Key result
Infusion of synthetic alpha-human ANF significantly reduced pulmonary artery pressure from 33 to 25 mmHg and systemic arterial pressure from 88 to 79 mmHg in patients with COLD.
Why the study?
Does synthetic alpha-human ANF infusion improve hemodynamics in patients with COLD and pulmonary hypertension?
Does synthetic alpha-human ANF infusion improve hemodynamics in patients with COLD and pulmonary hypertension?
Absolute Event Rate: 25% vs 33%
p-value: p=<0.001
ANF acts as a potent pulmonary vasodilator in patients with COLD and pulmonary hypertension, reducing pulmonary artery pressure and vascular resistance.
May lower PAP in COLD; hypothesis-generating and requires randomized confirmation before any clinical consideration.
To investigate the physiological role of atrial natriuretic factor (ANF) in patients with hypoxic pulmonary hypertension secondary to chronic obstructive lung disease (COLD), we infused synthetic alpha-human ANF in seven such patients, and investigated the physiological correlates to circulating peptide levels in 24 patients with COLD. ANF infusion, at incremental rates of 0.01, 0.03, and 0.1 micrograms/kg.min, increased basal plasma immunoreactive (ir) ANF (136 +/- 38 pg/ml) by 3-, 10-, and 26-fold, respectively, and reduced pulmonary artery pressure (from 33 +/- 3 to 25 +/- 2 mmHg, P less than 0.001) and systemic arterial pressure (from 88 +/- 4 to 79 +/- 4 mmHg, P less than 0.001) in a dose-related fashion. Cardiac index increased by 13.5% (P less than 0.01) while heart rate was unchanged. Cardiac filling pressures decreased at 0.1 micrograms/kg.min ANF. Pulmonary and systemic vascular resistance fell by 37% (P less than 0.001) and 19% (P less than 0.001), respectively. Arterial oxygenation was impaired during ANF infusion, suggesting partial reversal of hypoxic pulmonary vasoconstriction. Plasma renin activity remained unchanged but aldosterone fell by 44% (P less than 0.01). The levels of plasma irANF in 24 patients correlated directly with the degree of hemoconcentration (r = 0.67, P less than 0.001), respiratory acidosis (r = -0.65, P less than 0.001), and pulmonary hypertension (r = 0.52, P less than 0.01). The results suggest that ANF may serve as a potent pulmonary vasodilator involved in the circulatory homeostasis of patients with COLD.
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Adnot et al. (1989) studied Chronic obstructive lung disease with pulmonary hypertension (n=24). Synthetic alpha-human ANF vs. Baseline (pre-infusion) was evaluated on Pulmonary artery pressure (p=<0.001). Infusion of synthetic alpha-human ANF significantly reduced pulmonary artery pressure from 33 to 25 mmHg and systemic arterial pressure from 88 to 79 mmHg in patients with COLD.