Can a Chest X Ray Misdiagnosis an Aneurysm

Abstract

Acute aortic dissection (AAD) is the most mutual catastrophe to involve the aorta, resulting in high morbidity and mortality. Delayed diagnosis tin can adversely affect patient issue, therefore a high clinical index of suspicion is the first step. Absenteeism of the classical signs such as pulse defecit and chest radiograph changes should not falsely reassure clinicians. Availability of a biomarker to expedite and improve diagnosis of AAD would greatly benefit emergency section clinicians. Some promising novel biomarkers include calponin and elastin, merely their utilise in everyday do is still some time away. Bedside imaging including transthoracic and transesophageal echo is beingness increasingly used in the unstable patient suspected of AAD, while computed tomography (CT) appears to be the near accurate rapid imaging modality for its diagnosis. Expeditious diagnosis is crucial to ameliorate patient survival allowing for amend outomes.

Introduction

Astute aortic autopsy (AAD) as a clinical emergency was showtime described by Morgagni more than 200 years ago [ane]. The early detection of AAD is paramount given its significant morbidity and mortality. Recent studies have reported early bloodshed rates in the region of xviii–25 % with trivial alter over the by decade despite increasing applied science [ii]. Calculating the true incidence of AAD is hard due to the number of aortic catastrophies that result in sudden death and become undiagnosed. A large Swedish population-based study (1982–2002) has placed the incidence over a xvi-year period at iii.4 cases per 100,000 per twelvemonth [iii]. Early diagnosis and instigation of treatment is hampered by delayed or misdiagnosis in up to forty % of cases. This may be due to the lack of specificity and sensitivity of symptoms, signs, EKG and breast radiographs [four]. For Blazon A autopsy, the untreated mortality is currently 1–ii %/h with a 30-day mortality rate for the majority of patients approaching 100 % [two]. Current testify purports that diagnostic evaluation of patients farther delays the definitive diagnosis by a number of hours, thereby increasing mortality [5].

This article aims to review the current prove regarding the diagnosis of AAD in order to improve our management of this important condition.

History and Clinical Diagnosis

Although often presenting with the classical trigger-happy chest pain radiating through to the dorsum, AAD tin can present in whatever number of guises making it a challenging clinical diagnosis. Other symptoms and signs are often secondary to vascular compromise including pulse deficits, renal impairment and neurological signs, which can frequently mimic astute stroke. Less mutual symptoms include syncope, astute congestive eye failure and testify of myocardial ischemia [2]. Risk factors for AAD must exist taken into business relationship on initial presentation and raise clinical suspicion if present.

The nearly commonly associated factors are hypertension, atherosclerosis and previous cardiovascular surgery. Howard et al., in a population-based study of aortic dissection, reported 67.3 % of their study population having a known history of hypertension [6••]. AAD is more frequent in the 60th decade of life with a hateful age of 63 at the time of diagnosis [2]. Men are more than unremarkably affected, accounting for two/3 of patients in the IRAD cohort (International Registry of Acute Aortic Dissection). Marfan'due south disease results in approximately 5 % of all cases of aortic dissection, with a small-scale number of other collagen vascular diseases (including Ehler–Danlos syndrome) causing an even smaller per centum of aortic dissections. Bicuspid aortic illness too carries a high lifetime risk of AAD with 1 in 20 patients with a bicuspid aortic valve developing AAD [vii]. Cocaine has been recognized every bit a cause of AAD with the proposed mechanism mediated through profound catecholamine-induced superlative of the BP resulting in intimal tear [8].

Abrupt onset pain still remains the most common presenting clinical symptom. Hagan et al. conducted a case serial from 1996–1998 in which patients with AAD at presentation were enrolled from 12 international centers. Of the 464 patients enrolled in this study, 84.eight % of patients reported abrupt onset hurting. The majority of patients complained of chest hurting (72.seven %). Inductive chest pain was typical in patients with type A dissection, whereas patients with type B dissection more oftentimes experienced pain in the back and abdomen, although there was substantial overlap (P < 0.001) [ii].

