Patency of the false lumen is a strong independent prognostic factor for type B aortic dissection. Location of the most dilated aortic segment at the distal arch is a significant risk factor in the patients with a patent false lumen.

Background-The short-term clinical benefits of bone marrow mononuclear cell transplantation have been shown in patients with critical limb ischemia. The purpose of this study was to assess the long-term safety and efficacy of bone marrow mononuclear cell transplantation in patients with thromboangiitis obliterans. Methods and Results-Eleven limbs (3 with rest pain and 8 with an ischemic ulcer) of 8 patients were treated by bone marrow mononuclear cell transplantation. The patients were followed up for clinical events for a mean of 684Ϯ549 days (range 103 to 1466 days). At 4 weeks, improvement in pain was observed in all 11 limbs, with complete relief in 4 (36%). Pain scale (visual analog scale) score decreased from 5.1Ϯ0.7 to 1.5Ϯ1.3. An improvement in skin ulcers was observed in all 8 limbs with an ischemic ulcer, with complete healing in 7 (88%). During the follow-up, however, clinical events occurred in 4 of the 8 patients. The first patient suffered sudden death at 20 months after transplantation at 30 years of age. The second patient with an incomplete healing of a skin ulcer showed worsening of the lesion at 4 months. The third patient showed worsening of rest pain at 8 months. The last patient developed an arteriovenous shunt in the foot at 7 months, which spontaneously regressed by 1 year. Conclusions-In the present unblinded and uncontrolled pilot study, long-term adverse events, including death and unfavorable angiogenesis, were observed in half of the patients receiving bone marrow mononuclear cell transplantation. Given the current incomplete knowledge of the safety and efficacy of this strategy, careful long-term monitoring is required for future patients receiving this treatment.

cute aortic dissection (AAD) can be fatal and should be diagnosed as early as possible. Without treatment, mortality increases by 1% per hour during the first 48 h. 1 Acute aortic dissection has traditionally been diagnosed by computed tomography (CT) because a rapid laboratory test has not been available. However, if the possibility of AAD could be ruled out, contrast-enhanced CT, which is time-consuming and impairs renal function with contrast media, would be unnecessary. Both the coagulation and fibrinolytic systems are reportedly activated in cases of AAD. 2 Weber et al found that assay of D-dimer (DD), a specific degradation product of cross-linked fibrin, had 100% sensitivity but only 69% specificity for detection of AAD. 3 A rapid bedside DD assay (Cardiac D-dimer, Roche Diagnostics, Mannheim, Germany) was recently developed for detection of pulmonary embolism and deep vein thrombosis. 4,5 One characteristic of patients with AAD is elevated systolic blood pressure, 1 and we hypothesized that elevated blood pressure could serve as a diagnostic indicator in cases of suspected AAD. Therefore, the first goal of the present study was to show the utility of rapid bedside DD assay in the detection of AAD. The second goal was to clarify whether positive predictive value could be increased if the rapid bedside DD assay value and blood pressure reading upon admission were used in combination. Circulation Journal Vol.69, April 2005 Methods PatientsThe study group included consecutive patients in whom AAD was suspected or not ruled out, who were admitted to the coronary care unit during the period November 2002 through June 2004 and in whom the DD level was determined by rapid bedside assay. Acute aortic dissection was suspected in patients with sudden onset of chest and/or back pain and no definitive electrocardiographic findings of Background A rapid laboratory test for diagnosis of acute aortic dissection (AAD) has not been available. We performed this prospective study to determine the utility of a rapid bedside D-dimer (DD) assay for detection of AAD. Methods and ResultsPatients with suspected AAD were recruited and their DD levels were measured by rapid bedside assay. They were divided into 2 groups according to enhanced computed tomography findings: an AAD group (n=30) and a non-AAD group (n=48). The median DD level was higher in the AAD group (1.80 g/ml) than in the non-AAD group (0.42 g/ml) (p=0.000). The rapid bedside DD assay showed 100% sensitivity, 54% specificity, 58% positive predictive value and 100% negative predictive value for detection of AAD with a normal DD level of up to 0.5 g/ml. The combination of DD level >0.5 g/ml and systolic blood pressure ≥180 mmHg showed 86% positive predictive value for detection of AAD.Conclusions We conclude that the rapid bedside DD assay is a highly sensitive method for early exclusion of AAD in patients with chest and/or back pain suggestive of AAD. Acute aortic dissection is highly probable if a rapid DD assay shows the elevated DD level with systolic blood press...

Approximately 20% of aortic aneurysm and/or dissection (AAD) cases result from inherited disorders, including several systemic and syndromatic connective-tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome, which are caused by mutations in the FBN1, COL3A1, and TGFBR1 and TGFBR2 genes, respectively. Nonsyndromatic AAD also has a familial background, and mutations of the ACTA2 gene were recently shown to cause familial AAD. In the present study, we conducted sequence analyses of the ACTA2 gene in 14 unrelated Japanese patients with familial thoracic AAD (TAAD), and in 26 with sporadic and young-onset TAAD. Our results identified three mutations of ACTA2, two novel [p.G152_T205del (c.616+1G>T), p.R212Q] and one reported (p.R149C), in the 14 patients with familial TAAD, and a novel mutation (p.Y145C) of ACTA2 in the 26 sporadic and young-onset TAAD patients, each of which are considered to be causative for TAAD. Some of the clinical features of these patients were the same as previously reported, whereas others were different. These findings confirm that ACTA2 mutations are important in familial TAAD, while the first sporadic and young-onset TAAD case with an ACTA2 mutation was also identified.