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Background-Functional mitral regurgitation (MR) is common in patients with heart failure and left ventricular (LV) dysfunction, and its severity may vary over time, depending primarily on the loading conditions. Because dynamic changes in the severity of functional MR may affect forward stroke volume, we hypothesized that exercise-induced changes in MR severity influence the stroke volume response of patients with LV dysfunction to exercise, and hence their exercise capacity. Methods and Results-Heart failure patients (nϭ25; mean age 53Ϯ12 years) with LV dysfunction underwent dynamic bicycle exercise at steady-state levels of 30%, 60%, and 90% of predetermined peak V O 2 . During each exercise level, right heart pressures, cardiac output, V O 2 , and MR severity were measured simultaneously. During exercise, MR severity, as evaluated by the ratio of MR jet over left atrium area, increased from 15Ϯ8% to 33Ϯ15%. Peak V O 2 , exercise-induced changes in stroke volume, and those in capillary wedge pressure correlated with the changes in MR (rϭϪ0.55, Ϫ0.87, and 0.62, respectively, PϽ0.01). The changes in MR severity also correlated with those in end-diastolic (rϭϪ0.75, PϽ0.01) and end-systolic (rϭϪ0.72, PϽ0.01) sphericity indexes and those in the coaptation distance (rϭ0.86, PϽ0.01). Conclusions-Our data indicate that in patients with LV dysfunction, exercise-induced changes in MR severity limit the stroke volume adaptation during exercise and therefore contribute to limitation of exercise capacity.

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Background and Objectives: The 894T allele in exon 7 of the endothelial nitric oxide synthase (eNOS) gene has been inconsistently associated with hypertension in different racial groups. Because high-normal blood pressure (BP) confers an increased risk for the development of hypertension and other cardiovascular disorders, including left ventricular hypertrophy (LVH), we tested the hypothesis that the allelic variation (894T) in the eNOS gene would directly correlate with alterations in LV mass (LVM) in individuals with high-normal BP.Methods: Genotype distrbution of G894T was compared between 20 African Americans (10 females/1O males) with highnormal BP (systolic BP of 130-139 and/or diastolic BP of 85-89 mmHg) and 64 counterparts (37 females/27 males) with normal BP (<130/85 mmHg). Echocardiographic LVM was calculated (Devereux formula) and indexed to body surface area to define the presence of LVH (LVMI >134/1 10 g/m2 for men/women). Results: For the entire group, the 894T allelic frequencies (15,48%) and G894T genotype distributions were consistentwith the Hardy-Weinberg equilibrium expectations (estimated disequilibrium coefficient=0.01 18, P=0.40). LVMI was significantly higher in homozygous carriers (TT) of the rare 894T allele (n=3 females/0 males) than in heterozygous GT (n=1 3 females/7 males) and individuals bearing the GG (n=34 females/27 males) variant (124 ± 70 vs. 82 ± 24 and 82 ± 19 g/m2, respectively, P<0.05). The observed relationship between eNOS 894T allele and LVMI was restricted to individuals with high-normal BP (r=0.94, P=0.03) but not in those with normal BP (r=0.39, P=0.64), by analysis of variance (ANOVA) after adjusting for age, gender, body mass index, smoking and systolic BP. Conclusion: These findings, not previously described, provide important preliminary evidence to suggest an increased susceptibility to LVH in African Americans who carry the 894T variant of the eNOS gene and have high-normal blood pressure.