The majority of SVTs in stable OHT patients can be attributed to macro-reentrant tachycardias (flutter and scar reentry). Catheter ablation is effective in management of these SVTs. Atrial fibrillation was never encountered in stable patients in our series, and its occurrence should prompt an evaluation for acute rejection and/or vasculopathy.

Parasympathetic activation during AF ablation is associated with the presence of pre-ablation high-amplitude fractionated EGMs in sinus rhythm. Local acetylcholine release could potentially explain this phenomenon.

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One possible mechanism for neurohumoral activation after myocardial infarction may be the generation of an immune response against cardiac self-antigens. We hypothesize that if there is a T cell-mediated reaction to self-antigens, the transfer of splenic lymphocytes from postinfarct rats into syngeneic rats with normal hearts should result in a T cell-mediated autoimmune myocarditis in the healthy syngeneic rats. Rats were killed 6 weeks after coronary ligation. Splenocytes from animals with large and small infarcts were purified from spleens, activated with concanavalin A, and injected in varying doses into normal syngeneic rats. These recipient rats were killed 6 weeks later, and histopathological studies were performed. Our results demonstrate in vivo evidence of lymphocyte-mediated myocardial injury by adoptive transfer of sensitized lymphocytes from rats who developed congestive heart failure after acute myocardial infarction. The amount of infiltrate and necrosis in the recipient rats appeared directly related to the size of the infarct from the donor rats. This suggests that larger infarcts lead to a greater inflammatory response as well as a greater propensity for alteration of cardiac surface antigens or the emergence of previously sequestered antigens. None of the other organs (kidney, liver, lung, or brain) had evidence of infiltrates. Two-dimensional echocardiography did not reveal systolic dysfunction. This study provides direct evidence of autoimmune myocardial injury produced by adoptive transfer of concanavalin A-activated splenocytes after myocardial infarction. We propose that neurohumoral activation early in the postinfarction period triggers a series of specific inflammatory and immunological events that lead to formation of specific clones of T cells. When these are activated and transferred into normal rats, cardiac-specific cellular infiltration occurs, occasionally accompanied by myocardial necrosis. This model should help to further explore the link between neurohumoral activation after myocardial infarction and the subsequent immune alterations that might be associated with the development and/or progression of congestive heart failure. Additionally, this might be a useful model in which to study other immune-mediated cardiomyopathies.

The major coronary arteries lie in close proximity of the RVOT, and their anatomic course should be taken into consideration during ablation of ventricular tachycardias arising from the RV outflow tract.

Upon contacting each other, cells form gap junctions, in which each cell contributes half of the channel linking their cytoplasms, enabling them to share their metabolome up to a molecular weight of 1000. Each hemichannel (or connexon) is randomly inserted into the plasma membrane and then migrates to the site of cell-to-cell contact before pairing with the neighbouring cell's hemichannel to form a communicating conduit. This review summarizes the evidence for hemichannels in heart ventricular myocytes. Morphological findings are summarized describing how hemichannels are inserted into the plasma membrane. Once in the plasma membrane, hemichannels can be functionally detected electrophysiologically or by dye uptake assays. Each technique reveals specific aspects of hemichannel function. Using dye uptake studies, it is possible to investigate the biological regulation of hemichannels in vivo. Evidence is summarized which indicates that hemichannels are normally kept closed in the presence of normal extracellular Ca because they are phosphorylated at residues in the C-terminus regulated by the MAPK signalling pathway. When hemichannels are dephosphorylated, the channels open and allow dye uptake into the cells, as well as potentially deleterious ion exchange. Biological stresses, such as hyperosmolarity and metabolic inhibition, open hemichannels by this mechanism through activating phosphatases. The resulting ion fluxes may have important roles in heart physiology and pathophysiology.

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