Psychosomatic Medicine Faster Service from Outside North America
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baumert, J.
Right arrow Articles by Ladwig, K.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baumert, J.
Right arrow Articles by Ladwig, K.-H.
Related Collections
Right arrow Other Cardiovascular Medicine
Right arrow Pain
Right arrow Psychophysiology
Psychosomatic Medicine 68:591-597 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Psychophysiologic and Affective Parameters Associated With Pain Intensity of Cardiac Cardioverter Defibrillator Shock Discharges

Jens Baumert, MS, PhD, Claus Schmitt, MD and Karl-Heinz Ladwig, MD, PhD

From the Klinik und Poliklinik für Psychosomatische Medizin, Psychotherapie und Medizinische Psychologie, Klinikum rechts der Isar der Technischen Universität München, Munich, Germany (J.B., K.-H.L.); German Heart Center Munich, Munich, Germany (C.S.); GSF-National Research Center for Environment and Health, Institute of Epidemiology, Neuherberg, Germany (J.B., K.-H.L.).

Address correspondence and reprint requests to K.-H. Ladwig, PhD, MD habil, Prof., Klinik und Poliklinik für Psychosomatische Medizin, Psychotherapie und Medizinische Psychologie, Klinikum rechts der Isar der TUM, Langerstraße 3, 81675 München, Germany. E-mail ladwig{at}gsf.de


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 NOTES
 REFERENCES
 
Objective: Pain caused by intracardiac shock discharge of an implanted cardioverter defibrillator (ICD) is an important clinical issue in the treatment of ICD patients. The present study aimed to examine whether the strength of perceived shock pain is influenced by affective and psychophysiologic parameters.

Methods: Among 204 ICD patients drawn from the German Heart Center Munich, 95 patients (46.6%) experienced ≥1 shock discharge. Pain perception (PPC) was measured by a visual analog scale ranged from 0 to 100 points. Standard instruments were administered to measure psychological distress. A startle paradigm was assessed to measure psychophysiologic arousal with skin conductance responses (SCR) and electromyogram responses (EMG) as dependant variables. Classification and regression tree (CART) analysis was applied to assess the effects of psychodiagnostic and psychophysiologic parameters on pain perception.

Results: Mean ICD shock PPC was 53.7 points (SD 31.6), with a median of 59.0 points (interquartile range 30–80). Pain intensity was highly associated with shock discomfort (p < .001) but was largely uninfluenced by clinical and sociodemographic factors. CART analysis revealed patients with one shock and low EMG magnitude (≤4.15 µV) as subclass with the lowest mean PPC (21.9 points; 95% confidence interval [CI], 4.6–39.1), whereas patients with >one shock experience and an anxiety score >7 (Symptom Checklist-90) expressed the highest mean PPC (74.8 points; 95% CI, 60.5–89.2). Without heightened anxiety, an increased EMG amplitude and impaired EMG habituation yielded a mean PPC of 71.2 (95% CI, 61.6–80.9).

Conclusions: Augmented PPC of ICD shocks is predominantly associated with the number of perceived shocks, postshock anxiety, and accompanied by heightened levels of EMG magnitude and impaired EMG habituation, which points to sensitization of central neural structures.

Key Words: implanted cardioverter defibrillator • shock discharge • pain perception • psychophysiology • anxiety

Abbreviations: CART = classification and regression tree; CI = confidence interval; EMG = electromyogram; HAD-S = Hospital Anxiety and Depression Scale; ICD = implanted cardioverter defibrillator; SCL-90 = Symptom Checklist-90; SCR = skin conductance responses; SC = skin conductance; VAS = visual analog scale.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 NOTES
 REFERENCES
 
The implantable cardioverter defibrillator (ICD) has become the treatment of choice in patients at risk to suffer from potentially lethal ventricular arrhythmias. Compared with antiarrhythmic drug use, ICD therapy reduces mortality more effectively (1,2) and may also be superior in terms of quality-of-life effects (3,4), although fear of being shocked remains a virtually universal experience for patients with an ICD (5). The occurrence of ICD shocks is associated with increased psychological distress in both patients and families (6–9). Apparently, ICD shock applications compose the single most distressing aspect of ICD treatment (10).

However, to date, pain perception from internal electrical shocks is poorly understood. Nociceptive stimulation of the myocardium induced by intracardiac shock application and subsequent pain perception may only be poorly related (11,12). The variance of pain perception among unselected ICD patient populations range from estimates of ICD shocks as being hardly noticeable to being hit with a bat or stuck with a knife (11).

