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Cardiovascular Reactivity to Mental Stress in the Stockholm Female Coronary Risk Study

From the Department of Psychology (G.W.), State University of New York, Stony Brook, New York; Department of Health Psychology (C.-W.K.), University of Education, Schwäbisch-Gmünd, Germany; Departments of Preventive Medicine (M.H., S.P.W., K.O.-G.) and Cardiology (K.S.-G.), Karolinska Institute, Stockholm; Karolinska Hospital, Stockholm; and the Student Health Center (M.H.), University of Stockholm, Stockholm, Sweden.

Address reprint requests to: Gerdi Weidner, Preventive Medicine Research Institute, Sausalito, CA 94965. Email: gweidner{at}yahoo.com

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
OBJECTIVE: This study evaluated the ability of mental stress testing to discriminate between women with and without CHD, and among women with different disease manifestations, taking into account history of hypertension and ß-blocker use.

METHODS: Analyses were based on data from a community-based case-control study of women aged 65 years or younger. The study group consisted of 292 women who were hospitalized for an acute event of CHD, either AMI or unstable AP in Stockholm between 1991 and 1994. Controls were matched to cases by age and catchment area. Cardiovascular reactivity and emotional response to an anagram task solved under time pressure were measured 3 to 6 months after hospitalization.

RESULTS: Patients reacted with smaller increases in heart rate (4 bpm) than their controls (7 bpm). Results for the rate-pressure product were similar. Cardiovascular reactions did not distinguish patients with AP from those with AMI. History of hypertension (present in 50% of patients and 11% of controls) was related to enhanced diastolic blood pressure reactivity. Patients on ß-blockers (66%) had lower heart-rate levels throughout testing, but did not differ in their cardiovascular stress reactions when compared with the remaining participants.

CONCLUSIONS: Women with heart disease have somewhat lower heart-rate responses to stress than healthy age-matched controls. History of hypertension is related to enhanced diastolic blood pressure reactivity to mental stress in both patients and controls.

Key Words: cardiovascular stress reactivity, • coronary heart disease, • history of hypertension, • women.

Abbreviations: AP = angina pectoris;; (A)MI = (acute) myocardial infarction;; BMI = body mass index;; BP = blood pressure;; CHD = coronary heart disease;; DBP = diastolic blood pressure;; HR = heart rate;; RPP = rate-pressure product;; SBP = systolic blood pressure;; WHO = World Health Organization.

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
One of the most active areas in psychosomatic research has focused on cardiovascular reactivity to mental stress. The underlying assumption of this research is that excessive cardiovascular responses to stress play a role in the development of hypertension and CHD. Support for this hypothesis comes from several studies conducted with initially disease-free and mostly male samples (1–6). For example, Light and her colleagues (1) found that excessive blood pressure responses to stress predicted elevated blood pressure among initially normotensive young men with a familial history of hypertension more than 10 years later. Excessive cardiovascular responses to stress have also been implicated in the progression of intima-media thickness of the carotid arteries in the Kuopio Heart Study, a population study of middle-aged men in Eastern Finland (4–6). Similarly, a greater change in systolic blood pressure during a stressful task predicted progression of carotid atherosclerosis in an unmedicated sample of 136 volunteers (7).

The exploration of any factor believed to play a causal role in the development of a disease may benefit from an initial evaluation of that factor’s ability to distinguish those with the disease from those without the disease (8–10). Thus, the question is whether stress reactivity tests evoke responses that distinguish different clinical groups and discriminate between people with and without the disease. In a recent review of this literature we concluded that stress reactivity testing indeed discriminates between hypertensive and normotensive men: hypertensives (or persons at high risk for developing hypertension) show elevated cardiovascular responses to mental stress (11). However, when considering coronary patients, the situation is more complicated. Generally, methodological and procedural differences in early studies (eg, lack of representative patient groups and adequate control group; no distinction among various clinical manifestations of CHD; unspecified medication use and history of hypertension; and use of very small highly select samples) preclude conclusions about discriminatory validity of reactivity testing (11). For example, Sime et al. (12) found lower heart rates in response to a stressful quiz among 30 male MI patients when compared with 30 healthy age-matched controls. In contrast, Dembroski et al. (13) found elevated blood pressure reactivity to a quiz (but not an interview) among 31 male MI patients when compared with 33 control subjects. There were no differences in heart rates in that study. Similarly, Sundin et al. (14) report greater systolic blood pressure reactivity to mental stress in a highly select group of 30 nonsmoking, normotensive, and nonmedicated MI patients when compared with healthy age-matched controls. We currently lack information for women from both prospective and case-control studies.

