Diurnal, weekly and seasonal variations of chest pain in patients transported by emergency medical services

Abstract

Objectives

Chest pain is among the leading causes for emergency medical services (EMS) activation. Acute myocardial infarction (MI) is not only one of the most critical aetiologies of chest pain, but also one of few conditions encountered by EMS that has been shown to follow a circadian pattern. Understanding the diurnal relationship between the inflow of chest pain patients and the likelihood of acute MI may inform prehospital and emergency department (ED) healthcare providers regarding the prediction, and hence prevention, of dire outcomes.

Methods

This was a secondary analysis of previously collected data from an observational prospective study that enrolled consecutive chest pain patients transported by a large metropolitan EMS system in the USA. We used the time of EMS call to determine the time-of-day of the indexed encounter. Two independent reviewers examined available medical data to determine our primary outcome, the presence of MI, and our secondary outcomes, infarct size and 30-day major adverse cardiac events (MACE). We estimated infarct size using peak troponin level.

Results

We enrolled 2065 patients (age 56±17, 53% males, 7.5% with MI). Chest pain encounters increased from 9:00 AM to 2:00 PM, with a peak at 1:00 PM and a nadir at 6:00 AM. Acute MI had a bimodal distribution with two peaks: 10 AM in ST-elevation MI, and 10 PM in non-ST-elevation MI. ST-elevation MI with afternoon onset was an independent predictor of infarct size. Acute MI with winter and early spring presentation was an independent predictor of 30-day MACE.

Conclusions

EMS-attended chest pain calls follow a diurnal pattern, with the most vulnerable patients encountered during afternoons and winter/spring seasons. These data can inform prehospital and ED healthcare providers regarding the time of presentation where patients are more likely to have an underlying MI and subsequently worse outcomes.

INTRODUCTION

At least one-third of the 6 million annual chest pain cases in the USA present to the hospital by emergency medical services (EMS), and approximately half of deaths among patients with acute myocardial infarction (MI) occur prior to hospital arrival. In fact, deaths due to acute MI are 7-fold higher than deaths due to trauma.¹ This excessive burden is frequently complicated by limited resources available in the prehospital setting. Particularly, the number of emergency department (ED) visits for chest pain is increasing, while the percentage of these visits with a critical diagnosis is declining, increasing the complexity of prehospital triage. Furthermore, optimal management of patients with MI requires a coordinated effort between prehospital and in-hospital providers who must triage and engage downstream resources such as activation of the cardiac catheterisation laboratory.

Variability in time to treatment for patients transported by EMS with cardiac complaints have been linked to survival and other patient-centred outcomes during hospitalisation.² Clinical guidelines recommend that patients with ST-elevation MI (STEMI) receive coronary intervention with a first medical contact (FMC) to device time of <90 min, which is particularly difficult to achieve for patients arriving via EMS where FMC is measured at the initiation of EMS care. Off-hours activation of the catheterisation laboratory represents a unique challenge in staffing and resource utilisation. Managing patients with non-ST-elevation MI (NSTEMI) similarly requires additional hospital resources compared with patients with chest pain who are not having myocardial infarction. Understanding the diurnal, weekly and seasonal variations in chest pain transported by EMS across the spectrum of acute coronary syndrome may have important implications for the proper allocation of hospital and emergency resources, in addition to informing prehospital and in-hospital providers regarding the possibility of patients having an underlying critical diagnosis based on time of symptoms onset and presentation.