In the first place, characteristics of shock discharge, mainly the cumulative effect of repetitive shock delivery, may account for the degree of perceived pain intensity (13–15). However, reasons for this phenomenon have not been sufficiently elucidated so far. Basically, mechanisms that enhance or suppress afferent cortical processing of nociceptive stimuli (central sensitization) account for the degree of the perceived strength of a pain sensation. Thus, the psychophysiologic state of the patient may be an important condition for heightened intracardiac pain sensitivity (16).

In turn, the affective state of the patient—particularly anxiety and depression—may substantially affect both conditions. For patients with coronary artery disease, there is clear evidence for depression to amplify chronic chest pain of ischemia-induced conditions (17,18). Numerous studies have demonstrated positive relationships between anxiety and pain, with those less anxious patients experiencing less pain (19).

It is, however, less well established whether psychological and neurophysiologic factors also interfere with singular pain conditions of short duration like an electrical shock field, in which habituation and adaptation may be less likely (12). A better understanding of mechanisms that induce variations of interoceptive pain perception are urgently needed to highlight potential targets of intervention particularly in patients suffering from psychological side effects of ICD therapy. To identify possible risk factors for a malignant processing of therapeutic shocks may thus be crucial for preventive patient counseling.

We, therefore, conducted an investigation in patients who had experienced ICD shock applications and expected to identify subgroups with heightened and diminished intracardiac pain sensitivity, respectively. In an approach to elucidate pathways of a heightened pain perception, we aimed to analyze differences between subgroups of patients with low and amplified pain sensitivity, with focus on markers of psychological distress and psychophysiologic sympathetic arousability. In particular, we sought to investigate whether sustained sympathetic arousability and an impaired ability to habituate to afferent stimulation (and its interaction with negative affectivity) modifies ICD shock pain perception.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 CONCLUSIONS
 NOTES
 REFERENCES
 
Study Design
Patients were recruited consecutively from the LICAD (Living with an Implanted Cardioverter Defibrillator) study including initially 213 patients treated with an ICD. Patients attending the cardiology outpatient clinic of the German Heart Center Munich for routine ICD checkup were assessed between January and May 1998 (first wave) and between April and June 2002 (second wave). Patients were not included if the first implantation of the ICD was less than 3 months ago or age was ≤16 years. Written informed consent was obtained from all patients. The study was approved by the ethic committee of the Medical Faculty of the Technical University of Munich (TUM).

Seven patients refused to participate in the study, and two patients suffered from severe cognitive impairment. Among 204 patients with eligible data, a total of 95 (46.6%) subjects experienced at least one intracardiac shock discharge since implantation of the ICD device and were defined as the study population of the present analysis.

The majority of the study population was male (n = 80, 84.2%); the mean age was 59.5 years (SD, 12.3). Main indication for implantation of the ICD was ventricular tachyarrhythmia (n = 65; 68.4%). More than half of the patients had been resuscitated (n = 56; 58.9%). The most frequent cardiac diagnosis was a coronary heart disease (CHD) or an acute myocardial infarction (n = 60; 63.2%). For 13 patients (13.8%), ICD therapy started less than 1 year earlier at the time of the examination; mean time since ICD implantation was 33.6 months (SD, 23.9). For the majority of patients, the shock under investigation was not the first one; a total of 45.3% patients had even experienced ≥5 shocks. More details and a comparison to the no shock group can be drawn from Table 1.


View this table:
[in this window]
[in a new window]
  		TABLE 1. Clinical Characteristics of the ICD Study Patients (n = 204), Stratified in an ICD Shock (n = 95) and No-Shock (n = 109) Group

 

Patient and Clinical Data
The patient records, including ICD-treatment-specific data, were provided by the electrophysiologic outpatient clinic of the German Heart Center Munich. In a standardized interview, sociodemographic characteristics were assessed. Moreover, patients were asked whether they had experienced cardiac symptoms (palpitations, tachycardia, racing heart) or chest pain (exertional, at rest, at night) during the last 4 weeks before the examination.

Assessment of Pain Perception
Subjects rated the degree of pain perception on a visual analog scale (VAS) ranging from 0 to 100 points. Patients were asked to estimate the most recent ICD shock discharge. Discomfort of shock perception encompasses the affective component of pain perception (in contrast to the sensory component) and was assessed in the present study by a 5-point rating scale ranging from 1 ("bearable") to 5 ("unbearable").

Psychophysiologic Procedure
We applied the acoustic startle response (ASR) paradigm proposed by Shalev et al. (20). It comprised 15 loud tones as independent variables (trials). The acoustic startle stimulus was a 500-ms burst of 1000 Hz and 95 dB, with a near-instantaneous rise time presented binaurally through headphones (Panasonic). Intertrial intervals were randomly selected and ranged from 17 to 32 seconds. Signals were amplified and filtered by a bioamplifier (B-scope; Regensburg, Germany).

