Inhaled corticosteroids (ICS) have had a wild and controversial rollercoaster ride in chronic obstructive pulmonary disease (COPD). With the success of ICS in asthma and with the advent of the Dutch Hypothesis, suggesting that asthma and COPD had a similar pathogenic origin, there was great hope that ICS would be the saviour for millions of patients suffering from COPD, by palliating symptoms and changing its natural history. Based on this promise, by the mid 1980s, clinicians were routinely recommending ICS therapy to their patients, even though there was an absence of compelling grade A evidence from large randomised controlled trials (RCTs) demonstrating efficacy [1].By the late 1990s, the promise was shattered by the publication of several seminal RCTs that clearly showed that ICS did not modify the rate of decline in forced expiratory volume in 1 s (FEV1) and had only a modest effect on symptoms [2][3][4]. These data re-inforced the notion that COPD was a steroid-resistant state and many leading experts in the field concluded that ICS had no role in COPD, except during exacerbations [5]. Ostensibly, ICS were dead and buried.However, the new millennium brought new hope for ICS. Proponents argued that while ICS may not alter the rate of decline in FEV1, it improved patient based outcomes including survival. This optimism was fuelled by several large observational studies and meta-analyses [6][7][8][9] that demonstrated a distinct survival benefit for patients who were prescribed ICS. This enthusiasm, however, was dashed in 2007 by the publication of the long-awaited TORCH (TOwards a Revolution in COPD Health) Study, which failed to show an unequivocal survival advantage for patients assigned to a steroid-containing treatment strategy over a 3-yr period [10]. ICS were dead and buried for the second time.Yet almost immediately, ICS was resurrected from the dead, this time on the notion that COPD is an inflammatory disorder with multiple extrapulmonary manifestations, driven largely by a persistent systemic inflammatory process, which worsens during periods of exacerbation [11]. Although COPD is associated with many different comorbidities, cardiovascular disorders (CVDs) are of particular importance, as they are the leading causes of hospitalisation and a major contributor of total mortality, accounting for a quarter to a third of all deaths in COPD patients [12]. Since systemic inflammation is an important co-factor in the genesis of CVD, it was reasoned that ICS could mitigate the risk of CVD and, thus, reduce the overall health burden of COPD patients by attenuating the inflammatory load. Additional support for this theory came from large epidemiological studies and post hoc analyses of RCTs, showing the possible benefits of ICS in reducing the rate of myocardial infarctions, angina, stroke and heart failure morbidity and mortality in COPD patients [13][14][15][16].In this issue of the European Respiratory Journal, LOKE et al. [17] provide fresh data that challenge the notion that ICS reduce the risk of myoc...