The onset of acute MI has been shown to follow a diurnal pattern, with the majority of cases occurring between 6:00 AM and noon.³ Multiple studies report weekly and seasonal variations of MI events, with increased incidence on Mondays and during winter seasons.⁴ Infarct size and mortality also depend on the time of day, with worse outcomes when MI onset happens at night.⁵ However, prior studies have not focused on patients specifically being transported by EMS. Moreover, most studies have primarily focused on patients with STEMI, with little or no emphasis on NSTEMI. The latter group is distinct and includes older patients who may have more diffuse multivessel coronary artery disease and chronic comorbidities. Patients with STEMI and NSTEMI might have a different diurnal and seasonal pattern of onset. Additionally, no prior studies correlated the diurnal variation of acute MI with relation to diurnal variations in chest pain encounters. We hypothesised that, among patients presenting to the ED with chest pain, the likelihood of acute MI is highest during morning hours. Accordingly, we used existing data from our observational cohort study to (1) evaluate the diurnal variations of the inflow of EMS-activated chest pain encounters, (2) evaluate the diurnal variation of likelihood of acute MI in EMS-activated chest pain and (3) examine whether the time of day, day of week or season of presentation were associated with type of MI, infarct size and adverse cardiac outcomes.

METHODS

Sample and setting

This is a secondary analysis of the EMPIRE study (ECG Methods for the Prompt Identification of Coronary Events). The methods for this study were previously described in detail.⁶ Essentially, EMPIRE is an ongoing observational cohort study that enrolled non-selected, consecutive patients who called EMS with a chief complaint of non-traumatic chest pain or equivalent. Patients were subsequently treated and transported by City of Pittsburgh Bureau of EMS to one of three University of Pittsburgh Medical Center (UPMC)-affiliated tertiary care hospitals (UPMC Presbyterian, Shadyside and Mercy hospitals). For this analysis we are using data from the first study cohort that enrolled patients between May 2013 and August 2014 (n=2065). EMPIRE study enrolled all consecutive eligible patients and there were no modifications to routine medical care. The University of Pittsburgh Institutional Review Board approved this study with a waiver of the requirement for informed consent.

Data collection

We identified subjects who met the study criteria using custom reporting software in the prehospital electronic patient care record programme (emsCharts, Warrendale, Pennsylvania). We used both the call handler initial classification plus the EMS field evaluation to decide the eligibility. We manually linked the prehospital data with hospital records (PowerChart, Cerner Corporation, North Kansas City, Missouri, USA) using probabilistic linking via patient name, time and date of hospital arrival, age and sex. We abstracted clinically relevant data elements as recommended by the American College of Cardiology for measuring the management and outcomes of patients with suspected acute coronary syndrome: demographics, height, weight, past medical history, clinical presentation and course of hospitalisation, laboratory studies, including troponin measured by conventional cardiac troponin I assay (AccuTnI assay, manufactured by Beckman Coulter Inc; 99^th percentile cut-off at 0.1 ng/mL), imaging studies, cardiac catheterisation results, medical treatments and in-hospital complications.

Two independent reviewers retrospectively examined the in-hospital records to adjudicate the study outcomes. The primary outcome was the presence of acute MI based on the Universal Definition of Myocardial Infarction as elevation of cardiac troponin (>99^th percentile), with at least one of the following: (1) subsequent development of labile, ischaemic ECG changes (eg, ST-T changes, new bundle branch block or new Q wave) during hospitalisation, (2) imaging evidence of new loss of viable myocardium or new regional wall motion abnormalities or (3) coronary angiography or nuclear imaging demonstrating greater than 70% stenosis of a major coronary artery with or without treatment.⁷ We retrieved the type of MI (STEMI vs NSTEMI) from cardiac catheterisation report as determined by the interventional cardiologist at time of patient care. In addition, two secondary outcomes were evaluated in the subset of patients with acute MI: (1) infarct size, defined by a previously validated method of peak cardiac troponin level during hospitalisation,⁸ and (2) major adverse cardiac events (MACE), defined as in-hospital death, acute heart failure, cardiogenic shock, ventricular tachycardia/fibrillation, mechanical ventilation or re-infarction within 30 days of presentation. To ensure complete ascertainment of follow-up data, we used Cerner and EPIC, the UPMC electronic health records of in-hospital and out-hospital medical charts respectively, to identify all relevant subsequent medical visits within 30 days of the indexed admission. These electronic health records cover the entire UPMC healthcare network which means that we were able to access relevant follow-up data even if the patient was readmitted to a different centre.