Skin conductance (SC) was measured directly by a coupler using a constant 0.5 V through 8-mm (sensor diameter) electrodes (Beckman-type Ag/AgCl) placed on the subject’s nondominant palm. SC was analyzed in a spectrum from 15.9 mHz to 10 Hz. Response magnitude of the startle stimulus for each trial was defined by subtracting the average SC for the 2 seconds immediately preceding tone onset from the maximum level within 1 to 4 seconds after tone onset. SC values were measured in microsiemens. Skin conductance response (SCR) scores were square-root transformed before analysis in order to reduce the variance associated with unusually large responses. The average SCR across all 15 trials (SCR (1–15)) was used to measure SCR magnitude, which had a mean value of 0.48 microsiemens (SD 0.32), ranging from 0.02 to 1.58.

The left orbicularis oculi electromyogram (EMG) signal was recorded through 4-mm (sensor diameter) surface electrodes (Beckman-type Ag/AgCI) and filtered so as to retain a 90 to 500 Hz frequency range. Sampling frequency was 1000 Hz. EMG data were measured in µV. Response magnitude of the startle stimulus was defined by subtracting the mean EMG level during 2 seconds immediately preceding tone onset from the highest EMG measured within 40 to 200 ms after tone onset. EMG scores were square root transformed before analysis in order to reduce the variance associated with unusually large responses. The average EMG across all 15 trials (EMG (1–15)) was used to measure EMG magnitude (mean value of 5.29 µV [SD, 3.23], ranging from 1.35 to 16.87).

Habituation was defined in two ways: (1) as response slope of the regression equation Y = bX + a for trials 2 through 15, where Y is the magnitude of the response and X is the log trial number. To control for the individual level of response, the absolute value of the slope b was divided by intercept a of the regression line. (2) As trials-to-nonresponse: a SCR ≤0.15 microsiemens (nontransformed) and 18 µV (nontransformed) for the EMG was considered to constitute a nonresponse criterion. A patient was considered to reach the SCR/EMG nonresponse criterion when there were two consecutive nonresponse trials. The mean SCR habituation was 0.24 (SD, 0.10), ranging from 0 to 0.47. For EMG habituation, a mean of 0.25 was observed (SD, 0.62), with a range from 0 to 5.89.

The room temperature during the experiment was held at a constant level of 22°C, and humidity was kept automatically at 55%. The patient investigation was carried out in the time between 9:00 AM and 1:00 PM. The subjects underwent a hearing test and received a standard instruction while the electrodes were attached in accordance with published recommendations (21,22). In 88 patients, we received eligible psychophysiologic data.

Psychodiagnostic Assessment
Anxiety and depression symptoms were measured using the German version of the 14-item Hospital Anxiety and Depression Scale (HAD-S) (23,24) and the German version of Symptom Checklist-90 (SCL-90), which included assessment of phobic anxiety (25). To evaluate sleeping disturbance as an indicator for psychic distress, a four-item scale adapted from form A of the Maastricht questionnaire was used (26). The original scale was subtracted by four, leading to a parameter "sleeping disorders," ranging from 0 ("no sleeping disorders at all") to 12 ("strong sleeping disorders"). For all psychodiagnostic parameters, a missing value of an item was replaced with the mean of the other items if at least 70% of the other items were answered. Suggested cutoff points were used to define patients with high burden of symptoms. In case no suggested cutoff points were available, the median was chosen as the cutoff point. For most analyses, continuous scale values were applied.

Statistical Analysis
Group differences in mean pain perception were assessed by t test (for groups with two categories) or F test (for groups with more than two categories). Pearson correlations were used to describe univariate associations between continuous variables. To identify subgroups with heightened pain perception, we applied the regression and classification tree (CART) technique as described by Breiman et al. (27). A CART analysis is a tree-based approach with a sequence of tests to assess a significant difference in a response variable (i.e., mean pain perception) by an explanatory variable (i.e., sociodemographic, psychodiagnostic, and psychophysiologic variables). In each step, the explanatory variable with the lowest p value drawn from the test is chosen as the "node." This multivariate procedure allows the identification of different subclasses of the study population with respect to an outcome variable. By the minimum p value approach, the study population is divided into subsequent different dichotomous subclasses ("node"). In the present study, CART analysis was carried out to assess the impact of sociodemographic, clinical, psychiodiagnostic and psychophysiological parameters on the mean pain score perceived by the patient. Pain perception as a continuous variable was defined as outcome variable, and the subclasses were determined by subsequent t tests. The CART analysis included the covariates sex, age (continuous), partnership situation (living alone, living not alone), primary diagnosis (VT, others), cardiac diagnosis (CHD or acute myocardial infarction, others), reanimation (no, yes), time since ICD implantation (continuous), number of shocks (continuous), depression and anxiety assessed by HAD-S, depression, anxiety, phobic anxiety assessed by SCL-90, sleeping disorders (all continuous), and the psychophysiologic parameters SCR magnitude, SCR habituation, EMG magnitude, and EMG habituation (all continuous). In the final step, CART technique revealed a number of subclasses of patients with different mean pain perception values. Due to missing values, the CART analysis was restricted to patients with complete data on all covariates (n = 84).