A recent study by Lovy et al. sought clinical and diagnostic criteria to place depression-risk patients as an initial step in developing a clinical decision rule in Acute Aortic Syndome (AAS). AAS included aortic autopsy, rupture, intramural hematoma, and penetrating atherosclerotic ulcer. They retrospectively reviewed their institutional database for all adults initially presenting from January one, 2006, to Baronial 1, 2010, who underwent a CT browse for suspected AAS and who did not have a history of trauma, AAS, or aortic surgery. A full of 1,465 patients were included.

Chest hurting, acute onset of pain, radiation to the back, and astringent pain were all significant positive predictors of AAS. Acute chest pain had a sensitivity of 82.9 % with CI 66.four–94.4 %, a specificity of 70.7 %, a positive predictive value (PPV) of 0.07 % and a negative predictive value (NPV) of 99 % [ix••]. A review newspaper by Golledge et al. demonstrated similar results with 85 % of the patients included presenting with chest or back pain [ten].

Pulse deficits and the murmur of aortic regurgitation are clinical signs which are classically associated with AAD. Pulse arrears was reported in 44 % of the review patients [10]. Chua et al. conducted a retrospective nautical chart review of 68 patients with AAD, highlighting that 63.8 % did non display a pulse deficit on clinical test. This study also showed that emergency physicians are more likely to miss the diagnosis of AAD when pulse arrears was not detected on examination (OR 35.76; 95 % CI 3.lxx–345.34) [11•]. From IRAD aortic regurgitation and pulse deficit were noted in only 31.6 % and fifteen.1 % of patients, respectively [2]

Hypertension is a mutual presenting finding yet inter-arm blood pressure differences are non usually recorded. IRAD reported 49 % of patients were hypertensive at presentation with hypertension at initial presentation being more mutual among patients with type B dissection (seventy.1 vs 35.seven %, P < 0.001) [ii].

Neurological arrears is widely reported with some cases presenting with acute neurological findings in the absenteeism of pain [12, 13]. IRAD reports overall figures of 4.7 % of patients with an astute neurological deficit at presentation [2] with similar studies reporting figures of 12 % [x].

In isolation, breast hurting and indeed the nature of the pain may not be useful in aiding clinical diagnosis, but, in correlation, other clinical findings, patient risk factors such every bit known hypertension or the presence of conditions such equally Marfans' syndrome and X-ray findings may aid diagnosis. Attempts accept been fabricated to formulate pathways to identify high-risk patients that require imaging. The American Heart Association have published guidelines which identify high-risk clinical features to expedite a diagnosis [14•]. This grouped risk factors (e.one thousand. Marfan syndrome) with clinical features (violent breast hurting) and signs (pulse deficit) to run a risk stratify patients to immediate imaging. This guideline has since been applied to the IRAD database and is highly sensitive. However, this study did non permit for any testing of the specificity of the written report. Widespread implementation of such a guideline may result in over-investigation of patients [15••].

As AAD has many mimics and up to 10 % of patients may be pain free at presentation, a high clinical alphabetize of suspicion must be kept. The presence of signs such every bit pulse deficits, neurological symptoms and interim BP difference all raise the clinical suspicion of AAD; however, their absenteeism does not exclude the diagnosis every bit evidenced past the relevant figures above.

Investigations

A high index of clinical suspicion currently remains cardinal to the diagnosis of AAD. There is no betoken of intendance biochemical exam available now to accurately diagnose aortic autopsy. Some novel biomarkers are currently showing promise just are unlikely to impact on improving the fourth dimension to diagnosis.

Current Biomarkers

C Reactive Protein (CRP)

This is an acute stage protein which rises in response to inflammatory processes. Schillinger et al. found that CRP (and white cell count) were higher in those patients presenting with breast pain and subsequently diagnosed with AAD. Even so, due to its poor specificity, the rising was not found to be sufficient to modify diagnostic pathways [16].

D-Dimer

The likely usefulness of this fibrin degradation product is in its "rule out" and hazard stratification ability. When the dissection involves a coronary ostium and results in myocardial infarction (MI), elevated troponin and characteristic EKG changes may force the ED physician into treatment of an MI with anticoagulation therapy which would be disastrous for an AAD. The elevation of D-dimers coupled with an elevation in troponin should force the md to rethink the diagnosis. This is because an analysis of more than 700 patients with MI showed no correlation between raised D-dimers and MI [17].

