Defective Cardiac Parasympathetic Control in Patients with Heart Disease

TLDR

The study aimed to define the parasympathetic nervous system status in heart failure patients. The authors induced parasympathetic blockade with atropine after adrenergic blockade with propranolol in 12 normal subjects and nine heart‑disease patients, then measured baroreflex‑mediated heart‑rate responses to phenylephrine‑induced arterial pressure changes in 23 controls and 22 patients. Atropine raised heart rate by 55 % in normals but only 23 % in patients, and baroreceptor‑mediated heart‑rate slowing per mmHg systolic pressure was 16 ms in normals versus 3.7 ms in patients, indicating profound parasympathetic dysfunction in heart disease.

Abstract

To define the state of the parasympathetic nervous system in heart failure, parasympathetic blockade with atropine was induced after adrenergic blockade with propranolol in 12 normal subjects and in nine patients with heart disease. Atropine elevated heart rate by 55 ± 9 per cent in normal subjects, but by only 23 ± 8 per cent in patients with heart disease (p less than 0.05). In 23 control subjects and 22 patients, transient elevations in arterial pressure were produced by intravenous injections of phenylephrine, and successive R-R intervals were plotted as a function of systolic pressure. The slowing of heart rate per unit rise in systolic arterial pressure averaged 16.0 ±1.8 msec per millimeter of mercury in normal subjects but only 3.70 ± 0.8 msec per millimeter of mercury in the patients (p less than 0.001). Baroreceptor-induced slowing of heart rate in normal subjects was shown to be mediated by the parasympathetic nervous system since it could be abolished with atropine. These findings point to a profound abnormality in parasympathetic cardiovascular regulation in heart disease.