Circadian variation in the incidence of sudden cardiac death in the framingham heart study population

Willich, Stefan N.; Levy, Daniel; Rocco, Michael; Tofler, Geoffrey H.; Stone, Peter H.; Muller, James E.

doi:10.1016/0002-9149(87)91027-7

Cited by 612 publications

(277 citation statements)

References 34 publications

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“…As we hypothesized, the endogenous circadian trough in most of the cardiovascular risk biomarkers, as well as the circadian peak in "protective" vagal markers, occurred during the biological night (≈midnight-8:00 AM; ≈300°-50°) for most variables (except for cortisol: 10:30 PM; 270°; Table 1), possibly underlying the nighttime trough in adverse cardiovascular events in epidemiological studies (3)(4)(5)(6)(7)(8)(9)(10).…”

Section: Discussionmentioning

confidence: 92%

“…cardiovascular disease C ardiovascular disease is the leading cause of mortality in both men and women in developed countries (1,2). Epidemiological studies show a clear day/night pattern in risk for myocardial infarction (3)(4)(5)(6), stroke (7), angina (5), ventricular arrhythmias (8), and sudden cardiac death (9) with primary peaks in the morning (≈6:00 AM-noon), secondary peaks in the evening (≈6:00-10:00 PM), and lowest vulnerability during the night (≈midnight-6:00 AM) (reviewed in ref. 10).…”

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confidence: 99%

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Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Scheer

Evoniuk

et al. 2010

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

263

248

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The risk of adverse cardiovascular events peaks in the morning (≈9:00 AM) with a secondary peak in the evening (≈8:00 PM) and a trough at night. This pattern is generally believed to be caused by the day/night distribution of behavioral triggers, but it is unknown whether the endogenous circadian system contributes to these daily fluctuations. Thus, we tested the hypotheses that the circadian system modulates autonomic, hemodynamic, and hemostatic risk markers at rest, and that behavioral stressors have different effects when they occur at different internal circadian phases. Twelve healthy adults were each studied in a 240-h forced desynchrony protocol in dim light while standardized rest and exercise periods were uniformly distributed across the circadian cycle. At rest, there were large circadian variations in plasma cortisol (peak-to-trough ≈85% of mean, peaking at a circadian phase corresponding to ≈9:00 AM) and in circulating catecholamines (epinephrine, ≈70%; norepinephrine, ≈35%, peaking during the biological day). At ≈8:00 PM, there was a circadian peak in blood pressure and a trough in cardiac vagal modulation. Sympathetic variables were consistently lowest and vagal markers highest during the biological night. We detected no simple circadian effect on hemostasis, although platelet aggregability had two peaks: at ≈noon and ≈11:00 PM. There was circadian modulation of the cardiovascular reactivity to exercise, with greatest vagal withdrawal at ≈9:00 AM and peaks in catecholamine reactivity at ≈9:00 AM and ≈9:00 PM. Thus, the circadian system modulates numerous cardiovascular risk markers at rest as well as their reactivity to exercise, with resultant profiles that could potentially contribute to the day/night pattern of adverse cardiovascular events.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Scheer

Evoniuk

et al. 2010

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

263

248

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“…An emergent area of clinical research is focusing on circadian rhythms and cardiovascular disease (14). For example, it is well recognized that the incidence of several adverse cardiovascular events, like sudden cardiac death (18,35) and myocardial infarction (19), peak in the early morning hours. Recently, clinicians have begun to monitor daily rhythms in heart rate and blood pressure as an index for abnormal autonomic function (14).…”

Section: Discussionmentioning

confidence: 99%

Light phase-restricted feeding slows basal heart rate to exaggerate the type-3 long QT syndrome phenotype in mice

