Redo mitral surgery after coronary artery bypass grafts under hyperkalemic hypothermia using thoracotomy and axillary artery cannulation in a patient with functioning bilateral internal thoracic arteries and atheromatous aorta.

BACKGROUND: Redo mitral valve surgery using resternotomy after coronary artery bypass grafting (CABG) is challenging as previous CABG with patent internal thoracic artery (ITA) poses a risk of injury due to dense adhesion. It is paramount to have alternative method to minimize this risk. CASE PRESENTATION: We report a case of redo mitral and tricuspid valve repair via right thoracotomy under hypothermia and systemic potassium administration with axillary artery cannulation in a patient after CABG with patent bilateral ITA grafts crossing over the sternum. Herein, critical dissection around the aorta and functioning ITA grafts was avoided by performing the procedure under systemic hypothermia via thoracotomy. Furthermore, considering the presence of atheroma in the aorta, the axillary artery was used as a perfusion route to prevent stroke events. Postoperative course was uneventful and echocardiography demonstrated preserved cardiac function. CONCLUSION: Performing axillary artery cannulation and right thoracotomy under hypothermic cardiac arrest with systemic hyperkalemia without clamping the patent bilateral ITAs and aorta allowed us to perform redo mitral valve surgery after CABG without major postoperative cardiac or cerebral complications.

In vivo monitoring of peripheral circadian clocks in the mouse.

The mammalian circadian system is comprised of a central clock in the suprachiasmatic nucleus (SCN) and a network of peripheral oscillators located in all of the major organ systems. The SCN is traditionally thought to be positioned at the top of the hierarchy, with SCN lesions resulting in an arrhythmic organism. However, recent work has demonstrated that the SCN and peripheral tissues generate independent circadian oscillations in Per1 clock gene expression in vitro. In the present study, we sought to clarify the role of the SCN in the intact system by recording rhythms in clock gene expression in vivo. A practical imaging protocol was developed that enables us to measure circadian rhythms easily, noninvasively, and longitudinally in individual mice. Circadian oscillations were detected in the kidney, liver, and submandibular gland studied in about half of the SCN-lesioned, behaviorally arrhythmic mice. However, their amplitude was decreased in these organs. Free-running periods of peripheral clocks were identical to those of activity rhythms recorded before the SCN lesion. Thus, we can report for the first time that many of the fundamental properties of circadian oscillations in peripheral clocks in vivo are maintained in the absence of SCN control.