Aortic valve repair for isolated right coronary leaflet prolapse.

Objectives: Isolated right coronary leaflet prolapse is a common cause of nonaneurysmal aortic insufficiency, but can rarely occur in patients with proximal aortic aneurysms. Standardized techniques for routine autologous repair of this disorder are presented. Methods: Most aortic valve leaflet prolapse is isolated to the right coronary leaflet, with hypertension and annular dilatation being contributory. Echocardiographically, a posteriorly eccentric aortic insufficiency jet together with "fracture" of the right leaflet tip are diagnostic. Primary repair includes internal geometric ring annuloplasty to downsize and reshape the annulus, together with central plication of the prolapsing leaflet. Thickened, scarred, or retracted noduli are released using an ultrasonic aspirator. The goal is to achieve equivalent coaptation heights of ≥8 mm for all 3 leaflets. Results: Three videos of 6 cases are provided to illustrate these techniques. In the first, 3 patients are shown with classic isolated right leaflet prolapse. In the second and third videos, alternative pathologies are presented for contrast. Applying the reconstructive approaches of geometric ring annuloplasty, leaflet plication, and ultrasonic nodular release, excellent early and late repair outcomes are obtainable in most patients. Conclusions: The combination of aortic ring annuloplasty, central leaflet plication, and ultrasonic nodular release allows routine and standardized repair of right coronary leaflet prolapse, either isolated or concomitant with aneurysm surgery.

The effects of acute afterload change on systolic ventricular function in conscious dogs with normal vs. failing hearts.

BACKGROUND: To date, no data exist on the linearity and, therefore, the usefulness of the preload recruitable stroke work (PRSW) and end-systolic pressure-volume (ESPVR) relationships during acute afterload changes in heart failure. AIMS: Our aim was, therefore, to characterize both relationships in a model of ventricular pacing induced heart failure at baseline and during acute changes in afterload. METHODS: Dynamic left ventricular volume and transmural pressure were measured in 10 conscious dogs using sonomicrometry and micromanometry under control conditions and during heart failure produced by 3 weeks of rapid right ventricular pacing. Afterload was varied from baseline with intravenous infusions of nitroprusside and phenylephrine. Left ventricular function was assessed using the PRSW and ESPVR relationships. RESULTS: Cardiac output demonstrated a linear inverse relationship with afterload in both normal and failing hearts (r2>0.5, P<0.001) with failure producing a parallel, downward shift of the afterload (x) vs. cardiac output (y) relationship (P<0.01). Yet, afterload variation did not affect PRSW or ESPVR relationships in either normal or failing hearts (r2<0.12, P>0.05). CONCLUSION: Thus, the PRSW and ESPVR relationships are insensitive to acute afterload changes in both failing and normal hearts, and the failing left ventricle is no more afterload-sensitive than the normal heart.