The sensitivity of this biomarker has frequently been reported as approaching 100 % with a NPV of >97 % [18]. A recent meta-analysis of 349 cases provided a pooled sensitivity effect of 94 % [19]. Imitation negatives were almost likely in patients under 70, dissections which are shorter in length, and those with a thrombosed fake lumen [twenty].

Despite its limitations, the utilise of D-dimer testing is recommended by the task strength of European Society of Cardiology in the initial workup of those patients suspected of AAD [4]. A new betoken of care rapid latex agglutination test of whole blood providing a result within x min was shown to correlate well with laboratory testing [21]. This could take applied applications for usage within the ED as a screening tool when combined with an appropriate clinical presentation. Such a strategy volition require inquiry and validation earlier it is adopted given the probable utilization of resources.

Potential New Biomarkers

Smooth Muscle Myosin Heavy Chain (smMHC)

Enquiry as early equally 1995 past Katoh et al. suggested the use of this biomarker as a diagnostic tool for AAD [22, 23]. Levels rose chop-chop within the offset 24 h and ,when a cutoff value of 2.five ng/50 was used, the specificity was ninety % at 12 h and 85 % at 24 h. Those below the cutoff value who were after diagnosed with AAD had DeBakey type B aortic autopsy. At the ii.5-ng/ml cutoff, the biomarker had a specificity of 83 %, but at ten ng/ml the specificity rose to 100 %. Interestingly, astute MI was found non to cause a rise in smMHC [24]. It must exist noted that smMHC is present in uterine and abdominal polish muscle. Theoretically, it could therefore be raised in weather condition affecting these organs.

Calponin

Of the three isoforms (acidic, basic and neutral), two take shown some potential. During the first half-dozen h after AAD acidic calponin, at a value of 2.3 ng/ml, demonstrated a sensitivity of 50 % and specificity of 87 %, while the basic isoform provided sensitivity of 63 % and specificity of 73 % when using a cutoff value of 159 ng/ml. The PPV were 0.56 and 0.44 for acidic and basic calponin, respectively, at 6 h. The NPV of 0.84 (acidic) and 0.86 (bones) were of more clinical significance [25]. A drawback of the acidic isoform is its presence in neurological tissue, which therefore limits its accurateness for diagnosis in those with neurological signs.

Elastin (sELAF)

This biomarker measures the degradation product of elastin, i of the arterial wall'southward principal structural components. The study used a cutoff level of 3 standard deviations above mean at all ages and resulted in a specificity of 99.8 %. However, this figure roughshod to 88.ix % for those with a patent or partially thrombosed false lumen. Of significance, sELAF was negative in those with a completely thrombosed fake lumen. This was one of the marking's greatest limitations. A clear benefit above calponin and smMHC was that sELAF remained raised for upwards to 72 h post-dissection [26].

Novel biomarkers are unlikely to be available to EDs in the virtually future, and thus are unlikely to bear upon significantly on early diagnosis of AAD. Of those biochemical markers readily available, D-dimer would appear to be of sufficient specificity to prompt further diagnostic evaluation and imaging to facilitate expeditious diagnosis and treatment [27].

EKG

The EKG is frequently the first piece of diagnostic information obtained on patients with potential AAD. In IRAD, the EKG was reported as normal in 31 % of its 464 patients. Nonspecific ST and T wave changes were demonstrated in 42 % with show of ST elevation in 5 % of cases [2]. A retrospective study of 233 cases further confirms these findings. It demonstrated astute ST pinnacle in iv % of cases. ST segment low or T wave inversion were seen in 47 % of cases [28], while 30 % of EKGs had no significant finding. The principal pitfall of misdiagnosing AAD every bit ACS include the instigation of potentially harmful interventions such every bit anticoagulation, antiplatelet therapy and emergency catheter intervention. The mortality can climb to over lxx % from assistants of thrombolytic agents, manifested mainly by hemorrhage into the pericardial sac resulting in cardiac tamponade [29].

