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Ann Thorac Surg 2004;77:2012-2020
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Acute dissection of the descending aorta: noncommunicating versus communicating forms

Monvadi B. Srichai, MDa,b, Michael L. Lieber, MSc, Bruce W. Lytle, MDd, Jane M. Kasper, RNa, Richard D. White, MDa,b,d*

a Department of Radiology (Section of Cardiovascular Imaging), The Cleveland Clinic Foundation, Cleveland, Ohio, USA
b Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
c Department of Biostatistics and Epidemiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
d Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

Accepted for publication August 19, 2003.

* Address reprint requests to Dr White, Section of Cardiovascular Imaging, Departments of Radiology and Cardiovascular Medicine, Cleveland Clinic Foundation, Desk HB6, 9500 Euclid Ave, Cleveland, OH 44195, USA.
e-mail: whiter{at}ccisd1.ccf.org


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Noncommunicating dissecting intramural hematoma is an aortic dissection variant, characterized by absent flow within the false lumen. Noncommunicating dissecting intramural hematoma is thought to be more stable than communicating dissection when beginning in the descending aorta. This study assessed clinical characteristics, anatomic characteristics, and 1-year outcomes in acute descending noncommunicating dissecting intramural hematoma versus communicating dissection.

METHODS: Retrospective database review identified patients who underwent magnetic resonance or computed tomography imaging revealing acute descending noncommunicating dissecting intramural hematoma or communicating dissection. Comparisons of clinical and anatomic characteristics and 1-year outcomes were performed.

RESULTS: Twenty-four noncommunicating dissecting intramural hematoma and 36 communicating dissection cases were identified. Patients with noncommunicating dissecting intramural hematoma were older (68.5 ± 8.8 versus 61.8 ± 11.6 years; p < 0.05). Although noncommunicating dissecting intramural hematoma often showed abdominal aorta extension (50%), the infrarenal level was spared. Communicating dissection characteristically extended beyond the diaphragm (89%), including into the infrarenal aorta (28%). There was no significant difference in rates of adverse clinical events for noncommunicating dissecting intramural hematoma versus communicating dissection (13% versus 30%; 0.10 > p > 0.05). By follow-up imaging (87% of population), aortic deterioration was more frequent in noncommunicating dissecting intramural hematoma versus communicating dissection cases (60% versus 15%; p < 0.005).

CONCLUSIONS: Acute descending noncommunicating dissecting intramural hematoma and communicating dissection represent two variants, with differing clinical and anatomic characteristics, but comparable levels of 1-year morbidity.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Noncommunicating dissecting intramural hematoma (NCDIH) is a variant of aortic dissection characterized by absence of flow in the false lumen [1]. Noncommunicating dissecting intramural hematoma may result from vasa vasorum rupture with subsequent propagation of subintimal hemorrhage [2]. As the incidence of NCDIH compared with communicating dissection (CD) of the aorta is small, much remains unknown regarding its natural history and prognosis for affected patients.

Many regard NCDIH as a more stable form of aortic dissection and precursor to CD [3–5]. Although patients with NCDIH involving the ascending aorta have a high incidence of complications, similar to ascending CD (DeBakey I and II and Stanford A) [3, 6, 7], recent reports suggest a somewhat less complicated course for patients with descending NCDIH [8–10]. Thus, the relative clinical significance of NCDIH compared with CD remains unclear; this is particularly true for forms beginning in the descending thoracic aorta, beyond the left subclavian artery origin. With the advent of new interventions (eg, endovascular stenting) for treatment of dissections, insights into the urgency and intensity of initial diagnostic evaluation and requirements for therapy or monitoring of cases with NCDIH are needed.

In this imaging-based investigation, the clinical significance of acute descending NCDIH was assessed relative to the corresponding form of CD (DeBakey III and Stanford B). To this end, the following goals were set: (1) clinical characteristics of a patient group without histories of thoracic aortic disease presenting with acute descending NCDIH diagnosed with magnetic resonance imaging (MRI) or contrast-enhanced computed tomography (CT) were compared with a corresponding group with acute descending CD; (2) anatomic characteristics of acute descending NCDIH and CD on MRI or CT were compared; and (3) 1-year clinical and imaging outcomes of these two groups were determined.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
After institutional review board approval, the following methods were applied.