We used the automatically-stamped date and time of the EMS call from the EMS electronic patient care record programme (emsChart) to determine the time-of-day and day-of-week of the chest pain encounter. These data are automatically imported into the prehospital record from a computer-aided dispatch programme at the EMS call centre. To determine the exact onset of symptoms in patients with acute MI, an independent reviewer systematically reviewed the medical notes (eg, history of present illness) to determine the duration of symptoms and to manually compute the time of onset of symptoms as previously described in literature.⁹ We defined weekend onset from Friday at 5 PM to Sunday at midnight. We defined seasonal onset rounded to months as follows: winter (December 1^st to February 28^th), spring (March 1^st to May 31^st), summer (June 1^st to August 31^st) and fall (September 1^st to November 30^th), and analysed the distribution for a single year only to avoid double counting (1 September 2013 to 31 August 2014).

Statistical analysis

We report values as mean±SD for normally distributed variables, as median (25^thto 75^th percentile) for non-normally distributed variables, or n(%) for categorical variables. We log transformed clinically important variables (ie, peak troponin) to approximate the normal distribution when appropriate. We tested the diurnal, weekly and seasonal variations in the number of events using one-sample, goodness-of-fit, χ². Differences in distribution between various groups (acute MI vs non-MI or STEMI vs NSTEMI) were evaluated using independent samples X². The differences in peak troponin level between subgroups with STEMI and NSTEMI in relation to time-of-day were evaluated using two-way analysis of variance. Multivariate predictors of peak troponin (continuous response variable) were evaluated using generalised linear equation modelling, and the multivariate predictors of MACE (binary response variable) were evaluated using logistic regression. Important clinical variables significant in the univariate model for each outcome variable were entered in the multivariate model. Time of day, day-of-week and seasons were evaluated in the univariate model and if significant were entered in the multivariate model. All analyses were completed using SPSS V.24 (IBM SPSS Software, Armonk, New York) and alpha error was set at 0.05 for two-sided hypothesis testing.

RESULTS

Our sample included 2065 subjects with chest pain (mean age 56, SD 17 years, 58% male). Hypertension was the most prevalent comorbidity (50%), followed by known coronary artery disease (23%) and diabetes mellitus (18%). Figure 1 shows the diurnal, weekly and seasonal variations in chest pain transported by EMS. The frequency of chest pain cases varied with time-of-day (p=0.001, figure 1A) and day-of-week (p=0.001, figure 1B), but not season (p=NS, figure 1C). Frequency of chest pain encounters increased from 9 AM to 2 PM, with a peak at 1 PM and nadir at 6 AM. Frequency of chest pain encounters increased from Saturday nadir to Thursday peak. The diurnal variations across day-of-week and seasons are presented in the online supplementary figure 1. As noted in this figure, the afternoon peak (12:00 to 18:00) of chest pain encounters was most noticeable on Fridays and Sundays. On the other hand, there was a sharp increase in chest pain encounters on mornings (6:00 to 12:00) during the Spring season.

Figure 1.

Diurnal, weekly and seasonal variations in chest pain patients transported by EMS. This figure shows the diurnal (A), weekly (B) and seasonal (C) variations in the time of presentation in patients with chest pain transported by EMS. EMS, emergency medical services.

Around one-third of patients had undifferentiated musculoskeletal chest pain, and another third had non-ischaemic cardiopulmonary aetiologies (eg, pulmonary embolism). More importantly, a total of 155 subjects (7.5%) had a final diagnosis of acute MI (age 64±16 years; 58% male). Table 1 summarises the demographic and clinical characteristics of this group. Coronary risk factors and chronic comorbidities were very common (up to 70%) and the majority of subjects presented with typical chest pain (96%). Figure 2 compares the diurnal variations in encounters of subjects with acute MI versus those with non-MI related chest pain. There was no difference in distribution (Pearson X²=23.6, df=23, p=0.426), suggesting that chest pain generally follows a diurnal onset similar to that observed in patients with acute MI.

