Morning Sudden Cardiac Death

Mt, Guagnano; Davı̀, Giovanni; Sensi, S

doi:10.1177/039463200001300109

Cited by 7 publications

(6 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although the importance of neural mechanisms in the genesis of cardiac arrhythmias and onset of sudden cardiac death (SCD) has long been a topic of interest, 1 new findings have renewed expectations that improved understanding of cardiac neural connections will provide needed effective ways to treat and prevent ventricular arrhythmias and SCD. Diurnal changes in the occurrence of cardiac sudden death, for example, have been recognized, 2–4 and beta‐blocker use blunts the morning peak in SCD 5 . These findings and the results of several other basic and clinical studies suggest that the surge of sympathetic activity associated with wakefulness is important in ventricular arrhythmogenesis.…”

Section: Editorial Commentmentioning

confidence: 77%

Clearer Connections:

Lathrop

2004

Cardiovasc electrophysiol

View full text Add to dashboard Cite

Section: Editorial Commentmentioning

confidence: 77%

Clearer Connections:

Lathrop

2004

Cardiovasc electrophysiol

View full text Add to dashboard Cite

“…43 However, most of these counts were typically lower than the analytic imprecision of the cell counter, suggesting that improvement in analyzer performance is advisable before definitive conclusions can be drawn. 44 Platelet aggregability also undergoes a clear circadian rhythm, 45 which led some authors to hypothesize that the greater risk of sudden cardiac death (SCD) in the first hours after awakening may be at least partially due to platelet hyperresponsiveness in the morning. [46][47][48] Undar et al 49 reported an increase of platelet activity measured as membrane expression of P-selectin on platelets by flow cytometry from 6:00 to 9:00 AM, which was followed by a decrease from noon to midnight.…”

Section: Circadian Variation Of Platelet Functionmentioning

confidence: 99%

Circadian Variation within Hemostasis: An Underrecognized Link between Biology and Disease?

Montagnana

Salvagno

Lippi

2009

Semin Thromb Hemost

View full text Add to dashboard Cite

Biological rhythms are a universal phenomenon in living organisms and serve to help organisms adapt within a circadian cycle to the 24-hour-oscillating environment. The rhythmic modulation of selective pathways thus enables organisms to optimize their ability to store and generate chemical energy, to minimize environmental stresses, and to reproduce by cycles of cell growth and division. Remarkably, the onset of both cardiovascular disorders and venous thromboembolism also undergoes circadian oscillations, which might be closely related to an internal biological clock. A highly repetitive rhythmic cycle seems to modulate platelet and endothelial functions, as well as the concentration and activity of several proteins of the coagulation and fibrinolytic systems. Although it is currently unknown how the global hemostatic efficiency might be affected by these circadian variations, understanding the nature, clinical significance, and pathophysiologic consequences of our hemostatic clock may be helpful for the prevention and treatment of a variety of conditions where either the severity of the illness or therapeutic efficacy exhibit circadian rhythmicity. In this review, clinical and laboratory data describing the effects of these cyclical rhythms on the hemostatic system are discussed.

show abstract

“…Emerging experimental evidence suggests that calcium antagonists may block apoptosis in several cell lines (23,24) and in the kidney subjected to ischemia and reperfusion (25,26). The cardiovascular system is regulated by different paranmeters (27)(28)(29)(30)(31)(32)(33)(34)(35). There are however, few data regarding its effect during cardiac ischemia and reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Verapamil Reduces Coronary Endothelium Damage and Cardiomyocyte Necrosis but not Apoptosis after Ischemia and Reperfusion: Ex Vivo Study in Rat Hearts

Napoli

Taccardi²,

Grilli

et al. 2002

Int J Immunopathol Pharmacol

View full text Add to dashboard Cite

We tested the hypothesis of beneficial effects of the calcium-blocker verapamil in a model of ischemia-reperfusion, and investigated its effects against coronary microcirculation and cardiomyocyte apoptosis. Isolated working rat hearts were subjected to 15 min global ischemia and 22-180 min reperfusion in the presence or absence of verapamil (0.25 11M). We evaluated creatinephosphokinase (CK) in coronary effluent, heart weight changes, microvascular permeability (extravasation offluoresceinelabeled albumin), ultrastructural alterations, and cardiomyocyte apoptosis (by 1.5% agarose gel electrophoresis and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling technique). In this model, 0.25 11M verapamil significantly reduced myocardial damage, CK release and vascular hyperpermeabiIity, concomitant with a reduction in endothelial and cardiomyocyte lesions; on the contrary, 0.25 11M verapamil was unable to reduce cardiomyocyte apoptosis. In conclusion, in the absence of perfusing granulocytes, the acute administration of a pharmacologically relevant verapamil concentration reduces ischemia-reperfusion injury and prevents coronary endothelial cell and cardiomyocyte necrotic cell death but it is unable to reduce apoptotic cell death in isolated working rat hearts.

show abstract

Morning Sudden Cardiac Death

Cited by 7 publications

References 40 publications

Clearer Connections:

Clearer Connections:

Circadian Variation within Hemostasis: An Underrecognized Link between Biology and Disease?

Verapamil Reduces Coronary Endothelium Damage and Cardiomyocyte Necrosis but not Apoptosis after Ischemia and Reperfusion: Ex Vivo Study in Rat Hearts

Contact Info

Product

Resources

About