The underlying cause of EKG abnormalities involves hypoperfusion of the coronary arteries. A number of mechanisms have been suggested. These include a jutting false lumen which can cause apoplexy of the coronary orifice, a autopsy which can extend into the wall of the coronary artery, or the coronary artery itself tin can detach from the aortic root. In attempting to identify the vessel involved, retrospective studies have broken downwards the cases of ST elevation to suggest mainly right coronary artery and left master branch interest [28].

An important attribute of EKG changes in the setting of aortic dissection is their implication for the patient'due south consequence. Patients with ST segment changes had a higher prevalence of pericardial effusion, cardiac tamponade, moderate/severe aortic regurgitation, and shock on admission, resulting in higher in-infirmary mortality. On multivariate analysis, EKG changes were the but contained predictor of mortality. Fifty-fifty when the cases with ST elevation were removed from the equation, there remained an association with EKG changes and a higher in-hospital bloodshed [30•].

Imaging

The implications of a diagnosis of aortic dissection mandates that the imaging technique used be highly specific and sensitive. Information technology should as well provide acceptable data to plan for an emergent therapeutic strategy. Planning for a therapeutic strategy depends non but on the type of dissection but too on the site of entry, the extent of dissection, the involvement of the coronary arteries, arch branches, or visceral arteries, the involvement of the aortic valve, the presence and extent of pericardial effusion, false lumen patency, and the presence of thrombus in the faux lumen. Therefore, delineation of these features should be an important part of the diagnostic workup for patients with suspected aortic dissections. Imaging techniques range from the initial radiograph through to MRI.

Breast X-ray

The classic finding with aortic autopsy on x-ray is mediastinal widening. The mediastinum tin can be seen to bulge to the right with dissection of the ascending aorta and to the left with dissection of the thoracic aorta. Multiple other signs take been reported in cases of aortic dissection including widening of the aortic knob, aortic wall thickness, double aortic shadow and the presence of a pleural effusion, mainly on the left [31, 32]. All the same, while the absence of findings on a chest x-ray lowers the likelihood of the disease, it does non exclude its presence. In IRAD, absence of mediastinal widening was noted in 37.iv % of patients presenting with type A aortic dissection. No chest x-ray abnormality was noted in 12.4 % of patients [2]. Pooled information from 10 studies placed the predictive sensitivity of a widened mediastinum and aberrant aortic profile at 64 and 71 %, respectively. If all chest x-ray abnormalities were included, this increased the sensitivity to xc %; withal, this included modest breast x-ray changes including small pleural effusions [33]. A further prospective trial showed that the specificity of a breast radiograph for significant aortic affliction was 86 % [34].

These studies demonstrate that the absence of chest x-ray abnormalities makes the likelihood of significant aortic disease less likely. Notwithstanding, it is not powerful enough to be used alone as a rule-out test. Additional studies are required in almost all patients. In unstable patients, obtaining a breast x-ray can further filibuster the establishment of appropriate imaging and treatment

CT

CT is well established as the most used diagnostic modality in cases of suspected AAD. IRAD reported CT as the first imaging modality used in 61 % of cases [two]. Advantages of CT include its virtually universal availability and its speed of diagnosis. Information technology can also delineate branch vessel involvement and visualize the unabridged aorta. A further plus of CT is that an culling cause for chest hurting has been reported in upwardly to 21 % of cases scanned for suspected AAD [35].

Non-helical CT scanners were more than capable of diagnosing aortic dissection in the past. However, these machines were relatively tiresome and any patient motion resulted in significant artefact. The sensitivity of studies using non-helical CT have been shown equally close to 100 % but the specificity ranges from 87 to 100 %. The use of helical CT has improved this reported specificity. A systematic review of ane,139 patients in xvi studies suggested that helical CT had a sensitivity of 100 % and a specificity of 98 % in the diagnosis of aortic dissection [36]. Multidetector CT (MDCT) has added further speed and thus improved the utilize of CT as a diagnostic tool. This involves using multiple detectors to obtain simultaneous images of whatsoever part of the body in a single jiff-hold. MDCT allows authentic imaging of a large area in a curt conquering fourth dimension with high resolution. This improves the visualization of vascular structures as compared with conventional CT. It too facilitates breath holding, thus minimizing artefacts on images. A study on 57 patients showed sensitivities and specificities of upwardly to 100 % with MDCT [37].

