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The primary objective of thrombolytic therapy in patients with acute myocardial infarction (AMI) is the rapid opening of the thrombus. Delayed opening or reperfusion of the infarct-related artery is associated with an adverse prognosis. The temporal sequence of these two events has been elucidated by several investigators; a good thrombolytic therapy should reduce thrombus volume within the first 6 hours of AMI. However, several nonthrombogenic factors, particularly endothelium-derived factors, also need to be taken into account. These factors contribute to the stability of the thrombus and delay its detachment from the vessel wall. We have hypothesized that the prompt, early opening of AMI by thrombolysis eliminates the protective action of these factors. This hypothesis could be translated into the clinical setting in the form of adjunctive pharmacologic therapy targeted at endothelial cells or their products. Indeed, several pharmacologic strategies have been proposed based on the interaction between endothelial cells and platelets, involving the use of phosphodiesterase 3 inhibitors, matrix metalloproteinase inhibitors, urokinase, and nonthrombogenic compounds. Although promising in vitro data have stimulated basic and clinical research, there is no rigorous evidence for the efficacy of these strategies. I’d write an open letter to the Trump administration, and say, “Stop doing this. This is not America. You are hijacking this country’s values, it has never been this way. We are not some wide-open culture, we are not a country founded on religion, we

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