Background
Aortic dilatation may occur in some patients even after complete repair of tetralogy of Fallot (TOF). The progression rate of the aortic diameter is so slow, and the incidence of aortic dissection is so low that it is suspected that frequent imaging of the aorta may not be necessary.
Case presentation
We describe an asymptomatic 41-year-old man with hypertension in whom aortic dilatation was accidentally discovered 39 years after TOF repair. He underwent ambulatory follow-up without any difficulty for 21 years after the repair. Contrast-enhanced computed tomography revealed significant aortic dilatation (maximum diameter of 88 mm at the sinus of Valsalva), and echocardiography revealed severe aortic regurgitation, which seemed to progress during the last 18 years without any evaluation or follow-up. The Bentall procedure was successfully performed using a valved graft, under deep hypothermic circulatory arrest with antegrade cerebral perfusion, and his postoperative course was uneventful. Histopathological examination of ascending aorta specimens revealed severe cystic medial degeneration.
Conclusions
Keeping in mind that a patient with rapid progression of the aortic dilatation after TOF repair exist, periodic follow-up for evaluation of the aorta is essential in patients with TOF.
Myocardial ischemia/reperfusion (MI/R) injury leads to aggravated cardiac remodeling and heart failure. Previously, we reported that 2,5-dimethylelcelecoxib (DMC), a derivative of celecoxib without cyclooxygenase-2 inhibition, prevents cardiac remodeling in a non-ischemic cardiac fibrosis model. In this study, we examined whether DMC inhibited myocardial remodeling associated with MI/R injury. The left anterior descending coronary artery was ligatured for 0.5 hours and subsequently subjected to reperfusion for MI/R injury in male C57 BL/6 mice. Vehicle or DMC was administered orally (DMC: 150 mg/kg) immediately after awakening and followed by feeding (DMC: 1000 ppm). Echocardiographic evaluation showed significant improvement of left ventricular ejection fraction in the DMCtreated group compared to the Vehicle-treated group at 1-4 weeks after MI/R injury. In MI/R-injured hearts, protein expression of alpha-smooth muscle actin (myofibroblast marker) was significantly reduced by DMC treatment, as were mRNA expressions of fibronectin, connective tissue growth factor, and matrix metalloproteinase-9, 3 days after injury. Masson trichrome staining indicated that DMC significantly reduced cardiac fibrosis area 4 weeks after MI/R injury. This study revealed that DMC decreased myofibroblast appearance, and suppressed fibrosis and cardiac dysfunction associated with MI/R injury. DMC might be useful for preventing the development of heart failure associated with reperfusion therapy for acute myocardial infarction.
We previously reported that 2, 5-dimethylcelecoxib (DMC), a derivative of celecoxib, suppresses cardiac remodeling by suppression of fibroblast-myofibroblast transformation. However, its effects on the immunoreactive responses remain unclear. As macrophages are known to play critical roles in the process of fibrosis after myocardial damage, we evaluated the effect of DMC on macrophages using a cryoinjury-induced myocardial infarction (CMI) model mouse. The anterior left ventricular was cryo-injured by a liquid nitrogen-cooled aluminum probe in male C57 BL/6 mice. The mice were provided feed containing DMC or vehicle starting 3 days before the operation. Echocardiography showed that DMC attenuated the impairment of cardiac function, and Masson's trichrome staining of cross-section heart showed DMC reduced fibrosis area at the 14 days post-operation. In the cryo-injured damage area, DMC increased CD163-positive anti-inflammatory (M2) macrophages 3 days after operation, but not CD86-positive proinflammatory (M1) macrophages. Real-time PCR showed that DMC suppressed mRNA expression of interleukin (IL) -1β, IL-6, and monocyte chemoattractant protein (MCP) -1, which are known as inflammatory cytokines, in the damaged myocardium. These results suggested that DMC could attenuate impairment of cardiac function and fibrosis after the cardiac damage through increasing accumulation of M2 macrophages and decreasing inflammatory cytokines. Thus, DMC has potential against cardiac fibrosis and could be useful for the treatment of cardiac remodeling.
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