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Background: The association of aspirin loading with the risk of coronary no‐reflow (CNR) after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) has not been investigated. We assessed the association of aspirin loading before PCI with CNR in patients with AMI. Materials and Methods: This study included 3100 patients with AMI undergoing PCI. Of them, 2812 patients received aspirin loading (a single oral [or chewed] or intravenous dose of 150–300 mg) and 288 patients did not receive aspirin loading before PCI. The primary endpoint was CNR, defined as Thrombolysis in Myocardial Infarction blood flow grade of <3 after the PCI. Results: CNR occurred in 130 patients: 127 patients in the group with aspirin loading and 3 patients in the group without aspirin loading before PCI (4.5% vs. 1.0%; odds ratio [OR] = 4.50, 95% confidence interval, [1.42–14.21], p = 0.005). After adjustment, the association between aspirin loading and CNR was significant (adjusted OR = 4.49 [1.56–12.92]; p < 0.001). There was no aspirin loading‐by‐P2Y12 inhibitor (ticagrelor or prasugrel) interaction (pint = 0.465) or aspirin loading‐by‐chronic aspirin therapy on admission (pint = 0.977) interaction with respect to the occurrence of CNR after PCI. Chronic low‐dose aspirin therapy on admission was not independently associated with higher risk of CNR after PCI (adjusted OR = 1.06 [0.65–1.72]; p = 0.824). Conclusion: In patients with AMI undergoing PCI, aspirin loading before the PCI procedure at the guideline‐recommended doses was associated with higher odds of developing CNR. However, due to the limited number of events, the findings should be considered as hypothesis generating. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the "leukocyte supply chain" and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI. [ABSTRACT FROM AUTHOR]

Abstract: Tako-Tsubo cardiomyopathy is characterized by a transient and reversible left ventricular dysfunction possibly due to a catecholamine-mediated myocardial stunning. This form of cardiomyopathy is rarely associated with cardiogenic shock. Here we report on a patient with Tako-Tsubo cardiomyopathy induced low output failure in which blood flow disturbances in the thoracic aorta mimicked an acute type A aortic dissection. [ABSTRACT FROM AUTHOR]