Epidemiological Patterns of Acute Type-A Aortic Dissection in Regional New South Wales - A 10-year Analysis

doi:10.21203/rs.3.rs-2987473/v1

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Epidemiological Patterns of Acute Type-A Aortic Dissection in Regional New South Wales - A 10-year Analysis

https://doi.org/10.21203/rs.3.rs-2987473/v1

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Background:

Acute Aortic Dissection (AD) is a surgical emergency with significant mortality without prompt diagnosis and operative intervention. The management is time critical and regional Australia represents an area of interest owing to its large distances and often paucity of resources. No previous studies examining Type-A AD in regional Australia have been done. The aim of this study is to illustrate the epidemiological trends in Type-A AD within a regional population of Australia. The primary outcomes are prevalence and mortality. The secondary outcomes are assessment of risk factors, challenges in diagnosis and associated complications.

Methods:

A retrospective analysis was undertaken in the Hunter New England (HNE) health district of New South Wales (NSW), Australia. We retrospectively examined data from 2010 to 2020 in the population of the Hunter New England health district. The data was analysed using Microsoft Excel and Statistical Package for Social Sciences (SPSS).

Results:

The prevalence of Type-A AD in the HNE was 1.47 per 100,000 and mortality was 2.12 per 100,000 which was lower compared to previous studies. Five percent of patients identified as Aboriginal and Torres Strait Islander. Combined risk factors of smoking and hypertension, postoperative CVA and misdiagnosis demonstrated higher mortality which were statistically significant (p < 0.05).

Conclusion:

This study is the first study to illustrate Type-A AD in regional Australia. The epidemiological trends, analysis and risk factor profiles present a solid foundation for future prospective studies to be based on to ultimately allow better patient outcomes.

Aortic Dissection

Acute Aortic Syndrome

Stanford Type-A

Epidemiology

AD is a rare life-threatening pathology associated with a high morbidity and mortality. Owing to its rapid evolution in an acute setting, it remains a much-feared emergency presentation worldwide¹. Aortic dissection involving the ascending aorta is most lethal with mortality rising 1-3% per hourwithout surgical intervention^2-4. There are limited large multicentre observational registries which include International Registry of Acute Aortic Dissections (IRAD), German Registry for Acute Aortic Dissection Type-A (GERAADA) and the Nordic Consortium for Acute Type-A Aortic Dissection (NORCAAD). Australian studies are scarce with no literature representing regional areas^2-5.

Aortic Dissection

AD can be differentiated into classic/ spontaneous, limited intimal tear or iatrogenic/ traumatic. Classic or spontaneous aortic dissection is initiated with the formation of a tear in the aortic wall’s intimal layer, thereby exposing the underlying media layer to the pulsatile pressure of blood flow within the aortic lumen. Longitudinal cleaving of the aortic wall media causes the dissection, typically antegrade, from the intimal tear in the direction of the forwarding force of blood flow^6-9. This results in the division of the aortic lumen into a True Lumen (TL) and a False Lumen (FL), of which 90% of cases are communicated through entry and exit sites within the dissection flap¹⁰. Ischemic complications are a result of dynamic compression due to distension and pulsatile pressures within the FL compressing and narrowing the TL⁹. Aortic Regurgitation (AR), Acute Coronary Syndrome (ACS) and cardiac tamponade are potential complications of retrograde extension^6-8,10.

Limited Intimal Tear

Limited intimal tear or “limited intimo-medial tear” is a form of rare AD variant due to its low incidence, difficulty in detection with imaging and inconsistent terminology used to describe it across the English literature^7,8,10. It is defined as stellate or linear tear of the aortic intima and underlying superficial media thereby exposure of the deeper aortic media or adventitia in the absence of dissection⁷. They are commonly misreported as atherosclerotic aneurysms or pseudoaneurysms and are found intraoperatively in 5% of patients undergoing aortic aneurysm repair^7,8.

Intramural Hematoma (IMH)

Aortic IMH washistorically described by Krukenburg as a hematoma confined to the aortic wall media where the absence of an intimal tear was pathognomic. Non-enhanced CT imaging categorize IMH as a hyperdense, crescenteric lesion of the aortic wall without evidence of an intimal tear and either a retrograde or antegrade extension of hematoma⁸. Ambiguity surrounding IMH reflects either a radiological finding associated with a range of acute aortic diseases, a dissection variant or a separate disease entity in itself⁷. The author supports that IMH should be strictly considered as a non-specific but urgent radiological finding irrespective of underlying pathogenesis^7,8,10.

