Abstract:The study demonstrated a marked wake time-related circadian variation in the occurrence of angina pectoris attacks. To improve preventive strategies, type, dosage and particularly timing of cardiac medication appear of importance, as may be behavior modification.
“…It is also clear that, other than output from a central clock, the manner by which a given peripheral clock is synchronized with another, or the extent to which a peripheral clock can establish feedback to the SCN that it is, in fact, synchronized is not known. At present, the literature does support the premise that pathophysiologic conditions can both cause uncoupling of peripheral oscillators and be caused by uncoupling of peripheral clocks (Muller, 1999a , b ; Young et al, 2001a , b ; Willich et al, 2004 ; Lee et al, 2005 ; Fujino et al, 2006 ; Maywood et al, 2010 ; Tsimakouridze et al, 2012 ; Reddy and Rey, 2014 ; Robinson and Reddy, 2014 ; Wu and Reddy, 2014 ).…”
Section: Circadian Rhythm Biologymentioning
confidence: 94%
“…The significance of circadian rhythms to myocardial infarction has been identified in several studies in which onset of non-Q-wave angina, unstable angina, myocardial infarctions, and sudden cardiac death all show marked elevations in occurrence between the hours of 0600 and 1200 (Muller, 1999a , b ; Willich et al, 2004 ; Mosendane and Raal, 2008 ). Ethnic genetic, medications, co-morbidities, lifestyle, cultural, and/or social factors may shift the time of highest incidence (Kanth et al, 2013 ).…”
Section: Clinical Associations For Circadian Rhythms In Myocardial Inmentioning
Components of circadian rhythm maintenance, or “clock genes,” are endogenous entrainable oscillations of about 24 h that regulate biological processes and are found in the suprachaismatic nucleus (SCN) and many peripheral tissues, including the heart. They are influenced by external cues, or Zeitgebers, such as light and heat, and can influence such diverse phenomena as cytokine expression immune cells, metabolic activity of cardiac myocytes, and vasodilator regulation by vascular endothelial cells. While it is known that the central master clock in the SCN synchronizes peripheral physiologic rhythms, the mechanisms by which the information is transmitted are complex and may include hormonal, metabolic, and neuronal inputs. Whether circadian patterns are causally related to the observed periodicity of events, or whether they are simply epi-phenomena is not well established, but a few studies suggest that the circadian effects likely are real in their impact on myocardial infarct incidence. Cycle disturbances may be harbingers of predisposition and subsequent response to acute and chronic cardiac injury, and identifying the complex interactions of circadian rhythms and myocardial infarction may provide insights into possible preventative and therapeutic strategies for susceptible populations.
“…It is also clear that, other than output from a central clock, the manner by which a given peripheral clock is synchronized with another, or the extent to which a peripheral clock can establish feedback to the SCN that it is, in fact, synchronized is not known. At present, the literature does support the premise that pathophysiologic conditions can both cause uncoupling of peripheral oscillators and be caused by uncoupling of peripheral clocks (Muller, 1999a , b ; Young et al, 2001a , b ; Willich et al, 2004 ; Lee et al, 2005 ; Fujino et al, 2006 ; Maywood et al, 2010 ; Tsimakouridze et al, 2012 ; Reddy and Rey, 2014 ; Robinson and Reddy, 2014 ; Wu and Reddy, 2014 ).…”
Section: Circadian Rhythm Biologymentioning
confidence: 94%
“…The significance of circadian rhythms to myocardial infarction has been identified in several studies in which onset of non-Q-wave angina, unstable angina, myocardial infarctions, and sudden cardiac death all show marked elevations in occurrence between the hours of 0600 and 1200 (Muller, 1999a , b ; Willich et al, 2004 ; Mosendane and Raal, 2008 ). Ethnic genetic, medications, co-morbidities, lifestyle, cultural, and/or social factors may shift the time of highest incidence (Kanth et al, 2013 ).…”
Section: Clinical Associations For Circadian Rhythms In Myocardial Inmentioning
Components of circadian rhythm maintenance, or “clock genes,” are endogenous entrainable oscillations of about 24 h that regulate biological processes and are found in the suprachaismatic nucleus (SCN) and many peripheral tissues, including the heart. They are influenced by external cues, or Zeitgebers, such as light and heat, and can influence such diverse phenomena as cytokine expression immune cells, metabolic activity of cardiac myocytes, and vasodilator regulation by vascular endothelial cells. While it is known that the central master clock in the SCN synchronizes peripheral physiologic rhythms, the mechanisms by which the information is transmitted are complex and may include hormonal, metabolic, and neuronal inputs. Whether circadian patterns are causally related to the observed periodicity of events, or whether they are simply epi-phenomena is not well established, but a few studies suggest that the circadian effects likely are real in their impact on myocardial infarct incidence. Cycle disturbances may be harbingers of predisposition and subsequent response to acute and chronic cardiac injury, and identifying the complex interactions of circadian rhythms and myocardial infarction may provide insights into possible preventative and therapeutic strategies for susceptible populations.
