Natriuretic peptides to probe haemodynamic overload in hypertrophic cardiomyopathy.

sarily induce a large increase in left ventricular wall stress because of the obliterated left ventricular cavity in midto late systole as a result of hyperdynamic ejection. This reasoning was supported by micromanometer left ventricular and aortic pressure and flow measurements, but challenged by the outcome of myectomy surgery which resulted in significant improvement in symptoms and in radionuclide perfusion defects. Using plasma levels of natriuretic peptides to probe the mechanical overload in hypertrophic obstructive cardiomyopathy, the present study confirms the result of a previous study showing elevated levels, especially of brain natriuretic peptide, in patients with hypertrophic obstructive cardiomyopathy. The most straightforward interpretation of this finding is that the outflow tract gradient indeed contributes to systolic left ventricular overload. A confounding finding, however, is the significant correlation between brain natriuretic peptide and the extent of left ventricular hypertrophy. This correlation raises suspicions that the rise in brain natriuretic peptide was only a marker of hypertrophy-induced re-expression of the fetal gene programme and not necessarily of mechanical systolic overload. This suspicion is corroborated by a previous study which established a nice correlation between plasma brain natriuretic peptide levels and aortic valve gradients in patients with aortic stenosis, but failed to demonstrate a correlation between plasma brain natriuretic peptide levels and the outflow tract gradient in hypertrophic obstructive cardiomyopathy. It therefore seems prudent to await further studies, which should eventually establish a drop in brain natriuretic peptide following surgical myectomy or alcohol septal ablation, before interpreting the high brain natriuretic peptide levels in hypertrophic obstructive cardiomyopathy as an outflow tract gradient induced elevation in systolic wall stress. In patients with hypertrophic obstructive cardiomyopathy, it is often difficult to attribute a reduction in exercise tolerance to diastolic left ventricular dysfunction or to the outflow tract gradient. The study by Briguori et al. established an inverse relationship between peak exercise oxygen consumption and atrial natriuretic peptide plasma levels but not brain natriuretic peptide plasma levels. Since atrial natriuretic peptide plasma levels were closely related to diastolic left ventricular function and brain See page 1328 for the article to which this Editorial refers