Biological Psychiatry

Neuropsychobiology 1990-91;23:134-139

Risk Factors for Cardiovascular Illness in Panic Disorder Patients V.K. R. R. C. D. P.

Vikram K. Robert Richard Debra Paul

Yeragani Pohl Balon Ramesh Glitz Sherwood

Department of Psychiatry, Wayne State University School of Medicine and Lafayette Clinic, Detroit, Mich., USA Key Words Heart rate Blood pressure, supine, standing Smoking Nicotine Cholesterol Lipids Panic disorder Anxiety

Abstract Supine and standing heart rate (HR) and blood pressure measures were compared among 19 nonsmoking normal controls, 29 smoking patients and 36 nonsmoking patients with panic disorder. The smoking patients had a significantly higher supine HR, standing diastolic blood pressure, standing mean blood pressure and supine and standing cardiac load measures compared to both patient nonsmokers and controls. There was no significant difference between controls and nonsmoking patients for any of the above measures except for the higher standing HR and the ∆ increase in HR upon standing in female panic disorder patients which suggests increased adrenergic activity. When lipid values of panic disorder patients (n = 92) were compared to National Reference Values for their sex and age for an increased risk of cardiovascular illness, there was no significant risk with regard to plasma levels of total cholesterol, high-density lipoprotein cholesterol or low-density lipoprotein cholesterol. Dr. Vikram K. Yeragani, Department of Psychiatry, Lafayette Clinic, 951 East Lafayette Avenue, Detroit, MI 48207 (USA)

Introduction Panic disorder is a syndrome characterized by the sudden onset of anxiety associated with several somatic symptoms such as palpitations, chest discomfort, tremu-lousness, dizziness and other autonomic symptoms [1]. Panic disorder is relatively common; the current prevalence rate has been reported to be 0.4% [2] and the 1-year prevalence rate 1.2% [3]. Dysfunction of both sympathetic and parasympathetic systems may be associated with this condition [4–7]. Some recent reports have suggested a relationship between panic disorder and cardiac conditions such as mitral valve prolapse [8] and idio-pathic cardiomyopathy [9]. There is also evidence suggesting an increased incidence of mortality from cardiovascular illness in male panic disorder patients [10, 11]. Several studies suggest that patients with chronic anxiety are in a state of autonomic hyperarousal [12, 13]. Nesse et al. [14] and Roth et al. [15] have reported a significantly higher tonic heart rate (HR) in panic disorder patients. Weissman et al. [16] have found that the patients with panic attacks had greater increases in HR, blood pressure (BP) and cardiac load (CL), the product of HR and mean BP (MBP) during orthostatic stress compared to normal controls. Our previous work suggests that the HR, BP and subjective anxiety scores just before a provocative infusion to induce panic attacks were significantly higher in panic disorder patients compared to normal controls [17, 18]. Thus there appears to be an increased arousal in panic disorder patients in at least some situations. However, in another study [ 19], we did not find a significant difference in resting HR between panic disorder patients and normal controls, but the patients had a significantly higher diastolic BP (DBP). Recently Clark et al. [20] also found no significant differences in the mean waking or sleeping HR in panic disorder patients compared to controls. These authors attributed the previously reported differences in these measures to anticipatory anxiety. We have recently reported that the HR variability after a few minutes of quiet standing was significantly Panic Disorder and Cardiovascular Illness 135

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lower in panic disorder patients compared to normal controls which suggests an increased vagal withdrawal in patients upon quiet standing [21]. Such a decrease in HR variability has been previously reported in conditions such as diabetic autonomic neuropathy [22–25]. In the last few years, several reports on the fractal and nonlinear nature of HR variability in the healthy heart have suggested that a decrease in HR variability is associated with the development of cardiac illness [26, 27]. Thus there is a true need to investigate the risk of cardiovascular illness in panic disorder patients. Hayward et al. [28] recently reported a significantly higher than expected number of female panic disorder patients with cholesterol levels that exceeded the 75th percentile of National Reference Values. There is also some evidence suggesting that acute emotional arousal increases free fatty acids and in some cases, cholesterol levels [29]. However, Tancer et al. [30] compared serum cholesterol values in age- and sex-matched panic disorder patients and normal controls and did not find a significant difference between the two groups. There was no significant association between the state anxiety scores and serum cholesterol levels, either.

