A case of giant saphenous vein graft aneurysm followed serially after coronary artery bypass surgery.

Saphenous vein graft aneurysm (SVGA) is one of the chronic complications after coronary aorta bypass grafting (CABG) and may be caused by atherosclerosis-like phenomena of the vein graft, weakness around the vein valve, rupturing of the suture of the graft anastomosis, or perioperative graft injury. We describe a case of a large, growing saphenous vein graft aneurysm that was followed serially by chest radiography and computed tomography. Eighteen years after CABG, an SVGA (23 × 24 mm) was incidentally detected. The patient was asymptomatic and was followed conservatively. Four years later, coronary computed tomographic angiography showed that the giant aneurysm had grown to 52.1 by 63.8 mm and revealed a second, smaller aneurysm. Finally, the SVG was ultimately resected without bypass via off-pump surgery. Therefore, this case suggested that aggressive treatment that includes surgical intervention should be considered before the aneurysm becomes larger, even if it is asymptomatic.

Ryanodine receptor dysfunction and triggered activity in the heart.

Arrhythmogenesis has been increasingly linked to cardiac ryanodine receptor (RyR) dysfunction. However, the mechanistic relationship between abnormal RyR function and arrhythmogenesis in the heart is not clear. We hypothesize that, under abnormal RyR conditions, triggered activity will be caused by spontaneous calcium release (SCR) events that depend on transmural heterogeneities of calcium handling. We performed high-resolution optical mapping of intracellular calcium and transmembrane potential in the canine left ventricular wedge preparation (n = 28). Rapid pacing was used to initiate triggered activity under normal and abnormal RyR conditions induced by FKBP12.6 dissociation and beta-adrenergic stimulation (20-150 microM rapamycin, 0.2 microM isoproterenol). Under abnormal RyR conditions, almost all preparations experienced SCRs and triggered activity, in contrast to control, rapamycin, or isoproterenol conditions alone. Furthermore, under abnormal RyR conditions, complex arrhythmias (monomorphic and polymorphic tachycardia) were commonly observed. After washout of rapamycin and isoproterenol, no triggered activity was observed. Surprisingly, triggered activity and SCRs occurred preferentially near the epicardium but not the endocardium (P < 0.01). Interestingly, the occurrence of triggered activity and SCR events could not be explained by cytoplasmic calcium levels, but rather by fast calcium reuptake kinetics. These data suggest that, under abnormal RyR conditions, triggered activity is caused by multiple SCR events that depend on the faster calcium reuptake kinetics near the epicardium. Furthermore, multiple regions of SCR may be a mechanism for multifocal arrhythmias associated with RyR dysfunction.