For all statistical analysis, a p < .05 was considered to be statistically significant. The evaluations were performed with the statistical software package SAS (Version 8.02, SAS Institute, Inc., Cary, NC).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 CONCLUSIONS
 NOTES
 REFERENCES
 
The assessment of ICD shock pain intensity among 95 ICD patients revealed a roughly normal distribution of pain perception with a wide variability. The mean pain perception score, as assessed on the VAS, ranging from 0 to 100 points, was 53.7 points (SD, 31.6), with a median of 59.0 points (interquartile range [IQR], 30–80). Thirteen (13.7%) patients rated their pain perception as zero. The intensity of perceived shock pain was highly associated with the discomfort associated with shock pain. As can be seen in the box whisker plot in Figure 1, mean pain perception values increased significantly (p < .001) parallel to the perceived discomfort of shock discharges (n = 85).


Figure 112
View larger version (10K):
[in this window]
[in a new window]
  		Figure 1. Distribution of pain perception by discomfort of shock discharge as box whisker plot with 25% quantile to 75% quantile, including mean and median (box) and minimum and maximum (whisker).

 

Pearson correlation revealed no significant association of pain perception and depression with moderate Pearson correlation coefficients (HAD-S, 0.12; SCL-90, –0.02), anxiety (HAD-S, 0.18; and SCL-90, 0.16) and phobic anxiety (SCL-90, 0.13). Sleeping disorders were significantly correlated with pain perception, with a Pearson correlation coefficient of 0.22 (p = .033). Mean pain perception was largely uninfluenced by sociodemographic and clinical factors (Table 2). Additionally, mean pain perception was not associated with diabetes (p = .700), hypertension (p = .921), or prevalent stroke (p = .381) (data not shown). However, subjects who received ICD therapy for <1 year suffered more from shock application compared with those with ≥1 year. As is shown in Table 3, subjects with comorbid states of negative affectivity (depression, anxiety, sleeping disorders) had higher mean levels of pain perception; however, only phobic anxiety almost reached significance (p = .055). Defining a "score" with the sum of the five dichotomous psychodiagnostic variables (0 = not disturbed, 1 = disturbed), patients who reached a score of 4 or 5 (i.e., all or at most one on affective status) had a significant higher mean pain perception (76.3) than patients with lower score values (42.2 to 53.4), with a p = .037. No significant correlation was found between pain perception and psychophysiological factors (Table 4).


View this table:
[in this window]
[in a new window]
  		TABLE 2. Mean Pain Perception With SD by Sociodemographic and Clinical Factors in 95 ICD Patients

 

View this table:
[in this window]
[in a new window]
  		TABLE 3. Mean Pain Perception With SD by Psychodiagnostic Factors in 95 ICD Patients

 

View this table:
[in this window]
[in a new window]
  		TABLE 4. Correlation of Pain Perception With Psychophysiological Factors in 88 ICD Patients

 

The number of perceived shocks had a slightly significant influence on mean pain perception (p = .049). Time since last shock experience, which was available in 76 patients, was not associated with pain perception, with a Pearson correlation coefficient of 0.034 (p = .77).

The CART analysis for 84 patients with complete data on all covariates revealed subclasses with different mean pain perception scores. As can be seen in Figure 2, the experience of repetitive shock applications (versus one single ICD shock) had the most profound impact on pain perception. Mean pain perception ranged from 21.9 points (95% confidence interval [CI], 4.6–39.1) in subclass 1 (patients with one shock and EMG magnitude ≤4.15 µV, n = 12) to 74.8 points (95% CI, 60.5–89.2) in subclass 6 (patients with >one shock and anxiety (SCL-90) >7, n = 12). The psychophysiological parameters revealed an impact of the EMG magnitude and habituation on the mean pain perception in specific subclasses. Higher values of EMG magnitude and impaired EMG habituation led to a higher amount of pain perception in both shock groups (one, >one shock). In subclass 5 with subjects experiencing >one shock and having low anxiety symptoms (anxiety ≤7), patients (n = 18) with elevated EMG magnitude (EMMW >3.4 µV) and impaired EMG habituation (EMHAB ≤0.21 µV) yielded a mean perception of 71.2 (95% CI, 61.6–80.9), which was almost the same as for patients in subclass 6.


