Suppression of silent ischemia by metoprolol without alteration of morning increase of platelet aggregability in patients with stable coronary artery disease.

Willich, Stefan N.; Pohjola-Sintonen, Sinikka; Bhatia, Satinder J.S.; Shook, Thomas; Tofler, Geoffrey H.; Muller, James E.; Curtis, D G; Williams, Gordon H.; Stone, Peter H.

doi:10.1161/01.cir.79.3.557

Cited by 106 publications

(19 citation statements)

References 56 publications

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“…cardiac vulnerability ͉ circadian pacemaker ͉ locomotor activity ͉ scale invariance E pidemiological studies demonstrate that myocardial infarction (1)(2)(3)(4), stroke (5,6), and sudden cardiac death (7) have a 24-h daily pattern with a broad peak at 9-11 a.m. This 24-h pattern is widely assumed to be due to day/night patterns in behaviors that affect cardiovascular variables, such as autonomic balance, blood pressure, and platelet aggregability, in vulnerable individuals (8).…”

mentioning

confidence: 99%

Endogenous circadian rhythm in human motor activity uncoupled from circadian influences on cardiac dynamics

Ivanov

Hilton

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

110

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The endogenous circadian pacemaker influences key physiologic functions, such as body temperature and heart rate, and is normally synchronized with the sleep/wake cycle. Epidemiological studies demonstrate a 24-h pattern in adverse cardiovascular events with a peak at Ϸ10 a.m. It is unknown whether this pattern in cardiac risk is caused by a day/night pattern of behaviors, including activity level and/or influences from the internal circadian pacemaker. We recently found that a scaling index of cardiac vulnerability has an endogenous circadian peak at the circadian phase corresponding to Ϸ10 a.m., which conceivably could contribute to the morning peak in cardiac risk. Here, we test whether this endogenous circadian influence on cardiac dynamics is caused by circadian-mediated changes in motor activity or whether activity and heart rate dynamics are decoupled across the circadian cycle. We analyze high-frequency recordings of motion from young healthy subjects during two complementary protocols that decouple the sleep/wake cycle from the circadian cycle while controlling scheduled behaviors. We find that static activity properties (mean and standard deviation) exhibit significant circadian rhythms with a peak at the circadian phase corresponding to 5-9 p.m. (Ϸ9 h later than the peak in the scale-invariant index of heartbeat fluctuations). In contrast, dynamic characteristics of the temporal scale-invariant organization of activity fluctuations (long-range correlations) do not exhibit a circadian rhythm. These findings suggest that endogenous circadian-mediated activity variations are not responsible for the endogenous circadian rhythm in the scale-invariant structure of heartbeat fluctuations and likely do not contribute to the increase in cardiac risk at Ϸ10 a.m.cardiac vulnerability ͉ circadian pacemaker ͉ locomotor activity ͉ scale invariance E pidemiological studies demonstrate that myocardial infarction (1-4), stroke (5, 6), and sudden cardiac death (7) have a 24-h daily pattern with a broad peak at 9-11 a.m. This 24-h pattern is widely assumed to be due to day/night patterns in behaviors that affect cardiovascular variables, such as autonomic balance, blood pressure, and platelet aggregability, in vulnerable individuals (8). However, endogenous influences from the circadian pacemaker [suprachiasmatic nuclei of the hypothalamus (SCN)], independent from external behavioral effects, may also contribute to this daily pattern of adverse cardiovascular events. These circadian influences could occur via hormonal effects, direct neuronal links between the SCN and the sympathetic system (9) and through circadian modulation of the sympathovagal balance (10). Recently, we demonstrated (11) that dynamical scale-invariant features of heartbeat fluctuations [related to underlying mechanisms of cardiac control (12-17)], exhibit a significant endogenous circadian rhythm, independent from extrinsic scheduled behaviors and the sleep/wake cycle. These dynamical features of heartbeat fluctuations move closer to the features ob...

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mentioning

confidence: 99%

Endogenous circadian rhythm in human motor activity uncoupled from circadian influences on cardiac dynamics

Ivanov

Hilton

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

110

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“…These events do not occur randomly during the day. Epidemiological studies demonstrate that myocardial infarction (2-6), stroke (7,8), angina (9), ventricular arrhythmias (10), and sudden cardiac death (11, 12) have a 24-h day͞night pattern with a primary occurrence peak around 10 a.m. This 24-h pattern of cardiac risk is widely assumed to be caused by day͞night patterns in behaviors that affect cardiovascular variables such as autonomic balance, blood pressure, and platelet aggregability in vulnerable individuals.…”

mentioning

confidence: 99%

Endogenous circadian rhythm in an index of cardiac vulnerability independent of changes in behavior

