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ORIGINAL ARTICLES |
From the Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts (J.W.S., M.H.P.); Albert Einstein College of Medicine, Bronx, New York (S.W.-S.); the University of Nevada School of Medicine, Reno, Nevada (R.B.); the University of Hawaii, Honolulu, Hawaii (D.C.); the University of Iowa, Iowa City, Iowa (J.T.); Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama (A.O.); Department of Obstetrics and Gynecology, Wayne State University, Hutzel Women’s Hospital, Detroit, Michigan (S.L.H.); George Washington University Medical Center, Washington, DC (J.H.); and the University of Florida, Gainesville, Florida, and Malcom Randall VA Medical Center Gainesville, Florida (D.S.S.).
Address correspondence and reprint requests to Jordan W. Smoller, MD, ScD, Massachusetts General Hospital, Simches Research Building, 185 Cambridge Street, Suite 2200, Boston, MA 02114. E-mail: jsmoller{at}hms.harvard.edu
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ABSTRACT |
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Methods: The authors conducted a cross-sectional survey of 3063 community-dwelling, generally healthy postmenopausal women enrolled between 1997 and 2000 in the Myocardial Ischemia and Migraine Study in 10 clinical centers of the 40-center Women’s Health Initiative. Participants, ages 50 to 79 years, completed a questionnaire about occurrence of panic attacks in the previous 6 months and underwent 24-hour ambulatory electrocardiogram monitoring (AECG); 2705 women had valid AECG recordings and panic attack questionnaires. ST depression on AECG, heart rate variability (HRV), and chest pain episodes were compared among women with and without a 6-month history of panic attack.
Results: There was no difference in overall prevalence of ischemic episodes during AECG between women with and without panic attacks. Women with a recent history of panic were more likely to experience chest pain during AECG after controlling for potential confounders (odds ratio [OR] = 2.01; 95% confidence interval [CI] = 1.40–2.88), including both nonischemic (OR = 1.83; 95% CI = 1.26–2.65) and ischemic chest pain (OR = 4.94; 95% CI = 1.41–17.30). Although mean HRV was lower in those with panic attacks (p = .017), this was not significant after controlling for confounders.
Conclusions: Postmenopausal women with a recent history of panic attacks do not appear to have more daily life ischemia as measured by occurrence of ST depression during 24-hour monitoring, but do have more chest pain and possibly lower HRV, suggesting that even sporadic panic attacks may be related to cardiovascular risk.
Key Words: daily life ischemia • postmenopausal women • panic • chest pain • panic disorder
Abbreviations: PD = panic disorder; MIMS = Myocardial Ischemia and Migraine Study; WHI = Women’s Health Initiative; ECG = electrocardiogram; AECG = ambulatory ECG; HRV = heart rate variability; MI = myocardial infarction; CAD = coronary artery disease; CES-D = Center for Epidemiological Studies Depression Scale; CABG = coronary artery bypass surgery; CHD = coronary heart disease.
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INTRODUCTION |
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Anxiety has been associated with increased risk of fatal coronary heart disease and all-cause mortality, particularly among men (6–9). A recent analysis of data from the Nurses’ Health Study extended this finding to women (10). In that study, high scores on a measure of phobic anxiety were associated with increased risk of fatal myocardial infarction (MI) and sudden cardiac death but not nonfatal MI. Some studies have shown a high prevalence of coronary artery disease (CAD) in patients with panic disorder (11); however, a review by Katerndahl (12) of over 100 studies indicates wide variability in estimates of the association of panic disorder and coronary artery disease depending on the referral population studied. There are virtually no studies addressing the relationship of panic attacks to daily life ischemia. In a small study of 10 healthy young women (13), ischemia was not detected by ambulatory electrocardiogram (AECG) monitoring during panic attacks. More recently, a myocardial perfusion study of 65 patients with CAD (including 35 with PD and 30 without PD) provided evidence that panic attacks induced by carbon dioxide inhalation are associated with reversible perfusion defects (14). Whether generally healthy older women with a history of panic attacks are more prone to daily life ischemia not concurrent with the panic attack has not been studied.
Several studies have also documented a relationship between reduced heart rate variability (HRV), an index of autonomic dysregulation, and PD (15–17). Alterations in cardiac vagal tone may provide another pathophysiological link between panic and risk for increased cardiac morbidity and mortality. Whether a history of sporadic panic attacks is related to HRV has also not been explored previously.
