Left ventricular hypertrophy did not significantly affect peak oxygen uptake (33.6 vs 36.0 ml/min/kg) in hypertensive patients, though exercise-induced BNP rise predicted individualized capacity.
Cross-Sectional (n=49)
Does endogenous BNP release correlate with exercise capacity in hypertensive patients with and without left ventricular hypertrophy?
In hypertensive patients, a greater rise in BNP during exercise correlates with reduced exercise capacity, independent of the presence of left ventricular hypertrophy.
Absolute Event Rate: 33.6% vs 36%
Brain natriuretic peptide (BNP) is increased and it is also released during exercise in hypertension, but its biologic role is unclear. However, since BNP is released from the left ventricule and it is known to reduce left ventricular filling pressure, it is possible that it exerts a favorable effect on exercise performance. We studied the relationship between endogenous BNP release and exercise capacity in hypertension with reference to left ventricular hypertrophy (LVH). Cardiopulmonary exercise study was carried out in 2 groups of hypertensives, 24 16 men, aged 50 (SD 11) years of whom had echocardiographic LVH and 25 16 men, aged 41 ( 12) who did not have LVH. In multiple regression analyses, the major determinants of peak oxygen uptake (VO max) were age (-), sex (male), peak exercise systolic BP (+) and post-exercise BNP (-). For the predicted adjusted %VO max as a measure of individualised exercise capacity, the significant predictors were the exercise-induced BNP rise (-) (p = 0.0003) and peak exercise systolic BP (+) (p = 0.001). In other words, subjects with greater myocardial dysfunction had a greater rise in BNP during exercise. LVH did not however relate to exercise capacity. The baseline, post-exercise and the % rise in BNP (pmol/L) with exercise were not statistically different in those with LVH compared with those without (median values of 11.2, 14.6 and 133% versus 10.6, 11.5 and 120% respectively). Similarly, there were no significant differences in exercise capacity between the groups: exercise time, oxygen uptakes at ventilatory threshold and at peak exercise (VO max) were 10.8 (2.5) min, 15.8 (4.6) and 33.6 (7.6) ml/min/kg in the LVH group against 11.4 (2.9) min, 18.6 (5.2) and 36 (11.1) ml/min/kg in the non-LVH group respectively. The estimated VO max was not different from that predicted from age, sex, weight and height in either group suggesting preserved exercise capacity in these subjects as a whole. In Conclusion, BNP may potentially act as a homeostatic mechanism that helps to limit exercise incapacity in hypertension irrespective of LVH.
Lim et al. (Tue,) conducted a cross-sectional in Hypertension (n=49). Left ventricular hypertrophy (LVH) vs. No LVH was evaluated on Peak oxygen uptake (VO2 max). Left ventricular hypertrophy did not significantly affect peak oxygen uptake (33.6 vs 36.0 ml/min/kg) in hypertensive patients, though exercise-induced BNP rise predicted individualized capacity.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: