CIRCADIAN VARIATION OF TOTAL ISCHAEMIC BURDEN AND ITS ALTERATION WITH ANTI-ANGINAL AGENTS

doi:10.1016/S0140-6736(88)92414-2

The Lancet

Volume 332, Issue 8614, 1 October 1988, Pages 755-759

https://doi.org/10.1016/S0140-6736(88)92414-2 Get rights and content

Abstract

6264 hours of ambulatory ST segment monitoring of 150 unselected patients with proven coronary artery disease, who were off all routine anti-anginal treatments, showed 598 ischaemic episodes, of which 446 (75%) were silent (symptom-free). Most (68%) ischaemic episodes occurred between 0730 and 1930, with a peak in the morning and a lesser peak in the evening. Two subgroups were studied further in double-blind controlled trials: 33 patients had a total of 1313 hours of ST segment monitoring while treated with nifedipine; and 41 patients a total of 1581 hours while treated with atenolol. Nifedipine did not alter the circadian pattern of ischaemic episodes; atenolol abolished the morning peak, and the peak incidence of ischaemia then occurred in the evening. Circadian patterns for total duration of ischaemic episodes corresponded closely to those of episodes of ischaemia, and were similarly altered by treatment. The circadian pattern of silent ischaemic episodes and their total duration were very similar to those of total ischaemia for the group as a whole and the different subgroups. This circadian distribution of ischaemic episodes and the observed changes with treatment resemble the reported circadian variation of acute myocardial infarction and sudden death.