In our previous study [21], we did not have a sufficient number of smoking and nonsmoking patients for comparing the HR and BP variables. The aims of the present investigation were to find if the baseline resting HR, BP and CL (product of MBP and HR) are higher in panic disorder patients and if smoking influenced these measures. In this study, we have combined the physiological data on panic disorder patients from two different studies so that we had an adequate sample of smoking and nonsmoking patients. The other aims were to find if the increase in HR upon standing was higher in panic disorder patients compared to controls and if patients with panic disorder are at a higher risk for cardiovascular illness with regard to their serum lipid levels in comparison to National Reference Values.

Methods Subjects Patients. The patients in this study came from different studies, one dealing with the effects of postural changes [21] and the other on the effects of an isometric handgrip test on HR and BP in panic disorder patients. The patients in the isometric handgrip test in this study are different from the patients included in a previous study of ours on the isometric handgrip test [19]. The procedures for measuring the baseline supine and standing HR and BP were identical in both these studies. All patients met DSM III-R criteria for panic disorder during an interview with an experienced researcher. These patients did not have a current history of major depression or any other psychiatric illness. A written informed consent was obtained from each participant prior to the studies. The patients were physically healthy, and patients with cardiovascular, respiratory, endocrinological and other physical illnesses were excluded from the studies. The patients had not been taking any psychotropic medication for at least 2 weeks prior to the studies, either. There were 44 smokers (15 males, 29 females; age, 35.2 ± 7.4 years) and 49 nonsmokers (24 males, 25 females; age, 31.0 ± 7.5 years). The exact details of the number of cigarettes smoked and the duration of smoking are not completely available. Data on serum lipids were available for 44 smoking (15 males and 29 females) and 48 nonsmoking (24 males and 24 females) patients. HR and BP were available for 29 smoking (11 males and 18 females) and 36 nonsmoking (17 males and 19 females) patients. Controls. Eight females and 11 males participated in this study. The controls were physically healthy, and there was no history of any current or past psychiatric illness. Their age was 33.7 ± 4.9 years. All subjects were nonsmokers. All these subjects had participated in our previous study on the effects of postural changes on HR and BP [21]. Two male controls included in this study had also participated in a previous study of ours on the isometric handgrip test [19]. Recording ofHR and BP Thirty-three patients (20 females and 13 males) participated in the postural study and 32 patients (17 females and 15 males) participated in the isometric handgrip study. Both postural and isometric handgrip tests were done in the morning or afternoon after a light breakfast or lunch. The subjects were asked not to smoke or drink caffeinated beverages for at least 2 h prior to the test. HR and BP were monitored using a Hewlett Packard 78352 A patient monitor with a brachial artery cuff attached and a 78173 A EKG monitor (Palo Alto, Calif, USA). Patients were told in advance that the studies involved only HR and BP measurements in different postures and during isometric exercise. The patients’ anxiety was rated by the State and Trait Anxiety Inventories of Spielberger et al. [31]. No patient experienced a panic attack during the procedure. The subjects rested in the supine posture for 15 min prior to the recording of HR and BP. HR and BP were recorded every 1 and 2 min, respectively. Supine measures were the average of values at 1 and 3 min prior to active standing up. Standing measures were the average of values at 1 and 3 min after standing up. MBP was calculated by adding one third of the pulse pressure to the DBP. The product of HR and MBP was used as an indicator of CL as described in previous studies [16, 19]. Serum Cholesterol Measurement The data on plasma lipids was available for 92 patients (53 females and 39 males). Forty-four of these patients were smokers and 48 nonsmokers. The blood for the cholesterol assays was drawn from the antecubital vein while the patients were seated in a chair. Some patients were not in fasting state when the blood was drawn. Lipid profile assays were performed by Regional Clinical Laboratories, Dearborn, Mich., USA. Total cholesterol was measured using an AU 5000 analyzer (Olympus, New York, N.Y., USA) by the col-orimetric method. The high-density lipoprotein (HDL) cholesterol was measured by an RAXT analyzer (Technikon, New York, N.Y., 136 Yeragani/Pohl/Balon/Ramesh/Glitz/Sherwood

