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      Reduced Plasma NT-proBNP Levels Months after Myocardial Infarction Postconditioned with Lactate-Enriched Blood


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          Background: We recently reported a new approach, namely postconditioning with lactate-enriched blood (PCLeB), for cardioprotection in patients with ST-segment elevation myocardial infarction (STEMI). Objectives: We examined the effects of PCLeB on plasma NT-proBNP levels months after myocardial infarction (MI). Methods: The study included consecutive patients ( n = 31) undergoing percutaneous coronary intervention (PCI) for anterior STEMI within 12 h of symptom onset in our hospital between March 2014 and August 2018. We retrospectively compared plasma NT-proBNP levels several months after MI in these patients with those in historical control patients ( n = 32). The control patients included consecutive patients who underwent successful PCI without PCLeB for anterior STEMI within 12 h of symptom onset in our hospital between March 2009 and February 2014. We compared the highest plasma NT-proBNP values 6–10 months after MI in the postconditioned patients with the lowest plasma NT-proBNP values 6–10 months after MI in the control patients. In the PCLeB protocol, the duration of each brief reperfusion was increased stepwise from 10 to 60 s. Lactated Ringer’s solution (30 mL) was injected directly in the culprit coronary artery at the end of each brief reperfusion. Each ischemic episode lasted 60 s. Results: Plasma NT-proBNP levels in the postconditioned patients months after MI (211 ± 207 pg/mL) were significantly lower than those in the control patients (516 ± 598 pg/mL; p < 0.0001). Conclusion: PCLeB was associated with reduced plasma NT-proBNP levels months after MI.

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          Effect of Ischemic Postconditioning During Primary Percutaneous Coronary Intervention for Patients With ST-Segment Elevation Myocardial Infarction: A Randomized Clinical Trial.

           Thomas Engstrøm (corresponding) ,  Henning Kelbæk,  Steffen Helqvist (2017)
          Ischemic postconditioning of the heart during primary percutaneous coronary intervention (PCI) induced by repetitive interruptions of blood flow to the ischemic myocardial region immediately after reopening of the infarct-related artery may limit myocardial damage.
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            Is Open Access

            Effect of Ischemic Postconditioning on Infarct Size in Patients With ST‐Elevation Myocardial Infarction Treated by Primary PCI Results of the POSTEMI (POstconditioning in ST‐Elevation Myocardial Infarction) Randomized Trial

            Background Reduction of infarct size by ischemic postconditioning (IPost) has been reported in smaller proof‐of‐concept clinical studies, but has not been confirmed in other smaller studies. The principle needs to be evaluated in larger groups of ST‐elevation myocardial infarction (STEMI) patients before being implemented in clinical practice. This study assessed the effect of ischemic postcoditioning (IPost) on infarct size in patients with STEMI treated by primary percutaneous coronary intervention (PCI). Methods and Results Patients with first‐time STEMI, <6 hours from symptom onset, referred to primary PCI were randomized to IPost or control groups. IPost was administered by 4 cycles of 1‐minute reocclusion and 1‐minute reperfusion, starting 1 minute after opening, followed by stenting. In the control group, stenting was performed immediately after reperfusion. The primary endpoint was infarct size measured by cardiac magnetic resonance after 4 months. A total of 272 patients were randomized. Infarct size (percent of left ventricular mass) after 4 months (median values and interquartile range) was 14.4% (7.7, 24.6) and 13.5% (8.1, 19.3) in the control group and IPost group, respectively (P=0.18). No significant impact of IPost was found when controlling for baseline risk factors of infarct size in a multivariate linear regression model (P=0.16). The effects of IPost on secondary endpoints, including markers of necrosis, myocardial salvage, and ejection fraction, as well as adverse cardiac events during follow‐up, were consistently neutral. Conclusions In contrast to several smaller trials reported previously, we found no significant effects of IPost on infarct size or secondary study outcomes. Clinical Trial Registration URL: http://www.clinicaltrials.gov Unique identifier: NCT.No.PO1506.
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              Delayed recovery of intracellular acidosis during reperfusion prevents calpain activation and determines protection in postconditioned myocardium.

              Indirect data suggest that delayed recovery of intracellular pH (pHi) during reperfusion is involved in postconditioning protection, and calpain activity has been shown to be pH-dependent. We sought to characterize the effect of ischaemic postconditioning on pHi recovery during reperfusion and on calpain-dependent proteolysis, an important mechanism of myocardial reperfusion injury. Isolated Sprague-Dawley rat hearts were submitted to 40 min of ischaemia and different reperfusion protocols of postconditioning and acidosis. pHi was monitored by (31)P-NMR spectroscopy. Myocardial cell death was determined by lactate dehydrogenase (LDH) and triphenyltetrazolium staining, and calpain activity by western blot measurement of alpha-fodrin degradation. In control hearts, pHi recovered within 1.5 +/- 0.24 min of reperfusion. Postconditioning with 6 cycles of 10 s ischaemia-reperfusion delayed pHi recovery slightly to 2.5 +/- 0.2 min and failed to prevent calpain-mediated alpha-fodrin degradation or to elicit protection. Lowering perfusion flow to 50% during reperfusion cycles or shortening the cycles (12 cycles of 5 s ischemia-reperfusion) resulted in a further delay in pHi recovery (4.1 +/- 0.2 and 3.5 +/- 0.3 min, respectively), attenuated alpha-fodrin proteolysis, improved functional recovery, and reduced LDH release (47 and 38%, respectively, P < 0.001) and infarct size (36 and 32%, respectively, P < 0.001). This cardioprotection was identical to that produced by lowering the pH of the perfusion buffer to 6.4 during the first 2 min of reperfusion or by calpain inhibition with MDL-28170. These results provide direct evidence that postconditioning protection depends on prolongation of intracellular acidosis during reperfusion and indicate that inhibited calpain activity could contribute to this protection.

                Author and article information

                S. Karger AG
                April 2020
                04 February 2020
                : 145
                : 4
                : 199-202
                Department of Cardiology, Saitama Municipal Hospital, Saitama, Japan
                Author notes
                *Takashi Koyama, MD, Department of Cardiology, Saitama Municipal Hospital, 2460 Mimuro, Midori-ku, Saitama City, Saitama 336-8522 (Japan), koyamas@me.com
                505903 Cardiology 2020;145:199–202
                © 2020 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 1, Pages: 4
                CAD and AMI: Short Communication


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