What is the clinical evidence from this study?

Study design: Observational. Population: Chronic cardiac failure (n=43). Intervention: Chronic cardiac failure vs. Controls with normal cardiac function. Primary outcome: Overall levels of atrial natriuretic peptide (ng/L) (p=<0.001).

April 1, 1994

Variable patterns of atrial natriuretic peptide secretion in man

Q: What are the key findings of this study?

Chronic cardiac failure was associated with higher overall levels of atrial natriuretic peptide compared to controls (median 230 vs 26 ng/L; P<0.001), with both groups showing pulsatile secretion.

Resultado clave

Chronic cardiac failure was associated with higher overall levels of atrial natriuretic peptide compared to controls (median 230 vs 26 ng/L; P<0.001), with both groups showing pulsatile secretion.

Diseño del estudio

Tipo

Observational (n=43)

PICO estructurado

Does atrial natriuretic peptide secretion exhibit a pulsatile pattern with short-term variability in patients with and without cardiac failure?

Población

43 participants, comprising patients with chronic cardiac failure or valvular heart disease and healthy controls, undergoing frequent blood sampling over 90 minutes.

Exposición

Frequent blood sampling (every 2 min for 90 min) from the antecubital vein, pulmonary artery, and femoral artery to measure atrial natriuretic peptide levels.

Comparador

Healthy controls versus patients with cardiac failure or impaired cardiac function.

Resultado

Peripheral circulating levels and variability patterns (peaks, troughs, pulses) of atrial natriuretic peptide.surrogate

Atrial natriuretic peptide is secreted in a pulsatile manner with short-term variability that is preserved across different vascular beds in both healthy individuals and patients with heart failure.

Resultado numérico

Tasa de eventos absoluta: 230% vs 26%

valor p: p=<0.001

Resumen

Peripheral circulating levels of atrial natriuretic peptide may exhibit short-term variation compatible with a pulsatile pattern of secretion. We obtained samples every 2 min for 90 min from the antecubital vein of 16 patients with chronic cardiac failure and 13 controls. Overall levels were higher in the patients (median and quartiles 230 (125,325) vs. 26 (16,48) ng l-1; P 2 SD from the mean) and 16 (13-18) pulses (defined by computer) during the sampling period in controls, and a similar number in patients. We then carried out simultaneous sampling in the pulmonary artery, femoral artery and peripheral vein in eight subjects with normal cardiac function and six patients with impaired function due to valvular heart disease. The pattern of variability was preserved in all three sites in both groups, suggesting intermittent secretion rather than variable breakdown of the peptide in the lung. No changes in right atrial pressure or heart rate were observed to coincide with the variations, but levels of the peptide in the pulmonary artery correlated with right atrial pressure in patients (r = 0.87; P < 0.05). The mechanism of such periodicity and its pathophysiological importance remain unknown.

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