Administration of an intravenous contrast agent improves the ability to accurately assess LV volumes and EF in humans. Contrast enhancement is most useful in subjects with two or more adjacent endocardial segments not seen at baseline.

Abstract-A large body of clinical investigation implicates an important role for the sympathetic nervous system in linking obesity with hypertension. However, the experimental support for this hypothesis is derived from strictly white cohorts. The goal of this study was to determine whether being overweight begets sympathetic overactivity in black Americans, the ethnic minority at highest risk for hypertension. We recorded postganglionic sympathetic nerve discharge with microelectrodes in muscle nerve fascicles of the peroneal nerve in 92 normotensive young adult black men and women within a wide range of body mass index. The same experiments were performed in a control group of 45 normotensive white men and women of similar ages and body mass indices. The major new findings are 2-fold. First, in young, normotensive, overtly healthy black women, being overweight begets sympathetic overactivity (rϭ0.45, Pϭ0.0009), a putative intermediate phenotype for incident hypertension. Second, in black men, sympathetic nerve discharge is dissociated from body mass index (rϭ0.03, PϭNS). This dissociation is explained in part by a 20% to 40% higher rate of sympathetic nerve discharge in lean black men compared with lean white men and lean black and white women (28Ϯ3 versus 18Ϯ2, 21Ϯ2, and 17Ϯ2 bursts/min, respectively; PϽ0.05). Sympathetic nerve discharge in lean black men is comparable to that of overweight black men and women as well as white men and women. These data provide the first microneurographic evidence for tonic central sympathetic overactivity in blacks, both adiposity-related sympathetic overactivity in black women and adiposity-independent sympathetic overactivity in black men. Key Words: obesity Ⅲ sympathetic nervous system Ⅲ blacks Ⅲ blood pressure O besity is firmly established to be a major risk factor for hypertension, and a large body of clinical investigation implicates an important role for the sympathetic nervous system in linking adiposity with hypertension. [1][2][3][4][5][6] In numerous studies of normotensive young adults, increasing adiposity is accompanied by increased sympathetic nerve discharge (SND) to skeletal muscle, a major site of energy expenditure. 5-7 Overweight-related sympathetic overactivity is hypothesized to be a compensatory mechanism to burn fat and minimize weight gain but at the cost of increased sympathetic discharge to the peripheral vasculature, which could predispose to hypertension. 2,8 However, the experimental support for this hypothesis is derived from strictly white cohorts. 5,6 The importance of inclusion of minority subjects in this field of clinical investigation is underscored by recent studies of Pima Indians, an ethnic minority with a high prevalence of obesity but a comparatively low prevalence of hypertension. 4 Basal levels of skeletal muscle SND are lower in normotensive male Pima Indians than in whites and do not track with adiposity. This relative sympathetic underactivity constitutes a potential explanation for the surprisingly low prevalence of hypertensio...

The LVOT pressure gradient varies considerably from day to day in stable patients with HOCM. A single measurement of pressure gradient is not adequate to define the severity of dynamic LVOT obstruction in HOCM.

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Contrary to the results from in vitro studies, VCW is not load independent in patients with mitral regurgitation caused by dynamic changes in the regurgitant orifice. The origin of mitral regurgitation does not predict accurately whether the regurgitant orifice is fixed or dynamic. Finally, short-term vasodilation with nitroprusside may significantly worsen the severity of mitral regurgitation in some patients.