IMH as an AD variant is supported by a shared pathogenesis, demographics, clinical presentation and associated risk factors^6,7. However, there is uniform agreement upon the difference between IMH and AD as the presence or absence of a flap. 70% of cases diagnosed with IMH have identified intimal tears surgically and radiographically although 4% in an autopsy series exhibited no evidence of a primary intimal tear (PIT)^7,10,11. The traditional pathogenesis of spontaneous rupture of the vaso vasorum into the aortic media and subsequent thrombosis due to absent flow is an alternate pathogenesis albeit with limited evidence¹². Controversy between medical vs. surgical management have been described where the West is in unanimous support for immediate surgical intervention compared to parts of the East with variable views and conservative management have been reported with conflicting results ^7,8,10.

Penetrating Aortic Ulcer (PAU)

PAU is defined as an atherosclerotic ulceration that penetrates through a variable thickness of aortic intima, through the internal elastic lamina and haemorrhage into the aortic media. More than 90% of PAU occur in the descending thoracic aorta where atherosclerotic changes are most common⁷. PAU accounts for less than 5% of all AD and involvement of the ascending aorta is managed surgically¹⁰.

Periaortic Hematoma

Periaortic hematoma, or contained rupture, located around the site of aortic injury is associated with higher rates of shock, cardiac tamponade and syncope. IRAD reports higher mortality (33% vs 20%) in these patients³.

Impending Rupture of Aortic Aneurysm

Ueda et al suggest the inclusion of impending rupture of Aortic Aneurysm (AA) in Acute Aortic Syndrome (AAS) despite not being included in the original classification by Vila-costa¹³. A ‘true’ or ‘degenerative Aortic Aneurysm’ refers to dilatation of all layers of the aortic wall due to loss of elastin and smooth muscle. The argument supporting inclusion into AAS is largely based on its indistinguishable clinical presentation and diagnostic uncertainty on imaging.

Acute Aortic Syndrome

AAS traditionally comprises of AD, IMH, PAU however, the inclusion of impending rupture of AA of any aetiology and trauma is controversial^7-9. The important discussion to be had is how the term “syndrome” in this context is approached and by extension how we define AAS. It can either be a group of symptoms which consistently occur together therefore, compatible with the inclusion of impending rupture of AA. Alternatively, if we consider AAS as a condition characterized by a group of symptoms, the inclusion of all above mentioned becomes difficult and propagates unnecessary confusion. Application in the clinical context to aid diagnosis and prompt management is by far most important and the utilisation of AAS is better implemented with this in mind.

Classification

Classification of AD involves two fundamental anatomical variables which include origin and propagation of the FL. Commonly used systems in current practice include the DeBakey and Stanford classifications⁷. The 1970 Stanford Classification is the most used owing to its simplicity and is categorized based solely on the presence (Type-A) or absence (Type-B) of the dissection flap in the ascending aorta, irrespective of the location of the PIT^7-9,10. The Mount Sinai Medical Centre in New York have proposed a modified Stanford classification (see Table 1) which includes the addition of subcategories to incorporate all possible anatomical combinations of origin and propagation. Subcategorization conveys clinically relevant information including differences in clinical presentations, demographics and risk of rupture. This allows more consistent reporting in the literature and allows accurate comparisons between subtypes¹⁴. Majority of Stanford Type-A AD present in the hyperacute (<24hours), acute (1-14 days) and less commonly subacute (14-90 days) duration⁹. Chronic Type-A AD (>14 or >90 days) is a very rare and poorly understood process.

Epidemiology

Due to its rarity and high mortality, studies on AD are largely cohort studies. Population-based studies suggest an incidence rate of 2.5 to 3.5 per 100,000 people per year¹⁵. IRAD review concluded more than 60% of cases involve the ascending aorta and were distributed in a younger subset of patients (mean age 61.2 vs 66.3 years)⁶. The reported increase in incidence over time can be attributed to a combination of an aging population and improved diagnosis with imaging¹⁵. The proportions of dissections in patients over 75 years are estimated to reach 50% by 2030 and 57% by 2050 and may have profound implications on morbidity and mortality outcomes from previous as well as precluding a larger subset of patients from surgery⁶. These findings are supported by the GERAADA study.

Dinh et al is the only Australian AD study and calculated the incidence within NSW of 3.47 per 100,000 over 2017-2018. There were 273 cases of AD with a 30-day mortality of 35.53%¹. This study reported results of both Type-A and Type-B AD in an emergency department setting and results recorded without differentiation. There have been no studies representative of a regional, rural or remote setting.