We report on the relationship between history of recent panic attacks and results of 24-hour ambulatory electrocardiogram (ECG) monitoring in over 3000 postmenopausal women enrolled in the Myocardial Ischemia and Migraine Study (MIMS). This is the largest such study to date. We hypothesized that women with a recent history of panic attacks would be at increased risk of daily life ischemia and reduced HRV.
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METHODS AND DEFINITION OF VARIABLES |
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WHI Observational Study participants, after giving written informed consent, approved by each of the participating institutions’ Institutional Review Boards, completed questionnaires at baseline and annually, had a physical examination, and provided blood samples at baseline and again 3 years later. They were invited to join MIMS in most cases at their third year WHI clinic visit, or less frequently, at their WHI baseline visit, or between these visits; the median time between WHI baseline and MIMS enrollment was 3.1 years (interquartile range, 2.8–3.2 years). At their baseline and third year visits, participants were asked to bring in the original bottles of all the medications they were taking and the pill bottle data were entered into the computer database matched to the corresponding item in the Master Drug Data Base (MDDB; Medi-Span, Indianapolis, IN) and assigned a therapeutic class code provided by the American Hospital Formulary Service. MIMS participants completed a questionnaire about occurrence of panic attacks in the previous 6 months and about migraine headaches before being fitted with the Holter monitor.
Ambulatory Electrocardiographic Monitoring
Participants were fitted with a Holter monitor and were instructed to return the monitor to the local clinic the next day after undergoing 24-hour ambulatory ECG monitoring using a Zymed Model 3100–001 digital recorder with three bipolar leads. During ECG monitoring, they were asked to push a button for approximately 5 seconds if they experienced chest pain, pressure, or discomfort and to then record these events in a diary provided by the study. Analysis of the Holter recordings was done with the Zymed 0210, Model 108005–003 replay system. Recordings were transmitted for analysis to the AECG Core Laboratory at the University of Florida, Gainesville, Florida. Recordings with significant artifact, duration less than 12 hours, or duration entirely during sleep were not used. In addition, recordings were reviewed by one of the authors (D.S.) to judge whether episodes of ST depression were accompanied by chest pain (i.e., to determine if the chest pain button was pushed concurrently with the ischemia episode).
Definition of Variables
Panic episodes were defined on the basis of responses to a questionnaire adapted from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) Panic Disorder Field Trial (20) and administered at the clinic visit during which AECG monitor was initiated and before initiating recording. Full-blown panic attack was defined as reporting an attack of sudden fear, anxiety, or extreme discomfort during the past 6 months accompanied by four or more panic attack symptoms out of the 12-symptom checklist. Women reporting such an attack but with three or fewer panic attack symptoms were considered to have limited-symptom panic. Women who endorsed only a second screening question, which asked about an episode of sudden or irregular heartbeats in the past 6 months but not an attack of fear, anxiety, or extreme discomfort were classified as indeterminate. The indeterminate category was included in the DSM-IV Field Trial of Panic Disorder based on evidence that it might detect individuals with true panic attacks or panic disorder who do not endorse the traditional screening question about anxiety attacks. Thus, the group of women with these autonomic symptoms and four or more panic symptoms likely included some women with and some without true panic attacks, and their status was considered "indeterminate" with respect to panic. These women were excluded from the analyses. The no panic group, used as a comparison group, consisted of women who were classified as not having full panic attacks or limited-symptom panic attacks and who were not in the indeterminate category. Further details are provided in a previous publication (5).
Depression was defined as scoring above a standard cut point based on a regression equation derived from a shortened six-item version of the Center for Epidemiological Studies Depression Scale (CES-D), which asks about depressive symptoms in the past week and two questions asking about sad or depressed mood within the past 2 years described in more detail elsewhere (21). In multivariate analyses, the depression variable was used as a continuous measure. History of coronary heart disease before the MIMS (HxCHD) was defined as self-report of MI, coronary artery bypass surgery (CABG), or percutaneous transluminal coronary angioplasty (PTCA) before WHI baseline, or one of these outcomes after WHI baseline but before the AECG monitoring and the administration of the panic questionnaire. History of cardiovascular disease before MIMS was defined as HxCHD or stroke before the AECG monitoring.
