Ventricular constraint in dilated cardiomyopathy: A new, compliant textile mesh exerts prophylactic and therapeutic properties

BackgroundDilated cardiomyopathy is associated with a progressive decrease in cardiac function, leading to end-stage heart failure. We aimed to stop this process by mechanically constraining the heart with a new, compliant textile mesh.MethodsIn 16 male Munich minipigs (50 ± 7 kg), dilated cardiomyopathy with congestive heart failure was induced through 4 weeks of rapid ventricular pacing (220 beats/min). In the early-mesh group (n = 8), a polyvinylidene fluoride mesh was positioned around both ventricles before pacing was started. In the other group (n = 8), experimental dilated cardiomyopathy through rapid pacing was induced (no mesh). After mesh grafting, rapid pacing was continued (late mesh).ResultsRapid pacing in the no-mesh group (control group) significantly decreased both systolic (cardiac output, peak systolic pressure, and the derivative of pressure increase [dP/dtmax]) and diastolic (minimum rate of pressure rise [dP/dtmin] and left ventricular end-diastolic pressure) variables, whereas these variables remained almost unchanged in the early-mesh group. In the late-mesh group the passive-elastic constraint not only prevented further deterioration but even exerted reverse remodeling to some extent (dP/dtmax and left ventricular end-diastolic pressure, P < .05).ConclusionsVentricular constraint with the new mesh seems to be a prophylactic and therapeutic option in cardiac insufficiency caused by ventricular dilation. This passive-elastic cardioplasty induced reverse remodeling of dilated hearts and significantly improved diastolic and systolic ventricular function

Toll-like receptor 9 and the inflammatory response to surgical trauma and cardiopulmonary bypass

Objectives Cardiac surgery can lead to post-operative end-organ complications secondary to activation of systemic inflammatory response. We hypothesize that surgical trauma or cardiopulmonary bypass (CPB) may initiate systemic inflammatory response via release of mitochondrial DNA (mtDNA) signaling Toll-like receptor 9 (TLR9) and interleukin-6 production (IL-6). Materials and methods The role of TLR9 in systemic inflammatory response in cardiac surgery was studied using a murine model of sternotomy and a porcine model of sternotomy and CPB. mtDNA and IL-6 were measured with and without TLR9-antagonist treatment. To study ischemia-reperfusion injury, we utilized an ex-vivo porcine kidney model. Results In the rodent model (n = 15), circulating mtDNA increased 19-fold (19.29 ± 3.31, p < 0.001) and plasma IL-6 levels increased 59-fold (59.06 ± 14.98) at 1-min post-sternotomy compared to pre-sternotomy. In the murine model (n = 11), administration of TLR-9 antagonists lowered IL-6 expression post-sternotomy when compared to controls (59.06 ± 14.98 vs. 5.25 ± 1.08) indicating that TLR-9 is a positive regulator of IL-6 after sternotomy. Using porcine models (n = 10), a significant increase in circulating mtDNA was observed after CPB (Fold change 29.9 ± 4.8, p = 0.005) and along with IL-6 following renal ischaemia-reperfusion. Addition of the antioxidant sulforaphane reduced circulating mtDNA when compared to controls (FC 7.36 ± 0.61 vs. 32.0 ± 4.17 at 60 min post-CPB). Conclusion CPB, surgical trauma and ischemic perfusion injury trigger the release of circulating mtDNA that activates TLR-9, in turn stimulating a release of IL-6. Therefore, TLR-9 antagonists may attenuate this response and may provide a future therapeutic target whereby the systemic inflammatory response to cardiac surgery may be manipulated to improve clinical outcomes

Forty years of carabid beetle research in Europe - from taxonomy, biology, ecology and population studies to bioindication, habitat assessment and conservation

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