Coronary Artery Disease

Words: 701
Pages: 3

Cardiovascular diseases (CVD) are the leading cause of death and disability worldwide. The World Health Organisation estimates that by 2030 almost 24 million people will succumb to CVD. In Europe alone, it is responsible for over 4 million deaths per year accounting for almost 50 percent of all mortality. As such, research and development in modern medicine is largely focused on preventative and therapeutic strategies that will ultimately attenuate the scale of this mounting problem. The spectrum of CVD comprises coronary artery disease (CAD), which includes stable angina and acute coronary syndromes (ACS), ischaemic stroke and peripheral vascular disease (PVD). It is well established that platelets play an integral role in the onset, development …show more content…
The latter are an important patient group because coronary artery stenting can be associated with the potentially fatal complication of stent thrombosis (ST). Although the aetiology of ST is multifactorial, it is well recognised that suboptimal or premature discontinuation of APT is one of the leading and potentially avoidable causes. Nonetheless, the choice of APT regime and optimal duration of treatment in patients undergoing PCI remains to be established and is the subject of ongoing …show more content…
29!
Clinical studies have consistently demonstrated significant heterogeneity in individual patient responses to APT, determined using various laboratory tests of platelet function and, furthermore, a clear link between inadequate response and increased risk of adverse cardiovascular events has been established. Nonetheless, clinical guidelines recommend standard doses of APT in all patients rather than optimising pharmacotherapy by providing individually tailored treatment guided by platelet function testing. This is mainly due to the lack of consensus regarding the most appropriate and reliable test that can be employed in frontline clinical practice to measure individual responses to APT, as well as controversy surrounding the optimal definition of inadequate response to APT. Further data are required from large scale clinical studies to provide some clarity on these issues.
Thus, there remain several unanswered clinical questions in the vast field of APT prescribing in CVD. Specifically:
a) What is the optimal APT regime and duration of treatment in patients with CVD, particularly those patients undergoing PCI who may be at risk of ST?
b) Given the advent of newer, more potent APTs, should aspirin remain the default antiplatelet agent or can its role as the default APT now be