A further advancement on CT imaging has been the use of EKG gating. Movement of the eye throughout the cardiac cycle can produce movement artefacts in the epitome. The difficulty with interpreting cardiac motion can be helped with EKG gating. This is where information are simply caused during a specified portion of the cardiac cycle, typically during diastole. Images are created over a sequence of cardiac cycles, due east.g., R to R intervals. This has been shown to be valuable for reducing ascending aortic motion artefacts that can mimic dissection without increasing imaging time [38, 39].

Triple rule-out CTs are being used more and more by diverse institutions assuasive visualization of pulmonary arteries, aorta and coronary arteries in a single examination. This modality may safely eliminate the need for farther investigation in 75 % of patients in the appropriate population [xl]. The major disadvantages of this protocol are the utilize of increased dissimilarity with a college radiations dose. This limits its applicability to a unique subset of patients in which AAD, pulmonary embolism and acute coronary syndrome cannot exist reliably distinguished based on clinical history. Most triple rule-out CTs likewise do not include the abdominal aorta, thus the extent of a descending AAD may not be visualized. Continued clinical research is needed to ascertain the place of triple dominion-out CTs in the investigation of chest pain and AAD.

CT is an effective method of diagnosing an AAD with the completion of studies analyzing its effectiveness failing to maintain pace with the speed of increasing technology.

MRI

MRA tin can exist considered a very accurate tool for the diagnosis of AAD allowing the visualization of the aorta without the need for ionizing radiations. Both the sensitivity and specificity accept been reported as 100 % [36]. It is extremely accurate at identifying the site of entry, identifying thrombus and the presence of a pericardial effusion. Advantages include the assessment of functional cardiac information including left ventricular part and aortic regurgitation. There are pregnant limitations in the apply of MRA as a kickoff-line diagnostic tool, resulting in its utilise in but i % of cases in IRAD [2]. The availability of MRI and the length of time needed for a scan limit its employ in everyday do. The monitoring of critically ill patients is also much more hard in the MRI surroundings. Faster scanners are currently being explored and, equally the new generations of scanners are developed, MRA may be expected to play a more prominent office [41].

Transthoracic Echo

Although the electric current guidelines from the AHA would point to CT every bit the modality of option in ruling out AAD [4], transthoracic echo tin can often be overlooked equally a screening tool. It is portable, inexpensive, safe and tin can be of item benefit in the patient who is hemodynamically unstable. While an ascending aortic flap is diagnostic of AAD, other 'high-risk' features include aortic regurgitation, dilated aortic root (especially with a pericardial effusion), junior hypokinesia, and a bicuspid aortic valve. As well equally establishing a diagnosis of AAD, it can detect signs suggestive of an alternative diagnosis such as pericardial effusions, right heart dilatation (pulmonary embolus), and regional wall abnormalities (MI) [42].

High-adventure features for type A dissection on repeat tin prompt ED physicians to brand timely referrals to cardiothoracic surgery or arrange urgent transfer to an appropriate center. This minimizes delays in transfer of the patient within a facility, such as to and from the radiology department, which is of item importance in the hemodynamically unstable patient, in smaller centers with no cardiothoracic unit, and in those centers with limited access to CT scanners.

For the most time-critical dissection, type A, sensitivity is 78–100 %. For the less urgent type B dissection, sensitivity decreases to 31–55 % [43, 44].

Transesophageal Echo (TEE)

The current guidelines from the European Society of Cardiology advocate the apply of transesophageal echo for those hemodynamically unstable patients either prior to transfer or on inflow in the operating theatre [4]. The paradigm of AAD on TEE is an intimal flap. Reverberation artefacts take been reported to cause some misdiagnosis; still, the use of color menstruation imaging tin assist to recognize reverberation artefacts [42]. For those patients with Type A autopsy, TEE tin provide boosted information to assist in preoperative planning. This includes coronary, head or neck vessel involvement, presence of aortic regurgitation, site of entry tear, and the proximal extent of the dissection flap. It may also observe pericardial effusion or cardiac tamponade and make an assessment of left ventricular function [45].