Table 1.

Demographic and clinical characteristics of patients with acute MI

Clinical characteristics	(n=155)
Age (years)	64±16
Male sex	89 (58%)
Black race	45 (29%)
Past medical history
Ever smoked	94 (61%)
High cholesterol	81 (52%)
Hypertension	110 (71%)
Diabetes mellitus	50 (32%)
Known CAD	62 (40%)
Known heart failure	22 (14%)
Prior MI	43 (28%)
Prior PCI/CABG	50 (32%)
Duration of symptoms
<2 hours	64 (41%)
2–6 hours	55 (36%)
>6 hours	36 (23%)
Presenting vital signs
Heart rate	80 (65–95)
Respiratory rate	19 (17–22)
Oxygen saturation	97±3
Systolic blood pressure	139±27
Pain level	5.1±3.6
Diagnostic workup
Peak conventional troponin I level (ng/ml)	8.5 (1.5–36.1)
Glucose (mmol/L)	7.7 (6.2–10.2)
Creatinine (mg/dL)	1.0 (0.8–1.2)
Ejection fraction	55±12
Angiographic findings
LAD culprit lesion	85 (55%)
LCX culprit lesion	48 (31%)
RCA culprit lesion	64 (41%)
Course of hospitalisation
Length of stay (days)	3.2 (2.3–5.2)
Type of acute MI
STEMI	83 (54%)
NSTEMI	72 (46%)
PCI performed	131 (85%)
CABG performed	14 (9%)
30-day MACE	48 (31%)

Values are mean±SD; median (25^thto 75^th percentiles); or n(%).

CABG, coronary artery bypass grafting; CAD, coronary artery disease; LAD, left anterior descending artery; LCX, left circumflex artery; MACE, major adverse cardiac events; MI, myocardial infarction; NSTEMI, non-ST segment elevation myocardial infarction; PCI, percutaneous coronary intervention; RCA, right coronary artery; STEMI, ST-segment elevation myocardial infarction.

Figure 2.

Relationship between diurnal variations in chest pain and incidence of acute MI. This figure compares the diurnal variation in the time of presentation in patients with acute MI against those with non-MI related chest pain.EMS, emergency medical services, MI, myocardial infarction.

Figure 3 compares the diurnal, weekly and seasonal variations of onset of symptoms based on each subtype of acute MI. Among subjects with STEMI, there was a significant difference in frequency based on time-of-day, with a peak onset of 10 AM, but no differences based on day-of-week and season. Among subjects with NSTEMI, there was a significant difference in frequency based on time-of-day, with a peak onset of 10 PM, but no differences based on day-of-week and season.

Figure 3.

Diurnal, weekly and seasonal variations in acute myocardial infarction onset. This figure shows the diurnal (A), weekly (B) and seasonal (C) variations in the onset of symptoms in those with STEMI versus those with NSTEMI. MI, myocardial infarction; NSTEMI, non-ST segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction.

Finally, there was a total of 82 adverse events occurring in 48 out of 155 patients with acute MI (31%), including in-hospital death (n=9), acute heart failure (n=27), cardiogenic shock (n=8), cardiac arrest (n=17), mechanical ventilation (n=13), post-discharge re-infarction (n=6) and post-discharge death (n=2). Table 2 summarises the univariate and multivariate predictors of the secondary study outcomes in subjects with acute MI. A past medical history of hypertension, coronary artery disease and prior MI were associated with larger infarct size in univariate but not in multivariate analysis. Pain score on presentation, the presence of an left anterior descending artery culprit lesion on angiogram, and STEMI events with 12 PM to 6 PM onset were significant and independent predictors of infarct size in the final multivariate model (figure 4). On the other hand, a past medical history of heart failure, ischaemic time >6 hours, faster heart rate and lower oxygen saturation on presenting vital signs were associated with 30-day MACE in univariate but not in multivariate analysis. Elevated initial glucose level and MI events with winter/spring onset were significant and independent predictors of MACE in the final multivariate model.