Study patients
A retrospective review of our radiology database identified 28 cases with the diagnosis of acute descending NCDIH made by either MRI or CT between May 1991 and March 2001. All patients were urgently imaged because of symptoms (eg, acute chest pain) suggesting new aortic dissection, and were found to have acute NCDIH beginning beyond the left subclavian artery origin. In addition, a representative group of 47 symptomatic cases from the same period with MRI or CT diagnoses of acute descending CD was identified. No patients in either group had histories of significant thoracic aortic disease at the time of clinical presentation; those with confounding factors, including iatrogenic sources of dissection, aortic aneurysm, or penetrating aortic ulcer, were excluded. In addition, owing to patient identification from a combined MRI and CT database, patients with NCDIH or CD diagnosed by other means (eg, transesophageal echocardiography) during the same period were not represented. Last, patients with diagnoses of descending NCDIH or CD originally made using MRI or CT at a referring hospital were also excluded because of lack of availability of imaging data for reevaluation.

After retrospective review of each patient's clinical data in the hospital information system, the presence of specific risk factors associated with or predisposing to arterial disease was addressed. These risk factors included hypertension, diabetes mellitus, hyperlipidemia, tobacco use, and a positive personal or family history of coronary artery disease. Complete 1-year follow-up was available in 24 cases of descending NCDIH and 36 cases of descending CD; these 60 cases represent the study population.

Magnetic resonance imaging
Magnetic resonance imaging was performed with a 1.5-T scanner (Siemens Somatom Vision, Symphony or Sonata, Erlangen, Germany), using phased-array torso coil technology once developed. Electrocardiographically referenced static "dark-blood" and cine "bright-blood" imaging was performed. Absence of flow within the aortic wall in patients with NCDIH, representing fixed hematoma rather than flowing blood from CD, was supported with use of phase-contrast velocity mapping, dynamic tissue-tagging, or time-resolved contrast-enhanced (20 mL of Magnevist; Berlex Laboratories, Pine Brook, NJ) three-dimensional angiography. These MRI techniques have been described in greater detail elsewhere [11].

Imaging was performed in transaxial or oblique-sagittal orientations along the long axis of the thoracic aorta.

Computed tomography
Contrast-enhanced CT was performed with a helical scanner (Siemens Somatom Plus-4 or Volume Zoom). Test-contrast bolus administration (20 mL of Ultravist; Schering Pharmaceuticals, Berlin, Germany) during repetitive scanning at a mid-ascending or mid-descending thoracic aortic level was initially performed for determination of timing of diagnostic imaging with optimal blood-pool enhancement. This was followed by contrast-enhanced (100 mL of Ultravist) diagnostic helical scanning covering the thoracic and abdominal aorta, with (additional 50 mL of Ultravist) or without prospectively triggered sequential acquisition through the ascending aorta to overcome pulsation artifact. The basic details of these CT techniques have been previously described [12].

Diagnostic imaging criteria
Given the focus on forms of acute descending dissection, only cases with involvement of the thoracic aorta beginning beyond the left subclavian artery origin were included.

To ensure a "pure" population of acute descending NCDIH cases, most patients underwent MRI to confirm the absence of even slow flow within the false lumen. Diagnosis of NCDIH was based on evidence of formed hematoma within the aortic wall, manifested as an eccentric (crescent-shaped) to circumferential layer of smooth wall thickening with intermediate (≤7 days) to bright (>7 days) intensity on T1-weighted MRI (Fig 1) without evidence of intramural flow on the flow-sensitive acquisitions (Fig 2) [6]. On CT, NCDIH was manifested by the same cross-sectional patterns, but was characterized by baseline moderately high-attenuating smooth aortic wall thickening, without change after contrast administration (Fig 3) [13]. By either imaging modality, no focal intimal disruption allowing inflow into the hematoma was detected. In 2 patients, the diagnosis of NCDIH was made solely by MRI, and in 2 other patients, this diagnosis was made solely by CT. The diagnosis was supported by at least one complementary imaging examination (MRI, CT, transesophageal echocardiography, or conventional aortography) in the remaining 20 of 24 (83%) patients with NCDIH.



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  		Fig 1. Noncommunicating dissecting intramural hematoma beginning in the descending aorta on magnetic resonance imaging. Transaxial T1-weighted images of the aorta at the arch (left), mid-descending (center), and retrocardiac (right) segments show a crescentic to circumferential collection of relatively bright material representing intramural hematoma (arrows).

