Abstract
Introduction: Pulmonary arterial hypertension (PAH) is an acknowledged independent prognostic factor in patients with heart failure (HF). Beyond a “passive” component due to the increased left ventricular pressure, an “active” component due to pulmonary vascular reactivity is frequently observed. However, the mechanism behind pulmonary vasoconstriction is not fully understood. Hypothesis: We hypothesized that central apneas (Cheyne-Stokes respiration [[Unable to Display Character: &#8211;]] CSR) through chemoreflex stimulation may contribute to PAH in HF. Methods: we studied 56 HF patients (left ventricular ejection fraction <50%), on stable optimal pharmacological treatment, without increased left ventriculare pressure (excluding patients with severe mitral disease and severe diastolic dysfunction). All patients underwent echocardiographic and neurohormonal assessment, 24-hour cardiorespiratory screening for CSR (patients with obstructive events were excluded) and chemoreflex test for hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses (by rebreathing technique) . Results: Thirteen patients (23%) showed CSR, as defined by a 24 hour AHI > of 15. HF patients with CSR compared with patients with normal breathing, presented higher systolic arterial pulmonary pressure (SPAP: 40.1±7.6 vs 33.1±5.9, p<0.01) at echocardiography, despite similar systolic and diastolic function (data not shown). Furthermore, patients with central apneas also presented with enhanced HVR (median 0.78, interquartile range -IR 0.48-1.22 vs 0.43, IR 0.19-0.69 L/min/%, p<0.05) and HCVR (1.18, IR 0.98-1.35 vs 0.75, IR 0.51-0.95 L/min/mmHg, p<0.01) as well as increased plasma norepinephrine levels (546, IR 371-732 vs 393, IR 229-538 pg/mL, p<0.05). SPAP was indeed correlated with AHI (Spearman’s Rho, R=0.44, p<0.01), HCVR (R=0.48, p<0.001), HVR (R=0.33, p<0.05) and norepinephrine levels (R=0.31, p<0.05). Conclusions: In patients with systolic HF, the presence of diurnal-nocturnal CSR, likely via recurrent hypoxia and hypercapnia cycles, may determine a chemoreflex mediated adrenergic discharge and a consequent pulmonary vasoconstriction, responsible of the undesirable increase in pulmonary arterial pressure.
Published Version
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