A recent “state of the art” report on the no-reflow phenomenon (NRP) in patients with ST-segment elevation myocardial infarctions (STEMIs) who undergo primary percutaneous coronary intervention (PCI) brings up thoughts regarding efforts to protect the ischemic myocardium (an old therapeutic paradigm) in addition to the current scenario of providing immediate reperfusion for victims of heart attacks. Among the many factors contributing to the deleterious role of reperfusion, the investigators cited the “sarcolemmal Na ⁺ /Ca ⁺⁺ exchanger which produces calcium overload that triggers uncontrolled hypercontraction and stimulates opening of the mitochondrial permeability transition pore (m-PTP), which further enhances calcium overload.” They also referred to a report by Jaffe et al in which it is stated that ischemic preconditioning, among other things, might reduce eventual infarct size by the blockade of m-PTP. That report also postulates that postconditioning after primary PCI in patients with STEMIs may prevent no-reflow. Thus, preconditioning and postconditioning may prevent or ameliorate the NRP in patients with STEMI, which in turn may be translated to the salvage of myocardial tissue, smaller eventual infarct sizes, the prevention of ventricular remodeling, and higher left ventricular ejection fractions. A phenomenon relevant to “direct” preconditioning and postconditioning, that of “remote” preconditioning, refers to the salutary effect exerted on a particular vascular bed by the imposition of short repeated periods of 5 minutes of interrupted flow, interspersed with 5 minutes of reperfusion, in other than the particular, that is, “remote,” vascular territories. Such controlled brief curtailments of flow to an arm, using a blood pressure cuff, before the commencement of angioplasty and stenting have led to proved short- and long-term benefits for patients who undergo PCI. Looking at Figure 1 of the report that triggered these thoughts, one is shocked at the low rate (i.e., 35%) of patients with STEMIs eventually escaping the no-reflow state! While we are contemplating the paucity of definitive recommendations for dealing with the NRP, although many possibilities seem promising, one wonders whether “remote postconditioning” could find an application in the setting of patients with STEMIs who undergo PPCI, in an effort to minimize or prevent the NRP. To that effect, one could envision repeat applications of “remote preconditioning” and “remote postconditioning” by 5-minute periods of arterial flow interruption to the arms and legs in rotation (excluding the extremities encumbered by intravenous or intra-arterial catheters, at a particular time interval), starting immediately on admission to the hospital and extending to the period after primary PCI. The number of such sessions could be decided on, and the protocols of implementation could be borrowed from the experience with this therapeutic maneuver in patients who undergo elective PCI. Also, extrapolating further, one could envision applying the same complementary therapeutic protocol in other patients with STEMIs who undergo thrombolytic therapy. Common to these 2 groups of patients is the consideration that an acute STEMI constitutes a dynamic rather than static clinical entity amenable to therapeutic maneuvers aimed at protecting the myocardial tissue at risk from the NRP or ameliorating such condition if prevention fails. What is attractive in this proposal is its low-tech, universally available, noninvasive, and no-cost nature; it is worth giving a try. A registry of the patients who undergo this remote preconditioning and postconditioning could easily be established, and this could quickly provide evidence of whether such a method has therapeutic value or not. By taking advantage of large numbers of patients entering such a hypothetical registry and using the commonly employed outcome end points, one could forgo quantitative assessment of the extent of the protection of the ischemic myocardium afforded by this therapy.