Circadian Variation in Stroke Onset: Identical Temporal Pattern in Ischemic and Hemorrhagic Events

Abstract

Stroke is the culmination of a heterogeneous group of cerebrovascular diseases that is manifested as ischemia or hemorrhage of one or more blood vessels of the brain. The occurrence of many acute cardiovascular events--such as myocardial infarction, sudden cardiac death, pulmonary embolism, critical limb ischemia, and aortic aneurysm rupture--exhibits prominent 24 h patterning, with a major morning peak and secondary early evening peak. The incidence of stroke exhibits the same 24 h pattern. Although ischemic and hemorrhagic strokes are different entities and are characterized by different pathophysiological mechanisms, they share an identical double-peak 24 h pattern. A constellation of endogenous circadian rhythms and exogenous cyclic factors are involved. The staging of the circadian rhythms in vascular tone, coagulative balance, and blood pressure plus temporal patterns in posture, physical activity, emotional stress, and medication effects play central and/or triggering roles. Features of the circadian rhythm of blood pressure, in terms of their chronic and acute effects on cerebral vessels, and of coagulation are especially important. Clinical medicine has been most concerned with the prevention of stroke in the morning, when population-based studies show it is of greatest risk during the 24 h; however, improved protection of at-risk patients against stroke in the early evening, the second most vulnerable time of cerebrovascular accidents, has received relatively little attention thus far.

The importance of biological rhythms in drug treatment of hypertension and sex-dependent modifications

“…31 Pathophysiological events within the cardiovascular system do not occur at random either. [32][33][34][35][36] Thus, the onset of nonfatal or fatal myocardial infarction predominates around 6 am to 12 pm. A similar circadian time pattern has been shown for sudden cardiac death, stroke, ventricular arrhythmias, arterial embolism, and fatal pulmonary embolism.…”

Relationship Among Morning Blood Pressure Surge, 24-Hour Blood Pressure Variability, and Cardiovascular Outcomes in a White Population

“…[1][2][3][4] This has a pathophysiological explanation because transition from sleep to the wakefulness state is associated with an array of bodily modifications that have adverse effects on the cardiovascular system, that is, a marked and steep increase of blood pressure (BP) and heart rate, 5 a sympathetic activation and thus an increase of plasma catecholamines, 6,7 an increase of platelet adhesiveness, 8 and a reduction of fibrinolytic activity. 9 Two studies performed in Japan have reported the morning BP increase to be related to the incidence of hemorrhagic and thrombotic strokes, 10,11 thereby concluding that this increase has a role in the cardiovascular risk elevation that accompanies the sleep-wakefulness transition.…”

Circadian clock and vascular disease

“…57 Circadian oscillation has been shown not only in the factor VII level in blood, but also in the levels of fibrinogen, prothrombin, factor VIII and tissue factor pathway inhibitor, a direct inhibitor of the FXa/TF/FVIIa complex. 58,59 Microparticles from endothelium induce coagulation through the tissue factor-mediated pathway. 60 A recent report by Madden et al 61 showed that the number of vascular cell adhesion molecule-1-positive microparticles in human plasma had a significant diurnal variation with a peak at 9 in the morning.…”