The onset of acute myocardial infarction (AMI) has been shown to occur in a nonrandom pattern, with peaks in midmorning and on weekdays (especially Monday). The incidence of AMI has been shown to increase locally after natural disasters, but the effect of catastrophic events on AMI biorhythms is largely unknown. To assess the differences in the chronobiology of AMI in residents of New Orleans before and after Hurricane Katrina, the onset of AMI in patients at Tulane University Health Sciences Center in the 6 years before and the 3 years after Hurricane Katrina was retrospectively examined. Compared to the pre-Katrina group, the post-Katrina cohort demonstrated significant decreases in the onset of AMI during mornings (p = 0.002), Mondays (p <0.0001), and weekdays (p <0.0001) and significant increases in onset during weekends (p <0.0001) and nights (p <0.0001). These changes persisted during all 3 years after the storm. In conclusion, the normal pattern of AMI onset was altered after Hurricane Katrina, and expected morning, weekday, and Monday peaks were eliminated.
Acute myocardial infarction (AMI) occurs in distinct patterns with regard to time of day, day of the week, and season of the year, with morning, weekday (particularly Monday), and winter peaks. Several elements of psychosocial stress correlate with an increased risk for AMI. Hurricane Katrina struck the city of New Orleans on August 29, 2005. It was the third deadliest and most expensive hurricane to ever hit the United States. In the ensuing 3 years, the incidence of AMI at Tulane University Health Sciences Center (TUHSC) nearly tripled. It has been hypothesized that stresses associated with catastrophic events may also affect the timing of AMI, but to our knowledge, this relation has not been previously investigated. In the present study, we used the large TUHSC database to assess changes in the chronobiology of AMI after Hurricane Katrina. We hoped that this information would provide further insight into the pathogenesis of AMI.
Methods
The present investigation was a single-center retrospective study using data collected from medical records at TUHSC. Patients admitted with diagnoses of AMI were identified using International Classification of Disease, Ninth Revision, codes 410.1 to 410.9. The institutional review board at the Tulane Office of Human Research Protection approved the study, with a waiver of the requirement for informed consent. Our initial search results identified 1,183 AMIs. Included were all patients admitted with typical myocardial ischemic symptoms with troponin I levels exceeding the upper limits of normal (as defined by the TUHSC Biochemistry Laboratory). Specifically excluded were non–New Orleans residents (n = 193), patients transferred to TUHSC after being admitted elsewhere (n = 35), patients with symptom onset while hospitalized (n = 44), and patients with inadequate documentation of the day and time of symptom onset (n = 98). Also excluded were those with elevated serum troponin levels in the setting of severe noncardiac illness (n = 106), such as sepsis, renal failure, and hypovolemic shock, in whom ischemic symptoms could not be documented. Accordingly, the study population consisted of 698 patients and 707 total episodes of AMI.
Subjects were divided into 2 cohorts on the basis of the date of AMI. The pre-Katrina group consisted of patients admitted with AMIs from August 29, 1999, to August 28, 2005 (the day Hurricane Katrina struck the city of New Orleans). The post-Katrina group consisted of patients admitted with diagnoses of AMI from February 14, 2006 (the day TUHSC became the first downtown medical center to reopen) to February 13, 2009. The primary goal was to identify short- and/or long-term differences in the timing of AMI between cohorts (specifically the time of day, day of the week, and season). Subgroup analysis was based on whether admissions for AMI occurred in the first, second, or third year after Katrina following the reopening of TUHSC.
Patient medical records were reviewed for demographic, clinical, and laboratory data. Demographic data, when available, included age, gender, medical history, current medications, use of tobacco and illicit drugs, employment, and insurance status. Clinical data included date and time of symptom onset, type of AMI (ST-segment elevation myocardial infarction [STEMI] vs non-STEMI), and the presence and type of coronary intervention performed. The timing of symptom onset was obtained from notes provided by emergency room triage nurses and physicians, as well as internal medicine and cardiology admission notes. Although it was impossible to blind data gatherers to variables such as season and time of day, blinding to day of the week was implemented during data collection.
Study data were entered into a standardized Microsoft Excel worksheet (Microsoft Corporation, Redmond, Washington). All continuous data were calculated as mean ± SEM. Nonuniformity between cohorts and subgroups was performed using chi-square statistical tests. Differences between group means were compared using unpaired Student’s t tests. A p value <0.05 was considered statistically significant.