USA) by the colorimetric method after precipatation of other lipo-proteins. The lower-density Hpoprotein (LDL) cholesterol was then calculated by a formula. Comparison to National Reference Values The patients’ levels for total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides were compared with the reference values published by the Lipid Research Clinic Program, grouped according to age and sex [32]. As we did not have complete information on the use of sex hormones in females, we have compared the values to those of both the users and nonusers of sex hormones. According to the previous reports [28], total cholesterol, LDL-cho-lesterol and triglyceride values that exceeded the 75th percentile for age and sex were identified as associated with a greater risk of developing cardiovascular disease. Values of HDL-cholesterol below the 25th percentile were defined as being associated with such a risk. The observed versus expected numbers of subjects with risk-associated values were compared using χ2 statistic. Statistical Analysis BMDP software (Berkeley, Calif, USA) was used for the statistical analyses. Analysis of variance was used to compare ages between the groups. Analysis of covariance was used to compare controls, patient smokers and patient nonsmokers with regard to different variables with sex and age as covariates. When there was a significant difference, post-hoc t tests were used to compare the adjusted cell means of individual cells using BMDP software. Pearson’s product moment correlations were used to examine the relationship between anxiety measures and physiological variables and serum lipid levels, χ2 statistic was used for the comparison of frequency data.

Results

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Sixty-five (29 smokers and 36 nonsmokers) of the 93 patients had data on physiological measures, and 92 patients (44 smokers and 48 nonsmokers) had data on serum lipids. There was a significant difference in age among the groups (table 1; F = 4.21; d.f. = 2, 109; p < 0.02). Post-hoc t tests revealed that smoking patients were significantly older compared to nonsmoking patients (t = 2.73; d.f. = 91; p < 0.008). These differences in age were significant when the above subgroups with complete data on physiological measures and serum lip-ids were compared separately. Supine HR was significantly different among the groups (F ≈ 3.80; d.f. = 2, 79; p < 0.02). Post-hoc t tests for adjusted means revealed that the smoking patients had higher supine HR compared to both nonsmoking patients and controls (p < 0.05 and p < 0.01, respectively). There was no significant difference between patient nonsmokers and controls. Standing HR was significantly different among the groups (F = 6.02; d.f. = 2, 79;

p < 0.004). Post-hoc tests revealed that the HR of controls was significantly lower compared to both smoking and nonsmoking patients (p < 0.001 and p < 0.02, respectively). There was no significant difference in standing HR between smoking and nonsmoking patients. Though there was no significant difference for the ∆ HR (the increase in HR upon standing from supine posture) among the groups (F = 2.31; d.f. = 2, 79; p < 0.1), we have analyzed the males and females separately as our previous report [19] showed a significant difference in this measure only between female patients and female controls. Post-hoc tests revealed no significant differences in the ∆ HR for males. However, the female patient nonsmokers had significantly higher ∆ HR compared to the controls (t = 3.67; d.f. = 25; p < 0.002). The smoking patients also had higher ∆ HR, and this was approaching significance (t = 2.02; d.f. = 24; p = 0.06). There was no significant difference in the supine, standing or ∆ systolic BP between the groups. There was a significant difference in the supine DBP between the groups (F = 4.52; d.f. = 2, 79; p < 0.02). The supine DBP was significantly higher in patient smokers compared to controls (p < 0.005), and it was also higher compared to patient nonsmokers, but this difference was approaching significance (p < 0.06). There was no significant difference between patient nonsmokers and controls. There was also a significant difference in the standing DBP among the groups (F = 7.91; d.f. = 2, 79; p < 0.001). Post-hoc tests revealed that patient smokers had a significantly higher DBP compared to the patient nonsmokers and controls (p < 0.0006 and p < 0.003, respectively). There was a significant difference in the ∆ DBP among the groups (F = 3.43; d.f. – 2, 79; p < 0.04). Post-hoc tests revealed that the ∆ DBP was significantly higher in smoking patients compared to nonsmoking patients (p < 0.02). There was a significant difference in the supine MBP among the groups (F = 4.36; d.f. = 2, 79; p < 0.02). Post-hoc tests revealed that patient smokers had a significantly higher supine MBP than controls (p < 0.005). There was also a significant difference in the standing MBP among the groups (F = 5.77; d.f. = 2, 79; p < 0.006). Post-hoc tests revealed that the patient smokers had a significantly higher standing MBP compared to both nonsmoking patients and controls (p < 0.004 and p < 0.006, respectively). There was no significant difference in the ∆ MBP among the groups. There was a significant difference in the supine CL among the groups (F = 5.85; d.f. = 2, 79; p < 0.005). Post-hoc tests revealed that the smoking patients had a Panic Disorder and Cardiovascular Illness 137