Risk Factors

Risk factors for AD, or more accurately most associated factors, reflect a combination of inherited and acquired weakening of the aortic media and intimal disease. These include hypertension, old age, atherosclerosis, smoking, connective tissue disorder, bicuspid aortic valve and previous cardiac surgery, especially aortic surgery¹⁵.

IRAD reported 65% of patients were male and women were older at presentation (67 vs 60 years) as well as a vast majority of patients with systemic hypertension (72%) and atherosclerosis (31%). These commonly associated factors were less prevalent in patients under the age of forty and genetic predispositions were more apparent. Acute elevations in blood pressure by substances such as cocaine and methamphetamines as precipitating factors of AD have been described³. Links to circadian changes in blood pressure have been described with peak frequency reported between eight and nine in the morning and during winter corroborated with similar peak presentations in other acute cardiovascular presentations². Major predictors of thirty-day mortality were malperfusion, pre- and postoperative stroke or coma, acute kidney injury, massive bleeding and/ or transfusion, extensive dissection and surgery and cardiac tamponade or shock on presentation. Long term predictors of mortality included age, female gender and other comorbidity burden including coronary artery disease and diabetes³.

Global Burden of Disease

The most extensive study of Type-A AD's global and regional burden was studied by Sampson et al. from 1990 to 2010. Across 30 years, the authors studied regional deaths and years of life lost across 21 regions worldwide. The global mortality rate increased from the start of the study in 1990 to the end of the study 2010, 2.49 and 2.78 per 100,000, respectively¹⁶. The relative change in median death rate was +0.22 in developed nations versus +0.71 in developing nations across the period included in the study, alluding to the increasing Type-A AD burden in developing regions. In the study, men had a higher mortality rate from AD than women, and similar patterns were noted for years of life lost by sex in 1990 and 2010. At the regional level, the mortality rates and years of life lost increased consistently with advancing age across all 21 regions in both 1990 and 2010.

Our study aims to illustrate the epidemiological trends in Type-A AD within a regional population of NSW, Australia. The primary outcomes are prevalence and mortality. The secondary outcomes are assessment of risk factors, challenges in diagnosis and associated complications.

A retrospective study was undertaken of all cases with an ICD-10 diagnosis of Type-A AD in JHH from February 2009 to February 2019. Patient demographics, indigenous status, past medical history with a particular emphasis on known risk factors, time of the year, diagnostic modalities used, time to theatre data and mortality was collected. The data were analysed using Microsoft Excel and Statistical Package for Social Sciences (SPSS). The medial age with interquartile range was calculated. Chi-squared test for risk factors and their association with mortality was undertaken.

Demographics

Patient age at presentation ranged from 16 to 81 years, with a median age at 61 years old (IQR = 19.75). When categorized according to patient age by decade, the incidence was highest in the seventh decade (25.4%) of life with comparable results in both the eighth and sixth decades (23% and 24.6% respectively) of life (see Figure 1). Of all patients with Type-A AD, 25.4% (n=31) of patients were above the age of 70 years and 9.8% (n=12) were under the age of 40 years. Very young patients were majority male and very old patients were usually female. There was a male predominance with 69.7% (n=85) males, and 30.3% (n=37) were females. Females generally presented older with a mean of 63 years vs. 57 years in males. Of the 122 cases, 4% (n=5) of patients identified as Aboriginal and Torres Strait Islander (ATSI) and 117 as non-indigenous. There was a higher incidence noted in Summer (September – February) at 40.2% (n= 49) compared to Winter (June – August; 31.1%, n=38) and Spring (February – May; 28.7%, n=35). Prevalence was 1.47 per 100,000 per year. Patients aged 50-60 years had an incidence of 4.8 per 100,000 per year, which increased dramatically to 10.7 per 100,000 per year in patients over 60 years of age (see Table 2).

Risk Factors

There was a higher incidence of previous or active smoking history (53.8%, n=58) compared to no history of smoking (46.2%, n=54). Hypertension was present in over 50% of patients (56.7%, n=68) and 67.6% (n=46) were on a single antihypertensive agent, 18 (26.5%) were on two agents and 4 patients (5.9%) were on 3 or more agents. 25.4% of patients (n=31) were both previous and active smokers with hypertension. 7.3% (n=9) of patients had a known pre-existing aneurysm. Most patients did not have diabetes mellitus (87.7%, n=107), with only 15 patients having concurrent Type-2 Diabetes (12.3%) and no patients with Type-1 Diabetes. 3.3% (n=4) of patients had Marfan syndrome and this was the only congenital risk factor found in this cohort. Twenty-six patients (21.3%) had previous vascular disease. Other risk factors included the presence of atherosclerosis (16.4%, n =20), thoracic trauma (3.3%, n =4), and atrial fibrillation (11.5%, n=14). No patients were pregnant on presentation. There was one case as a result of iatrogenic injury during aortic cannulation for another procedure.