Table 2.

Predictors of specific outcomes in patients with acute MI (n=155)

	Multivariate β (95% CI)	P value
Infarct size
Hypertension	0.11 (−0.19 to 0.46)	NS
Known coronary artery disease	0.14 (−0.29 to 0.54)	NS
Prior myocardial infarction	0.12 (−0.30 to 0.58)	NS
LAD culprit lesion	0.48 (0.16 to 0.74)	0.001
STEMI with afternoon onset*	0.80 (0.13 to 1.46)	0.019
30-day MACE
Known heart failure	0.32 (−0.9 to 1.71)	NS
Ischaemic time >6 hours	0.45 (−0.5 to 1.41)	NS
Presenting heart rate	0.01 (−0.01 to 0.02)	NS
Presenting O2 saturation	–0.09 (−0.26 to 0.08)	NS
Glucose level (per 1 mg/dL)	0.01 (0.004 to 0.016)	0.015
Winter/spring presentation	1.01 (0.12 to 1.91)	0.028

^*Afternoon onset defined as 12 PM to 6 PM.

LAD, left anterior descending artery; MACE, major adverse cardiac events; MI, myocardial infarction; O2, oxygen; STEMI, ST-segment elevation myocardial infarction.

Figure 4.

Interaction between time-of-day and MI type in terms of infarct size. This figure shows the diurnal variation of infarct size (peak troponin level) with relation to myocardial infarction subtype (STEMI vs NSTEMI). Log transformation was used to approximate normal distribution in the positively skewed distribution of peak troponin. Error bars represent ±2 SE of the mean. P value based on the interaction term (time x MI type) of two-way ANOVA. ANOVA, analysis of variance; MI, myocardial infarction; NSTEMI, non-ST segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction.

DISCUSSION

In this study, we characterised the diurnal variations of inflow of chest pain and the likelihood of acute MI in patients transported by EMS. Our findings can be summarised in three main messages. First, the inflow of chest pain cases transported by EMS increases between 9 AM and 2 PM, with a peak onset of 1 PM and nadir of 6 AM. Second, this diurnal inflow of EMS-activated chest pain encounters was not generally different from the diurnal inflow observed in acute MI presentations. However, contrary to our hypothesis, the likelihood of acute MI remains the same throughout the day, with similar prevalence of acute MI among chest pain encounters across all times of day. Thus, the observed peak in the inflow of acute MI in the morning is likely driven by the sheer number of chest pain encounters during these hours. Third, cases with STEMI and NSTEMI have different diurnal inflow patterns, with peak onsets of 10 AM and 10 PM, respectively. STEMI events with afternoon onset were associated with larger infarct size, whereas acute MI events presenting in winter and spring seasons were associated with excess risk of 30-day MACE. To our knowledge, this is one of few studies to characterise and correlate the diurnal inflow of chest pain with the diurnal likelihood of acute MI and the incident of subsequent dire outcomes in patients transported by EMS.

