The first stage of the Arksey and O’Malley framework requires identification of an area of interest and an exploration of these concepts [17]. This stage of the scoping review framework aims to guide the search strategy. The research questions pertinent to this review were as follows:

What is the diagnostic time in patients with AD?

What factors influence diagnostic delay in patients with AD?

To ensure that sufficient information was obtained, the following databases were searched: PubMed, Web of Science, Cochrane Library, Bing, Wanfang Chinese, and Zhiwang or China National Knowledge Infrastructure Chinese database. The search strategy included a combination of the National Library of Medicine Medical Subject Headings (MeSH), in addition to exploring key words representing the concepts of “aortic dissection”, “diagnostic time”, and “diagnostic delay”. There were no restrictions on the language, date, or type of study.

A total of 3967 records were found by searching the databases; 953 duplicate records were deleted, and 27 records met the inclusion criteria according to the screening process. The screening process and the reasons for excluding studies are presented in Fig. 1.

There was a total of 27 articles included in this review of the diagnostic time for patients with AD (Table 1, Ref. [2, 5, 6, 9, 10, 11, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39]). Table 1 shows the details regarding first author, publication year, study design, patient period, patient source, patient type, number of patients, and diagnostic time. The time from symptom onset to diagnosis ranged from 40.5 min to 84.4 h, and the time from hospital presentation to diagnosis ranged from 0.5 h to 25 h.

Seven studies showed the predictors of delayed AD diagnosis using univariate analysis (Table 2, Ref. [5, 21, 23, 25, 31, 32, 40]). As shown in Table 2, the risk factors in relation to demographics and medical history were the female sex, North American versus European geographic location, initial AD, and transfer [21, 31, 32, 40]. In addition, TAAAD patients with preoperative coronary angiography (CA) were more likely to have a definitive diagnosis, as the time from symptom onset to diagnosis was longer among preoperative CA than among patients with non-preoperative CA. Preoperative CA is infrequently performed on patients with TAAAD, except, occasionally, on patients at high risk for myocardial ischemia, which may worsen the surgical outcome [23]. Regarding signs and symptoms, patients with chest and back pain, especially abrupt or radiating pain, were more frequent in the group with an early diagnosis. In contrast, syncope was more prevalent in patients with a delayed diagnosis [5, 25, 32]. These differences were deemed statistically significant.

Seven of the selected studies examined predictors of delayed AD diagnosis by employing multivariate analysis, as shown in Table 3 [2, 9, 20, 27, 29, 30, 39]. There was no clear definition of the duration of delayed diagnosis. Five studies used the 75th percentile as the cutoff time, and delayed diagnosis was defined as the time from presentation to diagnosis $>$75th percentile [9, 20, 29, 30, 39]. The cut-off values ranged from 4.5 h to 12 h. Only Du et al. [27] deemed a median presentation-to-diagnosis time of more than 12 h 40 minutes to be classified as a delayed diagnosis. Using multivariate analysis, Rapezzi et al. [20] found that age 70 years, dyspnea, pleural effusion, systolic blood pressure (SBP) $\le$105 mmHg, troponin positivity, and ACS-like electrocardiogram (ECG) results were associated with an increased likelihood of delayed diagnosis. Harris et al. [2] reported that delays in AD diagnosis occurred in women, those with an absence of atypical symptoms that were not abrupt or did not include chest, back, or any pain, patients with febrile diseases, those with an SBP $\ge$105 mmHg on admission, or those who transferred from a nontertiary care hospital. In addition, Hirata et al. [9] revealed that walk-in visits to the ED were the only predictors of delayed diagnosis. Du et al. [27] suggested that patients with dyspnea, troponin positivity, and ACS-like ECG findings were more likely to have a delayed diagnosis. In two studies by Vagnarelli et al. [29, 30], excessive risk was related to dyspnea, pleural effusion, troponin positivity, and a combination of troponin-positive and ACS-like ECG abnormalities, whereas back pain, pulse deficit, and SBP 90 mm Hg were protective against delayed diagnosis. In a recent study by Lim et al. [39], increased age, chest and back pain at presentation, evidence of malperfusion syndrome, and a history of congestive heart failure were associated with a decreased risk of delayed diagnosis. In contrast, a history of hyperlipidemia and a distressed communities index $>$60 were associated with an increased risk of diagnostic delay.

