Hypertrophic cardiomyopathy (HCM) is a clinically heterogeneous autosomal 
dominant heart disease characterised by left ventricular hypertrophy in the 
absence of another cardiac or systemic disease that is capable of producing 
significant wall thickening. Microscopically it is characterised by 
cardiomyocyte hypertrophy, myofibrillar disarray and fibrosis. The phenotypic 
expression of HCM is multifactorial, with the majority of cases occurring 
secondary to mutations in genes encoding the sarcomere proteins. In conjunction 
with the genetic heterogeneity of HCM, phenotypic expression also exhibits a 
high level of variability even within families with the same aetiological 
mutation, and may be influenced by additional genetic factors. Polymorphisms of 
the renin-angiotensin-aldosterone system (RAAS) represent an attractive 
hypothesis as potential disease modifiers, as these genetic variants alter the 
'activation status' of the RAAS, which leads to more left ventricular 
hypertrophy through different pathways. The main objective of this review is to 
provide an overview of the role of different polymorphisms identified in the 
RAAS, in patients with HCM.