Patients with combined risk factors of smoking and hypertension yielded 34.78% mortality in comparison to patients who had neither which was statistically significant (p<0.05). In contrast, patients with isolated risk factors of smoking or hypertension had mortality of 12.5% and 15.6% respectively and did not produce statistically significant results when compared to the non-smoker and no hypertension subset of patients (p>0.05).

Diagnosis

Of the 122 patients, 24.1% (n=28) had ECG changes and 30.3% (n=37) had changes on a plain chest film. Widened mediastinum was the most common abnormality on plain chest film (14.8%, n=18) followed by cardiomegaly and pleural effusion. Eighteen (15.1%) patients had a serum troponin elevation. 9.8% of patients were misdiagnosed of which majority were treated as acute coronary syndrome and carried a 33.3% mortality compared to 12.7% in the correctly diagnosed group which was statistically significant (p<0.05). Misdiagnosed patients had a higher rate of reopening within 24 hours (16.7% vs 8.1%) due to postoperative bleeding and/or tamponade. Acute kidney injury was noted in 11.7% (n=14) patients and deranged liver function in 8.3% (n=10).

The diagnostic modalities utilised include transthoracic echocardiogram (23.8%; n=29), CT angiogram (73%, n=89) and coronary angiogram (3.3%, n=4). IMH accounted for 4.9% (n=6) of which all patients were found to have a primary intimal tear intra-operatively. There were no cases of PAU reported in this cohort. 118 patients were operated on at the single tertiary referral centre with 47 patients (38.5%) requiring inter-hospital transfer to the referral centre.

Management and Complications

Overall, 30-day mortality was 14.75%. Four patients were not surgical candidates due to a combination of advanced age and multiple comorbidities. 118 patients underwent open repair with replacement of the ascending aorta and additionally had an aortic valve replacement (26.23%), coronary artery bypass graft (15.6%) and/ or hemiarch repair (22.1%). 11 patients had re-exploration within 24 hours due to postoperative bleeding and 7 cases were re-explored after 24 hours with the majority due to a large pericardial effusion, tamponade physiology and one case of sternal wound infection. Two patients had a CVA pre-operatively without mortality however, both patients required rehabilitation. Postoperative CVA occurred in 7.4% of patients and was associated with higher 30-day mortality (44% vs 12.4%, p<0.05). AKI occurred in 11.5% of patients and was associated with higher 30-day mortality (35.7% vs 12%, p<0.05).

This study represents the first epidemiological analysis of Type-A AD undertaken in regional Australia.

Prevalence

The prevalence within the HNE health district of Type-A AD was 1.47 per 100,000 per year. Our incidence is lower than the NSW study reported by Dinh et al, but these results are not comparable as they were reflective of both Type A and B AD. The incidence of Type A AD is still lower compared to global figures although the breakdown of data across metropolitan and regional areas have not been studied^2-4,16.

Mortality

Sampson et al. reported mortality rates at 2.49 (1990) and 2.78 (2010) per 100,000 per year. Australasia had the highest mortality with >8 deaths per 100,000 in 1990 and 2010²². Australia presents several challenges for the retrieval of critically ill patients which include the widespread decentralisation of health services and the sparse geographical distances needed to access health services²³. In our study covering regional NSW, the mortality rate was much lower than expected from literature at 2.12 per 100,000 per year with an overall thirty-day mortality of 14.75%. Two main reasons could explain this difference.

(i) Catchment Area of our Study

HNE has a single cardiothoracic surgery tertiary referral centre. In contrast to the large proportion of the rest of Australia, where distances to tertiary hospitals can vary from 10-12 hours by road, the furthest referring hospital from JHH is 495km or approximately 6 hours by road and 2 hours by air, making urgent transfers prompt. Therefore, in comparison to regional Australia as a whole, our mortality rates may be reduced due to the decreased transport distances specific to HNE.