Several studies have enumerated the factors associated with a delayed diagnosis of AD [2, 20, 21, 31, 39, 40]. Demographic and medical history predictors included the female sex, age 70 yrs, North American versus European geographic location, being the initial AD presentation, history of congestive heart failure, history of hyperlipidemia, distressed communities index $>$60, walk-in visit to the ED, transfer from a non-tertiary care facility, and preoperative CA.

More women than men waited for more than 24 h before diagnosis, and this was attributed to atypical presentation symptoms. Women appear likely to experience less typical or less severe pain perception, with less frequent abrupt onset and more frequently observed alterations in consciousness, partly accounting for the longer delay in diagnosis [40]. Harris et al. [2] also reported that women were diagnosed more slowly.

Patients 70 years of age had a higher risk of delayed diagnosis. This association may be attributed to a lower index of diagnostic suspicion of spontaneous AD in patients with fewer strong age-related risk factors and comorbidities [20]. Furthermore, in agreement with previous studies, Lim et al. [39] found that patient age was associated with delayed diagnosis.

Raghupathy et al. [21] observed a significant delay in presentation and diagnosis of AD in a North American patient cohort compared to that in European cohorts. North Americans have a higher percentage of atypical presenting symptoms and signs, ECG findings that suggest acute ischemia, and a tendency toward more normal-appearing chest radiographs. This may have contributed to the delayed diagnosis. In addition, differences were observed in the choice of the initial imaging test for patients between North American and European IRAD centers. More European centers use computed tomography (CT) scans as the first diagnostic test, obtaining the most readily available imaging data to confirm the diagnosis accurately and rapidly.

Isselbacher et al. [31] reported that compared to initial AD, the time from the onset of symptoms to diagnosis was significantly shorter in patients with recurrent AD. Therefore, recurrent AD is a protective factor against delayed diagnoses, probably because patients with recurrent AD have a better understanding of the disease and can reach the hospital more quickly when recurrence occurs. Their history of AD may also help doctors make a rapid diagnosis.

A history of congestive heart failure (CHF) was observed to be associated with a decreased risk of delayed diagnoses for AD [31]. Conversely, the presentation of CHF significantly prolonged AD diagnosis [2]. A larger sample size is required for further validation of this finding. In contrast, a history of hyperlipidemia and residence in a high-distressed communities index (DCI) zip code were associated with an increased risk of diagnostic delay [39]. Hyperlipidemia may increase the clinical suspicion of ACS. The DCI is an aggregate measure of community-based socioeconomic status (SES). To reduce diagnostic delay, improving our understanding of the patient, the patient environment, and the healthcare system treating this condition will be critical.

Walk-in visits to the ED were associated with a delayed diagnosis of AD [9]. The clinical manifestations of AD are diverse. If a patient with AAD presents to the ED with symptoms mimicking those of other diseases, the correct diagnosis may be missed or delayed. The walk-in mode of admission was also the strongest predictor of misdiagnosis in a study by Kurabayashi et al [11]. Although clinicians tend to regard walk-in patients as less likely to be seriously ill, the significance of the findings related to ED walk-in and delayed diagnosis of AD need to be remembered.

Strauss et al. [32] showed that patients with delayed diagnoses were more likely to be transferred from a referral hospital. Harris et al. [2] also found that delays in AD diagnosis occurred in patients transferred from non-tertiary hospitals. Owing to the high risk and complexity of AD, most non-tertiary hospitals are not equipped to treat AD, and the referral rate is extremely high, ranging from 68.2% to 79.0% [10, 21, 40, 41, 42]. The medical practice experience of clinicians, particularly related to aortic emergencies, may be especially relevant. It is not feasible to perform CTA for all ED patients presenting with chest or back pain, especially in non-tertiary hospitals. In a study by Pare et al. [28], patients with ascending AD who underwent emergency physician-focused cardiac ultrasound (EP FOCUS) were diagnosed more quickly. In addition, FOCUS is a rapid, noninvasive test, and Pare et al. [28] recommended that evaluation of the aorta be performed in patients with symptoms suggestive of AD. Improved physician awareness and recognition of AD and prompt transport are both important. Inter-hospital transfer requires coordination between hospitals, and a systematic approach to the diagnosis and management of AD will need to be developed and used as a reference. This includes the creation of regional networks where defined protocols allow for the most expedient diagnosis and transfer of patients with AD to Aortic Centers of Excellence for definitive treatment.

