[FFR-Guided Revascularisation - Pros and Cons]. / FFR-gesteuerte Revaskularisation ­ wann indiziert, wann überflüssig?

An invasive measurement of the fractional flow reserve (FFR) allows the valuation of the individual risk for ischemic events in patients with coronary artery disease. Therefore, FFR has become a valuable tool to guide coronary revascularisations. The cut-off value ≤ 0.80 has been validated in many different subsets of patients. However, FFR values describe a risk continuum with an inverse correlation between FFR value and the risk of events. So FFR should always be interpreted regarding the patient's clinical context, especially in patients with a high risk for rapid disease progression. As such, patients with diabetes mellitus and deferred revascularisation based on FFR > 0.80 had worse clinical outcomes compared to patients without diabetes. In addition, FFR shows methodical deficiencies concerning the quantification of serial stenoses as well as the valuation of residual ischemia of the culprit vessel early after myocardial infarction. This article highlights both the strengths and the pitfalls in the use and interpretation of FFR.

Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene.

The present study aimed to characterize cardiac hypertrophy induced by activation of the renin-angiotensin system in terms of functional alterations on the level of the contractile proteins, employing transgenic rats harboring the mouse renin gene (TGR(mREN2)27). Ca2+-dependent tension and myosin ATPase activity were measured in skinned fiber preparations obtained from TGR(mREN2)27 and from age-matched Sprague-Dawley rats (SPDR). Western blots for troponin I (TnI) and troponin T (TnT) were performed and the phosphorylation status of TnI were evaluated in myocardial preparations. TnT and myosin heavy chain (MHC) isoforms were analyzed by RT-PCR. The pCa/tension relationship was shifted to the right in TGR(mREN2)27 compared to SPDR as indicated by increased Ca2+-concentrations required for half maximal activation of tension (SPDR 5.80, 95% confidence limits 5.77-5.82 vs. TGR(mREN2)27 5.69, 95% confidence limits 5.67-5.72, pCa units), while maximal developed tension was unaltered. Even more pronounced was the shift in the relationship between pCa and myosin-ATPase (SPDR 6.01, 95% confidence limits 5.99-6.03 vs. TGR(mREN2)27 5.77, 95% confidence limits 5.73-5.79, pCa units). The maximal myosin-ATPase activity was reduced in TGR(mREN2)27 compared to SPDR, respectively (211.0 +/- 28.77 micromol ADP/s vs. 271.6 +/- 43.66 micromol ADP/s, P < 0.05). Tension cost (ATPase activity/tension) was significantly reduced in TGR(mREN2)27. The beta-MHC expression was significantly increased in TGR(mREN2)27. There was no isoform shift for TnT (protein and mRNA), as well as TnI, and no alteration of the phosphorylation of TnI in TGR(mREN2)27 compared to SPRD. The present study demonstrates that cardiac hypertrophy, induced by an activation of the renin-angiotensin system, leads to adapting alterations on the level of the contractile filaments, which reduce tension cost.