Figure 212
View larger version (11K):
[in this window]
[in a new window]
  		Figure 2. Mean pain perception in subclasses estimated by CART analysis (n = 84 patients). SHOCKS: number of shocks. ANXIETY: anxiety SCL-90 (0: no, 1: yes). EMMW: electromyogram magnitude (in µV). EMHAB: electromyogram habituation (in µV). Mean pain perception in end subclasses: Subclass 1 (SHOCKS = 1 and EMMW ≤4.15, n = 12): 21.9 (95% CI, 4.6–39.1). Subclass 2 (SHOCKS = 1 and EMMW >4.15, n = 14): 51.7 (95% CI, 34.2–69.3). Subclass 3 (SHOCKS >1 and ANXIETY ≤7 and EMMW ≤3.4, n = 11): 36.0 (95% CI, 19.0–53.0). Subclass 4 (SHOCKS >1 and ANXIETY ≤7 and EMMW >3.4 and EMHAB >0.21, n = 17): 51.1 (95% CI, 35.9–66.2). Subclass 5 (SHOCKS >1 and ANXIETY ≤7 and EMMW >3.4 and EMHAB ≤0.21, n = 18): 71.2 (95% CI, 61.6–80.9). Subclass 6 (SHOCKS >1 and ANXIETY >7, n = 12): 74.8 (95% CI, 60.5–89.2).

 

Using dichotomous psychodiagnostic variables, CART analysis revealed the same covariates with anxiety in patients with more than one shock and slightly different cutoff values for EMG magnitude or habituation.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
CONCLUSIONS
 NOTES
 REFERENCES
 
The ICD shock provides a largely homogeneous nociceptive stimulation of short duration. Nevertheless, the strength of the perceived pain among the ICD patients assessed in the present study varied considerably over the entire value spectrum of the 100-point VAS scale. Consistent with data from other studies dealing with pain from extreme short duration, these findings prove that a nociceptive stimulation resulting from the heart and the perceived pain intensity are only poorly correlated (11–15). What makes subjects perceive the same amount of nociceptive stimulation as unbearable on the one hand or almost not perceived on the other hand?

The present study adds several new findings to this scientific problem. Hyperalgesia, in the present study, was strongly associated with an aversive estimation of the shock experience: the more discomfort with the stimulus was reported, the more intense the shock application was perceived. Thus, patients who suffer from repeated presentations of an unconditioned threatening stimulus may subsequently develop perceptual habits of vigilance for this particular distress signal and may keep a constant vigil for the dreaded sensation (28).

The CART analysis basically separated the ICD shock receivers in those who experienced one shock and those who experienced more than one shock. This finding is in line with several other studies showing that a second delivered intracardiac shock is generally perceived as more uncomfortable than the first one, even when the second shock was delivered with less energy (13–15). Repetitive delivery of shocks also enhances the amplitude of startle responses in nonhuman (29,30) and human subjects (31) and may lead to sensitization in particular in ICD patients (32).

The present analysis further revealed that in patients with the experience of only one ICD shock, anxiety had no measurable influence on the reported pain intensity. This finding may explain why, in a recent investigation of 37 patients with chronic atrial fibrillation (AF) receiving a first homogenous low-energy intracardiac electrical shock of 60 V (0.1 J) under laboratory conditions, we confirmed a considerable variability of perceived strength but failed to find an association with depression and anxiety (12).

In patients with repetitive shock therapies (>one shock), however, elevated anxiety symptoms substantially increased pain threshold. Once the stimulus has shaped up to a perceptual focus, the perception of the threatening stimuli is indissolubly connected to higher brain regions, with important cortical networks within the limbic system (28), and conditioned responses, such as fear and anxiety, may interact with perception. One should not mistake the phenomenon of sustained anxiety associated with low pain tolerance with fear-induced hypoalgesia. Fear-induced hypoalgesia is a temporary state in which an alarm reaction to a threatening event decreases pain perception (33), whereas anxiety, as measured in the present study, is associated with apprehensive anticipation of pain, resulting in hypervigilance and somatic scanning subsequently increasing attention to pain and thereby increasing its perceived intensity (33).

Independent from anxiety, a similar effect emerged for increased mean EMG amplitude and even more striking for impaired habituation of EMG responses to the 15 acoustic test trials, both physiological parameters which serve as indicators of central neurophysiologic arousability (32,34–36). These findings suggest involvement of the amygdala in pain perception (35,36). Recently discussing the influence of emotion on pain, Rhudy and Meagher (37) concluded that the pain-modulating effects of emotion are best characterized by an interaction between valence and arousal. Negative emotions lead to pain inhibition when they are highly arousing; however, when coupled with low to moderate arousal, they may facilitate pain. The data of the present study add evidence to this assumption: in the startle experiment, patients with heightened pain perception exhibited a moderate amplified EMG response magnitude and an impaired EMG habituation compared with low-pain-perception patients. When integrating these data into the multivariate CART analysis, both parameters (again in patients with >one shock application) allowed effective identification of patients with hyperalgesia.

