The CV system is organized according to a specific oscillatory order, and most CV functions exhibit circadian changes. Thus, circadian differences in the physiological status of the CV system give rise to rhythmic—and predictable-in-time—variations either in the susceptibility of human beings to morbid and mortal events, or in the ability to precipitate the overt expression of disease [
1]. It is known that the occurrence of CV events exhibits peculiar temporal patterns that vary across 24 h of the day. These patterns coincide with the temporal variation in the (a) pathophysiological mechanisms that trigger CV events and (b) physiological changes in the body rhythms. A series of factors, not harmful if considered alone, are capable of triggering unfavourable events when they all occur within the same temporal window [
1]. An evident circadian (morning) rhythm for acute myocardial infarction (AMI) has been understood for more than 2 decades. It has been estimated that the incidence rate of AMI onset is 40% higher in the morning period than throughout the rest of the day, and nearly 28% of morning AMIs (accounting for approximately 9% of all AMIs) are attributable to the morning excess [
6]. Moreover, rupture or dissection of aortic aneurysms shows a circadian variation, with an evident morning preference, as well [
7]. The similarity of temporal patterns of such different acute CV and cerebrovascular events suggests that they share common underlying mechanisms. Several pathophysiologic phenomena, such as increased BP, HR, sympathetic activity, basal vascular tone, vasoconstrictive hormones, increased viscosity, fibrinogen, platelet aggregability, and reduced fibrinolytic activity, exhibit prominent circadian rhythms with phases positively correlated with the timing of excess in CV events [
7]. Moreover, the effect of stress on human cardiac, vascular, and haemostatic status appears to be circadian rhythmic, with the effects being greater in the morning [
1]. An exaggerated CV response to behavioural challenges has been suggested as a potential factor that enhances the risk of hypertension and CV disease. Thus, individuals who exhibit large increases in BP during acute psychological stress are at risk of atherosclerosis, probably secondary to endothelial damage by a BP surge, via increased flow turbulence, and a subsequent release of inflammatory and pro-atherogenic cytokines. Emotional stress can also play a pivotal triggering role for ischaemic heart disease, as shown for the morning onset of Takotsubo syndrome [
8].