Table 1. HR and BP in controls, smoking and nonsmoking panic disorder patients Controls Smoking Nonsmoking (n = 19) patients patients (n = 29) (n = 36) Table 2. Plasma lipid levels in panic disorder patients and a comparison to National Reference Values1 Lipid level mg/dl (mean ± SD) Patients with levels indicating greater risk of cardiovascular disease Age, years 33.7±5.O 36.3 ±7.0 30.3 ±6.8 HR Supine Standing ∆

68.1 ±10.1 78.4±ll.2 lO.3±6.9 76.5±IO.7 90.1 ± 11.7 l3.6±8.6 7l.4±lO.5 87.4±IO.5 l5.6±9.2 SBP Supine Standing ∆

H9.6±10.1 l27.4±ll.3 7.8±5.5 l26.6±l3.5 l32.3±l3.3 5.8±8.l I22.6±I3.8 I26.9±I4.7 4.3±8.6 DBP Supine Standing ∆

66.1 ±8.3 78.3±9.7 l2.2±5.7 73.1 ±9.6 85.7±9.8 l2.5±7.3 67.1 ±8.5 76.9±9.5 9.4 ±7.3 MPB Supine Standing Δ

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84.0 ±7.8 94.7±IO.3 lO.2±4.9 9l.O±9.7 lOO.9±9.8 9.9±6.O

85.8±9.6 93.5±IO.3 7.7±6.9 CL Supine Standing ∆

5,694 ±1,008 7,359± 1,568 l,685±876 6,935± 1,373 9, O55± 1,547 2,121 ±935 6, ll6±l, l37 8,088 ±1,200 1,973 ±942 SBP = Systolic BP. CL = HR × MBP. expected

% observed n% Women (n = 53, age =31.5 ± 7.9 years) Total cholesterol l86±3l 13.3 HDL-cholesterol 57±I6 13.3 LDL-cholesterol 109 ±26 13.3 Triglycerides 96 ±42 13.3

25 25 25 25

15 10 11 10

28.3 20 22 18.9

Men (n = 39; age = 34.8 + 7.24 years) Total cholesterol 203±41 HDL-cholesterol 45 ±12 LDL-cholesterol 120 ±34 Triglycerides 197 ±172

25 25 25 25

12 10 6 20

30.8 27 17.6 51.3

9.8 9.8 9.8 9.8

‘ Level of risk based on reference values from Lipid Research Clinics Program reference values [32], which are grouped by age and sex. For total cholesterol, LDL-cholesterol and triglycerides, greater risk = levels above 75th percentile; for HDL, greater risk = levels below 25th percentile.

significantly higher supine CL compared to nonsmoking patients and controls (p < 0.03 and p < 0.002, respectively). The standing CL was also significantly different among the groups (F = 8.95; d.f. = 2, 79; p < 0.0001). Post-hoc tests revealed that the smoking patients had a significantly higher standing CL compared to nonsmoking patients and controls (p < 0.009 and p < 0.0002, respectively). The difference between nonsmoking patients and controls was also approaching significance (p = 0.07). There was no significant difference in the Δ CL among the groups. Serum Lipids We were unable to find any significant differences for the comparisons of values of total cholesterol, HDL-cholesterol and LDL-cholesterol of male and female panic disorder patients to the national reference values (table 2). Though the observed frequency of values above the 75th percentile for triglycerides was significantly higher in male panic disorder patients compared to the reference values (p < 0.005), this may have been due to the fact that some of the patients in this study had not been fasting before the blood was drawn. There were no significant differences between patient smokers and paTable 3. Plasma lipid levels in smoking and nonsmoking panic disorder patients (means ± SD) Smoking patients (n = 44)

Nonsmoking patients (n = 48)

