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1 �� 0.6 versus sham 4.6 �� 0.04, n= 10, P this website In this regard, cardiac hypertrophy, as an adaptive condition that often precedes heart failure, is useful for studying the progressive changes that accompany the transition to failure (Mercadier, 2000). A limitation of most animal studies is that data are often collected only from a single time point following the surgical or drug-induced intervention. Progression of cardiac dysfunction is dynamic; therefore, it is essential that monitoring occurs over Ficain a period rather than taking a single snap-shot of what is a continually changing condition. As the heart responds to stress or injury, the adaptations are numerous, and it is essential that animal models reflect this complexity. Aortic banding has proved to be a reliable model of left ventricular pressure overload for studying compensated hypertrophy of the heart (Lompre et al. 1979; Mercadier et al. 1981; Izumo et al. 1987); however, this procedure is time consuming and technically find protocol complex because it involves mechanical ventilation and thoracotomy. Minimally invasive transverse aortic banding (MTAB) circumvents these requirements and can be performed very rapidly and reproducibly (Hu et al. 2003). Given the clear advantages of this model, it is surprising that so few laboratories have developed the technique. Of those that have, there are reports of high levels of mortality, which may be dependent on the sex of the mice used (Toischer et al. 2010). However, it remains to be established whether high mortality is associated with other particular aspects of the protocol, such as the anaesthetic regime. It is widely accepted that establishing any animal model of disease is time consuming, and that reproducing conditions established in another laboratory can prove difficult. It is therefore crucial that detailed reference material on optimization is available. Chronic pressure overload not only leads to cardiac hypertrophy, but can also result in fibrosis and stiffening of the myocardium. Increased stiffness leads to compromised relaxation or relengthening of cardiac myocytes and consequent problems with ventricular filling (Burlew & Weber, 2002).