Ischemia was defined as at least one episode during the 24-hour AECG of horizontal or downsloping ST depression of greater than 0.1 mV for at least 80 ms past the J point over a period greater than 1 minute. Presence of chest pain was indicated by at least one button press signal during Holter monitoring to indicate an episode of chest pain, pressure, or discomfort. Ischemic chest pain was considered to have occurred when the button was pressed concurrent with ischemic ST depression; nonischemic chest pain was an episode of chest pain not accompanied by ST depression. Heart rate variability was assessed as the standard deviation of the N-N interval on the AECG (22).
Statistical Methods
Baseline characteristics of women with full-blown panic attack history and those with no panic were compared by 
2 test for categorical variables. Similar analyses were done to compare occurrence of chest pain and ischemia among women with full panic compared with women with no panic. Fisher two-sided exact test was performed when the numbers in a given cell were too small to be used for a 2 test. Linear regression analyses were done to determine the effect of full panic on HRV controlling for age and race. Additional models also controlled for medications and for other confounding variables. Logistic regression analyses were done to determine the odds ratios for ischemia and chest pain associated with a history of full panic attacks compared with no panic attacks as well as for any type of panic attacks (full or limited panic) controlling for multiple relevant covariates from among the following: age at MIMS enrollment, WHI baseline data on race/ethnicity, education, income, smoking status, alcohol intake, history of hot flashes or night sweats, depression as a continuous variable, and life events in the past year; data from the third year WHI visit (closest to MIMS enrollment) on body mass index, any CHD before MIMS enrollment (which included a history of CHD at WHI baseline or a CHD event between WHI baseline and MIMS enrollment), and use of diuretic or beta-blockers or other antihypertensive medications and use of antianxiety or antidepressant medications. Independent variables entered in the multivariate analyses were confounders derived from the previously mentioned list that were significantly related both to panic attacks and to chest pain on Holter monitoring.
Identifying potential confounders in this way depends on associations in the current sample, although these may or may not have been observed in the source population; thus, it is possible that the model may be over- or underinclusive. Collinearity was assessed by examining the correlation matrix among these variables. No correlations were above 0.20 and most were less than 0.12, indicating no important collinearity (although it is possible that variables that do not demonstrate collinearity in bivariate correlations might exhibit collinearity in a multivariable model). In analyses of ischemia and chest pain, interactions of panic with age as well as panic with depression were tested in separate models, including main effects and the interaction term. These interactions were not significant and thus were not included in the multivariate models.
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RESULTS |
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Baseline Characteristics
Baseline characteristics determined at WHI screening are shown in Table 1 and have been previously reported (5). A greater proportion of women reporting full panic attacks compared with no panic attacks were younger, had lower income, and lower educational level. These differences were small but statistically significant as a result of the large sample size. Women with full panic were more likely to be smokers and heavier, but did not differ with respect to having either hypertension or high cholesterol that required medication. They were more likely to report menopausal vasomotor symptoms of hot flashes and night sweats, but did not differ in hormone use at WHI baseline. Women with full panic were more likely to be depressed and to have had three or more stressful life events in the year before WHI enrollment. Depression is commonly associated with panic attacks, as previously reported; 31% of those with full panic attacks were above the cut point for depression on the screening instrument compared with 7.6% of those with no panic. Women reporting panic attacks were also more likely to report a history of cardiovascular disease. Even among those whose panic attacks did not include chest pain as a symptom, women with panic reported a history of physician-diagnosed angina more frequently than did those with no panic (12.7% versus 3.5%, p < .005, data not shown). Women with limited-symptom panic more closely resembled the no panic group than the full panic group with respect to baseline characteristics.
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There were 305 women of the 2945 (10.4%) who reported at least one episode of chest pain during the AECG by pushing the button on the machine to indicate chest pain or discomfort. Most of these chest pain episodes were not accompanied by ST depression (N = 294). Women with full panic attacks had twice the rate of chest pain during AECG (18.8%) than did women with no panic attacks (9.3%) (p < .001). Those with limited-symptom panic had rates of ST depression and chest pain similar to those with no panic. The higher rate of chest pain among those with full panic attacks was also found among the 2831 women who did not have history of any cardiovascular disease before MIMS (18.9% among women with full panic and 9.4% among those with no panic attacks, p < .0001, data not displayed). There were very few cases (n = 11) judged at the ECG center to have episodes of chest pain accompanied by ST depression (ischemic chest pain), yet women with full panic were significantly more likely to experience ischemic chest pain (1.4%) than were women with no panic (0.3%, p = .024, Fisher two-sided exact test).
