 10.29	56.85 ± 11.69	0.0017
Men	203(72.76%)	276(63.30%)	473(60.95%)	898(60.52%)	0.0012
Heart rate (beats/min)	76.01 ± 13.33	78.74 ± 15.67	78.13 ± 14.94	79.65 ± 15.01	0.0010
SBP (mm Hg)	137.63 ± 21.59	131.11 ± 20.76	134.26 ± 19.93	130.58 ± 19.40	<0.0001
Diastolic BP (mm Hg)	80.99 ± 11.04	81.06 ± 12.06	81.28 ± 11.05	80.82 ± 11.28	0.8274
Hypertension	147(53.07%)	174(40.18%)	368(47.98%)	663(42.94%)	0.0008
Hyperlipidemia	88(31.77%)	86(19.91%)	177(23.11%)	341(22.09%)	0.0017
Diabetes mellitus	59(21.3%)	59(13.63%)	115(14.99%)	223(14.44%)	0.0226
Exercise time (s)	381.0(276.0–482.0)	421.0(300.0–540.5)	420.0(361.0–500.5)	427.0(361.0–541.0)	<0.0001†
Maximal heart rate achievable (%)	88.16(75.48–95.36)	89.97(76.66–97.98)	93.49(85.50–99.39)	92.61(85.71–99.39)	<0.0001†

Data are expressed as mean ± SD, number of patients (percentage), or median (quartiles 1 to 4).

There were total 346 deaths (11%) at the end of the 10-year follow-up, with 129 (4%) deaths from a cardiovascular cause. Most CVD mortalities included myocardial infarction, ischemic cardiomyopathy, congestive heart failure, and ischemic stroke. All-cause mortality and CVD mortality in each group are presented in Table 2. Taking patients in group 4 as controls, patients with paradoxical SBP increase and positive or negative ST-segment change (groups 1 and 2) had a higher CVD mortality rate. For all-cause mortality, patients with paradoxical SBP increase and ischemic ST-segment change (group 1) had a significantly higher incidence than those in the control group. Patients with isolated paradoxical SBP increase (group 2) also showed a trend toward increased all-cause mortality compared with those in the control group. After controlling for age, gender, pretest SBP and diastolic BP, hypertension, hyperlipidemia, and diabetes mellitus, patients in groups 1 and 2 had a higher hazard risk for CVD mortality, with odds ratios of 2.05 (95% confidence interval 1.21 to 3.47) and 1.80 (95% confidence interval 1.07 to 3.04), respectively, than the control group (Table 2, model 2). Patients with impaired exercise capacity, demonstrated by a short exercise time, also had a higher hazard risk for CVD and all-cause mortality. Exercise time significantly attenuated the effects of postexercise SBP change and age on CVD mortality (Table 2, model 3).

Table 2. Multiple logistic regression analysis for cardiovascular disease mortality and all-cause mortality

Variable	Model 1		Model 2		Model 3
	CVD Mortality	All-Cause Mortality	CVD Mortality	All-Cause Mortality	CVD Mortality	All-Cause Mortality
Group 1	3.18(1.94–5.20)‡	1.86(1.31–2.65)‡	2.05(1.21–3.47)†	1.24(0.84–1.83)	1.77(1.04–3.02)⁎	1.05(0.70–1.56)
Group 2	1.80(1.09–2.97)⁎	1.37(1.00–1.90)	1.80(1.07–3.04)⁎	1.39(0.98–1.96)	1.68(0.99–2.84)	1.27(0.89–1.81)
Group 3	1.24(0.78–1.97)	1.07(0.81–1.42)	1.13(0.70–1.81)	0.95(0.71–1.28)	1.14(0.71–1.83)	0.96(0.71–1.30)
Group 4	1	1	1	1	1	1
Age			1.04(1.02–1.06)‡	1.07(1.06–1.09)‡	1.01(0.99–1.03)	1.04(1.02–1.05)‡
Men			2.56(1.63–4.01)‡	2.32(1.76–3.06)‡	3.31(2.08–5.27)‡	3.21(2.39–4.30)‡
SBP			1.01(1.00–1.02)	1.01(1.00–1.02)⁎	1.01(1.00–1.020)	1.01(1.00–1.02)
Diastolic BP			0.98(0.96–1.00)⁎	0.98(0.97–0.99)‡	0.98(0.96–1.00)	0.98(0.97–1.00)†
Exercise time			—	—	1.00(0.996–1.00)‡	1.00(0.996–1.00)‡
Hypertension			1.61(1.08–2.39)⁎	1.23(0.95–1.58)	1.67(1.12–2.49)⁎	1.28(0.99–1.66)
Hyperlipidemia			2.97(2.04–4.30)‡	2.13(1.65–2.75)‡	2.74(1.88–4.00)‡	1.96(1.51–2.55)‡
Diabetes mellitus			1.95(1.30–2.93)‡	2.29(1.74–3.00)‡	1.81(1.20–2.73)‡	2.10(1.59–2.77)‡

