Background— Retrograde type A aortic dissection has been deemed a rare complication after endovascular stent graft placement for type B dissection. However, this life-threatening event appears to be underrecognized and is worth being investigated further. Methods and Results— Eleven of 443 patients developed retrograde type A aortic dissection during or after stent grafting for type B dissection from August 2000 to June 2007. Of these 11 patients, 3 had Marfan syndrome. The Kaplan–Meier estimate of the rate of freedom from this event at 36 months is 97.4% (95% confidence interval, 0.95 to 0.99). The new entry was located at the tip of the proximal bare spring of the stent graft in 9 patients, was within the anchoring area of the proximal bare spring in 1, and remained unknown in 1 patient. Eight patients were converted to open surgery, and 2 received medical treatment. One patient suddenly died 2 hours after the primary stent grafting, and 2 died within 1 week after the surgical conversion, so mortality reached 27.3%. During the follow-up from 3 to 50 months, type I endoleak was identified in 1 patient 3 months after the surgical exploration and disappeared at 6 months. Conclusions— Retrograde type A aortic dissection after stent grafting for type B dissection appears not to be rare and results from mixed causes. Fragility of the aortic wall and disease progression may predispose to it, whereas stent grafting–related factors make important and provocative contributions. Avoiding aortic arch stent grafting in Marfan patients, preferably selecting the endograft without the proximal bare spring for patients with a kinked aortic arch or with Marfan syndrome (if endografting is used), improving the device design, and standardizing endovascular manipulation might lessen its occurrence.

Acute myocardial infarction and stroke are more likely to occur in the early morning. Circadian pacemakers are considered to be involved in the process. Many peripheral tissues and cells also contain clock systems. In this study, we examined whether the primary cultured human plaque-derived vascular smooth muscle cells (VSMCs) process circadian rhythmicity; furthermore, we investigated the expression difference of clock genes between normal human carotid VSMCs and human plaque-derived VSMCs. Fifty-six human carotid plaques provided the atherosclerotic tissue, and 21 samples yielded viable cultured primary VSMCs. The normal carotid VSMCs were cultured from donors’ normal carotids. The mRNA levels of the target genes were measured by Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). After serum shock, both types of cells showed clear circadian expressions of Bmal1, Cry1, Cry2, Per1, Per2, Per3 and Rev-erbα mRNA; meanwhile the Clock mRNA show a rhythmic expression in plaque-derived SMCs but not in normal carotid VSMCs. The expression levels of these main clock genes were significantly attenuated in human plaque-derived VSMCs compared with normal human carotid VSMCs. The rhythm of Bmal1 mRNA in plaque-derived VSMCs was changed. The present results demonstrate that the human plaque-derived VSMCs possess different circadian rhythmicity from that of normal carotid VSMCs. The rhythm changes of clock genes in plaque-derived VSMCs may be involved in the process of atherosclerosis and finally promote the rupture of plaque.

Muscle necrosis and angiogenesis are two major challenges in the treatment of lower-limb ischemic diseases. In this study, a triple-functional Sr/Si-containing bioceramic/alginate composite hydrogel with simultaneous bioactivity in enhancing angiogenesis, regulating inflammation, and inhibiting muscle necrosis was designed to treat lower-limb ischemic diseases. In particular, sodium alginate, calcium silicate and strontium carbonate were used to prepare injectable hydrogels, which was gelled within 10 min. More importantly, this composite hydrogel sustainedly releases bioactive Sr²⁺ and SiO₃ ^2- ions within 28 days. The biological activity of the bioactive ions released from the hydrogels was verified on HUVECs, SMCs, C2C12 and Raw 264.7 cells in vitro, and the therapeutic effect of the hydrogel was confirmed using C57BL/6 mouse model of femoral artery ligation in vivo. The results showed that the composite hydrogel stimulated angiogenesis, developed new collateral capillaries, and re-established the blood supply. In addition, the bioactive hydrogel directly promoted the expression of muscle-regulating factors (MyoG and MyoD) to protect skeletal muscle from necrosis, inhibited M1 polarization, and promoted M2 polarization of macrophages to reduce inflammation, thereby protecting skeletal muscle cells and indirectly promoting vascularization. Our results indicate that these bioceramic/alginate composite bioactive hydrogels are effective biomaterials for treating hindlimb ischemia and suggest that biomaterial-based approaches may have remarkable potential in treating ischemic diseases.