“…Platelet aggregation and activation surface markers follow a circadian rhythm, with a peak between 6 AM to noon (5,6). This might play a role in the observed peak of acute CVD during morning hours, which is present in patients with-and without previous CVD (7)(8)(9)(10). Moreover, patients with a myocardial infarction during morning hours have larger infarct size than those with events dur-ing the rest of the day, which has a worse prognosis (11,12).…”
The risk of acute cardiovascular events is highest during morning hours, and platelet activity peaks during morning hours. The effect of timing of aspirin intake on circadian rhythm and morning peak of platelet reactivity is not known. It was our objective to evaluate the effect of timing of aspirin intake on circadian rhythm and morning peak of platelet reactivity. A randomised open-label cross-over trial in healthy subjects (n=14) was conducted. Participants used acetylsalicylic acid (80 mg) on awakening or at bedtime for two periods of two weeks, separated by a four-week wash-out period. At the end of both periods blood was drawn every 3 hours to measure COX-1-dependent (VerifyNow-Aspirin; Serum Thromboxane B2 [STxB2]) and COX-1-independent (flow cytometry surface CD62p expression; microaggregation) platelet activity. VerifyNow platelet reactivity over the whole day was similar with intake on awakening and at bedtime (mean difference: -9 [95 % confidence interval (CI) -21 to 4]). However, the morning increase in COX-1-dependent platelet activity was reduced by intake of aspirin at bedtime compared with on awakening (mean difference VerifyNow: -23 Aspirin Reaction Units [CI -50 to 4]; STxB2: -1.7 ng/ml [CI -2.7 to -0.8]). COX-1-independent assays were not affected by aspirin intake or its timing. Low-dose aspirin taken at bedtime compared with intake on awakening reduces COX-1-dependent platelet reactivity during morning hours in healthy subjects. Future clinical trials are required to investigate whether simply switching to aspirin intake at bedtime reduces the risk of cardiovascular events during the high risk morning hours.
“…Epidemiologic studies demonstrate the existence of circadian patterns in the incidence of cardiovascular disease. For example, the onset of non-Qwave angina, unstable angina, myocardial infarctions (MIs), and sudden cardiac death all show marked elevations in the occurrence between the hours of 6:00 AM and 12:00 PM, compared with any other time of day (27,44). A better understanding of the function of circadian genes in the heart and in response to injury may lead to innovative therapies for cardiovascular disease (9,29,46).…”
mentioning
confidence: 99%
“…However, all of these genes function essentially as reciprocally controlling transcription factors, and in many cases the expression of these genes is monitored by the modulation of many "noncircadian" proteins as readouts. Enzymes regulating cardiac metabolism (57), reactivity of vascular endothelial cells (22,50,54), modulation of inflammatory responses (3,27,33,34,44), bone marrow progenitor cell release (2), and apoptosis (25) all have circadian gene components of control, and all are associated with the myocardial response to coronary artery occlusion. However, the specific relationship between a circadian gene and the inflammatory response and injury associated with early MI has not been determined.…”
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