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J Am Coll Cardiol, 2007; 50:157-158, doi:10.1016/j.jacc.2007.03.032
(Published online 21 June 2007). © 2007 by the American College of Cardiology Foundation |
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Cardiovascular Center, Aalst, Belgium.
* Reprint requests and correspondence: Dr. Bernard De Bruyne, Cardiovascular Center Aalst, OLV-Clinic, Moorselbaan 164, B-9300 Aalst, Belgium. (Email: bernard.de.bruyne{at}olvz-aalst.be).
In this issue of the Journal, Ndrepepa et al. (5) go 1 step further in unraveling the factors that are associated with long-term recovery of LV function and survival after an AMI in the setting of contemporary patient care. The authors investigated the survival rate of over 600 patients who underwent primary PCI for a first AMI. Infarct size was assessed by 99mTc-sestamibi SPECT before revascularization, 1 to 2 weeks later, and 6 months later. Left ventricular angiography was obtained before and 6 months after revascularization.
The study provides a number of interesting points. The data presented confirm that in the majority of patients with an AMI treated by primary PCI, both substantial improvements in LV ejection fraction and reductions in the size of the perfusion defect can occur up to 6 months after the acute event. The authors also show that the larger the extent of LV dysfunction in the acute phase, the greater the potential for improvement (Fig. 1 in Ndrepepa et al. [5]). This does not really come as a surprise, because the larger the ischemic (dyskinetic) territory during the acute phase, the greater the potential for reperfusion-induced salvage ("the more you can lose, the more you can gain"). At the other end of the spectrum, patients with normal global LV ejection fraction during the acute phase often owe this preserved function to a hyperdynamic wall motion pattern in the noninfarcted segments secondary to a combination of low LV afterload and a hyperadrenergic state. These humoral and hemodynamic characteristics are no longer present after 6 months, which might counterbalance the effect of reperfusion on LV ejection fraction.
Ndrepepa et al. (5) further demonstrate that the reduction in infarct size predicts the extent of recovery in LV ejection fraction at 6 months. Importantly, the authors also suggest that the reduction in infarct size (6) and the improvement of LV ejection fraction (5) have a beneficial effect on long-term survival. In fact, it appears that in addition to the actual absolute value of infarct size and LV ejection fraction, the extent of change in both of these parameters are also important additional prognostic factors.
These changes somehow bring together the complex phenomena that occur soon after an AMI and persist for several months thereafter. Along the same lines, recent data also indicate that exercise capacity is a better predictor of both 2- and 5-year mortality than LV ejection fraction after AMI treated with primary angioplasty (7).
Several mechanisms play a role in improving LV function after primary PCI. Myocardial salvage is likely to be the main mechanism by which AMI patients benefit from reperfusion therapy. As indicated in the present study, this can be reliably quantified by deriving the "salvage index" (4). When 99mTc-sestamibi is injected intravenously before recanalization of the infarct-related artery, the perfusion defect assessed on the scintigram performed a few hours after recanalization reliably identifies the area at risk (8). The perfusion defect documented 7 to 14 days after re-establishment of antegrade coronary blood flow identifies the actual infarct size. The proportion of the area at risk that is salvaged by reperfusion is termed the "salvage index" (6).
The presence of myocardial stunning (9) after reperfusion is a second mechanism by which the time-dependent global and regional myocardial functional recovery can be explained. It is very likely that patients with improved LV function at follow-up had a significant amount of stunned myocardium. Indeed, this group of patients had the largest initial perfusion defect, the lowest LV ejection fraction, and yet the lowest creatine kinase peak (Tables 1 and 3 in Ndrepepa et al. [5]). The extensive regional LV dysfunction and low ejection fraction should therefore be viewed as a combination of the true infarct size, a significant stunned border zone, and additional tethering of the adjacent normal zones. In turn, the observed functional recovery is the result of not only salvage from ischemic cell death, but also recovery of the stunned segments together with diminished tethering of the normal myocardium.
Some limitations should be highlighted. The study population was retrieved from a number of multicentric randomized intervention trials in which all control patients were pooled for analysis. It is important to note that patients in cardiogenic shock as well as those presenting with congestive heart failure were excluded from the study. Information on those patients would have been helpful. Patients requiring repeat revascularization by PCI or coronary artery bypass grafting, requiring implantation of a biventricular pacing device, or experiencing recurrent MI or individuals who died within the first 6 months of follow-up were also excluded from the analysis. In addition, only data on global LV ejection fraction are provided, without details about regional wall motion and LV volumes and pressures, all parameters that could potentially hold additional prognostic information.
Should these findings have implications for the selection of patients with AMI for primary PCI? Probably not. It would be unrealistic to risk-stratify patients according to their infarct size before revascularization. A superficial analysis of Figure 1 in Ndrepepa et al. (5) might lead to the conclusion that patients with preserved LV ejection fraction in the acute phase of an AMI might not benefit from reperfusion. Yet the design of the study did not test the efficacy of primary PCI in patients with preserved LV ejection fraction. In contrast, the present data by Ndrepepa et al. (5) might have implications for the design and interpretation of trials that aim to evaluate the effects of therapeutic interventions in AMI patients after treatment by primary PCI. The dynamic nature of several parameters, including infarct size and LV ejection fraction, soon after primary PCI, as well as the magnitude and direction of these changes, might bear prognostic information over and above and well beyond the actual value of these parameters obtained during the acute phase of an infarction or before discharge from hospital. As suggested by the authors, the dynamics of these parameters, rather than actual values, might be factored in when evaluating the effects of intervention for treatment of AMI (although proper randomization of the patients should account for these phenomena).
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