Values are odds ratios (95% confidence intervals).

Model 1 = univariate logistic analysis; models 2 and 3 = multiple logistic regression models adjusting other covariates.

Figure 1 shows Kaplan-Meir survival curves for 10-year all-cause and cardiovascular mortalities in the 4 groups. Compared with patients in group 4, there were significant survival differences in patients in groups 1 and 2. These differences existed in all-cause mortality and CVD mortality. We further evaluated the characteristics of 346 mortality cases (Table 3). These subjects with paradoxical SBP increase during ETT were more likely to be men and to have diabetes mellitus and more severe CAD. Of these 346 deaths, after multivariate analysis, subjects who had ischemic ST-segment changes, paradoxical SBP increase, hypertension, hyperlipidemia, or younger age were more likely to have died from a cardiovascular cause (Table 4).

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• Figure 1. 

  Kaplan-Meir survival curves for 10-year all-cause and cardiovascular mortalities in the study population, stratified by 4 categories according to paradoxical SBP increase and ETT result. Group 1 = positive ischemic ST-segment change and negative paradoxical SBP increase; group 2 = negative ischemic ST-segment change and positive paradoxical SBP increase; group 3 = positive ischemic ST-segment change and negative paradoxical SBP increase; group 4 = negative ischemic ST-segment change and negative paradoxical SBP increase. The p values indicate the difference of survival curve between groups 1 (or 2, or 3) and group 4 (reference group).

Table 3. Baseline characteristics of mortality in four patient groups

Variable	Groups				p Value
	1	2	3	4
	(n = 48)	(n = 58)	(n = 83)	(n = 157)
Age (yrs)	64.04 ± 11.52	64.91 ± 10.45	63.05 ± 8.72	64.97 ± 8.49	0.4668
Men	38(79.17%)	48(82.76%)	63(75.90%)	116(73.89%)	0.5578
Diabetes mellitus	24(50%)	18(31.03%)	21(25.3%)	45(28.66%)	0.0211
Hypertension	30(62.5%)	31(53.45%)	47(56.63%)	90(57.32%)	0.8263
Hyperlipidemia	19(39.58%)	21(36.21%)	23(27.71%)	65(41.40%)	0.2096
Body mass index (kg/m2)	24.01 ± 2.58	24.78 ± 2.81	25.53 ± 4.18	24.50 ± 3.33	0.1811
Smoking habit	23(47.92%)	23(39.66%)	39(46.99%)	63(40.13%)	0.6148
CAD severity⁎
Mild	4(8.33%)	9(15.52%)	8(9.64%)	23(14.65%)	0.0029
Severe	18(37.50%)	11(18.97%)	12(14.46%)	18(11.46%)
Previous myocardial infarction	7(14.58%)	16(27.58%)	9(10.84%)	25(15.92%)	0.0636
Left ventricular ejection fraction (%)	56.16 ± 17.89	58.19 ± 14.78	61.17 ± 18.53	163.45 ± 14.43	0.1661
Uric acid (mg/dl)	7.31 ± 2.10	6.63 ± 1.89	6.31 ± 1.91	7.17 ± 2.01	0.0543
Creatinine (mg/dl)	1.36 ± 0.65	1.47 ± 0.93	1.26 ± 0.72	1.21 ± 0.34	0.1018
Exercise time (s)	298.02 ± 120.32	337.79 ± 125.09	335 ± 125.86	338.16 ± 142.69	0.3070

Table 4. Multiple logistic regression analysis for cardiovascular disease mortality in 10-year mortality subgroup

