Circadian pattern of arrythmic death in patients receiving encainide, Flecainide or moricizine in the cardiac arrhythmia

Peters, Robert W.; Mitchell, B.; Brooks, Maria M.; Echt, Debra S.; Barker, Allan H.; Capone, Robert J.; Liebson, Philip R.; Greene, H. Leon

doi:10.1016/0735-1097(94)90408-1

Cited by 52 publications

(15 citation statements)

References 21 publications

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“…The analysis of patients enrolled in the Cardiac Arrhythmia Suppression Trial (CAST) also demonstrated that sudden death began most frequently within 2 h after awakening. 21 A major methodological difficulty in studying possible triggers of sudden cardiac death is that first hand historical data are not available except in rare instances of successful resuscitation of the victim. Further studies are therefore needed in a larger number of patients to confirm these wake-time-adjusted analyses of time of death.…”

Section: Sudden Cardiac Deathmentioning

confidence: 99%

Circadian variation and triggering of cardiovascular events

Willich

1999

Vasc Med

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Myocardial infarction and sudden cardiac death demonstrate a marked circadian variation with an increased risk during the morning after awakening and arising. The recognition of the morning increase of acute cardiovascular events has convinced many that they may be triggered by morning activities. It is of note, however, that cardiovascular events occur throughout the day -even if at lower frequency compared with the morning.There is a strong association between external triggers and the onset of myocardial infarction and sudden cardiac death beyond what is to be expected by chance alone. The magnitude of this association (relative risk two-to threefold) is comparable with the known long-term risk factors of cardiac disease. Trigger factors occur relatively frequently and may play a causative role in up to 20% of cases of acute coronary syndromes. Physical exertion, bursts of anger and sexual activity have been proved to have triggering potential. Other possible triggers include external and environmental events such as earthquakes, war threat and climatic factors.The pathophysiological links between external triggers and the onset of cardiovascular events are important in addressing the question of a causal relationship between triggers and disease onset and in perhaps improving preventive strategies.

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Section: Sudden Cardiac Deathmentioning

confidence: 99%

Circadian variation and triggering of cardiovascular events

Willich

1999

Vasc Med

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“…The trial was terminated prematurely because of an unexpectedly high mortality rate in the active : ,- treatment group and showed a bimodal variation (midmorning and late-afternoon) of onset of arrhythmic death. Approximately 30% of all events occurred within 2h from awakening (38).…”

mentioning

confidence: 99%

Morning Sudden Cardiac Death

Mt¹,

Davı̀

Sensi³

2000

Int J Immunopathol Pharmacol

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A circadian variation of cardiac function with peak in the early morning was documented about twenty years ago. A circadian rhythm of platelet aggregability, in the same time of the day, was demonstrated in healthy young male subjects. The morning hours were also reported as crucial for sympathetic nervous system activity, for heart rate variability, and for the abrupt rise in blood pressure. Altogether, these trigger factors may explain the high incidence of sudden cardiac death during the morning.In the primary prevention of sudden death in patients with high cardiovascular risk, many strategies were proposed, such as implantable cardioverter-defibrillators, antiarrhythmic and antihypertensive therapies, particularly beta-blockers and more recently, aspirin. Also in subjects without cardiovascular risk factors, it is predictable that early and continuous administration of low-dose aspirin, by inhibiting platelet aggregation and thrombin formation, particularly in morning hours, may represent an effective therapy for the prevention of myocardial infarction and morning sudden cardiac death.

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“…20,[33][34][35][36][37] In the CAST, the time of onset of arrhythmic death in the active treatment group displayed a bimodal variation, with significant peaks in the midmorning and late afternoon/early evening. 3 It is likely that flecainide-induced sympathetic activation produced the detrimental effects in this group. Based on the results of the present study, the selection of anti-arrhythmic drugs for the treatment of arrhythmias in patients with myocardial infarction should also take into consideration their effects on the sympathetic nervous system.…”

Section: Discussionmentioning

confidence: 99%