Key result
HF and CCS with excess ventilation link to lower hyperoxic VRT versus healthy controls.
Why the study?
Increased ventilation/carbon dioxide production slope predicts progression and mortality in CCS, but increased chemosensitivity has rarely been assessed in these patients.
Does central and peripheral chemosensitivity differ in patients with inefficient ventilation and CCS or HF compared to healthy controls?
Case-Control (n=60)
No
Does central and peripheral chemosensitivity differ in patients with inefficient ventilation and CCS or HF compared to healthy controls?
p-value: p=0.004 and 0.01
Patients with heart failure or chronic coronary syndrome and excess ventilation exhibit reduced central chemoreflex ventilatory recruitment thresholds independently of heart failure presence.
Reduced chemoreflex thresholds may drive excess ventilation in HF/CCS; hypothesis-generating and leaves open therapeutic targeting.
Background In patients with chronic coronary syndromes (CCS), increased ventilation/carbon dioxide production ( V̇ E / V̇ CO 2 ) slope has been found to predict disease progression and mortality, similarly to patients with heart failure (HF); however, increased chemosensitivity, a well-established predictor for mortality in patients with HF, has rarely been assessed in patients with CCS. Method Patients with CCS, HF with reduced ejection fraction (EF < 50%), healthy controls (45+ years), and young healthy adults (<35 years) were recruited. For patients, a V̇ E / V̇ CO 2 slope ≥36 was an inclusion criterion. The Duffin rebreathing method was used to determine the resting end-expiratory partial pressure of carbon dioxide (P ET CO 2 ), ventilatory recruitment threshold (VRT), and slope (sensitivity) during a hyperoxic (150 mmHg O 2 ) and hypoxic (50 mmHg O 2 ) rebreathing test to determine the central and peripheral chemosensitivity. Results In patients with CCS, HF, controls, and young healthy adults, median V̇ E / V̇ CO 2 slopes were 40.2, 41.3, 30.5, and 28.0, respectively. Both patient groups had similarly reduced hyperoxic VRT (at P ET CO 2 42.1 and 43.2 mmHg) compared to 46.0 and 48.8 mmHg in the control and young healthy adults. Neither hypoxic VRT nor hyper- or hypoxic slopes were significantly different in patients compared to controls. Both patient groups had lower resting P ET CO 2 than controls, but only patients with HF had increased breathing frequency and rapid shallow breathing at rest. Conclusion In patients with HF and/or CCS and excess ventilation, central chemoreflex VRT was reduced independently of the presence of HF. Low VRTs were related to resting excess ventilation in patients with CCS or HF; however, rapid shallow breathing at peak exercise was present only in patients with HF. Clinical trial registration number NCT05057884.
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Eser et al. (2025) conducted a case-control in Chronic coronary syndrome or heart failure with inefficient ventilation (n=60). Chronic coronary syndrome or heart failure with inefficient ventilation vs. Healthy controls was evaluated on Hyperoxic ventilatory recruitment threshold (VRT) (p=0.004 and 0.01). Patients with heart failure or chronic coronary syndrome and excess ventilation had significantly lower hyperoxic ventilatory recruitment thresholds (median 42.1 and 43.2 mmHg, respectively) compared to healthy controls (46.0 mmHg).
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