Interestingly, EMG magnitude caused the only branching of the CART analysis in the one-shock group. Subjects with increased EMG levels rated the one shock perceived as more intense (>51.7 versus 21.9) compared with their low-reacting counterparts. These finding may point to a nonprovoked inherent hyperpotentiation of vulnerable subjects (38), which suggests a biological basis for susceptibility to shock pain sensitivity for a subgroup of patients.

Limitations
The strength of the present investigation is to combine clinical and psychological data with psychophysiologic measures of arousal in an attempt to determine sources of heightened ICD shock pain perception. However, there are limitations to be addressed. The present analysis is restricted to intracardiac shock pain perception and not to pain perception in general. Although time since last shock experience was not correlated to pain perception, it cannot be completely ruled out that intensity of negative affects at the time when study data were gathered may influence recall of pain sensitivity and discomfort. Moreover, the study applies a retrospective design, which makes directionality of effects difficult to determine. Prospective analyses are warranted to study whether those who are more anxious and hyperarousal may have an increased pain perception with shock or those who have experienced shocks as more painful may develop these characteristics.


   CONCLUSIONS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
NOTES
 REFERENCES
 
Recent evidence demonstrates that aversive emotional stress (39–42) and depression (43) can directly trigger potentially arrhythmias requiring ICD treatment. Although acceptance of the device is generally high, quality of life and psychological issues associated with use of the defibrillators deserve greater attention to improve outcomes (43,44). This paper demonstrated the deteriorating interrelationship of anxiety arousal and shock pain perception in ICD patients. Clinicians should be advised from these findings to acknowledge postshock anxiety as a serious adverse side effect of the therapy, which may both lead to a substantial reduction of the patients’ quality of life and may affect shock pain severity. It is recommended to record the patients’ rating of shock pain severity/intensity on a simple VAS scale (ranging from 0–100). All values above 50 should be taken seriously. Whether reduction of anxiety arousal is able to improve patient tolerability is yet to be established.

We are indebted to Anja Grethlein, Janin Schroth, Birgit Hofmann, Johannes Schapperer, and Claudia Wirsching for conducting the data collecting.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 NOTES
REFERENCES
 

Sources of Financial Support: This research project was supported by grants from the Deutsche Forschungsgemeinschaft (DFG) and the Medical Faculty of the Technische Universität München (KKF-H 18-97) and by a nonrestricted grant from Guidant Medical devices (grants to Dr. Ladwig).