The primary purpose of this report was to evaluate the ability of mental stress testing to discriminate between those with and without heart disease and among those with different disease manifestations. The present study was based on data from the Stockholm Female Coronary Risk Study, a population study consisting of all women aged 65 years or younger who were hospitalized with a diagnosis of an acute coronary disease event (myocardial infarction or unstable angina pectoris) in the greater Stockholm area during a 3-year period. Each patient was matched to a healthy control subject of the same age and from the same catchment area, randomly obtained from the Stockholm census register. Thus, the sample size of almost 600 women differing in disease manifestation allows for an evaluation of discriminatory validity of stress reactivity testing. In addition, assessment of history of hypertension and ß-blocker use among the patients makes it possible to explore their role in cardiovascular stress reactivity among women.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
Participants
The sample for this study consisted of all women aged 65 and under who were hospitalized with a diagnosis of an acute coronary disease event (unstable angina pectoris or myocardial infarction) in the greater Stockholm area between 1991 and 1994. The Swedish healthcare system provides care to all residents, regardless of income or insurance status. Thus, all patients who needed and sought hospital care for an acute CHD event during this time period were identified (N = 335). Thirteen percent (N = 43) could not be included in the study. Reasons for nonresponse included death, disability, and inability to speak Swedish fluently. Control subjects were randomly selected from the city census and were matched to patients by age and catchment area. The census register contains unique 10-digit identification numbers for each individual. It is based on birth date and sex. For each patient, a healthy woman was chosen who was born on the same day or another day as close as possible as the patient. "Healthy" was defined as being free of symptoms of heart disease and without hospitalization for any illness during the prior 5-year period. Of those eligible, 17% declined to participate, mostly due to administrative reasons (eg, difficulty scheduling time off work). In these instances, another woman was selected from the Census Registry. There were 292 patients and 292 matched controls.

Recruitment of patients was carried out by nurses at 10 existing coronary care units who reported on a weekly basis all hospitalized cases of suspected acute MI and stable or unstable angina pectoris. The criteria for admission to intensive coronary care units are the same at all 10 cardiology clinics. Patients were included in the study if their hospital records met any of the following criteria:

1. Definite or suspected AMI, based on the WHO criteria of typical chest pain, typical enzyme patterns, and diagnostic ECG changes (15), classified by the Minnesota code (16); or
   
2. Unstable AP, defined as severe AP of recent onset that had worsened during the 4 weeks before admission, with an increase in pain intensity and pain duration, or with pain at rest or after very low physical exertion (17).
   

For this report, the diagnosis at index event was categorized as either AP or AMI. Accordingly, there were 110 women with AMI and 182 with AP. A more detailed description of the study groups, recruitment procedures, nonresponse, and assessments has been given previously (18). Briefly, the mean age of the study groups was 56.7 (SD = 7) years, ranging from 30 to 65 years. There were no significant differences between the two groups in the number of premenopausal and postmenopausal women. However, patients were more likely to be less educated, more obese, have more unfavorable lipid profiles (18), and be "previous smokers," but were less likely to be "current smokers" when compared with the controls. Also, history of hypertension was more prevalent among the patients (50%) than among controls (11%). For this study, patients were divided into two groups: those with MI and those with AP. Characteristics of these two patient’s groups and those of their matched controls are presented in Table 1.

Because one or more cardiovascular assessment(s) were missing (due to malfunctioning of the measuring device) for either patient or control at any one of the three time points (baseline, anagram task, and recovery), there were 254 pairs (ie, patient- and matched-control) who had a complete set of readings for SBP, 253 pairs for DBP, and 231 pairs with complete readings for heart rate.