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Cardiovascular disease (CVD) represents the first cause of death globally. The nighttime is generally a period of relative protection from CVD events such as myocardial infarction, sudden cardiac death, and stroke, at least compared to the early morning period. The nighttime also generally entails lower values of arterial blood pressure (ABP) and heart rate (HR) and higher cardiac parasympathetic modulation. These day-night cardiovascular rhythms are ultimately driven by circadian molecular oscillators in the hypothalamic suprachiasmatic nucleus and in peripheral cells, including those in the heart, blood vessels, and kidneys. The wake-sleep states are intermediate mechanisms of circadian cardiovascular regulation, with non-REM sleep decreasing ABP and HR and increasing cardiac parasympathetic modulation at the beginning of the night. Obstructive sleep apnea, insomnia, and the restless legs syndrome have high prevalence in the general population and may increase nighttime cardiovascular activity and CVD risk. CVD risk is better predicted by ABP values during nighttime sleep than during daytime wakefulness. Higher nighttime values of ABP and HR increase cardiac work and vessel wall stress. During the night, circadian rhythms may enhance cardiac responses to hypertrophic stimuli, increase vascular smooth muscle Rho kinase activity and contractility, decrease endothelial nitric oxide production and vascular responses to vasodilators, and increase circulating monocytes with the potential to infiltrate atherosclerotic plaques. Together, these factors configure a “perfect storm” scenario that may make increased cardiovascular activity during the night a final common mechanism linking sleep disorders to CVD risk.
Relation between myocardial infarction and cyrcadian rhythm in patients attended in a prehospital emergency service
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El objetivo de este estudio es analizar la presencia de ritmo circadiano en la hora de inicio del infarto agudo de miocardio atendido por un sistema de emergencias prehospitalario, y la influencia en dicho ritmo de algunos factores de riesgo cardiovascular modificables y no modificables como posibles moduladores de ese patrón circadiano.
Análisis retrospectivo de 709 pacientes con diagnóstico clínico confirmado in situ de infarto agudo de miocardio. Se analizan las variables: hora de inicio de los síntomas, edad, sexo, cardiopatía isquémica previa, hipertensión arterial, diabetes mellitus, dislipidemia y tabaquismo. El análisis de ritmo se ha efectuado utilizando un test simple de igualdad de series basado en el análisis cosinor de múltiples sinusoides, eligiendo 3 armónicos (24,12 y 8 h) para su ajuste.
La hora de inicio del infarto muestra ritmo circadiano (p < 0,001), con un pico máximo a las 10.39 y un valle a las 4.28, mostrando una curva sinusoidal ajustada de aspecto bimodal, con un pico matinal predominante y otro vespertino de menor amplitud. Todos los subgrupos categorizados por la presencia de las variables analizadas presentaron ritmo circadiano, con una curva sinusoidal similar a la de la población global. Los pacientes fumadores muestran un pico vespertino predominante.
El infarto de miocardio presenta ritmo circadiano. El tabaquismo y la diabetes modifican el patrón de ritmo circadiano habitual del infarto.
The aim of this study is to analyze the presence of circadian rhythm in the time of onset of symptoms of acute myocardial infarction treated by a prehospital emergency system and the influence of modifiable cardiovascular risk factors and non-modifiable as modulators of that circadian rhythm.
Retrospective analysis of 709 patients clinically diagnosed with acute myocardial infarction on-site in the prehospital setting. The variables were time to onset of symptoms, age, sex, previous ischemic heart disease, hypertension, diabetes mellitus, hyperlipidemia and smoking. We analyzed the rhythm with cosinor multiple sinusoid method, with 3 harmonics (24, 12 and 8 h) for the adjustment.
The time of onset of pain showed circadian rhythm (P <,001), peaking at 10.39 and a valley at 4.28, showing a sinusoidal curve fitting bimodal aspect with a predominant morning peak and another evening one of lower amplitude. All subgroups categorized by the study variables showed circadian rhythm, with a cosine curve similar to the global infarction. Smokers had a predominantly evening peak.
Acute myocardial infarction shows a circadian rhythm. Smoking and diabetes mellitus can modify the standard incidence rate of occurrence of myocardial infarction.
Beta blocker therapy modifies circadian rhythm acute myocardial infarction
2011, International Journal of Cardiology
Sudden Cardiac Death: Epidemiology, Circadian Variation, and Triggers
2011, Current Problems in Cardiology
Sudden cardiac death (SCD) remains a major health issue accounting for over 5% of annual mortality in the Western world. There are several causes of SCD, most commonly, coronary artery disease. Although identifying the prodrome of SCD has attracted considerable interest, a large proportion of patients die before any medical contact is established. SCD onset seems to follow a circadian pattern, most likely because of exposure to endogenous and exogenous triggers. The aim of the present report is to review the current knowledge of epidemiology, patterns of onset, and triggers of SCD and present directions for future research with a focus on coronary artery disease.
Circadian Variation of Death in Hemodialysis Patients
2008, American Journal of Kidney Diseases
Citation Excerpt :
Jones-Crawford et al,25 in their recent retrospective analysis of in-hospital cardiopulmonary arrests, found no clear circadian distribution of events. β-Blocker use repeatedly was associated with absent or blunted circadian occurrence of cardiac morbid events in susceptible individuals.8,26,27 In our study, the association of β-blocker use with increased morning risk of death in prevalent dialysis patients extends the observation of Bleyer et al,13 who found that hemodialysis patients who died in the interval 60 to 72 hours after dialysis treatment were more likely to be on β-blocker therapy.
There is a circadian variation of death in nondialysis populations, with more cardiovascular events occurring in the morning. Whether this holds true in hemodialysis patients was never investigated.
Case series.
All prevalent (>3 months on hemodialysis therapy) and incident (≤3 months on hemodialysis therapy) patients of a dialysis network followed up prospectively for 18 months.
Patient characteristics and circumstances of death.
Time of death. Data for time of death were collected within 72 hours of the event. The frequency of deaths occurring in the morning hours (4:01 am to 12:00 noon) was compared with that expected by chance alone.
Time of death could be defined in 873 of 927 deaths (94.2%). In 459 prevalent hemodialysis patients, morning deaths occurred 24.8% more frequently than expected (P < 0.001). No similar excess was observed in the 414 incident hemodialysis patients (P = 0.9). In logistic regression, significant predictors of death occurring from 4:01 am to 12:00 noon in all subjects were being an outpatient (odds ratio [OR], 1.89; 95% confidence interval [CI], 1.24 to 2.88) and time since the end of the last dialysis treatment (postdialysis 49- to 72-hour period: OR, 1.73 [95% CI, 1.13 to 2.64] compared with 1 to 24 hours postdialysis). Considering prevalent hemodialysis patients only, being an outpatient (OR, 1.93; 95% CI, 1.17 to 3.18), postdialysis 25- to 48- and 49- to 72-hour periods (OR, 1.68; 95% CI, 1.05 to 2.68 and OR, 1.80; 95% CI, 1.03 to 3.12), diabetes (OR, 1.73; 95% CI, 1.14 to 2.63]), and β-blocker use (OR, 1.62; 95% CI, 1.08 to 2.43) were directly related and the presence of medical symptoms during the last dialysis treatment (OR, 0.53; 95% CI, 0.34 to 0.83) was inversely related to the risk of morning death.
No information for causes of deaths was gathered.
Prevalent hemodialysis patients have an excess of morning deaths, and its predictors suggest potential avenues for intervention studies.
A systematic review of the prothrombotic effects of an acute change in posture: A possible mechanism underlying the morning excess in cardiovascular events?
2007, Chest
Epidemiologic studies have demonstrated a morning excess of acute cardiovascular events, which has subsequently been refined to the 2 to 3 h after awakening. It is therefore reasonable to assume that some activity associated with awakening may trigger such cardiovascular events, with the assumption of an upright posture being of potential significance.
To identify and systematically review the literature to determine the effects of acute changes in posture on hemorheology and hemostasis.
Electronic databases MEDLINE, EMBASE, PSYCHINFO, and CINAHL (earliest date available to February 5, 2006) and conference abstracts were searched.
Studies examining the hemorheologic and hemostatic response to a change in posture from a supine position to an upright position were eligible for inclusion. Two reviewers independently selected the studies for inclusion.
The experimental evidence reviewed demonstrates that the assumption of an upright posture is associated with a significant degree of hemoconcentration, which is characterized by an increase in hematocrit and a decrease in plasma volume. Research examining the effect of postural change on hemostasis has been limited, although a small number of studies have demonstrated some significant changes in markers of coagulation, fibrinolysis, and platelet reactivity.
A sudden change in posture may act as a potential trigger for the onset of cardiovascular events occurring in the 3 h after awakening via effects on hemostasis and hemorheology. However, other possible triggering factors such as dehydration, mental stress, and physical exertion must also be considered.

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CIRCADIAN VARIATION OF TOTAL ISCHAEMIC BURDEN AND ITS ALTERATION WITH ANTI-ANGINAL AGENTS

Abstract

J Am Coil Cardiol

Lancet

Character of silent ischemia in angina pectoris

Am J Cardiol