Why we need intravenous antiplatelet agents.

Oral ADP-receptor antagonists combined with aspirin are the standard for dual antiplatelet therapy (DAPT) during percutaneous coronary intervention (PCI). However, the oral route of administration of ADP-receptor antagonists leaves them vulnerable to unpredictable and often inadequate platelet inhibition at the time of PCI, while their prolonged effects often lead to the decision not to load them prior to PCI. Intravenous antiplatelet agents, including glycoprotein IIb/IIIa inhibitors (GPI) and cangrelor, a reversible P2Y12 inhibitor, address these shortcomings.

Simulator training: The bridge between "primum non nocere" and "learning by doing".

Simulator training provides practice for trainees without exposing patients to potentially higher-risk operators early in their training. This study suggests that simulator training shortens the learning curve for femoral access and reduces complications. Commercial availability of inexpensive, realistic simulators would aid medical education and reduce the risk posed to patients.

Third universal definition of myocardial infarction: update, caveats, differential diagnoses.

Updated definitions of myocardial infarction (MI) reflect research on measuring cardiac troponin to diagnose MI. Elevations of this biomarker indicate cardiac injury but not always an acute coronary syndrome. Clinical judgment is needed to interpret increasingly sensitive biomarker assays appropriately.

Variations of coronary hemodynamic responses to intravenous adenosine infusion: implications for fractional flow reserve measurements.

Background: Continuous intravenous adenosine infusion reportedly produces stable and maximal hyperemia to allow for fractional flow reserve (FFR) measurement; however, several observers have noted variation of the coronary/aortic (Pd/Pa) pressure ratio during the course of an adenosine infusion.

Methods: Pd/Pa pressure recordings during continuous peripheral intravenous adenosine infusion were examined in 51 patients (68 measurements) with data collected for at least 150 sec and for at least 30 sec after the lowest Pd/Pa reading. The lowest recorded Pd/Pa ratio was used as the true FFR value at maximal hyperemia.