Ischemic postconditioning (IPCD) significantly reduces infarct size in healthy animals and protects the human heart. Because obesity is a major risk factor of cardiovascular diseases, the effects of IPCD were investigated in 8- to 10-wk-old leptin-deficient obese (ob/ob) mice and compared with wild-type C57BL/6J (WT) mice. All animals underwent 30 min of coronary artery occlusion followed by 24 h of reperfusion associated or not with IPCD (6 cycles of 10-s occlusion, 10-s reperfusion). Additional mice were killed at 10 min of reperfusion for Western blotting. IPCD reduced infarct size by 58% in WT mice (33+/-1% vs. 14+/-3% for control and IPCD, respectively, P<0.05) but failed to induce cardioprotection in ob/ob mice (53+/-4% vs. 56+/-5% for control and IPCD, respectively). In WT mice, IPCD significantly increased the phosphorylation of Akt (+77%), ERK1/2 (+41%), and their common target p70S6K1 (+153% at Thr389 and +57% at Thr421/Ser424). In addition, the phosphorylated AMP-activated protein kinase (AMPK)-to-total AMPK ratio was also increased by IPCD in WT mice (+64%, P<0.05). This was accompanied by decreases in phosphatase and tensin homolog deleted on chromosome 10 (PTEN), MAP kinase phosphatase (MKP)-3, and protein phosphatase (PP)2C levels. In contrast, IPCD failed to increase the phosphorylation state of all these kinases in ob/ob mice, and the level of the three phosphatases was significantly increased. Thus, although IPCD reduces myocardial infarct size in healthy animals, its cardioprotective effect vanishes with obesity. The lack of enhanced phosphorylation by IPCD of Akt, ERK1/2, p70S6K1, and AMPK might partly explain the loss of cardioprotection in this experimental model of obese mice.

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Introduction: Endocarditis on aortic prosthesis that we all fear as patients with heart valve prosthesis, is a rare disease less than 1% of cases.However, its evolution is very unfavorable when it occurs. The appearance of a fever, often insidious, is a sure sign of the disease. Diagnosis is based on blood cultures and echocardiography. This clinical case is an opportunity for us to recall the seriousness of this condition both for patients and for cardiac surgeons. Methods: We report the case of an adult aged 51 with two mechanical mitro-aortic prostheses implanted in 2001 presenting endocarditis on aortic prosthesis complicated by aortic leak, atrioventricular block (AVB) and stroke leaving as a sequela a hemiplegia with infectious aneurysm of the right sinus ruptured in the right atrium (RA) in cardiac decompensation with persistent fever and orthopnea despite well-conducted triple anti-staphylococcal antibiotic therapy with clinical examination: aortic systolic murmur with crackling rales. Chest X-ray: cardiomegaly, flaky opacities, transthoracic echocardiography: large aneurysm on the right coronary side fistulized in the right atrium (RA), desinsertion of the aortic prosthesis with grade IV paraprosthetic aortic leak, left ventricular (LV): 52/32 mm, an undilated right ventricular (RV), an ejection fraction (EF) at 64 %, and finally a systolic arterial pulmonary pressure (SAPP) at 68 mmHg. Positive blood cultures: staphylococcus. Intraoperative exploration: voluminous vegetation next to the exit orifice of the aorta-right atrium fistula, desinsertion of the aortic prosthesis on the peri-annular abscess and vegetation on the aortic wings, destruction of the mitro-aortic junction with the presence of a fistula aorta-right atrium. He benefited from explantation of the aortic prosthesis, vegetation sent to bacteriology, reconstitution of the aortic annulus on the right coronary-left coronary (RC-LC) side by a Dacron® patch, closure of the entry orifice of the fistula on the aortic side by separate points and reconstruction of the mitro-aortic junction with a triangular Dacron® patch, implantation of an aortic prosthesis