Variable	CVD Mortality
	Model 1	Model 2
Group 1	2.66(1.33–5.33)†	2.63(1.31–5.30)†
Group 2	1.69(0.88–3.23)	1.68(0.88–3.22)
Group 3	1.30(0.72–2.34)	1.29(0.72–2.33)
Group 4	1	1
Age	0.97(0.95–1.00)⁎	0.97(0.95–1.00)
Men	1.12(0.63–1.98)	1.14(0.63–2.07)
Diabetes mellitus	0.89(0.54–1.47)	0.88(0.53–1.46)
Hypertension	1.64(1.02–2.63)⁎	1.64(1.02–2.63)⁎
Hyperlipidemia	2.02(1.26–3.25)‡	2.01(1.25–3.24)‡
Smoking habit	1.43(0.88–2.30)	1.43(0.88–2.30)
Exercise time	—	1.00(0.99–1.00)

Values are odds ratios (95% confidence intervals).

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Discussion 

The major findings of this study indicated that postexercise SBP change had a superior and independent role in long-term CVD mortality. In routine clinical practice, we use ETT as a tool to predict CAD and focus mainly on exercise duration and ST-segment changes. Amon et al¹⁶ reported that an abnormal postexercise SBP response during ETT accurately identified patients with CAD, which was significantly better than using criteria of ischemic ST depression only. Several subsequent studies have indicated using the 3-minute postexercise SBP ratio (SBPR; calculated by dividing SBP 3 minutes into recovery phase of ETT by SBP at peak exercise) to express the rate of decrease in postexercise SBP. These studies found that SBPR values were associated with presence and extent of CAD as documented by coronary angiogram¹⁴, ¹⁷, ¹⁸ and thallium-201 scintigram.¹⁹ In a Japanese study,²⁰ an abnormal SBPR value was the most important risk factor for cardiac mortality, with a relative risk of 15.4.

In a study by Ellis et al,²¹ 12,379 patients were followed for 6 years. The 3-minute SBPR (range 0.36 to 1.62) was divided into 4 quartiles. Compared with patients in the lowest quartile of SBPR, patients in the highest quartile were at increased risk for all-cause mortality. However, this association was significantly attenuated after adjusting for age. In our study, the association of paradoxical SBP increase with all-cause mortality also was attenuated after adjusting other CVD risk factors. However, our study clarified its independent role in long-term cardiovascular mortality. We chose “paradoxical SBP increase” instead of “3-minute SBPR” because peak-exercise SBP is difficult to record in a timely fashion and correctly and this ratio needs to be further calculated. Defining the cut-point ratio at 1 makes interpreting this important risk factor more convenient for physicians.

The mechanism of an abnormal postexercise SBP response has been investigated in several studies.¹³, ²² Studies evaluating intracardiac hemodynamics and their relation to the SBPR have been helpful in determining the mechanism of an abnormal 3-minute SBPR. They found that higher values of calculated SBPR were associated with a significantly higher pulmonary capillary wedge pressure and a lower cardiac index at peak exercise. By 3 minutes into the recovery phase, these patients also had greater vascular resistance, increased catecholamine levels, and a pronounced delay in the return of the stroke index to baseline, a reflection of overactivity of the sympathetic nervous system and attenuated vagal reactivation.

Exercise capacity has been documented as a powerful prognostic indicator in previous studies.²³ Peterson et al²³ demonstrated that decreased exercise capacity was an independent predictor for nonfatal cardiovascular events and mortality. This significant role in long-term CVD mortality and all-cause mortality also was found in our study. Other increased co-morbidities were associated with decreased exercise capacity and might contribute to this poor outcome. However, the mechanisms remain unclear. Higher pulmonary capillary wedge pressure and lower cardiac index at peak exercise might also be contributors, and these may explain why a paradoxical SBP increase effect attenuated after further controlling exercise capacity.

There are some limitations in our study. First, BPs were measured by using indirect arm cuff sphygmomanometry, which is somewhat inaccurate during exercise. Second, we included patients taking hypertensive medications and did not put this factor into the final covariate analysis. It would be difficult to delineate between effects of medications and effects of native BP regulatory mechanisms on BP recovery immediately after exercise.

In conclusion, our findings indicated the superior added value of applying postexercise SBP changes as an important prognostic predictor in clinical practice, in addition to the routine standard criterion of ischemic ST-segment change. For these patients with paradoxical SBP increase after exercise, more aggressive lifestyle modification and medical treatment are reasonable recommendations.

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Acknowledgment 

We thank the information systems office and the medical records office, National Taiwan University Hospital, for help in data collection for this study.

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