(ii) Access to Retrieval Services

Retrieval services have significantly improved in Australia since the study in 2010²³. The Hunter Retrieval Service is an in-house round-the-clock retrieval at JHH. It plays a central role in assessment, triage and timely transfers of critically ill patients across the entire HNE catchment area. The team consists of a Senior Intensive Care Nurse and a Consultant or Senior Trainee from Emergency, Anaesthetics or Intensive Care, allowing rapid recognition and management of critically ill patients such as those included in our study. Although this service was established 25 years ago, the service was extended from purely fixed-wing air transport to introduce helicopter retrieval in 2014 and road transport in 2015. Therefore, our mortality rate may also reflect improved retrieval mechanisms now in place compared to the 1990s and 2010.

Our study reflects that more robust retrieval systems and local cardiothoracic units can potentially improve patient outcomes. The HNE represents a unique model of an in-house retrieval system with an accessible catchment area. If utilised and implemented in larger, more sparsely populated Australian states, this model has the potential to improve patient outcomes significantly.

Risk factors

(i) Age

In our study, advancing age is associated with an increased prevalence of acute Type-A AD. Patients over the age of 50 had a higher incidence than the average recorded in our population. Patients aged 50-60 years had an incidence of 4.8 per 100,000 per year, which increased dramatically to 10.7 per 100,000 per year in patients over 60 years of age. In the largest study done in elderly patients over 70 (n=55) who suffered a Type-A AD, expected risk factors of hypertension, atherosclerosis, and iatrogenic dissection were more common in the elderly population compared to age 70 or less. Mortality was also significantly higher in the older population than the younger population (43% vs 28%, p = 0.0006). Logistic regression analysis identified age>or=70 years as an independent predictor of hospital death for acute Type-A AD (OR 1.7, 95% CI 1.1-2.8; p = 0.03). Our study showed that almost half the cases in our cohort were aged 60 and older. The ageing Australian population in part explains this. In the 2016 census, 1 in 7 people was over 65, with a projection to increase steadily. More local Australian studies are required to investigate Type-A AD in the elderly population specifically. This could have far-reaching benefits in one of the most rapidly growing populations within Australia and provide much-needed lobbying for cardiovascular preventative health funding targeting the elderly.

(ii) Indigenous Population

In our study of 122 patients, 4 (5%) identified themselves as an Australian Aboriginal and Torres Strait Islander (ATSI). Australia has long faced challenges in combating poor ATSI health outcomes¹. Numerous factors include barriers in cultural communication, functional view of health and reduced access to healthcare in remote and rural areas of Australia, where the ATSI populations predominantly live. Our study did not see a predominance of ATSI populations being affected by Type-A AD. However, it is interesting to see a similar percentage of ATSI patients in our cohort compared to the broader Australian population. Although no comparable previous studies of Type-A AD in the ATSI population exist, it is of significance that they are not underrepresented in our population.

(iii) Misdiagnosis

Previous studies show a misdiagnosis rate of up to 40%. In a review of 68 patients, 26 (38%) patients were misdiagnosed as an acute coronary syndrome (ACS) with subsequent treatment with antiplatelet, fibrinolytic or anticoagulant therapy^2-4. In this study, 12 of 122 (9.8%) patients were initially diagnosed with acute myocardial infarction and subsequently associated with a delay in diagnosis of Type-A AD (p =0.003). Management with subsequent antithrombotic agents was associated with higher rates of major bleeding (38% vs 13%) compared to no antithrombotic agents and associated with more significant in-hospital mortality (27% vs 13%, p=0.02). The use of antithrombotic agents was also associated with increased haemorrhagic pericardial fluid, haemorrhagic pleural effusion and haemodynamic instability. Our study demonstrates a lower rate of misdiagnosis than literature (9.8% vs 40%), although there seems to be a clear correlation with a perioperative bleeding event. 2 of the patients misdiagnosed required urgent re-opening and 4 died intraoperatively due to significant bleeding and friable tissue. The correlation between misdiagnosis and mortality was statistically significant in our study (p<0.05).

(iv) Smoking and Hypertension

It is well-known from IRAD that hypertension is common and is considered the most crucial risk factor in mortality for AD³. Although our study did not show a significant correlation between hypertension and mortality, there was a statistically significant association between hypertensive smokers with mortality from Type-A AD in our population. It can be speculated that the oxidative stress from smoking creates a further insult to an arterial wall that is already under stress from hypertension. Although the numbers in our study were limited, they provide a starting point for more extensive studies.

