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Background— Patent false lumen in aortic dissection has been associated with poor prognosis. We aimed to assess the natural evolution of this condition and predictive factors. Methods and Results— One hundred eighty-four consecutive patients, 108 surgically treated type A and 76 medically treated type B, were discharged after an acute aortic dissection with patent false lumen. Transesophageal echocardiography was performed before discharge, and computed tomography was performed at 3 months and yearly thereafter. Median follow-up was 6.42 years (quartile 1 to quartile 3: 3.31–10.49). Forty-nine patients died during follow-up (22 type A, 27 type B), 31 suddenly. Surgical or endovascular treatment was indicated in 10 type A and 25 type B cases. Survival free from sudden death and surgical-endovascular treatment was 0.90, 0.81, and 0.46 (95% CI, 0.36–0.55) at 3, 5, and 10 years, respectively. Multivariate analysis identified baseline maximum descending aorta diameter (hazard ratio [HR]: 1.32 [1.10–1.59]; P =0.003), proximal location (HR: 1.84 [1.06–3.19]; P =0.03), and entry tear size (HR: 1.13 [1.08–1.2]; P <0.001) as predictors of dissection-related adverse events, whereas mortality was predicted by baseline maximum descending aorta diameter (HR: 1.36 [1.08–1.70]; P =0.008), entry tear size (HR: 1.1 [1.04–1.16]; P =0.001), and Marfan syndrome (HR: 3.66 [1.65–8.13]; P =0.001). Conclusions— Aortic dissection with persistent patent false lumen carries a high risk of complications. In addition to Marfan syndrome and aorta diameter, a large entry tear located in the proximal part of the dissection identifies a high-risk subgroup of patients who may benefit from earlier and more aggressive therapy.

Cross-sectional imaging techniques allow excellent visualization of the cardiophrenic space. Under normal conditions, the cardiophrenic space is occupied by fat, the amount of which is usually increased in overweight individuals. It has been suggested that this fat accumulation correlates with the risk of cardiovascular disease. Several alterations originating above or below the diaphragm can affect the cardiophrenic space. Inflammatory lesions such as pericardial fat necrosis and tumoral masses are sometimes seen. Lymphoma is a major but not exclusive cause of cardiophrenic adenopathy and must be differentiated from lymphatic seeding of supradiaphragmatic and infradiaphragmatic malignancies. In patients with portal hypertension, cardiophrenic space varices are not uncommon. Other masses or pseudomasses occurring in this region include pericardial cysts, mediastinal tumors, and diaphragmatic hernia. Computed tomography and magnetic resonance imaging of the thorax are helpful in characterizing cardiophrenic lesions initially identified at plain radiography. Such characterization helps narrow the differential diagnosis when lesions are detected in this location.

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Aortic wall stiffness, tear size and location and the presence of abdominal side branches arising from the false lumen (FL) are key properties potentially involved in FL enlargement in chronic aortic dissections (ADs). We hypothesize that temporal variations on FL flow patterns, as measured in a cross-section by phase-contrast magnetic resonance imaging (PC-MRI), could be used to infer integrated information on these features. In 33 patients with chronic descending AD, instantaneous flow profiles were quantified in the FL at diaphragm level by PC-MRI. We used a lumped-parameter model to assess the changes in flow profiles induced by wall stiffness, tear size/location, and the presence of abdominal side branches arising from the FL. Four characteristic FL flow patterns were identified in 31/33 patients (94%) based on the direction of flow in systole and diastole: BA = systolic biphasic flow and primarily diastolic antegrade flow (n = 6); BR = systolic biphasic flow and primarily diastolic retrograde flow (n = 14); MA = systolic monophasic flow and primarily diastolic antegrade flow (n = 9); MR = systolic monophasic flow and primarily diastolic retrograde flow (n = 2). In the computational model, the temporal variation of flow directions within the FL was highly dependent on the position of assessment along the aorta. FL flow patterns (especially at the level of the diaphragm) showed their characteristic patterns due to variations in the cumulative size and the spatial distribution of the communicating tears, and the incidence of visceral side branches originating from the FL. Changes in wall stiffness did not change the temporal variation of the flows whereas it importantly determined intraluminal pressures. FL flow patterns implicitly codify morphological information on key determinants of aortic expansion in ADs. This data might be taken into consideration in the imaging protocol to define the predictive value of FL flows.