Real-time three-dimensional echocardiography-derived MV annular, tenting, and papillary muscle parameters vary widely in normal subjects. When used clinically, normal values of parameters that are age- and/or BSA-dependent need to be adjusted accordingly.

Although bioavailability of NO in the coronary circulation is commonly evaluated by acetylcholine (ACh)-induced vasodilation, a change in plasma NO concentration and its relation to the flow response after injection of ACh are still unknown. Thus, we directly measured the concentration of NO in the coronary sinus by using a catheter-type NO sensor for coronary sinus. An NO-sensitive sensor was located and fixed in a 4-Fr catheter with a soft tip for protection of vascular wall. After calibration with an NO-saturated pure water, the catheter-type NO sensor was located in the coronary sinus in anesthetized dogs. The coronary flow velocity (CFV) was measured with a Doppler guide wire. Intracoronary injection of ACh (0.4 and 1.0 g͞kg) increased plasma NO concentration in a dose-dependent manner (3-10 nM). Although ACh increased CFV by 95%, there was no significant difference between the two ACh doses. After ACh, the peak value of plasma NO concentration was observed significantly later than CFV. N G -methyl-L-arginine (NO synthase inhibitor) decreased basal NO concentration by 3 nM and suppressed the ACh-induced NO synthesis with no significant change in average peak velocity. We conclude that production of NO in the coronary circulation can be evaluated in the coronary sinus. Although ACh increases both CFV and NO concentration, CFV dose not reflect NO concentration in terms of magnitude and time course. Direct measurement of plasma NO concentration by the catheter-type NO sensor is useful to evaluate bioavailability of NO in the coronary circulation.nitric oxide synthase ͉ nitric oxide-selective sensor ͉ acetylcholine ͉ coronary blood flow ͉ endothelial function N itric oxide (NO) released by endothelial cells is formed from L-arginine by nitric oxide synthase (NOS) (1). NO release is augmented by mechanical stimulation such as shear stress (2-6), pulsatile flow (7, 8), and axial strain (9). Such mechanical stresses, which are produced by the periodic myocardial contraction and relaxation, directly influence the coronary blood vessels, acting as an overwhelmingly dominant factor of the coronary blood flow regulation (10-12). Under the stimulatory influences by the mechanical stresses, coronary endothelial cells produce NO on a beat-to-beat basis (13). In the coronary circulation, endothelium-derived NO plays fundamental roles in the regulation of blood flow, exerting a tonic vasodilator influence at rest and with increasing myocardial metabolism (14).However, bioavailability of NO is diminished in the subjects with a wide range of cardiac risk factors and pathologic conditions, such as aging, gender, smoking, hypertension, hypercholesterolemia, diabetes mellitus, hyperhomocystinemia, heart failure, infections, and polymorphisms of the endothelial NOS (15-23). Importantly, endothelial dysfunction, characterized by decreased bioavailability of NO, is a predictor of cardiovascular risk and outcome (24-28).Several techniques have been used to evaluate the endothelial function or bioavailability of NO (29). Coronary en...

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The degree of MV coaptation can be quantified using 3D echocardiography. The coaptation index should be a useful parameter in the assessment of functional MR.

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