After 2 decades of follow-up, the Mitroflow pericardial aortic valve continues to be a valve of choice with a predictable low rate of valve-related events, particularly for patients over the age of 65 to 70 years and others with comorbidities.

Our surgical strategy for right-sided infective endocarditis is based on three principles: (1) debridement of the infected area or vegetectomy; (2) valve repair whenever possible, avoiding artificial material; (3) if valve replacement is unavoidable, use of a biological substitute without any artificial material that might become infected. Following these strategies surgery of right-sided infective endocarditis with or without left-side involvement can be performed with good early, mid-term and long-term results. Patients with involvement of the left side showed not only worse preoperative conditions but also a significantly poorer clinical outcome than those with isolated right-sided infective endocarditis.

Cannulation of the right axillary artery improved the outcome of surgery for acute type A aortic dissection. However, postoperative complications occurred after both axillary and femoral artery cannulation.

The survival of patients differs significantly in dependence on their surgical urgency. Better outcome could have been achieved if patients had been referred earlier for surgery and operated upon before heart failure or septic shock developed. Long-term survival was better in patients without abscess formation. The low reinfection rate of Shelhigh bioprostheses in AIE is promising and the early and mid-term results achieved need to be verified in the long-term course.

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The Mitroflow external mounted, pericardial aortic bioprosthesis with documented excellent haemodynamics (especially for the small aortic root), demonstrates that prosthesis-patient mismatch in moderate and severe categories can essentially be eliminated, with durability performance comparable to other heterograft (porcine and pericardial) bioprostheses.

Keywords► cardiac surgery in Africa ► rheumatic and congenital heart surgery ► development models for cardiac programs ► pioneers in cardiac surgery AbstractBackground Current data on cardiac surgery capacity on which to base effective concepts for developing sustainable cardiac surgical programs in Africa are lacking or of low quality. Methods A questionnaire concerning cardiac surgery in Africa was sent to 29 colleagues-26 cardiac surgeons and 3 cardiologists in 16 countries. Further, data on numbers of surgeons practicing in Africa were retrieved from the Cardiothoracic Surgery Network (CTSNet).Results There were 25 respondents, yielding a response rate of 86.2%. Three models emerged: the Ghanaian/German model with a senior local consultant surgeon (Model 1); surgeons visiting for a short period to perform humanitarian surgery (Model 2); and expatriate surgeons on contract to develop cardiac programs (Model 3). The 933 cardiothoracic surgeons listed by CTSNet translated into one surgeon per 1.3 million people. In North Africa, the figure was three surgeons per 1 million and in sub-Saharan Africa (SSA), one surgeon per 3.3 million people. The identified 156 cardiac surgeons represented a surgeon to population ratio of 1:5.9 million people. In SSA, the ratio was one surgeon per 14.3 million. In North Africa, it was one surgeon per 1.1 million people. Open heart operations were approximately 12 per million in Africa, 2 per million in SSA, and 92 per million people in North Africa.

The contribution of the angiotensin (Ang) II type 2 receptor (AT2R) to cardiac hypertrophy is still controversial. Here we examined the effect of overexpressing the human AT2R in cultured porcine cardiac fibroblasts (pFib) on proliferation, procollagen I mRNA expression, and - as putatively underlying signal-transduction pathways - on mitogen-activated protein kinase ERK1/ERK2 and phosphotyrosine phosphatase activities. As quantitated by 125I-(Sar1,Ile8)-Ang II binding, transduction of cardiac fibroblasts with the adenoviral AT2R expression vector led to a six- to tenfold higher AT2 than endogenous Ang II type 1 receptor (AT1R) expression. The overexpressed AT2R had the same apparent molecular mass as the endogenous AT2R in rat PC12W cells. Proliferation was not significantly lower in AT2R expressing pFib than in antisense-transduced controls (TA2) upon stimulation with Ang II (AT2R 110.5+/-4.8% vs. TA2 110.2+/-5.5%), Ang II plus the AT1R blocker Irbesartan (97.1+/-1.4% vs. 108.0+/-5.0; P=0.052) and the partial AT2R antagonist CGP42112 at the agonistic concentration of 50 nM (92.1+/-2.7% vs. 99.8+/-3.1%; P=0.053). Procollagen Ialpha2 (COL1A2) mRNA levels were quantitated by (a) northern blot analysis and (b) reverse transcriptase polymerase chain reaction. COL1A2/GAPDH (a) and COL1A2/beta-actin (b) ratios revealed no differences between AT2R-transduced fibroblasts and antisense controls when stimulated with Ang II (1 microM, 24 h) plus Irbesartan and 10 ng/ml transforming growth factor beta1. Ang II stimulation of the endogenous AT1R increased extracellular signal regulated kinase 1/2 activities. This response was reduced by Irbesartan, but PD123319 had no effect. Time course and magnitude of Ang II stimulated ERK1/ERK2 activation was identical in AT2R-transduced and control cells. Also, neither simultaneous nor Ang II pre-stimulation, suggested to induce gene expression of the MAP kinase phosphatase 1, modulated phorbol myristate acetate-stimulated ERK1/ERK2 activation in AT2R-transduced pFib, in AT2R-transduced human umbilical vein endothelial cells, and in PC12W cells. By the use of a tyrosine phosphatase assay we observed an inhibition of phosphotyrosine phosphatase activity by 30.8% (P=0.009, n=5) after 5 min Ang II stimulation of AT2R-expressing pFib. Immunoprecipitation-tyrosine phosphatase assays revealed that inhibition of phosphotyrosine phosphatase 1B, which regulates insulin signaling, contributed to this effect. In conclusion, stimulation of the overexpressed human AT2R in porcine cardiac fibroblasts inhibited tyrosine phosphatase activity but had no significant effect on fibroblast functions related to cardiac fibrosis. It is conceivable that possible antifibrotic AT2R effects are species specific and/or require the interaction between fibroblasts and cardiomyocytes, probably via paracrine factors, or mechanical load.