As left ventricular dilatation and the impairment of left ventricular systolic function due to replacement fibrosis only appear in very advanced stages, we assume that myocardial wall thickening and diastolic dysfunction are the main contributors to cardiac wall stress and elevations of NT-proBNP in patients with mild or moderate cardiac involvement of Fabry disease. Here, NPPB is linked to Left ventricular dilatation.