The sensitivity of TEE is 94–100 % with a specificity of 77–100 % for identifying the intimal flap. One meta-analysis concluded information technology had like sensitivity and specificity for AAD detection of helical CT and MRI [36]. However, the accurateness of TEE is also dependent on the operator with its availability limited in many settings.

It must exist emphasized that the absence of such factors does not rule out the presence of an aortic dissection.

The imaging modality of choice remains CT. MRI has a higher sensitivity simply its availability in the emergency situation results in CT becoming a more acquiescent diagnostic tool. TTE and TEE accept been included in AHA and European society of Cardiology guidelines every bit a tool in the unstable patient. However, this is dependent on the operator and availability with a high level of skill involved.

Conclusion

The diagnosis of AAD is challenging for the emergency physician with potentially devastating consequences. A high index of suspicion must be maintained in order to ensure expedient and authentic diagnosis. The presence of risk factors and signs including pulse deficits or neurological symptoms propel the clinician to investigate further. There is currently no single biomarker that can be used to diagnose aortic autopsy, but the judicious use of D-Dimers tin can aid clinicians in take chances stratification and inquiry is ongoing in this field. The future may allow novel biomarkers to exist incorporated into a guideline with known gamble factors and clinical features. This would significantly expedite and reduce mortality from AAD. CT remains the imaging of choice with increasing input from TTE.

References

Recently published papers of item involvement have been highlighted as: • Of importance •• Of major importance

1. Acierno LJ. The history of cardiology. New York: Parthenon; 1994.

   Google Scholar

2. Hagan PG, Nienaber CA, Isselbacher EM. The international registry of acute aortic dissection (IRAD): new insights into an onetime disease. JAMA. 2000;283:897–903.

   Google Scholar

3. Olsson C, et al. Thoracic aortic aneurysm and dissection increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14 000 cases from 1987 to 2002. Circulation. 2006;114:2611–18.

   Google Scholar

4. Erbel R, Alfonso F, Boileau C. Diagnosis and management of aortic dissection: task strength on aortic dissection, European society of cardiology. Eur Heart J. 2001;22:1642–81.

   Google Scholar

5. Raghupathy A, Nienaber CA, Harris KM. Geographic differences in clinical presentation, treatment, and outcomes in blazon A acute aortic dissection (from the International Registry of Acute Aortic Dissection). Am J Cardiol. 2008;102:1562–66.

   Google Scholar

6. •• Howard DP, et al. Population-based study of incidence and outcome of astute aortic dissection and premorbid risk factor command: 10-year results from the Oxford Vascular Study. Circulation. 2013;127(twenty):2031–7. A study highlighting the significance of pre-existing hypertension in a big 10 yr report.

7. Elefteriades JA, et al. Thoracic aortic aneurysm: Reading the enemy'south playbook. World J Surg. 2008;32:366–74.

   Google Scholar

8. Fisher A, Holroyd BR. Cocaine-associated autopsy of the thoracic aorta. J Emerg Med. 1992;10:723–seven.

   Google Scholar

9. •• Lovy AJ, et al. Preliminary evolution of a clinical decision rule for acute aortic syndromes. Am J Emerg Med. 2013;31:1546–fifty. A report which attempted to identify low risk patients as an initial pace in the development of a clinical decision rule for the diagnosis of aortic dissection.

10. Golledge J, et al. Acute aortic dissection. The Lancet. 2008;372(9632):55–66.

    Google Scholar

11. • Chua M, et al. Acute aortic dissection in the ED: risk factors and predictors for missed diagnosis. Am J Emerg Med. 2012;30:1622–6.

12. Colak N, et al. Painless aortic dissection presenting as paraplegia. Tex Heart Inst J. 2012;39(2):273–six.

    Google Scholar

13. van Zeggeren L, et al. Painless transient paraparesis as the lone manifestation of aortic autopsy. J Vasc Surg. 2011;54(5):1481–4.

    Google Scholar

14. • Hiratzka LF, Bakris GL, Beckman JA, et al. American college of cardiology foundation/american heart clan task force on do guidelines. Guidelines for the direction of patients with thoracic aortic affliction. Circulation. 2010;121:e266–e369. A Guideline which identifies high-adventure features to expedite a diagnosis of aortic dissection.

