Inducible cardiac-specific overexpression of cyclooxygenase-2 (COX-2) confers resistance to ischemia/reperfusion injury.

The role of cyclooxygenase-2 (COX-2) in cardiovascular biology remains controversial. Although COX-2 has been reported to mediate the protective actions of late preconditioning, other studies show that it is also an important mediator of inflammation, toxic shock, and apoptosis, resulting in significant dysfunction and injury in several tissues. To determine whether increased myocardial COX-2, in itself, is protective, cardiac-specific, inducible (Tet-off) COX-2 transgenic (iCOX-2 TG) mice were generated by crossbreeding α-MyHC-tTA transgenic mice (tetracycline transactivator [tTA]) with CMV/TRE-COX-2 transgenic mice.

Paradoxical Thromboembolism/ST-Elevation Myocardial Infarction via a Patent Foramen Ovale in Sub-Massive Pulmonary Embolism Following an Upper Extremity Deep Venous Thrombosis: Is It Time for a Change in the Standard of Care?

The objective of this case study is to discuss a rare case of proven paradoxical thromboembolism captured in-transit. A 23-year-old female with a diagnosis of right internal jugular deep vein thrombus who developed acute onset chest pain, dyspnea and hypotension, was selected for the study. Sub-massive PE and STEMI were diagnosed.

The COX-2/PGI2 receptor axis plays an obligatory role in mediating the cardioprotection conferred by the late phase of ischemic preconditioning.

Background: Pharmacologic studies with cyclooxygenase-2 (COX-2) inhibitors suggest that the late phase of ischemic preconditioning (PC) is mediated by COX-2. However, nonspecific effects of COX-2 inhibitors cannot be ruled out, and the selectivity of these inhibitors for COX-2 vs. COX-1 is only relative.