 


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  		Fig 2. Dark-blood (left), bright-blood (center), and systolic tissue-tagged (right) oblique-sagittal magnetic resonance imaging images confirm an immobile (ie, no grid movement on tissue-tagging) intramural thrombus mass (arrows).

 


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  		Fig 3. Noncommunicating dissecting intramural hematoma beginning in the descending aorta on computed tomography. Contrast-enhanced transaxial images at the arch (top left), proximal descending (top right), mid-descending (bottom left) and retrocardiac segment (bottom right) of the thoracic aorta demonstrate a spiraling crescentic to circumferential collection of moderately high-attenuating material within the aortic wall, representing intramural hematoma (arrows). Its attenuation was unchanged from precontrast scans owing to lack of communication with the central aortic lumen.

 
The diagnosis of descending CD was made if the typical double-channel appearance of the aortic lumen, because of an intimal flap separating flows within the true and false lumens, was observed on MRI or CT [14, 15]. Twenty-four of 36 (67%) patients diagnosed with CD had complementary imaging studies supporting the diagnosis.

Various anatomic characteristics of both acute descending NCDIH and CD were evaluated. First, the longitudinal extent of dissection was assessed. Note was made of the maximal thickness of the hematoma-filled false lumen in NCDIH cases. Measurements of the maximal total aortic diameter in both NCDIH and CD cases were standardized by assessment in the mid-descending thoracic aorta, performed at the pulmonary artery bifurcation level. Involvement and compromise of aortic side branches, including the renal arteries, was also addressed.

Assessment of the MRI and CT data was retrospectively performed by the most experienced investigator (R.D.W.) without knowledge of other imaging findings or clinical data.

Follow-up assessment
One-year clinical follow-up was accomplished by retrospective review of subsequent clinical and imaging data on each patient in the hospital information system and by direct contact with their primary-care physician. Clinical complications considered include end-organ ischemia, aortic rupture, and aorta-related death. Interventional needs include surgical or endovascular grafting procedures used to treat these complications.

After excluding patients who had an early aortic intervention (except for stenting of an individual affected artery for ischemia) or died, 46 of 53 patients (87%; 20 NCDIH and 26 CD) had subsequent imaging by MRI or CT during the follow-up period. Adverse imaging end points identified included dissection progression, further aortic wall deterioration, and significant interval dilatation (eg, diameter increase > 1 cm in 1 year).

Statistical analysis
Group comparisons of categorical variables were made using {chi}2 tests. Continuous variables were represented as mean ± standard deviation and compared using a standard Student's t test.

Univariate logistic regression identified predictors of adverse events by 1 year for each group. Probability values, c statistics, and odds ratios with corresponding 95% confidence intervals were calculated. C statistics measured the ability of each predictor to discriminate between two possible outcomes; it is equivalent to the nonparametric estimate of area under a receiver-operating characteristics curve. A p value less than 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Initial clinical and imaging findings
Comparison of baseline clinical characteristics of the 24 patients with acute descending NCDIH with those of the 36 patients with acute descending CD revealed that NCDIH patients were significantly older (68.5 ± 8.8 versus 61.8 ± 11.6 years; p < 0.05; Table 1). On the other hand, frequency of tobacco use was significantly higher in the CD group (78% versus 50%; p < 0.05).


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  		Table 1. Baseline Clinical Characteristics

 
Initial imaging studies in both the NCDIH and CD groups were performed urgently within a day of presentation, although in some cases there was delay between symptom onset and patient presentation. In NCDIH and CD patients, initial diagnostic MRI or CT imaging was performed a mean of 0.5 days (range, 0 to 6 days) and a mean of 1.2 days (range, 0 to 14 days) after symptom onset, respectively.

Initial imaging studies revealed that 50% of cases with descending NCDIH extended beyond the diaphragm, but none extended distal to the renal artery origins (Table 2). The pattern of extension of CD was significantly different, with cases more often showing involvement beyond the diaphragm level (89%), and a notable proportion (28%) extending beyond the renal artery level. The thickness of the hematoma-filled false lumen of NCDIH cases ranged from 0.5 to 2.0 cm (mean, 1.0 cm) with average maximum mid-descending thoracic aortic diameter of 3.8 ± 0.6 cm, comparable to 3.8 ± 0.5 cm in CD patients.


