Long-term Follow-up of Patients Undergoing Postconditioning During ST-Elevation Myocardial Infarction
Rent the article at a discountRent now
* Final gross prices may vary according to local VAT.Get Access
Reperfusion injury may offset the optimal salvage of myocardium achieved during primary coronary angioplasty. Thus, coronary reperfusion must be combined with cardioprotective adjunctive therapies in order to optimize myocardial salvage and minimize infarct size. Forty-three patients with their first ST-elevation myocardial infarction were randomized to myocardial postconditioning or standard of care at the time of primary coronary angioplasty. Postconditioning was performed immediately upon crossing the lesion with the guide wire and consisted of four cycles of 30 s occlusion followed by 30 s of reperfusion. End-points included infarct size, myocardial perfusion grade (MPG), left-ventricular ejection fraction (LVEF), and long-term clinical events (death and heart failure). Despite similar ischemic times (≅4.5 h) (p = 0.9) a reduction in infarct size was observed among patients treated with the postconditioning protocol. Peak creatine phosphokinase (CPK), as well as its myocardial band (MB) fraction, was significantly lower in the postconditioning group when compared with the control group (CPK—control, 2,444 ± 1,928 IU/L vs. PC, 2,182 ± 1,717 IU/L; CPK-MB—control, 242 ± 40 IU/L vs. PC, 195 ± 33 IU/L; p = 0.64 and p < 0.01, respectively). EF in the postconditioning group was improved when compared with the control group (control, 43% ± 15 vs. PC, 52% ± 9; p = 0.05). After a mean follow-up of 3.4 years, a 6-point absolute difference in LVEF was still evident in the postconditioning group (p = 0.18). MPG was better among patients treated with the postconditioning protocol compared with control (2.5 ± 0.5 vs. 2.1 ± 0.6; p = 0.02). Due to the small sample size no significant differences in clinical events were detected (p value for death = 0.9; p value for heart failure = 0.2). A simple postconditioning protocol applied at the onset of mechanical reperfusion, resulted in reduction of infarct size, better epicardial and myocardial flow, and improvement in left ventricular function. The beneficial effects of postconditioning on cardiac function persist beyond 3 years.
- Lloyd-Jones, D., Adams, R. J., Brown, T. M., et al. (2010). Heart disease and stroke statistics—2010 update: a report from the American Heart Association. Circulation, 121, e46–e-215. CrossRef
- Gruppo Italiano per lo Studio dell Streptochinasi nell’Infarcto Miocardico (GISSI). (1990). GISSI-2: a factorial randomised trial of alteplase versus streptokinase and heparin versus no heparin among 12 490 patients with acute myocardial infarction. Lancet, 336, 65–71.
- ISIS-3 (Third International Study of Infarct Survival Collaborative Group). (1992). ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin and heparin vs heparin alone among 41 299 cases of suspected acute myocardial infarction. Lancet, 339, 753–770. CrossRef
- Grines, C. L., Browne, K. F., & Marco, J. (1993). A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The New England Journal of Medicine, 328, 673–679. CrossRef
- Keeley, E. C., Boura, J. A., & Grines, C. L. (2003). Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet, 361, 13–20. CrossRef
- Henry, T. D., Unger, B. T., Sharkey, S. W., Lips, D. L., Pedersen, W. R., Madison, J. D., et al. (2005). Design of a standardized system for transfer of patients with ST-elevation myocardial infarction for percutaneous coronary intervention. American Heart Journal, 150, 373–338. CrossRef
- Henry, T. D., Sharkey, S. W., Burke, M. N., et al. (2007). A regional system to provide timely access to percutaneous coronary intervention for ST-elevation myocardial infarction. Circulation, 116(7), 721–728. CrossRef
- US Department of Health and Human Services. Website: http://www.hospitalcompare.hhs.gov/Hospital/Search/Welcome.asp?version=default&browser=Safari%7C5%7CMacOSX&language=English&defaultstatus=0&MBPProviderID=&TargetPage=&ComingFromMBP=&CookiesEnabledStatus=&TID=&StateAbbr=&ZIP=&State=&pagelist=Home. Accessed on June 30th 2010.
