Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction

作者：Bhella Paul S; Prasad Anand; Heinicke Katja; Hastings Jeff L; Arbab Zadeh Armin; Adams Huet Beverley; Pacini Eric L; Shibata Shigeki; Palmer M Dean; Newcomer Bradley R; Levine Benjamin D^*

来源：European Journal of Heart Failure, 2011, 13(12): 1296-1304.

DOI：10.1093/eurjhf/hfr133

• Cardiac output response to exercise
• Haemodynamic response to exercise
• Heart failure with preserved ejection fraction
• Exercise capacity
• Myocardial contractile reserve
• Oxygen consumption

Aims Peak oxygen uptake (VO(2)) is diminished in patients with heart failure with preserved ejection fraction (HFpEF) suggesting impaired cardiac reserve. To test this hypothesis, we assessed the haemodynamic response to exercise in HFpEF patients.
Methods and results
Eleven HFpEF patients (73 +/- 7 years, 7 females/4 males) and 13 healthy controls (70 +/- 4 years, 6 females/7 males) were studied during submaximal and maximal exercise. The cardiac output (Q(c), acetylene rebreathing) response to exercise was determined from linear regression of Q(c) and VO(2) (Douglas bags) at rest, similar to 30% and similar to 60% of peak VO(2), and maximal exercise. Peak VO(2) was lower in HFpEF patients than in controls (13.7 +/- 3.4 vs. 21.6 +/- 3.6 mL/kg/min; P < 0.001), while indices of cardiac reserve were not statistically different: peak cardiac power output [CPO = Q(c) x mean arterial pressure (MAP); HFpEF 1790 +/- 509 vs. controls 2119 +/- 581 L/mmHg/min; P = 0.20]; peak stroke work [SW stroke volume (SV) x MAP; HFpEF 13 429 +/- 2269 vs. controls 13 200 +/- 3610 mL/mmHg; P = 0.80]. The Delta Q(c)/Delta VO(2) slope was abnormally elevated in HFpEF patients vs. controls (11.2 +/- 3.6 vs. 8.3 +/- 1.5; P = 0.015).
Conclusion Contrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO(2), increased Delta Q(c)/Delta VO(2) slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.

• 出版日期2011-12