Summary Visual information is conveyed to the brain by axons of >30 retinal ganglion cell (RGC) types. Characterization of these types is a prerequisite to visual perception understanding. Here we identify a family of RGCs that we call F-RGCs based on expression of the transcription factor Foxp2. Intersectional expression of Foxp1 and Brn3 transcription factors divides F-RGCs into four types, comprising two pairs, each composed of closely related cells. One pair, F-miniON and F-miniOFF, shows robust direction selectivity. They are among the smallest RGCs in the mouse retina. The other pair, F-midiON and F-midiOFF, are larger and not direction-selective. Together, F-RGCs comprise >20% of RGCs in the mouse retina, halving the number that remain to be classified and doubling the number of known direction-selective cells. Co-expression of Foxp and Brn3 genes also marks subsets of RGCs in macaques that could be primate homologues of F-RGCs.

Background: The relation between ventricular arrhythmia and fibrosis in mitral valve prolapse (MVP) is reported, but underlying valve-induced mechanisms remain unknown. We evaluated the association between abnormal MVP-related mechanics and myocardial fibrosis, and their association with arrhythmia. Methods: We studied 113 patients with MVP with both echocardiogram and gadolinium cardiac magnetic resonance imaging for myocardial fibrosis. Two-dimensional and speckle-tracking echocardiography evaluated mitral regurgitation, superior leaflet and papillary muscle displacement with associated exaggerated basal myocardial systolic curling, and myocardial longitudinal strain. Follow-up assessed arrhythmic events (nonsustained or sustained ventricular tachycardia or ventricular fibrillation). Results: Myocardial fibrosis was observed in 43 patients with MVP, predominantly in the basal-midventricular inferior-lateral wall and papillary muscles. Patients with MVP with fibrosis had greater mitral regurgitation, prolapse, and superior papillary muscle displacement with basal curling and more impaired inferior-posterior basal strain than those without fibrosis ( P <0.001). An abnormal strain pattern with distinct peaks pre–end-systole and post–end-systole in inferior-lateral wall was frequent in patients with fibrosis (81 versus 26%, P <0.001) but absent in patients without MVP with basal inferior-lateral wall fibrosis (n=20). During median follow-up of 1008 days, 36 of 87 patients with MVP with >6-month follow-up developed ventricular arrhythmias associated (univariable) with fibrosis, greater prolapse, mitral annular disjunction, and double-peak strain. In multivariable analysis, double-peak strain showed incremental risk of arrhythmia over fibrosis. Conclusions: Basal inferior-posterior myocardial fibrosis in MVP is associated with abnormal MVP-related myocardial mechanics, which are potentially associated with ventricular arrhythmia. These associations suggest pathophysiological links between MVP-related mechanical abnormalities and myocardial fibrosis, which also may relate to ventricular arrhythmia and offer potential imaging markers of increased arrhythmic risk.

This dialog between a cardiac surgeon (C.L.) and cardiac imager (J.W.W.) provides an overview of cardiac MRI (CMR) methods relevant to cardiac surgery. Major areas of focus include logistics of performing a CMR exam, as well as established and emerging methods for assessment of cardiac structure, function, valvular performance, and tissue characterization. Regarding tissue characterization, a major area of focus concerns CMR assessment of viability, for which this modality has been shown to provide incremental utility to conventional techniques for detection of presence and transmural extent of infarction, as well as powerful predictive utility of recovery of left ventricular systolic function as well as long term clinical prognosis in patients with an array of clinical conditions, including coronary artery disease and valvular heart disease both before and following cardiac surgery.