Ramanath et al. [23] observed significantly increased time delays from symptom onset to diagnosis during preoperative CA before the surgical repair of TAAAD. Fortunately, preoperative CA was not associated with significant changes in in-hospital or long-term mortality rates.

Patients presenting without typical symptoms of AD or hemodynamic instability are more likely to experience diagnostic delays and be initially treated for more common etiologies. The median interval from symptom onset to diagnosis was 29 h in AAD with no pain and 10 h in patients with pain [5]. When patients do not have typical pain, clinicians may not initially consider AD, and this delays the diagnosis. A delayed diagnosis of painless AD is probably responsible for the higher mortality rate observed in patients without pain. This is consistent with the results reported by Tolenaar et al. [25]. Furthermore, previous reports have shown that 6.4%–15% of patients with AAD presented without severe or worst-ever pain [5, 24]. Clinicians should be aware of this rare condition.

Chest and back pain, especially when abrupt or radiating, occurred more frequently in the early diagnosis group. In contrast, syncope was more prevalent in patients with a delayed diagnosis [32]. In a study by Vagnarelli et al. [29, 30], patients with back pain were identified earlier. Similarly, typical presenting symptoms, such as chest and back pain expedited the diagnostic process [39]. Diagnostic delays occurred in patients with atypical symptoms that were not abrupt or did not include chest, back, or any other pain [2]. Moreover, fever at presentation is not a common symptom of AD, and so may lead to an alternative diagnosis [2].

In a study by Rapezzi et al. [20], two strong clinical confounders appeared to be pleural effusion and dyspnea which were associated with a three to fourfold elevated risk of delayed diagnosis. In a study by Vagnarelli et al. [29, 30], the increased risk of diagnostic delay was also related to dyspnea and pleural effusion. These two clinical presentations may prompt clinicians to formulate a primary diagnostic hypothesis for pulmonary or cardiac diseases.

A low SBP (105 mmHg) was associated with a significantly decreased risk of diagnostic delay [20]. Likewise, an admission SBP $\ge$105 mmHg delay diagnosis [2]. In another study, SBP 90 mmHg was associated with earlier recognition of AD [30]. Additionally, the presence of malperfusion syndrome expedited the diagnostic process [39]. Pulse deficits were protective from delayed diagnoses [2, 29]. In patients with life-threatening limb ischemia, shock, syncope, or altered consciousness, the diagnosis of AD was achieved more quickly because multiple diagnostic tests were conducted concurrently [2].

Troponin positivity and ACS-like ECG lead to delays in the diagnosis of AD [20]. This observation is consistent with the findings of reports by Vagnarelli et al. [30] and Du et al. [27]. An initial suspicion of ACS was the most common reason for a missed or delayed diagnosis of AD [43]. An ECG is routinely performed when patients present with chest pain. The incidence of AAD is far lower than that of ACS [3]. In the absence of a specific biomarker for AD, troponin positivity is used, given the high frequency of ACS among emergency patients and shared causal risk factors for AAD and ACS. Notably, in many cases of AD, electrocardiographic repolarization abnormalities and/or increased troponin levels reflect the coexistence of myocardial ischemia [20]. These findings emphasize the need for clinicians to suspect AD whenever plausible, even in cases where the initial diagnostic hypothesis is ACS. The American College of Cardiology/American Heart Association aortic guidelines suggest that clinicians should focus on high-risk conditions that place patients at risk as well as typical historical and examination features to diagnose AD earlier [43].