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  		Table 2. Anatomic Characteristics

 
After initial clinical stabilization, patients were followed for at least 1 year for clinical events, interventions, and changing imaging characteristics.

Clinical complications
Clinical complications of NCDIH (Fig 4) included related end-organ ischemia soon after symptom onset in 3 patients (13%), including renal (day 0; Fig 5), mesenteric (day 11), and spinal (day 0) ischemia. There were 2 aorta-related deaths in the NCDIH group: 1 patient with small bowel infarction (despite small bowel resection), and 1 patient who had distant ascending aortic CD within 24 hours of myocardial revascularization surgery followed by death owing to progressive multisystem organ failure (despite aortic surgical grafting).



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  		Fig 4. Flow diagram of complications and interventional needs in the noncommunicating dissecting intramural hematoma (NCDIH) group. Day number refers to the number of days after the initial onset of symptoms that the event occurred. Patients may have presented late to the treating institution leading to the delay in interventional treatment. (f/u = follow-up.)

 


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  		Fig 5. Noncommunicating dissecting intramural hematoma patient exhibiting acute end-organ ischemia. Two original images (top left, top middle), a maximum-intensity projection (top right), and a curved-multiplanar reconstruction (bottom) of a time-resolved contrast-enhanced magnetic resonance imaging angiography series confirm occlusion of the right renal artery (arrows) by the nonenhancing thickened portion of the abdominal aorta, representing the intramural hematoma. This results in lack of a right nephrogram (circles), whereas the left kidney is perfused by a patent left renal artery.

 
In CD patients (Fig 6), clinical complications included acute (all within day 3 of symptom onset) end-organ ischemia in 6 patients (17%), including 2 renal, 3 mesenteric, and 1 lower-extremity ischemia cases; there was also 1 (3%) patient with remote (day 150) lower-extremity ischemia. Early aortic rupture (all within day 30 of symptom onset, including 3 within day 10) occurred in 4 CD patients (11%). Aorta-related deaths occurred in 3 CD patients during the 1-year follow-up; early (day 4 and day 8) rupture accounted for 2 deaths (despite surgical grafting in 1), whereas the remaining death was caused by bowel infarction from mesenteric ischemia (despite stent grafting; Fig 6).



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  		Fig 6. Flow diagram of complications and interventional needs in the communicating dissection (CD) group. Day number refers to the number of days after the initial onset of symptoms that the event occurred. Patients may have presented late to the treating institution leading to the delay in interventional treatment. (f/u = follow-up.)

 
Although a strong trend was observed, there was no statistically significant difference in the rate of these adverse clinical events (13% for NCDIH versus 30% for CD; 0.10 > p > 0.05).

Interventional needs
After the initial presentation, patients were treated medically (eg, antihypertensives) unless dissection-related complications developed, for which acute or semielective intervention was performed.

Interventions for NCDIH (Fig 4) consisted of descending aortic surgical grafting in the patient with early renal ischemia; 1 patient underwent small bowel resection for mesenteric ischemia, whereas 1 patient with spinal ischemia received no intervention and remained paraplegic. No aortic graftings were performed for any patients in whom saccular outpouchings from the central lumen were demonstrated on follow-up imaging, although it was planned in the patient who had distant ascending CD after myocardial revascularization.

In the CD group, interventions included emergency surgical graftings in 2 of 4 patients developing aortic rupture; of the remaining 2 patients with rupture, 1 underwent urgent stent grafting and the other died before intervention. Semielective surgical grafting was performed in 3 CD patients with significant interval dilatation found by imaging. Six of 7 CD patients with evidence of ischemic complications underwent urgent stenting of the affected artery.

Adverse imaging end points
Excluding patients who had an early aortic intervention (except for stenting of an individual affected artery for ischemia) or died, 46 of 53 study patients (87%) had subsequent imaging by MRI or CT during the 1-year follow-up period. The results of at least one follow-up examination were available in 20 of 23 patients (87%) with NCDIH and 26 of 30 patients (87%) with CD (Figs 4 and 6).

Subsequent stabilization or improvement (eg, decreased hematoma thickness for NCDIH or increased false lumen thrombosis for CD) in the appearance of affected aortic segments was seen in 8 (40%) of NCDIH patients and 22 (85%) of CD patients during the subsequent 1-year period (p < 0.005); only 1 patient in each group demonstrated complete regression with restoration of relatively normal appearing aortic wall. No NCDIH or CD patients demonstrated progression of the dissection process, with direct extension into new segments.

