Such systems have been used for many years in the assessment of the effects of novel pharmacological agents on cardiovascular electrophysiological and contractile function ( Habeler et al., 2009). An advantage of these integrated models is that they can maintain their physiological integrity for long periods of time. Such models have yet to be used in research in atherosclerotic cardiovascular disease, but they may lend themselves well to modelling the long-term disease processes which occur in smoking-related

Cell Cycle inhibitor cardiovascular disease. Clearly, a number of in vitro cardiovascular disease models have the potential for use in an approach to assess the biological effects of cigarette smoke from modified cigarettes, and these have been summarised in Table 2. What we have not discussed in this article are the practicalities of use of these models, particularly in terms of

model validation and experimental standards. With respect to the latter, any data and conclusions derived from the use of these models would have greater strength if studies were conducted following the principles of Good Laboratory Practise, which would ensure the quality, integrity and reproducibility of experimental findings ( Gupta et al., 2006). Model validation is an area which needs a great deal of development in order to ensure that the C59 wnt concentration models used Telomerase are fit-for-purpose, in terms of the model used being relevant to the disease being examined and linked to pathogenic processes. Validation would further ensure that data from models was robust, reproducible

and repeatable and that similar findings could be obtained from independent laboratories using the same model and test agents. Of further importance is verification of the identity of the cells used in any given model, to ensure that they are in fact authentic and what the investigator believes them to be ( Freshney, 2008). While in vitro models are powerful assessment tools, a thorough testing strategy may be enhanced with in vivo models. In the realm of cardiovascular disease studies, many animal models have been used over several decades and include a range of species from pigeons to non-human primates. Early animal models relied on atherogenic diets to drive the pathogenesis of cardiovascular disease and typically were time-consuming and expensive. However, important understandings of disease processes resulted from the use of these models. Current in vitro models are poor predictors of events that lead to plaque formation, destabilisation, rupture and thrombotic events.