Participants with full panic attacks had significantly lower heart rate variability as indexed by the standard deviation of the N-N intervals (113.9), in a univariate comparison, than did those with no panic attacks (118.6) (t test, p = .017, Table 3); however, this effect was not apparent after controlling for multiple confounders. Although regression analyses (Table 4) indicated a significant regression coefficient for full panic versus no panic controlling for age and race (p = .006), the regression coefficient was no longer significant when additional adjustment was made for antihypertensive, antianxiety, or antidepressant medications (p = .09) and completely disappeared with further adjustment for all confounding variables (p = .60).
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Multiple Logistic Regression Analyses
Multiple logistic regression analyses indicated no significant effect of full panic attacks or of any type of panic attacks on ST segment depression; the odds ratio adjusting for age, race, education, income, WHI baseline smoking, alcohol intake, body mass index, moderate or severe hot flashes or night sweats, any stressful life events in the year before WHI baseline, depression, and history of CHD before MIMS baseline was 1.18 (95% confidence interval [CI] = 0.78–1.78). However, women with full panic attacks had 2.25-fold higher odds of chest pain (95% CI = 1.63–3.11) during the Holter monitoring compared with women with no panic. Adjustment for age at AECG and race did not change this odds ratio. Further adjustment for the variables noted above reduced the odds ratio only slightly to 1.79 (95% CI = 1.24–2.59) (Table 5). Excluding the 114 women who had a history of prior cardiovascular disease from the analyses did not change the results. Despite the small number of ischemic chest pain episodes, women with full panic attacks were nearly five times more likely to experience ischemic chest pain than those with no panic, adjusting for age at AECG and race/ethnicity, although the confidence intervals are wide (odds ratio = 4.94; 95% CI = 1.41–17.30).
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DISCUSSION |
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Prior studies have suggested a link between panic or phobic anxiety and cardiovascular morbidity (7,10,12,23). Although the precise mechanisms underlying this connection remain to be defined, proposed mediators have included anxiety-related increases in sympathetic outflow, altered autonomic reactivity, microvascular angina, or increased prevalence of cardiovascular risk factors among individuals with anxiety (10,12,17).
Although there was a lower mean HRV among women with panic attacks in our study, we found no effect of panic on HRV after controlling for multiple covariates. A lower HRV among those with panic attacks has been shown in other reports that related HRV to panic disorder (16,17). A recent report from the Nurses’ Health Study (10) indicated that elevated scores on a measure of phobic anxiety were associated with incident fatal MI and sudden cardiac death, which may be related to reduced HRV in a large cohort that included older women. Lower HRV has been associated with depression (24) and with cardiovascular events after a myocardial infarction (25,26). In our study, women with vasomotor symptoms compared with those women without such symptoms had lower HRV (112.6 versus 118.0, p = .025) whether they had panic attacks or not (data not displayed). To our knowledge, there are no reports on heart variability in relation to vasomotor symptoms, although, in one study, postmenopausal women have been reported to have lower HRV than premenopausal women (27), but the number of women monitored in that study was small (n = 88).
Most prior studies of the connection between panic and cardiovascular disease have focused on the prevalence of PD among patients presenting with chest pain to emergency rooms, cardiology practices, or primary care settings and among those with documented coronary artery disease (12,28). These studies have generally found a high prevalence or odds ratio of PD among patients with chest pain compared with controls. However, in contrast to the focus in previous studies on patients with cardiovascular disease, our study focuses on the prevalence of ischemia and chest pain among generally healthy women in an unreferred population reporting a recent (6 months) history of panic attacks.
