Duration of Symptoms Is the Key Modulator of the Choice of Reperfusion for ST-Elevation Myocardial Infarction

Time has been transformed, and we have changed; it has advanced and set us in motion; it has unveiled its face, inspiring us with bewilderment and exhilaration . —Kahlil Gibran1 The intense focus at the nexus between elapsed time and outcomes in patients with ST-elevation myocardial infarction (STEMI) signals its far-reaching implications for public health and the healthcare system. In this perspective, we demonstrate not only the time dependence of the 2 principal forms of reperfusion therapy but also how the efficacy of each depends on the baseline risk of the individual in whom it occurs, as well as where the event unfolds in time, space, and context. These variables play a crucial role in determining the choice of best therapy, thereby confirming the admonition that 1 size does not, and could not, fit all individuals in all circumstances at all times.2–4 A central issue that bears on the interpretation of the reperfusion literature is which of the various definitions of time is used. We will use the terminology summarized in Table 1 and explore opportunities to modulate the delay incumbent with STEMI treatment. View this table:Table 1. Time Definitions and Clinical Reperfusion Response by Bogaty p 1303 An ironic divide exists between the precision of time-dependent laboratory observations on the extent of myocardial injury and the frustrating imprecision of this metric when applied to humans. The notion of reversible ischemic cell damage after coronary occlusion was framed more than half a century ago.5 Subsequent canine experiments demonstrated that ischemic necrosis begins in the subendocardium within 20 minutes of coronary occlusion and subsequently proceeds in a transmural wave front of cell death that maximizes within 3 to 6 hours (Figure 1).6 Although reperfusion achieved within the first hour salvages nearly two thirds of the myocardium at risk, …