15. •• Rogers AM, et al. Sensitivity of the aortic dissection detection chance score, a novel guideline-based tool for identification of acute aortic dissection at initial presentation: results from the international registry of astute aortic dissection; IRAD Investigators. Circulation. 2011;123(20):2213–8. Highlighting the loftier sensitivity of the guideline produced by the AHA but also outlines limitations of lack of enquiry into specifity of same.

16. Schillinger M, Domanovits H, Bayegan K. C-reactive protein and bloodshed in patients with astute aortic disease. Intens Care Med. 2002;28:740–v.

    Google Scholar

17. Weber T, Hogler S, Auer J, Berent R, Lassnig Due east, Kvas E, et al. D-dimer in acute aortic dissection. J Am Coll Cardiol. 2004;44:804–9.

    Google Scholar

18. Lippi One thousand, Filippozzi L, Montagnan M, Salvango GL, Guidi GC. Diagnostic value of Ddimer measurement in patients referred to the emergency section with suspected myocardial ischaemia. J Thromb Thrombolysis. 2007;25(iii):247–50.

    Google Scholar

19. Marill KA. Serum D–dimer is a sensitive test for the detection of acute aortic dissection: a pooled meta-assay. J Emerg Med. 2008;34:367–76.

    Google Scholar

20. Hazhui H, Nishimoto One thousand, Hoshiqa One thousand, Negoro North, Muraoka H, Murai M, et al. Young adult patients with short autopsy length and thrombosed false lumen without ulcer-like projections are liable to take false negative results of d-dimer testing for astute aortic dissection based on a study of 113 cases. Circ J. 2006;70(12):1598–601.

    Google Scholar

21. Akutsu K, Sato Northward, Yamamoto T. A rapid bedside D-dimer assay (cardiac D-dimer) for screening of clinically suspected astute aortic autopsy. Circ J. 2005;69:397–403.

    Google Scholar

22. Katoh H, Suzuki T, Hiroi Y. Diagnosis of aortic autopsy by immunoassay for circulating smoothen muscle myosin. Lancet. 1995;345:191–2.

    Google Scholar

23. Katoh H, Suzuki T, Yokomori K. A novel immunoassay of smooth muscle myosin heavy chain in serum. J Immunol Meth. 1995;185:57–63.

    Google Scholar

24. Suzuki T, Katoh H, Watanabe M. Novel biochemical diagnostic method for aortic dissection: results of a prospective study using an immunoassay of shine muscle myosin heavy chain. Circulation. 1996;93:1244–9.

    Google Scholar

25. Suzuki T, Distante A, Zizza A. Preliminary experience with the smooth muscle troponin-like protein, calponin, as a novel biomarker for diagnosing acute aortic dissection. Eur Heart J. 2008;29:1439–45.

    Google Scholar

26. Shinohara T, Suzuki K, Okada M. Soluble elastin fragments in serum are elevated in acute aortic dissection. Arterioscler Thromb Vasc Biol. 2003;23:1839–44.

    Google Scholar

27. Ranasinghe A, Bonser R. Biomarkers in acute aortic dissection and other aortic syndromes. J Am Coll Cardiol. 2010;56(19):1535–41.

    Google Scholar

28. Hirata K, Wake M, Kyushima M, Takashi T, Nakazato J, Mototake H, et al. Electrocardiographic changes in patients with type A acute aortic dissection incidence, patterns and underlying mechanisms in 159 cases. J Cardiol. 2010;56(2):147–53.

    Google Scholar

29. Kamp TJ, Goldschmidt-Clermont PJ, Brinker JA, Resar JR. Myocardial infarction, aortic dissection, and thrombolytic therapy. Am Heart J. 1994;128:1234–7.

    Google Scholar

30. • Kimura Thousand, et al. Frequency and implication of ST-T abnormalities on hospital access electrocardiograms in patients with type A astute aortic autopsy. Am J Cardiol. 2013;112(iii):424–9. Identifies the relationship between EKG changes and a higher in hospital mortality.

31. Earnest F, Muhm JR, Sheedy PF. Roentgenographic findings in thoracic aortic dissection. Mayo Clin Proc. 1979;54:43–l.