Given the rarity of Type-A AD, our study sample is small, making it difficult to extract strong conclusions and generalisations without the aid of extrapolation of data or speculation. The study is a retrospective cohort study and is open to selection bias, missing records and misclassification of data. Selection bias is reduced as the data was collected with an established ICD-10 diagnosis of Type-A AD, however, can still exist during the actual data collection phase. Although generalisations may not be possible from this study, it does provide a strong direction for future prospective studies.

Our study illustrates the epidemiological trends and risk factor profiles for Type-A AD which carries a high mortality if not treated in a timely manner. Further prospective and large-scale studies are needed in both regional and metropolitan Australia to understand measures needed to keep mortality from Type-A AD as low as possible.

AD – Aortic Dissection

HNE – Hunter New England

NSW – New South Wales

SPSS - Statistical Package for Social Sciences

IRAD - International Registry of Acute Aortic Dissections

GERAADA - German Registry for Acute Aortic Dissection Type-A

NORCAAD - Nordic Consortium for Acute Type-A Aortic Dissection

TL – True Lumen

FL – False Lumen

AR – Aortic Regurgitation

ACS – Acute Coronary Syndrome

IMH – Intramural Haematoma

PIT – Primary Intimal Tear

PAU – Penetrating Aortic Ulcer

AA – Aortic Aneurysm

AAS – Acute Aortic Syndrome

Ethics approval and consent to participate

Ethics approved by the University of Newcastle's Human Research Ethics Committee (HREC) and in conjunction with the Hunter Medical Research Institute (HMRI).

Consent for publication

Not applicable

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Competing interests

The authors declare that they have no competing interests

Funding

Not applicable

Authors' contributions

AR– Data collection and Writing of Manuscript

OC– Data Collection

TN– Supervisor, Editor

RM– Supervisor, Editor

Acknowledgements

Not applicable

Dinh, Michael M et al. “Incidence and Outcomes of Aortic Dissection for Emergency Departments in New South Wales, Australia 2017–2018: A Data Linkage Study.” Emergency medicine Australasia 32.4 (2020): 599–603.
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Rudenick, Paula A et al. “A Multi-Method Approach Towards Understanding the Pathophysiology of Aortic Dissections – The Complementary Role of In-Silico, In-Vitro and In-Vivo Information.” Statistical Atlases and Computational Models of the Heart. Berlin, Heidelberg: Springer Berlin Heidelberg. 114–123.
Vilacosta, Isidre, And José Alberto San Román. “Acute Aortic Syndrome.” Heart (British Cardiac Society) 85.4 (2001): 365–368.
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Chin, Anne S., and Dominik Fleischmann. “State-of-the-Art Computed Tomography Angiography of Acute Aortic Syndrome.” Seminars in ultrasound, CT, and MRI 33.3 (2012): 222–234.
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Hynes, Conor F et al. “Chronic Type-A Aortic Dissection.” Aorta (Stamford, Conn.) 4.1 (2016): 16–21.
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Table 1: Modified Stanford Type A AD with Subtypes of Acute AD

Type A

Type B

Ascending

Arch

Descending

Multiple Tears

No Tear

Arch

Descending

Multiple Tears

No Tear

Lansmen et al. Department of Cardiothoracic Surgery, Mount Sinai Medical Centre, New York, New York

Table 2: Prevalence of AD across age groups per year per 100,000

Population Age Group (years)	<20	20-40	40-50	50-60	>60
Prevalence per year per 100,000	0.35	0.75	2.6	4.8	10.7

Table 3: Risk Factor Profile

Risk Factor	Number of Patients	Percentage (%)
Smoker	58	53.8
HTN	68	56.7
Smoker + HTN	31	25.4
DM Type 2	15	12.3
DM Type 1	0	0
Marfan Syndrome	4	3.3
PVD	26	21.3
Atherosclerosis	20	16.4
Trauma	4	3.3
Atrial Fibrillation	14	11.5
Iatrogenic	1	<1

Table 4: Comparison of Smoking and Hypertension in Mortality

	Smoking + Hypertension	Smoking Only	Hypertension Only	Non-Smoker + No Hypertension
Number of Patients	31	27	37	27
30 Day Mortality	8	3	5	1
Mortality (%)	34.78	12.5	15.6	3.7

Table 5: Correlation between Misdiagnosis with Mortality and Reopen

Diagnosis	Number of Patients	Mortality	Reopen within 24 hours
Misdiagnosis/ Delayed diagnosis	9.8%	33.3%	16.7%
Correct diagnosis	90.2%	12.7%	8.1%

No competing interests reported.

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Epidemiological Patterns of Acute Type-A Aortic Dissection in Regional New South Wales - A 10-year Analysis

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