A morning peak of acute MI is reported in various observational studies.^10,11 Although we did find a similar morning peak of acute MI in our study, this was primarily driven by the higher inflow of chest pain patients during morning hours, and was not associated with an increased likelihood of acute MI, which remained similar throughout the day. Other studies also found a morning peak in various acute cardiac complaints,^12,13 and sudden cardiac arrest events.¹⁴ The reasons for such morning peak in chest pain, acute MI and other cardiac complaints is unknown and is most likely multifactorial. Mahmuda et al recently developed a grounded theory to explore why people call EMS services.¹⁵ They noticed that exacerbation of illness in patients with chronic comorbidities are key determinants in patients’ decision to call EMS. A post-hoc analysis of our data shows that, compared with the nadir period, patients presenting during peak period were more likely to have a significant cardiac history (30% vs 23%, p=0.032) and more likely to be older (59±16 vs 54±18, p=0.001). It can then be speculated that symptom exacerbations that build up a few hours after waking up and starting the activities of daily living, especially among the elderly with chronic comorbidities, might partially explain the peak of chest pain calls attended by EMS between 9 AM and 2 PM observed in this study.

We further compared the diurnal variability between STEMI and NSTEMI events and noticed a significant difference. STEMI events had a morning peak at 10 AM whereas NSTEMI had an evening peak around 10 PM. The majority of prior studies either exclusively included patients with STEMI or studied acute MI as a whole.^3,9,11 The reason behind our observed discrepancy remains unknown, but the fact these previous studies utilised Creatine Kinase MB assays to detect MIs, compared with the more sophisticated current guideline-recommended troponin assays, makes it possible that a considerable number of NSTEMIs were undetected or considered unstable anginas at that time,¹⁶ and therefore not included in their analysis. We speculate that the diurnal variability between STEMI versus NSTEMI could be related to the distinct clinical pathophysiology associated with each subtype of infarct. STEMI is largely known as a complete occlusion of a coronary artery due to plaque rupture. Thus, the cumulative increase of circulating levels of homoeostatic and clotting agents throughout midday¹⁷ would explain why STEMI events are triggered during the day. On the contrary, NSTEMI is associated with progressive worsening of partial coronary occlusion in patients with multivessel disease. Physical exertion could trigger acute MI,¹⁸ especially within the first 24 hours, which would possibly explain why NSTEMI events are more frequently observed at night. These speculations can be supported by a few studies that noticed a biphasic pattern of MI onset, with two peaks separated by 12 hours.^19,20 These studies interestingly noticed that patients presenting with MI at night were older, and more likely to have a prior history of MI, peripheral vascular disease or stroke, all of which are known clinical characteristics of the NSTEMI population.⁶

Similar to previous studies, we noticed that infarct size is influenced by the time of symptom onset. We observed the largest infarct size in patients with STEMI presenting in the afternoon, even after controlling for other demographic and clinical variables. Although we did not control for door-to-balloon time, similar diurnal pattern was observed in patients with NSTEMI who did not receive immediate percutaneous coronary intervention. This suggests that our findings might have a plausible physiological basis. Prior studies have described that circulating fibrinogen, fibrin D-dimer and C-reactive protein have an afternoon peak (2 to 3 PM) in middle age adults.¹⁷Compared with previous studies, infarct size was found to be largest in patients presenting around midnight or early morning,²¹compared with afternoon in our study. One methodological difference in our study that could explain such discrepancy in findings is that we only enrolled patients calling EMS for chest pain. Prior studies primarily looked at unselected patients hospitalised with acute MI. Frequent EMS users who call EMS are known to be older with more prevalent comorbidities compared with those who self-transport to the ED.²²

Our data also show that seasonal variability of MI onset is associated with 30-day MACE, with patients presenting in winter and spring seasons having significantly worse outcomes. The variability in terms of post MI adverse events has been previously reported, with higher mortality rates occurring during the winter season across multiple climates.^23,24 Multiple mechanisms of such excess risk have been suggested, including an increase in sympathetic tone and platelet aggregation.²⁵

