A case of infected left atrial myxoma with concomitant mitral valve endocarditis.

Myxoma is the most common primary tumor in the heart. Cardiac myxomas can present in various manners including embolization and fever, sometimes simulating endocarditis. However, they are rarely infected. We report here a case of an infected left atrial myxoma that seeded a normal mitral valve and atypically presented with multiple embolic events in the lower extremities along with multiple splenic and a cerebellar infarction.

A Case of Cogan's Syndrome With Angina.

Cogan's syndrome is a rare systemic inflammatory disease and can be diagnosed on the basis of typical inner ear and ocular involvement with the presence of large vessel vasculitis. We report a case of Cogan's syndrome with stable angina resulting from coronary ostial stenosis caused by aortitis.

Cases of swallow syncope induced by the activation of mechanorecepters in the lower esophagus.

Swallowing is a rare cause of neurally mediated syncope. The mechanism of swallow syncope that contributes to hypotension, bradycardia, or to both is complex. A 59-year-old man had experienced a recurrent loss of consciousness during swallowing of carbonated beverages or sticky foods. Another 59-year-old man had complained of intermittent syncope just after eating foods. These two patients had no significant structural or functional abnormalities in the esophagus or heart. Both cases showed bradycardia when the lower esophagus was stretched by balloon inflation. The activation of mechanoreceptors in the lower esophagus can be regarded as an initiating factor of these cardioinhibitions. The patients were treated with permanent pacemaker implantation and instructed to change eating habits, respectively.

Calpain and mitochondria in ischemia/reperfusion injury.

Studies of ischemia/reperfusion (I/R) injury and preconditioning have shown that ion homeostasis, particularly calcium homeostasis, is critical to limiting tissue damage. However, the relationship between ion homeostasis and specific cell death pathways has not been investigated in the context of I/R. Previously we reported that calpain cleaved Bid in the absence of detectable caspase activation (1). In this study, we have shown that an inhibitor of the sodium/hydrogen exchanger prevented calpain activation after I/R. Calpain inhibitors prevented cleavage of Bid as well as the downstream indices of cell death, including DNA strand breaks, creatine kinase (CK) release, and infarction measured by triphenyl tetrazolium chloride (TTC) staining. In contrast, the broad spectrum caspase inhibitor IDN6734 was not protective in this model. To ascertain whether mitochondrial dysfunction downstream of these events was a required step, we utilized a peptide corresponding to residues 4-23 of Bcl-x(L) conjugated to the protein transduction domain of HIV TAT (TAT-BH4), which has been shown to protect mitochondria against Ca2+-induced deltaPsi(m) loss (2). TAT-BH4 attenuated CK release and loss of TTC staining, demonstrating the role of mitochondria and a pro-apoptotic Bcl-2 family member in the process leading to cell death. We propose the following pathway. (i) Reperfusion results in sodium influx followed by calcium accumulation. (ii) This leads to calpain activation, which in turn leads to Bid cleavage. (iii) Bid targets the mitochondria, causing dysfunction and release of pro-apoptotic factors, resulting in DNA fragmentation and death of the cell. Ischemia/reperfusion initiates a cell death pathway that is independent of caspases but requires calpain and mitochondrial dysfunction.