Key result
Remote Ischemic Preconditioning prior to TF-TAVI did not significantly reduce necrosis or apoptosis markers, but significantly lowered the increase in IL-1b levels at 24 hours (p < 0.01).
Why the study?
It was unclear whether remote ischemic preconditioning confers protective effects against cardiac injury and inflammation in patients undergoing TF-TAVI.
Does Remote Ischemic Preconditioning (RIPC) reduce myocardial injury and inflammation in patients with severe aortic valve stenosis undergoing TF-TAVI?
RCT (n=55)
random consecutive
Does Remote Ischemic Preconditioning (RIPC) reduce myocardial injury and inflammation in patients with severe aortic valve stenosis undergoing TF-TAVI?
p-value: p=< 0.01
Remote ischemic preconditioning prior to TF-TAVI reduced post-procedural inflammation (IL-1b) but did not significantly affect markers of myocardial necrosis or apoptosis.
RIPC does not reduce myocardial injury markers in TF-TAVI; challenges preconditioning efficacy and does not support routine use.
BACKGROUND: Remote ischemic preconditioning (RIPC) is being evaluated as a strategy to reduce cardiac injury and inflammation in patients undergoing diverse cardiac invasive and surgical procedures. However, it is unclear whether RIPC has protective effects in patients undergoing the transfemoral- transcatheter aortic valve implantation (TF-TAVΙ) procedure. METHODS: Between September 2013 and September 2015, 55 random consecutive patients were prospectively assigned to receive SHAM preconditioning (SHAM, 22 patients) or Remote Ischemic Preconditioning (RIPC) (4 cycles of 5 min intermittent leg ischemia and 5 min reperfusion, 33 patients) prior to TF-TAVI. The primary endpoint was to determine the serum levels of: hs-cTn-I (necrosis), CK-18 (apoptosis), and IL-1b (inflammation). Quantification was performed using commercially available ELISA kits. Patients were sampled 1-day pre TF-TAVΙ and 24-hours post TF-TAVΙ. Secondary endpoints included: total mortality, incidence of periprocedural clinical acute myocardial infarction (AMI), acute kidney injury (AKI), and stroke. RESULTS: 22 SHAM patients and 33 RIPC patients were finally analyzed. Our data revealed no significant difference in serum levels of hs-cTn-I and CK-18 among various groups. However, in the RIPC group, the increase in IL1b level was significantly lower for 24-h post TF-TAVΙ, (p < 0.01). There were no significant differences between groups in the secondary endpoints at the follow-up interval of one month. RIPC-related adverse events were not observed. CONCLUSIONS: Our data suggest that RIPC did not exhibit significant cardiac or kidney protective effects regarding necrosis and apoptosis in patients undergoing TF-TAVΙ. However, an important anti-inflammatory effect was detected in the RIPC group.
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Halapas et al. (2021) conducted an RCT in severe aortic valve stenosis undergoing Transcatheter Aortic Valve Replacement (TF-TAVI) (n=55). Remote Ischemic Preconditioning (RIPC) vs. SHAM preconditioning was evaluated on Serum levels of hs-cTn-I (necrosis), CK-18 (apoptosis), and IL-1b (inflammation) at 24-hours post TF-TAVI (p=< 0.01). Remote Ischemic Preconditioning prior to TF-TAVI did not significantly reduce necrosis or apoptosis markers, but significantly lowered the increase in IL-1b levels at 24 hours (p < 0.01).
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