    Google Scholar

32. Jagannath AS, Sos TA, Lockhart SH, et al. Aortic autopsy: a statistical assay of the usefulness of plain chest radiographic findings. AJR Am J Roentgenol. 1986;147:1123–half-dozen.

    Google Scholar

33. Klompas Thousand, et al. Does this patient take an acute thoracic aortic dissection? JAMA. 2002;287(17):2262–72.

34. Von Kodolitsch Y, Nienaber CA, Dieckmann C, et al. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med. 2004;116:73–seven.

    Google Scholar

35. Thoongsuwan N, Stern EJ. Chest CT scanning for clinical suspected thoracic aortic dissection: beware the alternate diagnosis. Emerg Radiol. 2002;9(v):257–61.

    Google Scholar

36. Shiga T, Wajima Z, Apfel CC, et al. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic autopsy: systematic review and meta-analysis. Arch Intern Med. 2006;166:1350–6.

    Google Scholar

37. Yoshida S, Akiba H, Tamakawa M, et al. Thoracic involvement of type A aortic dissection and intramural hematoma: diagnostic accurateness—comparison of emergency helical CT and surgical findings. Radiology. 2003;228(2):430–5.

    Google Scholar

38. Roos JE, Willmann JK, Weishaupt D, Lachat Thousand, Marincek B, Hilfiker PR. Thoracic aorta: motion artifact reduction with retrospective and prospective electrocardiography-assisted multidetector row CT. Radiology. 2002;222(1):271–7.

    Google Scholar

39. Schertler T, Glucker T, Wildermuth South, Jungius KP, Marincek B, Boehm T. Comparison of retrospectively ECG-gated and nongated MDCT of the chest in an emergency setting regarding workflow, image quality, and diagnostic certainty. Emerg Radiol. 2005;12(1-ii):19–29.

    Google Scholar

40. Halpern EJ. Triple-rule-out CT angiography for evaluation of astute chest pain and possible acute coronary syndrome. Radiology. 2009;252(2):332–45.

    Google Scholar

41. Pereles FS, McCarthy RM, Baskaran V, et al. Thoracic aortic dissection and aneurysm: evaluation with nonenhanced true FISP MR angiography in less than iv minutes. Radiology. 2002;223(1):270–4.

    Google Scholar

42. Meredith E, Masani N. Echocardiography in the emergency cess of acute aortic syndromes. Eur J Echocardiogr. 2009;10:131–nine.

    Google Scholar

43. Appelbaum A, Karp R, Kiklin J. Ascending vs descending aortic dissections. Ann Surg. 1976;183:296–300.

    Google Scholar

44. Daily PO, Trueblood H, Stinson EB, Wuerflein R, Shumway Due north. Management of astute aortic dissections. Ann Thorac Surg. 1970;10:237–47.

    Google Scholar

45. Evangelista A, Gonzalez-Alujas M, Garcia del Castillo H, Anivarro I, Angel J, Salas A, et al. Transoesophageal echocardiography in the diagnosis of aortic autopsy. Revista Espanola de Cardiologia. 1993;46:805–ix.

    Google Scholar

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Author data

Affiliations

1. Retrieval, Emergency and Disaster Medicine Research and Evolution Unit of measurement (REDSPoT), Emergency Department, University Hospital Limerick, Dooradoyle, Limerick, Ireland

   Siobhan Coyle, Tadgh Moriarty, Laura Melody & Damien Ryan

2. Centre for Prehospital Inquiry, Graduate Entry Medical School, Academy of Limerick, Composition, Ireland

   Damien Ryan

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Correspondence to Damien Ryan.

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Coyle, S., Moriarty, T., Tune, L. et al. Diagnostic Testing in Astute Aortic Dissection. Curr Emerg Hosp Med Rep 2, 97–103 (2014). https://doi.org/x.1007/s40138-014-0044-8

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• Published: 19 April 2014

• Issue Date: June 2014

• DOI : https://doi.org/x.1007/s40138-014-0044-viii

Keywords

• Acute aortic dissection
• Biomarkers
• Imaging
• TEE
• MRI

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Source: https://link.springer.com/article/10.1007/s40138-014-0044-8

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