Ivanov

Hilton

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

131

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There exists a robust day͞night pattern in the incidence of adverse cardiac events with a peak at Ϸ10 a.m. This peak traditionally has been attributed to day͞night patterns in behaviors affecting cardiac function in vulnerable individuals. However, influences from the endogenous circadian pacemaker independent from behaviors may also affect cardiac control. Heartbeat dynamics under healthy conditions exhibit robust complex fluctuations characterized by self-similar temporal structures, which break down under pathologic conditions. We hypothesize that these dynamical features of the healthy human heartbeat have an endogenous circadian rhythm that brings the features closer to those observed under pathologic conditions at the endogenous circadian phase corresponding to Ϸ10 a.m. We investigate heartbeat dynamics in healthy subjects recorded throughout a 10-day protocol wherein the sleep͞wake and behavior cycles are desynchronized from the endogenous circadian cycle, enabling assessment of circadian factors while controlling for behavior-related factors. We demonstrate that the scaling exponent characterizing temporal correlations in heartbeat dynamics does exhibit a significant circadian rhythm (with a sharp peak at the circadian phase corresponding to Ϸ10 a.m.), which is independent from scheduled behaviors and mean heart rate. Cardiac dynamics under pathologic conditions such as congestive heart failure also are associated with a larger value of the scaling exponent of the interbeat interval. Thus, the sharp peak in the scaling exponent at the circadian phase coinciding with the period of highest cardiac vulnerability observed in epidemiological studies suggests that endogenous circadian-mediated influences on cardiac control may be involved in the day͞night pattern of adverse cardiac events in vulnerable individuals.detrended fluctuation analysis ͉ forced desynchrony protocol ͉ heartbeat dynamics ͉ correlations ͉ scaling A dverse cardiac events are the leading cause of mortality in the United States (1). These events do not occur randomly during the day. Epidemiological studies demonstrate that myocardial infarction (2-6), stroke (7,8), angina (9), ventricular arrhythmias (10), and sudden cardiac death (11, 12) have a 24-h day͞night pattern with a primary occurrence peak around 10 a.m. This 24-h pattern of cardiac risk is widely assumed to be caused by day͞night patterns in behaviors that affect cardiovascular variables such as autonomic balance, blood pressure, and platelet aggregability in vulnerable individuals. The suprachiasmatic nuclei of the anterior hypothalamus contain the principal endogenous circadian pacemaker, which is normally synchronized with the light͞dark cycle and the sleep͞wake cycle but also has independent effects on the sympathovagal balance of the autonomic nervous system (13, 14). These last effects raise the possibility that the circadian pacemaker contributes to the 24-h pattern of adverse cardiac events in vulnerable individuals.Recent studies based on approaches derived from statisti...

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“…[7][8][9][10] Analysis of this circadian variations is important to clarify the triggering mechanisms of AMI.Although the precise underlying mechanisms of the circadian variation of AMI are still unclear, the morning peak appears to be associated with surges of blood pressure, 11-13 neurohumoral factors 14,15 and platelet aggregability; [16][17][18] that is, it appears to be associated with an inherent biologic rhythm. However, the second peak in the evening is more associated with socioeconomic factors, such as the timing of the evening meal, 19 mental stress 20-22 and overtime work, 23 but it is unclear which population is more susceptible to the morning surge or to the nighttime socioeconomic factors.…”

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confidence: 99%

Circadian Variation of the Onset of Acute Myocardial Infarction in the Osaka Area, 1998-1999

Kinjo

Sato

et al. 2001

Jpn Circ J

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he time of onset of acute myocardial infarction (AMI) has a characteristic circadian variation, 1-10 with a definite morning peak and a vague evening peak. [7][8][9][10] Analysis of this circadian variations is important to clarify the triggering mechanisms of AMI.Although the precise underlying mechanisms of the circadian variation of AMI are still unclear, the morning peak appears to be associated with surges of blood pressure, 11-13 neurohumoral factors 14,15 and platelet aggregability; [16][17][18] that is, it appears to be associated with an inherent biologic rhythm. However, the second peak in the evening is more associated with socioeconomic factors, such as the timing of the evening meal, 19 mental stress 20-22 and overtime work, 23 but it is unclear which population is more susceptible to the morning surge or to the nighttime socioeconomic factors.Serious economic recession has existed for several yearsJapanese Circulation Journal Vol.65, July 2001 in Japan and so the circadian variation of AMI, especially the nighttime peak, may have altered in Japan. The present study had 2 aims: (1) to examine the recent circadian variation of AMI in Osaka, Japan and (2) to examine which specific population/s shows the morning peak or nighttime peak predominantly. Methods Organization and SubjectsWe conducted a district based survey named the 'Osaka Acute Coronary Insufficiency Study' (OACIS) to assess the clinical variables, therapeutic procedures and consequent clinical events in patients with AMI in the Osaka area. The study group comprised 1,609 consecutive patients with AMI who were admitted to 25 collaborating hospitals within 1 week of onset between April 1998 and January 2000. The diagnosis of definite AMI required 2 of the following 3 criteria: (1) a clinical history of central chest pressure, pain, or tightness lasting for 30 min or more, (2) ST-segment elevation greater than 0.1 mV in at least one standard or 2 precordial leads, and (3) a rise in serum creatine kinase concentration to greater than twice the normal laboratory value. Standard clinical variables, including the timing of the onset of AMI, therapeutic procedures and clinical events, were assessed during the patient's stay in hospital. When written informed consent for entering the OACIS study was obtained from the patient, all in-hospital data were transmitted to the OACIS office located at the The onset of acute myocardial infarction (AMI) shows characteristic circadian variations; that is, a definite morning peak related to biologic rhythms and a vague nighttime peak related to socioeconomic factors. The recent economic recession in Japan may change the circadian variation, especially the nighttime peak. This study evaluated the recent circadian variation of AMI in Osaka and specified the patient subgroups showing either a morning or nighttime peak predominantly. Of 1,609 consecutive patients with AMI registered from April 1998 to January 2000, 1,252 whose onset of AMI was definitely identified were studied. The day was divided into six 4-...

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Suppression of silent ischemia by metoprolol without alteration of morning increase of platelet aggregability in patients with stable coronary artery disease.

Cited by 106 publications

References 56 publications

Endogenous circadian rhythm in human motor activity uncoupled from circadian influences on cardiac dynamics

Endogenous circadian rhythm in human motor activity uncoupled from circadian influences on cardiac dynamics

Endogenous circadian rhythm in an index of cardiac vulnerability independent of changes in behavior

Circadian Variation of the Onset of Acute Myocardial Infarction in the Osaka Area, 1998-1999

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