Emotions.
To arrive at an indicator of emotional reactivity, participants were asked to rate to which degree they felt frustrated, angry, and anxious. These ratings were obtained at the end of the baseline and immediately after the two-minute anagram task. All ratings were made on visual analog scales (100 mm), with one end of the scale indicating the opposite dimension of the other end of the scale (eg, not angry at all to very angry). Scores were summed to yield one index of negative emotional affect of acceptable internal consistency ( = 0.61). One control participant did not complete the emotion measure, resulting in 291 pairs of observation.

Stressor.
The stressor consisted of 15 anagrams presented on a sheet of paper. Participants were told that they had 2 minutes to solve the anagrams (please refer to Ref. 11 for a list of the anagrams).

Task perceptions and performance.
Participants were asked to indicate how difficult they felt the experimental task was, how much effort they put into solving it, and how well they thought they had solved the task. All ratings were made on 100-mm visual analog scales (eg, very easy to very difficult). Two measures of task performance were constructed: number of anagrams solved correctly and number of anagrams attempted.

History of hypertension.
Participants were classified as having a history of hypertension if they had a systolic blood pressure above 140 mm Hg or diastolic blood pressure above 90 mm Hg, or if a physician had diagnosed hypertension in the past.

Beta-blockers therapy.
Medication use among patients was obtained from hospital charts, or based on interviews for the controls. Table 1 provides descriptive information on history of hypertension, ß-blockers, and other blood pressure-affecting medications, such as ACE inhibitors and calcium channel blockers.

Procedure
Reactivity testing took place early in the morning on the second day of the 2-day baseline assessment period. Participants were told that this session was concerned with physiological changes while solving "fairly easy anagrams that most people can solve," and that their blood pressure and pulse would be monitored while they performed the task. When scheduling participants for this session, they were asked to abstain from caffeine-containing beverages and smoking for at least ten hours before the experiment. All tests were run individually by the female experimenter (M.H.), who was blind to each participant’s diagnosis. Participants were invited to sit comfortably on an examination table (leaning against a support, legs straight). The experimenter measured midarm circumference and positioned the appropriate blood pressure cuff over the brachial artery in the upper portion of the participant’s nondominant arm. After brief orienting instructions, an initial blood pressure reading was taken to make sure the equipment was operating properly and to familiarize participants with the procedure. Participants were informed that it was important for them to be in a relaxed state to get accurate measures of their BP and HR. The experimenter offered several suggestions to ensure proper relaxation (see Ref. 19 for details). The experimenter told the participants that several blood pressure readings would be taken until their blood pressure stabilized. Participants were reminded to remain as relaxed as they could so that stable readings could be obtained, and to focus on their breathing or heartbeat to keep thoughts from entering their minds. SBP, DBP, and HR were measured once every minute for a period of 10 minutes. If the last three readings differed by 10 mm Hg or more, additional readings (no more than five) were taken until blood pressure stabilized.

After baseline, each participant was asked to rate "how you feel right now" (ie, baseline emotion ratings). Participants were then introduced to the anagram task and were shown one example. They were told that they had exactly 2 minutes to solve the problems. They were instructed to remain silent throughout the procedure. SBP, DBP, and HR were measured twice during the anagram task. After 1 minute, participants were reminded that they had 1 minute left to solve the problems. After the 2-minute task period, they were told to stop, and indicate how many anagrams they worked on by putting a check mark beside each one. Participants were asked to fill out the questions regarding their perceptions of the anagrams and to rate their emotions again. Finally, participants were instructed to relax again (recovery period) while three measures of blood pressure and heart rate were taken.

