Circadian Variation and Triggers of Cardiovascular Disease

Abstract

It has recently been shown that approximately 90% of cases of non-fatal myocardial infarction and many cases of sudden cardiac death are caused by disruption of a coronary atherosclerotic plaque, followed by occlusive thrombus formation. Secondly, the circadian pattern of myocardial infarction is well known to feature a prominent increase in the morning hours. Taken together, these factors may provide an opportunity to reduce deaths caused by cardiovascular disease. Findings indicate that, in many cases, plaque disruption and thrombus formation are triggered by the activities of the patient. It is postulated that onset occurs when a ‘vulnerable’ atherosclerotic plaque becomes disrupted and occlusive thrombus formation occurs. The occurrence of a myocardial infarction in the morning hours could result from the synchronization of a number of potential triggers. The importance of the recognition of the circadian variation of acute onset of myocardial infarction is that pharmacologic protection can be directed at the early waking hours. It would seem reasonable to propose that long-acting anti-ischemic agents would have an advantage over short-acting agents in providing protection against the morning occurrence of myocardial infarction. A future goal would be to design therapeutic regimens that would have the ability to sever the linkage between a potential triggering activity and the development of myocardial infarction.

The influence of age on heart rate variability during morning wakefulness

“…Conversely, a dynamic system may also be disadvantageous. For example, excessive surges in sympathetic activity, with concurrent vagal withdrawal is associated with the waking process [15], and these changes may account for the increased occurrence of adverse cardiac events towards the end of the sleep period and during wakefulness following sleep [20,24,31,32].…”

Circadian Variation in the Timing of Stroke Onset

“…1 Some believe this morning excess of cardiovascular risk parallels the usual circadian pattern of physical activity, blood pressure, plasma catecholamines, and/or plasma cortisol. [2][3][4][5] Early studies of the timing of acute stroke, however, indicated that many afflicted patients reported awakening with new neurologic deficits, and several reports indicated that acute strokes tended to occur either during the evening hours or during sleep. [6][7][8] This led to the conclusion that especially because acute therapies for stroke-in-evolution were not particularly effective, there was little reason to consider acute stroke as a medical emergency because the onset of symptoms was thought to occur during sleep, when most patients would not recognize them.…”

Differences between amlodipine and lisinopril in control of clinic and twenty-four hour ambulatory blood pressures

“…16 Tolerability was good during both treatment phases and there were no serious adverse events. Similar numbers of patients reported adverse events following amlodipine and lisinopril and there were 95% confidence intervals (CI) relate to differences in mean % changes in BP between treatments;…”