The prevalence of chest pain among women not seeking medical attention is uncertain. In the Royal College of General Practitioners’ Oral Contraception Study (29), the lifetime prevalence of any exertional chest pain was 10.1%, whereas our estimates of chest pain during the Holter monitoring ranged from 9.3% of those with no panic to 18.8% of those with full panic attacks. Chest pain and palpitations have been reported to increase after menopause (30). In the current sample, a recent history of panic attacks was an independent predictor of chest pain during AECG, adjusting for potential confounders, and those with full panic attacks were nearly twice as likely to experience chest pain during ambulatory monitoring as those with no panic attacks. The independent association of panic with chest pain in our study suggests that evaluation for panic attacks, which can be done with a screening instrument, and perhaps for PD, which requires more in-depth psychiatric diagnostic methods, may be helpful in older women with chest pain. Because effective pharmacologic intervention is available for treatment of PD, making this diagnosis has practical implications.
Although most episodes of chest pain on AECG among these generally healthy women were nonischemic, a 6-month history of panic was also significantly associated with ischemic chest pain. These results are consistent with previous studies reporting that panic anxiety is associated both with noncardiac chest pain (31,32) and with studies suggesting a link between anxiety and ischemic heart disease (6,7,9,23,31,32). They also suggest that, by itself, a history of panic attacks does not distinguish women whose chest pain is more or less likely to be ischemic. Importantly, however, panic attack history was not associated with an increased risk of ischemia overall during AECG. We had sufficient power to detect a 5% higher difference in rate of ST depression corresponding to an odds ratio of approximately 1.6 or higher. Thus, although our finding of no significant association of panic attacks and ST depression does not rule out the possibility of a smaller effect, it is highly unlikely the effect is at least this high. The association between panic and ischemia may be stronger in patients with preexisting CAD. In a study of 65 patients with documented CAD (35 with PD), Fleet and colleagues (14) performed a provocative challenge to induce panic attacks by inhalation of a mixture of 35% carbon dioxide and 65% oxygen and examined myocardial perfusion by single photon emission computed tomography. In that study, induced panic attacks were associated with reversible myocardial perfusion defects in 21 of 26 (81%) patients with PD and 13 of 28 (46%) patients without PD. In our study, however, the results were not substantially different when controlling for a history of CHD (Table 5).
Our study should be interpreted in light of several limitations. Panic attack history was assessed just before the AECG and concerned the occurrence of at least one panic attack in the previous 6 months. Thus, we are not able to determine whether women with panic experienced frequent or infrequent attacks or what proportion may have met criteria for PD. In addition, our results pertain to generally healthy postmenopausal women. We do not know whether women had ischemia during their panic attacks. Because the prevalence of panic attacks in a 6-month period is approximately 10%, a well-powered study of panic attacks during AECG monitoring might require ambulatory monitoring of an unfeasibly large number of women to capture the occurrence of a panic attack.
In summary, in the largest study of its kind, we found an increased risk of chest pain (both ischemic and nonischemic) but no overall increase in daily life ischemia during AECG monitoring among older women with a recent history of panic attack.
Myocardial Ischemia and Migraine Study Investigators and Clinical Centers
David Sheps, MD, MIMS Principal Investigator, University of Florida at Gainesville, Florida.
Clinical Sites Principal Investigators
David Curb, MD, University of Hawaii at Manoa, Manoa, Hawaii; Sandra Daugherty, MD, PhD (deceased), University of Nevada, Reno, Nevada; Julius Gardin, MD, St. John’s Hospital and Medical Center, Detroit, Michigan; Susan Hendrix, DO, Wayne State University, Detroit, Michigan; Hsia, MD, George Washington Medical Center, Washington, DC; Rebecca Jackson, MD, Ohio State University Medical Center, Columbus, Ohio; Albert Oberman, MD, MPH, University of Alabama at Birmingham, Birmingham, Alabama; Carla A. Sueta, MD, PhD, University of North Carolina, Chapel Hill, North Carolina; James Torner, MD, University of Iowa College of Medicine, Iowa City, Iowa; and Sylvia Wassertheil-Smoller, PhD, Albert Einstein College of Medicine, Bronx, New York.
Short List of Women’s Health Initiative Investigators
Program Office
National Heart, Lung, and Blood Institute, Bethesda, Maryland: Barbara Alving, Jacques Rossouw, and Linda Pottern.