Clear signs of further aortic wall degeneration were characteristic of only the NCDIH group; although no NCDIH patients showed evolution into a typical CD, 11 (55%, representing 46% of total NCDIH group) were found on follow-up imaging to have new focal saccular outpouchings of the central aortic lumen protruding into the residual hematoma with variable degrees of focal dilatation along the descending thoracic aorta (Fig 7).



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  		Fig 7. Noncommunicating dissecting intramural hematoma patient exhibiting subacute dilatation with saccular outpouchings. Corresponding dark-blood (left), bright-blood (center), and maximum-intensity projection (right) oblique-sagittal images on the day of acute presentation (top) and 20 days later (bottom) demonstrate the rapid development of large saccular outpouchings (arrows) into the intramural hematoma.

 
Significant interval dilatation was found by imaging in 1 (5%, representing 4% of total NCDIH group) NCDIH patient, but in 3 (12%, representing 10% of total CD group) CD patients.

Clinical and imaging predictors of adverse outcomes
By 1 year after their acute presentation, the 24 patients with descending NCDIH reached a clinical complication or adverse imaging end point at least as often as the 36 patients with descending CD (58% versus 39%; p > 0.05). In the NCDIH group, no significant predictors were found to account for the high incidence of these problems during the 1-year follow-up (Table 3). However, characteristics that were found to be marginally statistically significant predictors (p ≤ 0.10, c ≥ 0.67) of subsequent problems in NCDIH patients included age and initial hematoma thickness. In the CD group, only the initial diameter of the mid-descending aorta at presentation significantly predicted (p = 0.01, c = 0.74) an unfavorable outcome during the subsequent 1-year period.


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  		Table 3. Identification of Predictors of Adverse Events by 1 Year

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
Krukenberg [1] first described aortic NCDIH in 1920 as "dissection without intimal tear." In the absence of penetrating aortic ulcer [16], it is believed to result from spontaneous rupture of the aortic vasa vasorum with propagation of subintimal hemorrhage [2]. The resulting weakening of the aortic wall, which exhibits less distensibility [17], may lead to either outward wall rupture or inward intimal disruption.

The prevalence of NCDIH is 3% to 13% of all patients with acute aortic syndromes by remote autopsy studies [2, 18], but more recent prospective imaging studies suggest a higher occurrence of 13% to 53% [3, 4, 19, 20]. These data may reflect heightened awareness and detection of this disease entity, but could alternatively represent an overestimation as a result of inability to adequately visualize an intimal tear or slow flow within the false lumen from CD by some imaging modalities.

Initial clinical studies described NCDIH as a precursor to classic CD with a high rate of conversion [1–5]. On the other hand, recent studies suggest that NCDIH is distinctly different from CD with characteristic clinical features and prognosis [9, 10], and have led to growing concern that the etiology, clinical environment, anatomic traits, and clinical behavior of these two entities may differ considerably. Other dissection variants, including penetrating atherosclerotic ulcer [16], have been recognized as having differing pathogenesis, clinical features, and prognosis.

Given the similar clinical presentations of patients with acute NCDIH and those with acute CD, most are initially managed as CD. Similar to CD, NCDIH can be classified as Stanford type A (involvement of ascending aorta ± arch and descending aorta) or type B (beginning in descending portion of the thoracic aorta beyond the left subclavian artery) for planning therapy [21, 22]. Like their CD counterparts, forms of type A NCDIH have worse outcomes than forms of type B NCDIH [3, 8, 23]. Nevertheless, a great deal of controversy regarding the optimal treatment for NCDIH remains, but, in general, type A is treated surgically and type B is treated medically [22].

Prior studies have suggested that among patients with type B dissections, those with NCDIH have a more favorable prognosis than those with CD [8–10]. These studies have shown the overall in-hospital death rate to be lower for NCDIH [8]. Additionally, type B NCDIH was found more often to be associated with complete resolution and therefore a more benign prognosis over 6 months follow-up [9, 10].

Our results compare similarly with prior studies showing that NCDIH patients are significantly older than CD patients [8, 9, 16]. However, a significantly higher proportion of CD patients showed extension of the dissection into the abdominal aorta, including the infrarenal portion, compared with NCDIH patients.

