International journal of cardiology · 2015
Hemodynamic, not ventilatory, inefficiency is associated with high VE/VCO2 slope in repaired, noncyanotic congenital heart disease.
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Mezzani Alessandro, Giordano Andrea, Moussa Nidhal Ben, Micheletti Angelo, Negura Diana, Saracino Antonio, Canal Elena, Giannuzzi Pantaleo, Chessa Massimo, Carminati Mario
Аннотация
BACKGROUND: A high slope of the ventilation vs. carbon dioxide relationship (VE/VCO₂ slope) during incremental exercise has been reported in several congenital heart disease (CHD) types, but it is not clear whether the main cause of high VE/VCO₂ slope is excessive ventilation or reduced perfusion.
METHODS: We studied 169 adolescent and adult patients with repaired, noncyanotic CHD, divided into 2 groups according to VE/VCO₂ slope %predicted values (≤120 and >120), and 15 age- and sex-matched normals. VCO₂/VE max and VO₂/VE max were considered proxies of the perfusion/ventilation relationship, with VCO₂ and VO₂ as indirect descriptors of cardiac output.
RESULTS: VCO₂/VE max was significantly and inversely related to VE/VCO₂ slope (r=-0.73, p<0.0001), and higher in normals and ≤120 than in >120 (39.6 ± 7.7, 36.1 ± 5.3 and 28.5 ± 4.1, respectively, p<0.0001). Similarly, VCO₂ at VCO₂/VE max was higher in normals and ≤120 than in >120 (1701 ± 474, 1480 ± 492 and 1169 ± 388 ml/min, respectively, p<0.0001), whereas ventilation at VCO₂/VE max showed no changes (43 ± 8, 41 ± 12, 41 ± 11 and 41 ± 9l/min, respectively, p=0.82) between groups. Thus, differences in VCO₂/VE max and VE/VCO₂ slope between groups were due mostly to changes in VCO₂, i.e. in cardiac output, rather than ventilation. The same behavior was observed for VO₂/VE max.
CONCLUSIONS: A high VE/VCO₂ slope observed in patients with repaired, noncyanotic CHD seems not to depend on excessive ventilation but on hypoperfusion due to impaired cardiac output response to incremental exercise. This finding should focus researchers' attention mainly on the heart when addressing exercise pathophysiology of this patient population.
METHODS: We studied 169 adolescent and adult patients with repaired, noncyanotic CHD, divided into 2 groups according to VE/VCO₂ slope %predicted values (≤120 and >120), and 15 age- and sex-matched normals. VCO₂/VE max and VO₂/VE max were considered proxies of the perfusion/ventilation relationship, with VCO₂ and VO₂ as indirect descriptors of cardiac output.
RESULTS: VCO₂/VE max was significantly and inversely related to VE/VCO₂ slope (r=-0.73, p<0.0001), and higher in normals and ≤120 than in >120 (39.6 ± 7.7, 36.1 ± 5.3 and 28.5 ± 4.1, respectively, p<0.0001). Similarly, VCO₂ at VCO₂/VE max was higher in normals and ≤120 than in >120 (1701 ± 474, 1480 ± 492 and 1169 ± 388 ml/min, respectively, p<0.0001), whereas ventilation at VCO₂/VE max showed no changes (43 ± 8, 41 ± 12, 41 ± 11 and 41 ± 9l/min, respectively, p=0.82) between groups. Thus, differences in VCO₂/VE max and VE/VCO₂ slope between groups were due mostly to changes in VCO₂, i.e. in cardiac output, rather than ventilation. The same behavior was observed for VO₂/VE max.
CONCLUSIONS: A high VE/VCO₂ slope observed in patients with repaired, noncyanotic CHD seems not to depend on excessive ventilation but on hypoperfusion due to impaired cardiac output response to incremental exercise. This finding should focus researchers' attention mainly on the heart when addressing exercise pathophysiology of this patient population.