Myocardial Salvage beyond Recanalization of the STEMI Lesion

As rapid global progress is being made to reduce door-to-balloon times (D2B) for primary percutaneous coronary intervention (PCI) by improving the ST-elevation myocardial infarction (STEMI) procedure and the D2B process, it is imperative to look beyond recanalization of the infarct-related STEMI lesion. Restoration of left ventricular (LV) function remains critical and therapies that may supplement the restoration of thrombolysis in myocardial infarction (TIMI) flow and myocardial blush grade (MBG) by thrombectomy, local drug delivery and stenting, need urgent exploration. Despite current optimal therapy, the 1-year mortality rate for STEMI patients remains significant: about 10% at 1 year, with 25% of patients going on to develop heart failure, indicating that clinical outcomes need to be further improved.1 The abrupt restoration of coronary artery flow to ischemic myocardium has the ability to exacerbate myocardial injury and trigger cardiomyocyte death by two important processes: coronary no-reflow and lethal reperfusion injury. The restoration of blood flow to the infarct-related artery, as visualized by coronary angiography, does not in itself guarantee that ischemic myocardium is actually being perfused. Obstruction of blood flow at the level of the microvasculature can impede myocardial perfusion, a phenomenon termed microvascular obstruction (MVO), which manifests clinically as no-reflow. Furthermore, the abrupt restoration of coronary blood flow to previously ischemic myocardium is capable of independently triggering cardiomyocyte death, a phenomenon termed lethal reperfusion injury.1 Critically, the presence of these two reperfusion phenomena in STEMI patients has the potential to negatively affect myocardial infarct size, LV remodeling and clinical outcomes, underlining the importance of these two factors as critical targets for myocardial protection. In the context of this critical pathophysiological imperative, the work by Wang et al2 reported in this issue of the Journal is of paramount importance, particularly as it pertains to the gradual restoration of flow through the infarct-related vessel and to the previously ischemic myocardium, and in its potential for limiting lethal reperfusion injury. Wang et al have taken a step forward in STEMI reperfusion therapies by assessing myocardial ischemic postconditioning in real-world practice by designing a protocol based on the physiologic principles discovered during the past two decades in the experimental phases. Postconditioning refers to brief, intermittent cycles of artery occlusion (inflation) with reperfusion (deflation) performed at the onset of reflow following a prolonged ischemic insult.3,4 In their retrospective study that enrolled 85 patients out of a population of 433, the authors divided this cohort into two groups according to the number of times the balloon was inflated, after reflow (≥ 3 and ≤ 2 times), which was obtained by guidewire passage or balloon predilatation. The variables chosen were peak CK, ST-segment resolution, MBG, LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), and LV ejection fraction (LVEF). Comparing both groups, there was a significant decrease in the LVESV in the patients who had ≥ 3 balloon inflations (33.1 mL/m2 ± 7.9 vs. 37.5 ± 11.2 mL/m2; p = 0.036). LVEF significantly increased in the group with ≥ 3 inflations (50.4% ± 6.3 vs. 46.1% ± 8.5; p = 0.009); the 4-inflations group and the ≥ 5-inflations group had significantly higher values (p From the University of Miami, Miami, Florida. The authors report no conflicts of interest regarding the content herein. Address for correspondence: Sameer Mehta, MD, FACC, the University of Miami, Miami, Florida. E-mail: mehtas@bellsouth.net

1. Hausenloy DJ, Yellon DM. Treatment strategies for preventing lethal reperfusion injury. In: Mehta S (ed.).Textbook of STEMI Interventions. 2008, HMP Communications, Chapter 15, pp 327–346.

2. Wang G, Zhang, MD, Joggerst SJ, et al. Effects of the number and interval of balloon inflations during primary PCI on the extent of myocardial injury in patients with STEMI: Does postconditioning exist in real-world practice? 2009;21:451–455.

3. Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: Comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol 2003; 285:H579–H588.

4. Thibault H, Piot C, Staat P, et al. Long-term benefit of postconditioning. Circulation 2008; 117:1037–1044.

5. Staat P, Rioufol G, Piot C, et al. Postconditioning the human heart. Circulation 2005; 112: 2143–2148.