35.2±7.4 3l.2±7.4

Age, years Lipids, mg/dl Total cholesterol 201.3 ±35.9 185.8 ±36.0 HDL-cholesterol 53.7 ±18.5 50.8 ±12.9 LDL-cholesterol 118.5 ±28.8 107.9 ±30.1 Total cholesterol/HDL-cholesterol4.1 ± 1.5 4.0± 1.8 Triglycerides 137.1 ±95.5 l4O.3± 149.7

tient nonsmokers for any of the lipid variables (table 3). There was no significant difference between the smokers and nonsmokers for the scores on the State Anxiety Inventory (49 ± 13 vs. 48 ± 12) or Trait Anxiety Inventory (52 ± 12 vs. 52 ± 11). There were no significant correlations between the state and trait anxiety scores and the physiological variables or serum lipids (table 4). 138 Yeragani/Pohl/Balon/Ramesh/Glitz/Sherwood

Supine HR

Supine SBP

score and HR, Supine DBP

BP and values of serum lipids

Supine MBP

Supine CL

Total cholesterol

HDLcholesterol

LDLcholesterol

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Table 4. Correlation between anxiety

SAI 0.20 (n = 62)

0.10 (n = 62)

0.02 (n = 62)

-0.04 (n = 62)

0.13 (n = 62)

0.09 (n = 89)

-0.12 (n = 84) 0.05 (n = 81)

TAI 0.09 (n = 53)

0.13 (n= 53)

0.05 (n = 53)

-0.04 (n= 53)

0.06 (n = 53)

0.10 (n = 80)

0.00 (n = 75)

0.09 (n = 72)

SBP = Systolic BP; SAI = State Anxiety Inventory; TAI = Trait Anxiety Inventory.

Discussion The results of this study suggest that smoking is a very important confounding variable in the interpretation of comparison of physiological measures such as HR and BP between panic disorder patients and controls. We were unable to find any significant differences between nonsmoking patients and nonsmoking controls with regard to resting HR and BP measures. On the other hand, the smoking patients had significantly higher resting HR, DBP, MBP and CL compared to both controls and nonsmoking patients. It should be noted that age and sex were covaried out in all the analyses. In addition the ∆ DBP increase after standing was significantly greater in smoking patients compared to nonsmoking patients which could be due to the increase in peripheral vascular resistance in the smoking patients. When we compared the ∆ increase in HR upon standing in males and females separately, we did not find any differences in males among the three groups (patient smokers: 13; patient nonsmokers: 14; controls: 13). However, this increase was significantly higher in nonsmoking female patients compared to female controls (18 vs. 7; p < 0.002), and this was also higher in smoking female patients compared to female controls (14 vs. 7; p < 0.06). It is possible that the increase in HR upon standing in smoking patients, which was smaller than that of nonsmokers, was due to the higher increase in DBP in smoking patients upon standing. It is interesting to note that in our previous report [19], we also found such a higher increase in HR upon standing only in a different group of female panic disorder patients. It should also be noted that all female controls and the patients in this report are different from our previous study [19]. Recently Stein et al. [33] also reported that panic disorder patients had greater increases in HR upon standing in a study of age- and gender-matched patients and controls. Thus these findings suggest an increase in ß-adrenergic activity at least in a subgroup of panic disorder patients. The other important finding of this study is that there may not be an increased risk of cardiovascular illness in panic disorder patients with regard to the levels of serum lipids, when compared to the National Reference Values. This is in agreement with the report of Tancer et al. [30]. However, the report by Hayward et al. [28] suggests that there may be a higher risk for cardiovascular illness in female panic disorder patients. Thus it appears that further studies are needed before any definite conclusions can be drawn. Finally, we should point out the problems in this study. This was not a prospective study designed to answer the questions raised. Patients were included from two different studies, and there was no group of smoking controls. We also did not have detailed information on the history of smoking in patients who were smokers. The control sample size was also smaller compared to the smoking and nonsmoking patients. Thus these results should be considered preliminary. However, this study suggests that the status of smoking is an important factor in the interpretation of data on physiological variables between panic disorder patients and controls. Acknowledgements The authors wish to thank Renee Kareus, Barbara Merlos, Paula Weinberg and Mary Schemm for their assistance in the preparation of this manuscript.

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Risk factors for cardiovascular illness in panic disorder patients.

Supine and standing heart rate (HR) and blood pressure measures were compared among 19 nonsmoking normal controls, 29 smoking patients and 36 nonsmoki...
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