Schroder

Burgess

Manning

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Light phaserestricted feeding slows basal heart rate to exaggerate the type 3 long QT syndrome phenotype in mice. Am J Physiol Heart Circ Physiol 307: H1777-H1785, 2014. First published October 24, 2014 doi:10.1152/ajpheart.00341.2014.-Long QT syndrome type 3 (LQT3) is caused by mutations in the SCN5A-encoded Nav1.5 channel. LQT3 patients exhibit time of day-associated abnormal increases in their heart rate-corrected QT (QTc) intervals and risk for life-threatening episodes. This study determines the effects of uncoupling environmental time cues that entrain circadian rhythms (time of light and time of feeding) on heart rate and ventricular repolarization in wild-type (WT) or transgenic LQT3 mice (Scn5a ϩ/⌬KPQ ). We used an established light phase-restricted feeding paradigm that disrupts the alignment among the circadian rhythms in the central pacemaker of the suprachiasmatic nucleus and peripheral tissues including heart. Circadian analysis of the RR and QT intervals showed the Scn5a ϩ/ ⌬KPQ mice had QT rhythms with larger amplitudes and 24-h midline means and a more pronounced slowing of the heart rate. For both WT and Scn5a ϩ/⌬KPQ mice, light phase-restricted feeding shifted the RR and QT rhythms ϳ12 h, increased their amplitudes greater than twofold, and raised the 24-h midline mean by ϳ10%. In contrast to WT mice, the QTc interval in Scn5a ϩ/⌬KPQ mice exhibited time-ofday prolongation that was flipped after light phase-restricted feeding. The time-of-day changes in the QTc intervals of Scn5a ϩ/⌬KPQ mice were secondary to a steeper power relation between their QT and RR intervals. We conclude that uncoupling time of feeding from normal light cues can dramatically slow heart rate to unmask genotypespecific differences in the QT intervals and aggravate the LQT3-related phenotype.long QT syndrome; heart rate; feeding; circadian rhythms; SCN5A CONGENITAL LONG QT SYNDROME (LQTS) is primarily an autosomal-dominant disease that delays ventricular repolarization and increases the risk for polymorphic ventricular tachycardia, which can cause syncope, seizures, and sudden cardiac arrest (26). The majority of LQTS cases are linked to mutations in three different cardiac ion channel genes: KCNQ1 (LQT1), KCNH2 (LQT2), or SCN5A (LQT3) (27). These three major types of LQTS show differences in disease penetrance, electrocardiographic characteristics, symptomatic risk, triggers for events, and responsiveness to treatment (23,29). In particular, LQT3 is more lethal than LQT1 or LQT2, and LQT3 patients typically exhibit an abnormal increase in their heart ratecorrected QT (QTc) intervals and risk for life-threatening episodes at night (28,30, 33).Despite this strong time-of-day association between lifethreatening events in the LQT3 phenotype, the role that manipulating circadian rhythms has on the expressivity of the LQT3 phenotype has not yet been investigated. Circadian rhythms are Ϸ24-h rhythms that are regulated at the cellular level by a transcription-translation feedback loop referred to as the molecular clock. The mol...

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“…There is prominent circadian variability in SCD occurrence with a peak incidence during the waking hours in the morning (Willich et al 1987) which corresponds to the abrupt reduction in heart rate variability during the same time period, signifying the surge in sympathetic activity and withdrawal of vagal activity (Bonnemeier et al 2003). Cardiac diseases such as chronic heart failure (Nolan et al 1998) and myocardial infarction (La Rovere et al 1998) are associated with abnormal cardiac autonomic control including high levels of sympathetic activity, impaired parasympathetic control and subnormal arterial baroreflex sensitivity.…”

Section: Autonomic Nervous System and Sudden Cardiac Deathmentioning

confidence: 99%

“…Left cardiac sympathetic denervation has been shown to be effective in treating and reducing arrhythmia burden in patients with refractory ventricular arrhythmias (Schwartz 2014). Epidemiological studies and studies in patients with implantable cardioverter defibrillators have shown that a high proportion of ventricular arrhythmias and SCD occurs in the early hours of the morning suggesting a strong link with the diurnal changes seen in autonomic nerve activity (Willich et al 1987). Clinical measures of vagal tone (heart rate variability and baroreflex sensitivity) are powerful predictors of mortality in heart failure (Nolan et al 1998) and patients with previous myocardial infarction (MI) (La Rovere et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Neuro-cardiac interaction in malignant ventricular arrhythmia and sudden cardiac death

2016

Autonomic Neuroscience

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Sudden cardiac death as a result of lethal ventricular arrhythmias is a major cause of death in cardiac diseases such as heart failure and prior myocardial infarct. Activity of the autonomic nervous system is often abnormal where sympathetic activity is upregulated and vagal activity reduced in these conditions. The abnormal autonomic state has been shown to be a strong prognostic marker of increased mortality and propensity to lethal arrhythmias, for which there is no effective prevention. Research effort over the years has established good evidence for a causal link between autonomic disturbance and ventricular arrhythmias. However, the detailed electrophysiological mechanisms by which ventricular fibrillation occurs are still not clear and molecular processes which are modulated by autonomic nerve influences that either predispose the heart to or protect it from these arrhythmias are not fully understood. This review presents data from studies investigating the link between activity of the autonomic nervous system and ventricular arrhythmias, from seminal findings in classical studies to ongoing investigations, in the quest for a better understanding of the arrhythmogenic mechanisms underlying neurocardiac interactions with a view to the development of effective preventative and therapeutic strategies which are very much needed.

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Circadian variation in the incidence of sudden cardiac death in the framingham heart study population

Cited by 612 publications

References 34 publications

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Light phase-restricted feeding slows basal heart rate to exaggerate the type-3 long QT syndrome phenotype in mice

Neuro-cardiac interaction in malignant ventricular arrhythmia and sudden cardiac death

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