Statistical Analyses
The analytical procedure for the split-plot design consisted of a series of MANOVAs (20, 21) with the following between factors: patient diagnosis (AMI vs. AP), ß-blocker use among patients (yes/no), history of hypertension among patients (yes/no), and history of hypertension among matched controls (yes/no). The within factors were group (patient vs. matched control) and time (at three levels for the cardiovascular measures, baseline, stress, and recovery; at two levels for the emotion measures, baseline, and stress). Whenever a significant interaction with time (followed by post hoc comparisons) indicated significant differences between baseline and stress values, the term "reactivity" is used to describe this effect. The time factor was eliminated from analyses of performance and task perception data. Additionally, all analyses involving cardiovascular measures were re-run excluding data from women taking ACE inhibitors and/or calcium channel blockers, resulting in 133 pairs of observation.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
Cardiovascular Measures
Highly significant effects for time emerged for all the cardiovascular measures,¹ confirming increases in cardiovascular arousal during the stressor and subsequent returns to baseline level during recovery; SBP: Wilks’ = 0.42, F(2,223) = 151.71; DBP: Wilks’ = 0.40, F(2,222) = 163.72; HR: Wilks’ = 0.47, F(2,201) = 112.44; RPP: Wilks’ = 0.44, F(2,200) = 126.36; all p values < .001. There were no significant effects for patient diagnosis. Therefore, data from all patients were combined into one group for purposes of illustration. Table 2 displays mean levels of BP, HR, and RPP for patients and their matched controls during baseline, stress, and recovery.

The significant main effects involving HR (and consequently RPP) were due to ß-blocker use among the patients, as indicated by significant interaction terms involving both ß-blocker status and group: HR: F(1,202) = 12.79; RPP: F(1,201) = 9.22; all p values < .004. Throughout the experimental procedure, patients on ß-blockers had significantly lower levels of HR and RPP than the remaining participants (mean HR for patients on ß-blockers = 64 bpm; mean HR for their matched controls, patients without ß-blockers, and their matched controls was either 74 or 75 bpm. The corresponding RPP values were 76 for patients on ß-blockers, and ranged from 89 to 91 for the three other groups).

While ß-blockers influenced patients’ overall HR levels, history of hypertension was a significant factor influencing blood pressure levels, affecting patients and their controls in the same manner. The respective effects of history of hypertension among patients, F(1,224) = 3.84, p = .05, and history of hypertension among controls, F(1,224) = 16.06, p < .001, indicated that women with a history of hypertension had higher levels of SBP throughout the experimental period than those without a history of hypertension (patients: those with history [N = 119], M = 122 mm Hg, those without history [N = 121], M = 114 mm Hg; controls: those with history [N = 26], M = 133 mm Hg, those without history [N = 214], M = 117 mm Hg).

Similar effects for history of hypertension emerged among controls only for DBP, F(1,223) = 13.96, p < .001 (DBP levels across the three experimental periods: controls with history of hypertension, M = 84 mm Hg, those without history of hypertension, M = 73 mm Hg), and RPP, F(1,201) = 4.20, p < .05 (the corresponding RPP levels were M = 104 for controls with history of hypertension and M = 88 for those without history of hypertension).

Furthermore, history of hypertension interacted significantly with time, revealing greater DBP reactivity to the anagram task among those with a history of hypertension in both patients, Wilks’ = 0.97, F(2,222) = 3.17; and controls, Wilks’ = 0.97, F(2,222) = 3.25; p values < .05. For patients with a history of hypertension, baseline, stress, and resting values were 72, 82, and 74 mm Hg (reactivity effect from baseline to stress period: 10 mm Hg). The corresponding values for patients without a history of hypertension were 69, 77, and 69 mm Hg (stress reactivity: 8 mm Hg). Among the controls, respective values for those with a history of hypertension were 79, 94, and 79 mm Hg (stress reactivity: 15 mm Hg). For those controls without a history of hypertension, they were 70, 80, and 70 mm Hg (stress reactivity: 10 mm Hg).

When we eliminated data from patients on ACE inhibitors and/or calcium channel blockers from the analyses (resulting in N = 133 pairs), the pattern of results was similar, but reduced to a nonsignificant level in some instances. For example, patients still had lower average SBP levels (p = .048) and RPP levels (p = .016), but differed little in their overall DBP and HR levels (p > .17) from their controls. Also, group (patient vs. control) by time results remained the same for HR and RPP (p values < .01), but were reduced to nonsignificant levels for SBP (p = .11) and DBP (p = .15). Finally, the original effects for history of hypertension on blood pressure remained significant among controls (p values < .05), but were nonsignificant among the patients (p values > .30).