- Yellon, D. M., & Hausenloy, D. J. (2007). Myocardial reperfusion injury. The New England Journal of Medicine, 357(11), 1121–1135. CrossRef
- Mahaffey, K. W., Puma, J. A., Barbagelata, N. A., et al. (1999). Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlled trial: the Acute Myocardial Infarction STudy of Adenosine (AMISTAD) trial. Journal of the American College of Cardiology, 34, 1711–1720. CrossRef
- Ross, A., Gibbons, R., Kloner, R. A., et al. (2002). Acute Myocardial Infarction Study of Adenosine (AMISTAD II). Journal of the American College of Cardiology, 39, 883–886. CrossRef
- Granfeldt, A., Jiang, R., Wang, N.-P., Mykytenko, J., Eldaif, S., Deneve, J., et al. (2008). Inhibition of neutrophils is critical to the in vivo cardioprotection of postconditioning. Circulation, 118, S403.
- Shandelya, S., Kuppusamy, P., Weisfeldt, M. L., & Zweier, J. L. (1993). Evaluation of the role of polymorphonuclear leukocytes on contractile function in myocardial reperfusion injury. Circulation, 87, 536–546.
- Kevin, L. G., Camara, A. K. S., Riess, M. L., Novalija, E., & Stowe, D. F. (2003). Ischemic preconditioning alters real-time measure of O2 radicals in intact hearts with ischemia and reperfusion. American Journal of Physiology Heart and Circulatory Physiology, 284, H566–H574.
- Sun, H. Y., Wang, N. P., Kerendi, F., Halkos, M., Kin, H., Guyton, R. A., et al. (2005). Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload. American Journal of Physiology Heart and Circulatory Physiology, 288, H1900–H1908. CrossRef
- Kin, H., Wang, N. P., Mykytenko, J., Reeves, J., Deneve, J., Jiang, R., et al. (2008). Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-κ B translocation and TNF α release. Shock, 29, 761–768.
- Kin, H., Zhao, Z. Q., Sun, H. Y., et al. (2004). Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovascular Research, 62, 74–85. CrossRef
- Zhao, Z.-Q., Corvera, J. S., Halkos, M. E., Kerendi, F., Wang, N.-P., Guyton, R. A., et al. (2003). Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. American Journal of Physiology Heart and Circulatory Physiology, 285, H579–H588.
- Murry, C. E., Jennings, R. B., & Reimer, K. A. (1986). Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation, 74, 1124–1136.
- Staat, P., Rioufol, G., Piot, C., et al. (2005). Postconditioning the Human Heart. Circulation, 112, 2143–2148. CrossRef
- Thibault, H., Piot, C., Staat, P., Bontemps, L., Sportouch, C., Rioufol, G., et al. (2008). Long-term benefit of postconditioning. Circulation, 117, 1037–1044. CrossRef
- Lonborg, J., Kelbaek, H., Vejlstrup, N., Jorgensen, E., Helqvist, S., Saunamaki, K., et al. (2010). Cardioprotective effects of ischemic postconditioning in patients treated with primary percutaneous coronary intervention, evaluated by magnetic resonance. Circ Cardiovasc Interv, 3, 34–41. CrossRef
- Antman, E. M. (2008). Time is muscle: translation into practice. Journal of the American College of Cardiology, 52, 1216–1221. CrossRef
- Stone, G. W., Witzenbichler, B., Guagliumi, G., et al. (2008). Bivalirudin during primary PCI in acute myocardial infarction. The New England Journal of Medicine, 358, 2218–2230. CrossRef
- Gibson, C. M., Cannon, C. P., Murphy, S. A., et al. (2000). Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs. Circulation, 101, 125–130.
- Vinten-Johansen, J., Yellon, D., & Opie, L. (1005). Postconditioning. A simple, clinically applicable procedure to improve revascularization in acute myocardial infarction. Circulation, 112, 2085–2088. CrossRef
- Yellon, D. M., & Downey, J. P. (2003). Preconditioning the myocardium: from cellular physiology to clinical cardiology. Physiological Reviews, 83, 1113–1151.