Contrary to prior studies, we found no statistically significant difference in the rate of adverse clinical outcomes between the two groups of patients, not more favorable outcomes for NCDIH as suggested by earlier studies. Clinical complications did show a strong trend toward more frequent occurrence in the CD compared with NCDIH group (30% versus 13%; 0.10 > p > 0.05), which compares similarly with the reported literature [8]. Overall 1-year mortality was 8% for both NCDIH and CD groups, which again compares similarly with other studies [8, 23, 24]. However, after exclusion of patients who underwent early aortic intervention or death, in the 87% of patients with follow-up imaging, NCDIH showed significantly more frequent signs of aortic deterioration compared with CD (60% versus 15%; p < 0.005). In NCDIH, 1 patient had progressive aneurysmal dilatation and 11 patients had saccular outpouchings with degradative dilatation, a phenomenon previously reported as an early complication of NCDIH [25]. Because it lacks accompanying acute symptoms and demonstrates different anatomic characteristics from type B CD, it is our opinion that some investigators have incorrectly labeled this complication of NCDIH as representing CD [7]. No specific interventions were performed on NCDIH patients exhibiting outpouchings, but 1 patient died after experiencing distant aortic complications (ie, ascending aortic dissection) immediately after coronary artery bypass grafting. Most patients with CD showed little change in aortic appearance, although 3 patients had progressive aneurysmal dilatation requiring surgical grafting.

Interestingly, no patient initially diagnosed with NCDIH progressed to CD. This lends support to the belief that each is a distinct entity. This concept is supported by observations that early complications occur more commonly in CD, but subacute or remote complications frequently occur in NCDIH. Also, initial aortic diameter in CD, but not NCDIH, predicted adverse clinical or imaging outcomes whereas patient age and hematoma thickness were marginally predictive (0.05 < p ≤ 0.10) of further clinical or imaging events in NCDIH.

Currently, patients diagnosed with acute type B NCDIH are medically treated with antihypertensives and ß-blockers in a similar manner to patients diagnosed with acute type B CD. Our findings of subacute and remote complications occurring frequently in NCDIH suggest that these patients should be monitored closely in the months after the acute event with follow-up imaging studies to assess progression. It is unclear whether the presence of saccular outpouchings on follow-up imaging represents a stable lesion or portends more serious outcomes, but is likely that future intervention will be required.

There were several limitations to this study. First, although the diagnoses of descending aortic NCDIH or CD were made prospectively at the time of presentation, the identification, review, and follow-up of these patients was accomplished by retrospective database search, chart review, or primary-care physician contact. Identification of cases from the institutional MRI and CT database facilitated the needed access to imaging data for aortic characterization; this was a prerequisite to study-patient inclusion. Hence, patients whose diagnoses of acute NCDIH or CD were made in intensive care unit or surgical suite settings by transesophageal echocardiography owing to clinical instability precluding transportation for MRI or CT are not represented. Thus, the low incidence of clinical complications seen in our CD patients may be underestimated. However, with the increasing appreciation of imaging attributes of MRI and CT, including the simultaneous complete visualization of the thoracic and abdominal aorta, and with improvements in life support and monitoring during such imaging, their utilization for evaluation of even acutely ill patients should continue to grow. In addition, clinical instability related to type B dissection remains very uncommon, and the impact of this bias was probably minimal. Second, the high proportion of NCDIH compared with CD in this study population probably represents the nature of care at a tertiary hospital center to which patients are often referred for further assessment when a diagnosis is unclear such as with NCDIH more so than with CD, which is often treated medically at the local hospital. Third, follow-up imaging data were available in many but not all study patients; this failure was largely because of transfer of clinical care after the initial admission back to the local physician. Fourth, to ensure a truly representative NCDIH population, without any evidence of false lumen flow, the original goal was to obtain MRI on all patients with the presumptive diagnosis of NCDIH; however, with the introduction of multidetector CT technology in recent years, allowance was made for the inclusion of 3 additional patients.

In conclusion, NCDIH and CD beginning in the descending aorta represent two distinct disease entities, with differing clinical characteristics, anatomic characteristics, and outcomes, but with comparable levels of 1-year morbidity. Importantly, the results of this investigation indicate that acute descending NCDIH does not represent a precursor to acute or late descending CD and does not necessarily carry a more favorable prognosis.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
Dr Srichai was supported by an unrestricted training grant from Berlex Laboratories (Pine Brook, NJ).


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

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