Circadian Variation Of Acute Myocardial Infarction Research Articles

Contents of second peak in the circadian variation of acute myocardial infarction in the Japanese population

Circadian variation has been accepted as a factor in acute myocardial infarction (AMI). An increased incidence of cardiac events in the morning has been reported for a long time. Recent reports have indicated that the onset of AMI shows two peaks, which occur in the morning and evening. It has also been demonstrated that circadian pattern of AMI may vary with sex and age. We investigated 522 consecutive patients who underwent primary percutaneous coronary intervention (PCI) for ST segment elevation myocardial infarction (STEMI) between 2000 and 2010. The patients were classified into 3 age groups: younger (≤59 years old), intermediate (60-79 years old), and older (≥80 years old). Clinical data were investigated, including the age and sex, angiographic characteristics, and time of onset of STEMI. There were two peaks in the onset of STEMI throughout the day, which were at 7:00-10:00 and 19:00-21:00 h, among all patients (male and female). Stratified analysis showed that older females formed the main part of the second peak. There were two peaks in the onset of STEMI in a Japanese population in Tokyo. The second peak was significantly dominated by the older female group. Age and gender influenced the second peak in the circadian variation of AMI in a Japanese population in Tokyo.

Influence of statin therapy on circadian variation of acute myocardial infarction

Strong evidence has suggested that there is a circadian periodicity of acute coronary event. Beta-blockers, aspirin and angiotensin-converting enzyme inhibitors decrease the rate of acute myocardial infarction (AMI) and blunt the peak incidence in the morning. However, such effect has not been evaluated for statins. Accordingly, the present study aimed to evaluate the influence of statin therapy on circadian variation of AMI. This retrospective study consisted of 451 consecutive patients with acute ST segment elevation AMI. The patients were divided into two group based on prior statin usage. In statistical analysis t test, Chi-square test and Mann Whitney U test were used for comparison of groups. We used harmonic regression models to evaluate the circadian variation of onset of MI symptoms in patients receiving statin and patients not receiving statin. In all study participants, the highest incidence of AMI was between 6.00 and 12.00; the odds ratio was 1.34 (95% CI 1.20 to 1.46, p=0.001). In the non-statin group, the highest incidence of AMI occurred between 0:00 A.M. and 06.00. There was still a peak incidence between 6.00 A.M. and noon in the statin therapy receiving group; the odds ratio was 1.61 (95% CI 1.34 to 1.80, p=0.001). Accordingly, there was no statistical difference between the statin and non-statin groups regarding circadian variation of AMI. Prior usage of statin did not blunt the peak incidence of AMI in the morning. Prior usage of statin does not seem to play a role in the circadian periodicity of AMI.

Circadian variation of plaque rupture in acute myocardial infarction

Studies have reported a circadian variation in the onset of acute myocardial infarction (AMI). Pathologic studies have revealed that plaque rupture is 1 of the major causes of AMI, but none of these has looked specifically at the circadian variation of plaque rupture. The aim of this study was to use intravascular ultrasound (IVUS) to investigate the circadian variation of plaque rupture in AMI. This study included 174 consecutive patients with AMI who underwent preinterventional IVUS. All patients were assigned to either a rupture group or a nonrupture group according to the preinterventional IVUS. In the 81 patients (47%) in the rupture group, the frequency of the onset of AMI increased significantly in the period from 6 a. m. to 12 p. m. compared with all other time periods (p <0.05). The clinical features of AMI in the rupture group were characterized as occurring significantly more at rest (67% vs 31%, p <0.01) and after significantly less preinfarction angina (22% vs 57%, p <0.01) compared with the nonrupture group. A different circadian variation was identified in the nonrupture group, characterized as a significant nocturnal nadir (12 to 6 a. m. compared with all other periods, p <0.05). The circadian variation of AMI is the result of a morning increase in incidence of plaque rupture.