- Yang, X. M., Proctor, J. B., Halkos, M. E., et al. (2004). Multiple, brief coronary occlusions during early reperfusion Project rabbit hearts by targeting cell signaling pathways. Journal of the American College of Cardiology, 44, 1103–1110. CrossRef
- Tsang, A., Hausenloy, D. J., Mocanu, M. M., & Yellon, D. M. (2004). Postconditioning: a form of “modified reperfusion” protects the myocardium by activating the phosphatidylinositol 3-kinase-Akt pathway. Circulation Research, 95, 230–232. CrossRef
- Downey, J., & Cohen, M. (2005). We think we see a pattern emerging here. Circulation, 11, 120–121. CrossRef
- Okamoto, F., Allen, B. S., Buckberg, G. D., Bugyi, H., & Leaf, J. (1986). Reperfusion conditions: importance of ensuring gentle versus sudden reperfusion during relief of coronary occlusion. Journal of Thoracic and Cardiovascular Surgery, 92, 613–620.
- Sato, H., Jordan, J. E., Zhao, Z. Q., Sarvotham, S. S., & Vinten-Johansen, J. (1997). Gradual reperfusion reduces infarct size and endothelial injury but augments neutrophil accumulation. The Annals of Thoracic Surgery, 64, 1099–1107. CrossRef
- Argaud, L., Gateu-Roesch, O., Raisky, O., Loufouat, J., Robert, D., & Ovize, M. (2005). Postconditioning inhibits mitochondrial permeability transition. Circulation, 111, 194–197. CrossRef
- Schulman, D., Latchman, D. S., & Yellon, D. M. (2002). Urocortin protects the heart from reperfusion injury via upregulaiton of p42/p44 MAPK signaling pathway. American Journal of Physiology Heart and Circulatory Physiology, 283, H1481–H1488.
- Juhaszova, M., Zorov, D. B., Kim, S.-H., Pepe, S., Fu, Q., Fishbein, K. W., et al. (2004). Glycogen synthase kinase-3ß mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore. Journal of Clinical Investigation, 113, 1535–1549.
- Gomez, L., Paillard, M., Thibault, H., Derumeaux, G., & Ovize, M. (2008). Inhibition of GSK3beta by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion. Circulation, 117, 2761–2768. CrossRef
- Cohen, M. V., Yang, X. M., & Downey, J. M. (2007). The pH hypothesis of postconditioning: staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosis. Circulation, 115, 1895–1903. CrossRef
- Inserte, J., Barba, I., Hernando, V., Abellan, A., Ruiz-Meana, M., Rodriguez-Sinovas, A., et al. (2008). Effect of acidic reperfusion on prolongation of intracellular acidosis and myocardial salvage. Cardiovascular Research, 77, 782–790. CrossRef
- Ovize, M., Baxter, G. F., Di Lisa, F., et al. (2010). Postconditioning and protection from reprfusion injury: where do we stand? Position paper from the working group of cellular biology of the heart of the European society of cardiology. Cardiovascular Research, 87, 406–423. CrossRef
- Piot, C., Croisille, P., Staat, P., Thibault, H., Rioufol, G., Mewton, N., et al. (2008). Effect of cyclosporine on reperfusion injury in acute myocardial infarction. The New England Journal of Medicine, 359, 473–481. CrossRef
- Long-term Follow-up of Patients Undergoing Postconditioning During ST-Elevation Myocardial Infarction
Journal of Cardiovascular Translational Research
Volume 4, Issue 1 , pp 92-98
- Cover Date
- Print ISSN
- Online ISSN
- Springer US
- Additional Links
- Acute myocardial infarction
- Industry Sectors
- Author Affiliations
- 1. Minneapolis VA Medical Center, Minneapolis, MN, USA
- 3. University of Minnesota Medical School, Minneapolis, MN, USA
- 2. Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, 920 East 28th Street, Suite 300, Minneapolis, MN, 55407, USA
- 4. Hennepin County Medical Center, Minneapolis, MN, USA