DOI:10.1097/01.psy.0000221379.17371.47


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 NOTES
 REFERENCES
 

  1. National Institute for Clinical Excellence. Guidance on the Use of Implantable Cardioverter Defibrillators for Arrhythmias. London: NICE Technology Appraisal Guidance; 2000:11.
  2. Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, Kerber RE, Naccarelli GV, Schoenfeld MH, Silka MJ, Winters SL, Gibbons RI, Antman EM, Alpert JS, Hiratzka LF, Faxon DP, Jacobs AK, Fuster V, Smith SC Jr. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). J Cardiovasc Electrophysiol 2002;13:1183–99.[CrossRef][Medline]
  3. Schron EB, Exner DV, Yao Q, Jenkins LS, Steinberg JS, Cook JR, Kutalek SP, Friedman PL, Bubien RS, Page RL, Powell J. Quality of life in the antiarrhythmics versus implantable defibrillators trial: impact of therapy and influence of adverse symptoms and defibrillator shocks. Circulation 2002;105:589–94.[Abstract/Free Full Text]
  4. Irvine J, Dorian P, Baker B, O’Brien BJ, Roberts R, Gent M, Newman D, Connolly SJ. Quality of life in the Canadian Implantable Defibrillator Study (CIDS). Am Heart J 2002;144:282–9.[Medline]
  5. Sears SF Jr, Conti JB. Quality of life and psychological functioning of ICD patients. Heart 2002;87:488–93.[Free Full Text]
  6. Dougherty CM. Psychological reactions and family adjustment in shock versus no shock groups after implantation of internal cardioverter defibrillator. Heart Lung 1995;24:281–91.[CrossRef][Medline]
  7. Hegel MT, Griegel LE, Black C, Goulden L, Ozahowski T. Anxiety and depression in patients receiving implanted cardioverter-defibrillators: a longitudinal investigation. Int J Psychiatry Med 1997;27:57–69.[Medline]
  8. Herrmann C, Mühen V F, Schaumann A, Buss U, Kemper S, Wantzen C, Gonska BD. Standardized assessment of psychological well-being and quality of life in patients with implanted defibrillators. Pacing Clin Electrophysiol 1997;20:95–103.[CrossRef][Medline]
  9. Kamphuis HC, de Leeuw JR, Derksen R, Hauer RN, Winnubst JA. Implantable cardioverter defibrillator recipients: quality of life in recipients with and without ICD shock delivery: a prospective study. Europace 2003;5:381–9.[Abstract/Free Full Text]
  10. Pauli P, Wiedemann G, Dengler W, Blaumann-Benninghoff G, Kuhlkamp V. Anxiety in patients with an automatic implantable cardioverter defibrillator: what differentiates them from panic patients? Psychosom Med 1999;61:69–76.[Abstract/Free Full Text]
  11. Ahmad M, Bloomstein L, Roelke M, Bernstein AD, Parsonnet V. Patients’ attitudes toward implanted defibrillator shocks. Pacing Clin Electrophysiol 2000;23:934–8.[CrossRef][Medline]
  12. Ladwig KH, Marten-Mittag B, Lehmann G, Gündel H, Simon H, Alt E. Absence of an impact of emotional distress on the perception of intracardiac shock discharges. Int J Behav Med 2003;10:56–65.[CrossRef][Medline]
  13. Lok NS, Lau CP, Tse HF, Ayers GM. Clinical shock tolerability and effect on different right atrial electrode locations on efficacy of low energy human transvenous atrial defibrillation using an implantable lead system. J Am Coll Cardiol 1997;30:1324–30.[Abstract]
  14. Steinhaus DM, Cardinal DS, Mongeon L, Musley SK, Foley L, Corrigan S. Internal defibrillation: pain perception of low energy shocks. Pacing Clin Electrophysiol 2002;25:1090–3.[CrossRef][Medline]
  15. Jung J, Hahn SJ, Heisel A, Buob A, Schubert BD, Siaplaouras S. Defibrillation efficacy and pain perception of two biphasic waveforms for internal cardioversion of atrial fibrillation. J Cardiovasc Electrophysiol 2003;14:837–40.[CrossRef][Medline]
  16. Bruehl S, Chung OY. Interactions between the cardiovascular and pain regulatory systems: an updated review of mechanisms and possible alterations in chronic pain. Neurosci Biobehav Rev 2004;28:395–414.[CrossRef][Medline]
  17. Ladwig KH, Röll G, Breithardt G, Borggrefe M. Sources of amplified chest pain perception in cardiac patients six months after acute myocardial infarction. Am Heart J 1999;137:528–34.[CrossRef][Medline]
  18. Watkins LL, Schneiderman N, Blumenthal JA, Sheps DS, Catellier D, Taylor CB, Freedland KE. ENRICHD Investigators: cognitive and somatic symptoms of depression are associated with medical comorbidity in patients after acute myocardial infarction. Am Heart J 2003;146:48–54.[CrossRef][Medline]
  19. Carr EC, Nicky Thomas V, Wilson-Barnet J. Patient experiences of anxiety, depression and acute pain after surgery: a longitudinal perspective. Int J Nurs Stud 2005;42:521–30.[CrossRef][Medline]
  20. Shalev AY, Scott PO, Peri T, Schreiber S, Pitman RK. Physiologic responses to loud tones in Israeli patients with posttraumatic stress disorder. Arch Gen Psych 1992;49:870–5.[Abstract]
  21. Fridlund AJ, Cacioppo JT. Guidelines for human electromyographic research. Psychophysiology 1986;23:567–89.[Medline]
  22. Fowles DC, Christie MJ, Edelberg R, Grings WW, Lykken DT, Venables PH. Publication recommendations for electrodermal measurements. Psychophysiology 1981;18:232–9.[Medline]
