Myocardial adrenergic nervous activity is intensified in patients with heart failure without left ventricular volume or pressure overload

Objectives. To clarify whether myocardial adrenergic activity is different in patients with heart failure without left ventricular volume or pressure overload, we used iodine-123 metaiodobenzylguanidine (MIBG) imaging to study patients with mitral stenosis. Background. In patients with heart failure due to cardiomyopathy or to valve diseases with volume or pressure overload, or both, myocardial adrenergic nerve activity is accelerated independent of underlying cause. However, it is not clear whether this change in myocardial adrenergic nerve activity is present in patients without left ventricular volume or pressure overload. Methods. The study patients were 20 men and women with normal left ventricular function and heart failure due to mitral stenosis. Planar MIBG images obtained from these patients were compared with images from nine age-matched healthy subjects (control group). Myocardial uptake of MIBG was calculated as the heart/mediastinal activity ratio. Storage and release of MIBG were calculated as percent myocardial MIBG washout from 15 min to 4 h after isotope injection. All 20 study patients underwent echocardiography, and 16 underwent right heart catheterization. Results. The heart/mediastinal activity ratio in the immediate images (15 min) did not show any significant difference between the patient and control groups. Myocardial washout was increased in patients with severe heart failure. The level of myocardial washout correlated with left atrial diameter (r = 0.51, p = 0.02) and mitral valve area calculated with Doppler echocardiography (r = -0.61, p < 0.01) and mitral valve area calculated with cardiac catheterization (r = -0.62, p = 0.02), The closest correlation existed between myocardial washout and cardiac output (r = -0.80, p < 0.01). Conclusions. In heart failure due to mitral stenosis, myocardial adrenergic nerve activity is intensified. A decrease in cardiac output associated with mitral stenosis acts as a potent stimulus for this intensification.