Put your chips on transcriptomics.

The course of any disease is determined by a complex interplay between innate characteristics and environmental triggers. Accordingly, evidence-based risk factor assessment in heart disease requires a detailed family history to gauge inherited features and accurate estimates of smoking, diet, exercise, and other aspects that constitute important extrinsic disease modifiers. The value of traditional risk assessments for individual prognostication is limited, however, by lack of a precise family history to reveal specific genetic makeup on one hand and by interindividual variation in response to environmental events on the other. In diseases such as familial hypertrophic or dilated cardiomyopathies, in which the innate component is far more important than external factors in determining disease onset and progression, genetic testing is increasingly being used to assess individual risks for developing disease and to personalize therapy.1 However, although there have been some intriguing potential applications,2,3 the clinical utility of genetic profiling is less clear in nonischemic or idiopathic heart failure syndromes that are polygenic in origin or for which there is greater contribution of environmental factors. Thus, there is a need for clinical tests that not only will reveal a patient’s static genetic makeup but also will define the dynamic changes in gene transcript and protein expression that are a consequence of gene-environment interactions.