Emotional Reactivity
With regard to negative emotions, a main effect for time indicated a significant increase in negative emotions in response to the anagram task [F(1,260) = 143.12, p < .001]. The mean for negative emotions at baseline was 5.6 and increased to 25.9 during the anagram task. There were no other significant effects for this variable.

Task Perceptions and Actual Performance
No significant differences between patients and their matched controls were obtained with regard to task perceptions (for means, see Table 2). With regard to performance, differences between patients and their matched controls were also nonsignificant (for means, see Table 2).

	SUMMARY

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
The above results confirm that the anagram stressor elicited significant increases in cardiovascular arousal as well as negative affect. There were no significant effects for patient diagnosis, indicating that AMI patients did not differ from MI patients in regard to the variables measured in the present study.

Patients’ baseline blood pressure levels did not differ from that of their controls, indicating that their blood pressure levels were adequately controlled. However, patients had lower heart-rate levels, on average, than controls. This finding seemed to be due to ß-blocker use among the patients. Heart rates of patients without ß-blockers were similar to those of the controls.

With respect to reactivity differences between patients and controls, the results from the present study indicate that patients evidenced lesser increases in HR and RPP to the anagram task than the controls, regardless of whether they were on ß-blockers or not.

History of hypertension was an important variable for blood pressure of patients as well as controls. Those with a history of hypertension had higher levels of blood pressure throughout the experimental period and reacted with greater DBP increases in response to the anagram task than those having no history of hypertension. No significant differences for task performance and task perceptions were found.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
The present study found no evidence for enhanced cardiovascular stress reactivity among coronary patients either by disease manifestation or when compared with their controls. Rather, if group differences were found, they were consistent with Sime et al.’s study of 30 men (12), indicating lesser heart-rate reactivity among coronary patients than controls. To further explore whether this general lack of group difference in reactivity was due to medication use (2/3 of our patients were taking ß-blockers), additional analyses of our data, selecting patients who were not on medications (ie, ß-blockers, ACE inhibitors, calcium channel blockers) showed that these patients did not differ significantly from their controls with respect to any of the cardiovascular measures. Considering that our study is based on data from all women (ie, the population) who were hospitalized with a diagnosis of an acute coronary disease event in the greater Stockholm area over a specific time period and carefully matched healthy controls, it is reasonable to assume that the findings obtained in the present study will generalize to other samples that are representative of the population.

It is important to point out that our finding of diminished HR and RPP responses to stress among the patients (as compared with their controls) does not indicate that patients were not reacting. In fact, patients as a group showed significant increases in all response parameters, including negative emotions, when compared with their baseline values. Furthermore, considering the nature of the mental stress task employed—an anagram task performed under time pressure without requiring verbalization—it is unlikely that any group differences are due to potential group differences in voice characteristics, a problem inherent in many studies employing mental stress tests. We also found no group differences in task perceptions or task performance.

In our previous review of the literature on diagnostic and prognostic validity of stress reactivity testing, the following two medical variables were deemed important influences on cardiovascular parameters: ß-blocker use and history of hypertension (11). With regard to ß-blocker use among the patients (none of the controls were taking ß-blockers), those on ß-blockers had overall lower heart rate and RPP levels. However, neither blood pressure nor heart rate reactivity differed by ß-blocker use. This finding is consistent with the conclusions of Mills and Dimsdale (22), which was based on their review of the effects of ß-blockade on blood pressure reactivity. There is some speculation that ß-blockade could inhibit atherogenesis independently of any effects on blood pressure through reductions in heart rate (see Ref. 23 for review). For example, ß-blockade may attenuate or postpone plaque rupture (reinfarction) by reducing overall heart-rate levels and thus reducing the rate of progression of atherosclerosis (23). Thus, it may not be surprising to find an increase in ß-blocker prescriptions to prevent reinfarction.

Patients on ß-blockers had substantially lower heart-rate levels than both patients not on ß-blockers and the healthy controls. However, having a personal history of hypertension (at currently normotensive levels) was associated with blood pressure reactivity in both patients and controls. Fifty percent of the patients and 11% of the controls had a history of hypertension. The finding of excessive blood pressure responses among the controls not only supports the conclusions Fredrikson and Matthews (24) reached in their meta-analysis based on predominantly male samples but also extends this finding to women. These findings confirm the importance of history of hypertension in the etiology of heart disease and point to excessive blood pressure reactions as a potential pathophysiological mechanism linking history of hypertension (even in the presence of controlled blood pressure levels) to heart disease (also see Ref. 1).