This study has some important clinical implications. First, the similar likelihood of a diagnosis of acute MI throughout the day suggests that prehospital providers and clinicians should always have a high index of suspicion when evaluating chest pain patients, regardless of time of presentation. The morning peak seems to be primarily driven by the high volume of chest pain cases presenting during these hours, implying that the pretest probability remains the same throughout the day, therefore, time of presentation should not directly alter patient evaluation or management. Second, STEMI events, especially those with largest infarct size, are more likely to present to the ED during ‘rush’ hours and ED overcrowding periods. EMS and hospital systems need to be aware of this issue to plan and implement strategies to avoid system-related delays in door-to-balloon time. Specifically, off-hours and peak-time challenges in meeting guideline-directed prehospital FMC to device times make understanding the distribution of patients presenting with chest pain over the course of the day important. Our findings suggest hospitals should consider evaluating their individual distribution of patients presenting with chest pain over the course of a day to optimise the allocation of staff and other resources, which could potentially benefit from adjustments of only a couple of hours in the afternoon or evening periods. Third, the rate of adverse events is higher in patients presenting during winter and early spring season, independent of MI type. Such patients could need closer follow-up and more aggressive preventive therapy to improve their clinical outcomes.

Finally, this study has some limitations. First, although the prevalence of acute MI events was consistent with the expected distribution in real-world clinical populations, the absolute number of MI events was relatively small. This could have led to a larger margin of error in estimating the diurnal variability. Second, despite adjudicating for the type of MI in terms of STEMI versus NSTEMI, we did not further analyse the data with respect to whether the MIs were in fact Type I or Type II MIs. While Type I MI is caused by an atherothrom-botic coronary artery disease and is usually precipitated by an atherosclerotic plaque disruption, Type II MI, on the other hand, occurs in the context of a mismatch between oxygen supply and demand to the heart when no acute atherothrom-botic plaque disruption is involved (ie, acute blood loss or tachyarrhythmia). The difference in the pathophysiological mechanism of these two types of MIs could lead to a difference in onset and distribution of presenting cases, which we were not able to describe in our study.⁷ Third, we used retrospective chart review to estimate the time of symptom onset in patients with acute MI. This approach, although acceptable in literature, would lead to some inaccuracies in the results. Finally, 30-day MACE was based on the review of the electronic health records system of UPMC healthcare network, meaning we could have missed events that occurred outside of our catchment area, for example, events occurring during travel of patients or those who otherwise live in a different city and happened to be in town during their initial visit.

CONCLUSLON

In this study, we examined the diurnal variations of inflow of chest pain encounters transported by EMS with relation to the diurnal likelihood of acute MI. We found that EMS-activated chest pain encounters follow a diurnal pattern with a peak onset of 1 PM and nadir of 6 AM. This diurnal pattern was proportionately similar to that observed with acute MI onset, however, the likelihood of acute MI remains the same throughout the day, with similar prevalence of acute MI among EMS-activated chest pain encounters across all times of day. In addition, the inflow of acute MI cases followed two peaks that was mainly influenced by the type of MI: morning peak for STEMI and night peak for NSTEMI. More importantly, infarct size and adverse cardiac outcomes were found to be independently associated with the diurnal and seasonal onset of acute MI. These findings suggest that while the time of presentation does not influence the pretest probability of diagnosing an Acute MI, however, patients with MI’s presenting during peak hours have worse outcomes. This suggests that prehospital providers, clinicians and hospital systems need to operate at maximum efficiency during these times.

Key messages.

What is already known on this subject

• It is well documented that the onset of acute MI, including subsequent cardiac arrests, follows a circadian pattern with the majority occurring during morning hours.

• It is unknown if EMS-activated chest pain calls follow a similar diurnal pattern, which may indicate potential for prevention of dire outcomes and EMS systems improvement.

What this study adds

• In this secondary analysis of a prospectively collected data, we found that EMS-activated chest pain encounters follow a diurnal pattern that mirrors actual MI events with a peak onset of 1 PM and nadir of 6 AM.

• ST-elevation MI had a peak onset of 10 AM whereas non-ST-elevation MI had a peak onset of 10 PM.

• Both infarct size and 30-day adverse cardiac outcomes were associated with the diurnal and seasonal onset of acute MI.