  23. Zigmond AS, Snaith RP. The Hospital Anxiety and Depression Scale. Acta Psychiatr Scand 1983;67:361–70.[Medline]
  24. Herrmann CH, Buss U, Snaith RP. Psychologisches Screening von Patienten einer kardiologischen Akutklinik mit einer deutschen Fassung der "Hospital Anxiety and Depression (HAD) Scale." Psychother Psychosom Med Psychol 1991;41:83–92.[Medline]
  25. Franke GH. Die Symptom-Checkliste von Derogatis (SCL-90-R), Deutsche Version. Weilheim: Beltz-Test Manual; 2002.
  26. Appels A, Hoppener P, Mulder P. A questionnaire to assess premonitory symptoms of myocardial infarction. Int J Cardiol 1987;17:15–24.[CrossRef][Medline]
  27. Breiman L, Friedman JH, Olshen A, Stone CJ. Classification and Regression Trees. Belmont, CA: Wadsworth; 1984.
  28. Chapman CR. Pain: the perception of noxious events In: Sternbach RA, ed. The Psychology of Pain. New York, NY: Raven Press; 1978:169–202.
  29. Boulis NM, Davis M. Footshock-induced sensitization of electrically elicited startle reflexes. Behav Neurosci 1989;103:504–8.[CrossRef][Medline]
  30. Davis M. Sensitization of the acoustic startle reflex by footshock. Behav Neurosci 1989;103:495–503.[CrossRef][Medline]
  31. Hamm AO, Stark R. Sensitization and aversive conditioning: effects on the startle reflex and electrodermal responding. Integr Physiol Behav Sci 1993;28:171–6.[Medline]
  32. Ladwig KH, Marten-Mittag B, Deisenhofer I, Hofmann B, Schapperer J, Weyerbrock S, Schmitt C. Exaggerated electrodermal startle responses after intracardiac shock discharge. Psychosom Med 2003;65:222–8.[Abstract/Free Full Text]
  33. Rhudy JL, Meagher MW. The role of emotion in pain modulation. Curr Opin Psychiatry 2001;14:241–5.[CrossRef]
  34. Lee Y, Lopez DE, Meloni EG, Davis M. A primary acoustic startle pathway: obligatory role of cochlear root neurons and the nucleus reticularis pontis caudalis. J Neurosci 1996;16:3777–89.
  35. Rosen JB, Davis M. Enhancement of acoustic startle by electrical stimulation of the amygdala. Behav Neurosci 1988;102:195–202.[CrossRef][Medline]
  36. Hitchcock JM, Davis M. The efferent pathway of the amygdala involved in conditioned fear as measured with the fear potentiated startle paradigm. Behav Neurosci 1991;105:826–42.[CrossRef][Medline]
  37. Rhudy JL, Meagher MW. Individual differences in the emotional reaction to shock determine whether hypoalgesia is observed. Pain Med 2003;4:244–56.[CrossRef][Medline]
  38. Globisch J, Hamm AO, Esteves F, Öhman A. Fear appears fast: temporal course of startle reflex potentiation in animal fearful subjects. Psychophysiology 1999;36:66–75.[CrossRef][Medline]
  39. Lampert R, Joska T, Burg MM, Batsford WP, McPherson CA, Jain D. Emotional and physical precipitants of ventricular arrhythmia. Circulation 2002;106:1800–5.[Abstract/Free Full Text]
  40. Steinberg JS, Arshad A, Kowalski M, Kukar A, Suma V, Vloka M, Ehlert F, Herweg B, Donnelly J, Philip J, Reed G, Rozanski A. Increased incidence of life-threatening ventricular arrhythmias in implantable defibrillator patients after the World Trade Center attack. J Am Coll Cardiol 2004;44:1261–4.[Abstract/Free Full Text]
  41. Shedd OL, Sears SF Jr, Harvill JL, Arshad A, Conti JB, Steinberg JS, Curtis AB. The World Trade Center attack: increased frequency of defibrillator shocks for ventricular arrhythmias in patients living remotely from New York City. J Am Coll Cardiol 2004;44:1265–7.[Abstract/Free Full Text]
  42. Whang W, Albert CM, Sears SF Jr, Lampert R, Conti JB, Wang PJ, Singh JP, Ruskin JN, Muller JE, Mittleman MA, TOVA Study Investigators. Depression as a predictor for appropriate shocks among patients with implantable cardioverter-defibrillators: results from the Triggers of Ventricular Arrhythmias (TOVA) study. J Am Coll Cardiol. 2005;45:1090–5.[Abstract/Free Full Text]
  43. Dunbar SB. Psychosocial issues of patients with implantable cardioverter defibrillators. Am J Crit Care 2005;14:294–303.[Abstract/Free Full Text]
  44. Ladwig KH, Deisenhofer I, Simon H, Schmitt C, Baumert J. Characteristics associated with low treatment satisfaction in patients with implanted cardioverter defibrillators: results from the LICAD study. Pacing Clin Electrophysiol 2005;28:506–13.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 EuropaceHome page
C. Marquie, A. Duchemin, D. Klug, N. Lamblin, F. Mizon, H. Cordova, M. Boulo, D. Lacroix, A. Pol, and S. Kacet
Can we implant cardioverter defibrillator under minimal sedation?
Europace, July 1, 2007; 9(7): 545 - 550.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baumert, J.
Right arrow Articles by Ladwig, K.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baumert, J.
Right arrow Articles by Ladwig, K.-H.
Related Collections
Right arrow Other Cardiovascular Medicine
Right arrow Pain
Right arrow Psychophysiology

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS