Circadian variation of plaque rupture in acute myocardial infarction

Tanaka, Atsushi; Kawarabayashi, Takahiko; Fukuda, Daiju; Nishibori, Yoshiharu; Sakamoto, Tsunemori; Nishida, Yukio; Shimada, Kenei; Yoshikawa, Junichi

doi:10.1016/j.amjcard.2003.09.002

« Previous Next »American Journal of Cardiology
Volume 93, Issue 1 , Pages 1-5, 1 January 2004

Circadian variation of plaque rupture in acute myocardial infarction

Atsushi Tanaka, MD
- Baba Memorial Hospital, Sakai, Japan
- Address for reprints: Atsushi Tanaka, MD, Department of Cardiology, Baba Memorial Hospital, 4-244, Hamadera-funao-cho Higashi, Sakai, 592-8555 Japan.
Takahiko Kawarabayashi, MD
- Baba Memorial Hospital, Sakai, Japan
Daiju Fukuda, MD
- Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan
Yoshiharu Nishibori, MD
- Baba Memorial Hospital, Sakai, Japan
Tsunemori Sakamoto, MD
- Baba Memorial Hospital, Sakai, Japan
Yukio Nishida, MD
- Baba Memorial Hospital, Sakai, Japan
Kenei Shimada, MD
- Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan
Junichi Yoshikawa, MD
- Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan

Received 9 June 2003; received in revised form 2 September 2003; accepted 2 September 2003.

Abstract

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.