Prolonged (> 60 minutes) deep hypothermic circulatory arrest with retrograde cerebral perfusion was not a risk factor for mortality and stroke in patients who underwent surgery for aneurysms of the aortic arch. However, the prevalence of transient delirium necessitates further investigations.

The Impella microaxial-flow pump can directly unload left ventricle (LV) in cases of acute heart failure. Extracorporeal membrane oxygenation (ECMO) is widely used for circulatory support. Although the clinical effectiveness of ECMO has been demonstrated, insufficient LV loading reduction may not be advantageous for myocardial recovery. The objective was to compare ventricular loading reduction and reversibility of ventricular fibrillation (VF) with either Impella or ECMO. Six dogs were used. Extracorporeal membrane oxygenation was established by the femoral artery and right atrium. The Impella LD was inserted in LV by the ascending aorta. An acute failing heart was created by sequential coronary artery ligations. Pressure-volume (PV) relationships were acquired without a device and with ECMO or Impella. When VF occurred, direct cardioversion was performed while supported by either ECMO or Impella. The PV area, which is a measure of ventricular unloading and is correlated with myocardial oxygen consumption, decreased more with Impella than with ECMO. Successful defibrillation was achieved more effectively while under Impella support. Superior ventricular unloading with the Impella device may provide higher recovery potential to damaged hearts than ECMO and may have a significant impact not only on intensive care of patients with heart failure but also on resuscitation.

The long-term survival after surgery for atypical aortic coarctation was satisfactory. However, our study showed that complications associated with cardiovascular system or the operation could occur at any time after surgery; thus, life-long follow-up is mandatory. Further, the absence of normalization of blood pressure after surgery was a poor prognostic factor. Our results demonstrate the need for an intimate preoperative evaluation of renal and carotid artery lesions, which often coexist and may also cause secondary hypertension, to fully manage hypertension by surgery.

SUMMARYChanges in the expression levels of several genes have been described in aortic aneurysm specimens, however, the spectrum of diverse molecular alterations remains to be elucidated. We attempted to identify key molecules that modulate the pathogenesis of aortic aneurysm, using a complimentary DNA microarray carrying approximately 13,000 human genes.Segments of thoracic aortic aneurysms (TAA) and adjacent normal thoracic aortic tissues without aneurysmal changes (NTA) were obtained from 20 patients undergoing graft surgery. RNA obtained from five pairs of TAA and NTA samples was compared to determine aneurysm-specific alterations using microarray. Further, the expression levels of several genes of interest were verified in the remaining specimens by real-time reverse transcription-polymerase chain reaction (RT-PCR).In microarray assays, several types of the matrix metalloproteinases were upregulated as reported previously. Also, 220 genes suggested to be involved in protein degradation, inflammation, apoptosis, stress response, intracellular signaling, and other processes were significantly upregulated. Many of these genes have not been previously implicated in cardiovascular disease. The real time RT-PCR independently confirmed that the expression levels of MMP-2, MMP-9, ADAMTS-1, and caspase 4 were consistently increased in TAA.The results indicate that many genes are involved in a complicated manner in the pathogenesis of TAA. Investigation of these genes will help clarify the pathogenesis of this disease, and may lead to the discovery of novel therapeutic targets. (Int Heart J 2005; 46: 265-277)

Marfan syndrome is an inherited disorder characterized by genetic abnormality of microfibrillar connective tissue proteins. Endothelial dysfunction is thought to cause aortic dilation in subjects with a bicuspid aortic valve; however, the role of endothelial dysfunction and endothelial damaging factors has not been elucidated in Marfan syndrome. Flow-mediated dilation, a noninvasive measurement of endothelial function, was evaluated in 39 patients with Marfan syndrome. Aortic diameter was measured at the aortic annulus, aortic root at the sinus of Valsalva, sinotubular junction and ascending aorta by echocardiography, and adjusted for body surface area (BSA). The mean value of flow-mediated dilation was 6.5 ± 2.4 %. Flow-mediated dilation had a negative correlation with the diameter of the ascending thoracic aorta (AscAd)/BSA (R = -0.39, p = 0.020) and multivariate analysis revealed that flow-mediated dilation was an independent factor predicting AscAd/BSA, whereas other segments of the aorta had no association. Furthermore, Brinkman index had a somewhat greater influence on flow-mediated dilation (R = -0.42, p = 0.008). Although subjects who smoked tended to have a larger AscAd compared with non-smokers (AscA/BSA: 17.3 ± 1.8 versus 15.2 ± 3.0 mm/m(2), p = 0.013), there was no significant change in flow-mediated dilation, suggesting that smoking might affect aortic dilation via an independent pathway. Common atherogenic risks, such as impairment of flow-mediated dilation and smoking status, affected aortic dilation in subjects with Marfan syndrome.