Clinical Coordinating Center
Fred Hutchinson Cancer Research Center, Seattle, Washington: Ross Prentice, Garnet Anderson, Andrea LaCroix, Charles L. Kooperberg, Ruth E. Patterson, and Anne McTiernan; Wake Forest University School of Medicine, Winston-Salem, North Carolina: Sally Shumaker; Medical Research Labs, Highland Heights, Kentucky: Evan Stein; University of California at San Francisco, San Francisco, California: Steven Cummings.
Clinical Centers
Albert Einstein College of Medicine, Bronx, New York: Sylvia Wassertheil-Smoller; Baylor College of Medicine, Houston, Texas: Jennifer Hays; Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts: JoAnn Manson; Brown University, Providence, Rhode Island: Annlouise R. Assaf; Emory University, Atlanta, Georgia: Lawrence Phillips; Fred Hutchinson Cancer Research Center, Seattle, Washington: Shirley Beresford; George Washington University Medical Center, Washington, DC: Judith Hsia; Harbor-UCLA Research and Education Institute, Torrance, California: Rowan Chlebowski; Kaiser Permanente Center for Health Research, Portland, Oregon: Evelyn Whitlock; Kaiser Permanente Division of Research, Oakland, California: Bette Caan; Medical College of Wisconsin, Milwaukee, Wisconsin: Jane Morley Kotchen; MedStar Research Institute/Howard University, Washington, DC: Barbara V. Howard; Northwestern University, Chicago/Evanston, Illinois: Linda Van Horn; Rush-Presbyterian St. Luke’s Medical Center, Chicago, Illinois: Henry Black; Stanford Prevention Research Center, Stanford, California: Marcia L. Stefanick; State University of New York at Stony Brook, Stony Brook, New York: Dorothy Lane; The Ohio State University, Columbus, Ohio: Rebecca Jackson; University of Alabama at Birmingham, Birmingham, Alabama: Cora E. Lewis; University of Arizona, Tucson/Phoenix, Arizona: Tamsen Bassford; University at Buffalo, Buffalo, New York: Jean Wactawski-Wende; University of California at Davis, Sacramento, California: John Robbins; University of California at Irvine, Orange, California: Allan Hubbell; University of California at Los Angeles, Los Angeles, California: Howard Judd; University of California at San Diego, LaJolla/Chula Vista, California: Robert D. Langer; University of Cincinnati, Cincinnati, Ohio: Margery Gass; University of Florida, Gainesville/Jacksonville, Florida: Marian Limacher; University of Hawaii, Honolulu, Hawaii: David Curb; University of Iowa, Iowa City/Davenport, Iowa: Robert Wallace; University of Massachusetts/Fallon Clinic, Worcester, Massachusetts: Judith Ockene; University of Medicine and Dentistry of New Jersey, Newark, New Jersey: Norman Lasser; University of Miami, Miami, Florida: Mary Jo O’Sullivan; University of Minnesota, Minneapolis, Minnesota: Karen Margolis; University of Nevada, Reno, Nevada: Robert Brunner; University of North Carolina, Chapel Hill, North Carolina: Gerardo Heiss; University of Pittsburgh, Pittsburgh, Pennsylvania: Lewis Kuller; University of Tennessee, Memphis, Tennessee: Karen C. Johnson; University of Texas Health Science Center, San Antonio, Texas: Robert Brzyski; University of Wisconsin, Madison, Wisconsin: Gloria E. Sarto; Wake Forest University School of Medicine, Winston-Salem, North Carolina: Denise Bonds; Wayne State University School of Medicine/Hutzel Hospital, Detroit, Michigan: Susan Hendrix.
The WHI program is funded by the National Heart, Lung and Blood Institute, US Department of Health and Human Services. The Myocardial Ischemia and Migraine Study (MIMS) was funded by Glaxo Wellcome (now GlaxoSmithKline). We acknowledge with appreciation Victor Kamensky for programming the statistical analyses. Dr. Smoller has received honoraria from Hoffman-La Roche, Inc. and is a member of the Roche Diagnostics Psychiatric Advisory Board.
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NOTES |
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Because co-author David S. Sheps is Editor-in-Chief of this journal, the review of this paper was overseen by a guest editor, Nancy Frasure-Smith, who was chosen by other editors of the journal. He was not involved in the decision-making process and like all authors was blinded to the identity of the peer reviewers.
DOI:10.1097/01.psy.0000244383.19453.c5
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