Results
A total of 707 events were examined. The population was predominantly male (62.5%), with a mean age of 62.7 ± 13 years (range 27 to 94). The demographic and clinical historical characteristics of the population are listed in Table 1 , separated into the 2 cohorts. The post-Katrina group was significantly younger (p <0.05) and had higher rates of smoking (p <0.001), unemployment (p <0.0001), and lack of medical insurance (p <0.001). There were more men in the post-Katrina group, but this trend did not quite achieve statistical significance (p = 0.07). No significant differences were found in race, substance abuse, medical co-morbidities, or medications on admission. Table 2 depicts the type of AMI and the nature of the coronary intervention that occurred during hospitalization. The percentage of patients with STEMIs and the percentage who underwent percutaneous intervention increased slightly, but these differences were not statistically significant. The percentage of patients found to have significant coronary disease on arteriography decreased slightly after Hurricane Katrina (from 94% to 91%), but this was not statistically significant.
| Variable | Pre-Katrina (n = 299) | Post-Katrina (n = 408) | p Value |
|---|---|---|---|
| Age (yrs) | 64 ± 14 | 62 ± 13 | <0.05 |
| Men | 169 (57%) | 276 (67%) | 0.07 |
| White | 142 (48%) | 183 (45%) | 0.61 |
| Black | 138 (46%) | 197 (48%) | 0.69 |
| Asian | 3 (1%) | 5 (1%) | 0.78 |
| Substance abuse | 29 (10%) | 52 (13%) | 0.24 |
| Smokers | 103 (34%) | 208 (51%) | 0.001 |
| Unemployed | 21 (7%) | 73 (18%) | <0.0001 |
| Uninsured | 25 (8%) | 79 (19%) | <0.001 |
| Previous AMI | 108 (36%) | 153 (38%) | 0.76 |
| Previous percutaneous intervention | 82 (27%) | 118 (29%) | 0.71 |
| Previous coronary artery bypass | 61 (20%) | 76 (19%) | 0.60 |
| Hypertension (systolic blood pressure >140 mm Hg or therapy) | 212 (71%) | 296 (73%) | 0.80 |
| Hyperlipidemia (low-density lipoprotein >160 mg/dl or therapy) | 134 (45%) | 186 (46%) | 0.88 |
| Diabetes mellitus | 93 (31%) | 137 (34%) | 0.57 |
| Heart failure | 51 (17%) | 77 (19%) | 0.58 |
| Aspirin | 119 (40%) | 155 (38%) | 0.70 |
| β blockers | 111 (37%) | 144 (35%) | 0.69 |
| Statins | 109 (36%) | 135 (33%) | 0.45 |
| Angiotensin-converting enzyme inhibitors/angiotensin receptor blockers | 114 (38%) | 156 (38%) | 0.98 |
| Diuretics | 101 (34%) | 127 (31%) | 0.54 |
| Variable | Pre-Katrina (n = 299) | Post-Katrina (n = 408) | p Value |
|---|---|---|---|
| STEMI | 130 (44%) | 191 (47%) | 0.51 |
| Coronary arteriography performed | 236 (79%) | 351 (86%) | 0.31 |
| Incidence of significant coronary disease (≥50% in ≥1 vessel) | 222 (94%) | 319 (91%) | 0.694 |
| Percutaneous intervention after AMI | 155 (52%) | 256 (63%) | 0.06 |
| Coronary artery bypass after AMI | 39 (13%) | 53 (13%) | 1.0 |
The circadian, septadian (day of the week), and seasonal distribution of AMI onset is listed in Table 3 . Notable findings included a significant decrease in mornings (5:59 to 11:59 a.m. ) (p = 0.002), a twofold increase in evenings (6 to 11:59 p.m. ) (p <0.0001), and a nonsignificant increase in AMIs in the hours between midnight and 6 a.m. The most dramatic septadian changes included a more than twofold decrease in AMIs on Mondays (p <0.0001) and a more than twofold increase in AMIs on Saturdays (p <0.001). Sunday AMIs also increased (p = 0.032). The onset of AMI was also analyzed using selected parameters that combined circadian and septadian rhythms ( Table 3 ). The percentages of night (6 p.m. to 5:59 a.m. , Monday through Friday) and weekend (12 a.m. Saturday to 11:59 p.m. Sunday) AMIs increased significantly, while the percentage of weekday (6 a.m. to 6 p.m. , Monday through Friday) events decreased (p <0.0001). Seasonal variation in AMI was notable for increases in winter and summer and decreases in spring and fall, but none of the differences were statistically significant.
| Time Period | Pre-Katrina (n = 299) | Post-Katrina (n = 408) | p Value |
|---|---|---|---|
| 12 to 5:59 a.m. ∗ | 47 (16%) | 89 (21.8%) | 0.07 |
| 6 to 11:59 a.m. ∗ | 135 (45%) | 126 (30.9%) | 0.002 |
| 12 to 5:59 p.m. ∗ | 73 (24%) | 78 (19.1%) | 0.132 |
| 6 to 11:59 p.m. ∗ | 42 (14%) | 115 (28.2%) | <0.0001 |
| Monday | 70 (23%) | 42 (10%) | <0.0001 |
| Tuesday | 42 (14%) | 65 (16%) | 0.525 |
| Wednesday | 49 (16%) | 48 (12%) | 0.10 |
| Thursday | 50 (17%) | 62 (15%) | 0.614 |
| Friday | 40 (13%) | 68 (17%) | 0.27 |
| Saturday | 20 (7%) | 64 (16%) | <0.001 |
| Sunday | 28 (9%) | 62 (15%) | 0.032 |
| Weekday † | 180 (60%) | 160 (39%) | <0.0001 |
| Weekend ‡ | 48 (16%) | 126 (31%) | <0.0001 |
| Night § | 89 (30%) | 204 (50%) | 0.00005 |
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