Several limitations of the study should be noted. First, findings regarding ß-blocker use need to be interpreted with caution, because patients were not randomized to ß-blocker use in the present study. Thus, it is likely that patients who were on ß-blockers also differed in other characteristics from those who were not. Obviously, similar reservations apply when assessing a history of heart disease and when comparing patients to controls. For example, comparisons between patients and healthy controls could be hampered by the fact that some patients have experienced damage to their myocardium, which may have influenced their cardiovascular reactions to stress, thus contaminating the true measure of risk. This problem is inherent in any exploratory study that uses the case-control design to detect new risk factors. Taking these difficulties into account, we attempted to recruit representative samples of both cases (all patients) and controls, which were representative of healthy women aged 30 to 65 years in Stockholm. We have previously compared the same cases with their controls on several other risk factors (18, 25–27). In an editorial accompanying one of these reports, our case-control design, which "is most likely to produce representative samples of both cases and noncases," was considered "most useful in the study of uncommon diseases, including coronary disease in young women" (28). Furthermore, the effects of acute myocardial infarction on reactivity were minimized by examining patients at least 3 months after their acute event, so that damage to the cardiac muscle was mostly healed. Thus, it may not be too surprising that cardiovascular reactivity among patients with acute myocardial damage (AMI) did not differ from that obtained from patients with transient ischemia (AP).

In regard to our laboratory assessment of cardiovascular reactivity, one might argue that cardiovascular responses elicited in one experimental session may not be representative of cardiovascular reactivity in everyday life. However, there is some evidence that cardiovascular stress reactions elicited in the laboratory generalize to those in the field when ambulatory measures are used (29). In any case, it would be desirable to measure cardiovascular reactivity to everyday stressors in natural settings using ambulatory procedures (30). It is also still unknown whether enhanced cardiovascular reactivity plays a role in the prognosis of recurrent events. The two available studies, based on predominantly male patients, have reported contradictory results (31, 32). Preliminary analyses of 5-year follow-up data from the present study indicate that the magnitude of DBP responses to the anagram task was found to predict "hard events," such as recurrent AMI and cardiovascular death, independent of age, smoking, history of hypertension, and ß-blocker use (33).

To conclude, with the exception of somewhat reduced heart rate reactivity, patients with heart disease differed little in the cardiovascular parameters assessed in the present study when compared with their age-matched controls. Our finding that persons with a history of hypertension had higher DBP reactivity (even in the presence of normotensive baseline levels), together with the fact that history of hypertension is highly prevalent among heart disease patients may have important implications for prognosis of the disease. Future investigations, especially those focusing on the role of cardiovascular reactivity in prognosis and disease progression, will benefit from including an assessment of this variable.

	ACKNOWLEDGMENTS

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Preparation of this article was supported by Grants HL45785 and HL62156 from the National Heart, Lung, and Blood Institute (National Institutes of Health); Grant CRG921325 from NATO; Grants B93 to 19X-10407 from the Swedish Medical Research Council; and grants from the Swedish Labor Market Insurance Company and the Swedish Heart and Lung Foundation. We thank Dr. N.R. Mendell for statistical advice and J. Skirving for editorial assistance.

	NOTES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
Because of missing data on some of the grouping variables and cardiovascular assessment time points (see Methods), analyses of SBP were based on 240 pairs of observations, of DBP on 239, of HR on 218, and of RPP on 217 pairs of observations. Missing data were evenly distributed among MI and AP patients and their matched controls, and there were no statistically significant differences between those who had complete BP and HR data and those who had missing data for any of the variables listed in Table 1, except for BMI and weight; those with greater BMI (and body weight) were more likely to miss a HR reading (p values < .05) and tended to be more likely to lack a BP reading (p values < .10).

Received for publication July 29, 1999.

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TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS SUMMARY DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 

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