© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Mechanoelectric contributions to sudden cardiac death
aCardiologie B, CNRS UMR 6542, Hôpital Trousseau, 37044 Tours Cedex, France
bNational Heart and Lung Institute, Imperial College School of Science Technology and Medicine, Charing Cross Campus, London W6 8RF, UK
* Corresponding author. Tel.: +33-2-4747-4687; fax: +33-2-4747-5919 d.babuty@chu.med.univ-tours.fr
Received 28 September 2000; accepted 7 February 2001
KEYWORDS Arrhythmia (mechanisms); Mechanotransduction; Sudden death; Ventricular arrhythmias
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1 Introduction |
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Sudden death, a major problem in developed countries and increasingly so in some underdeveloped countries, justifies research on the mechanisms and identification of patients at high risk of sudden death. Most sudden deaths are secondary to ventricular tachyarrhythmias [1,2]. Primary electrical disturbances, such as Brugada syndrome, long QT syndrome, are rare and account for few sudden deaths. Sudden death as a rule complicates the situation with an underlying cardiac disease with different classes of heart failure [2]. The alteration of the cardiac mechanical properties developing early in heart failure is accompanied by action potential lengthening [3], which is modulated by acute stretch [4–6].
The English theologian and philosopher William of Occam (1280–1349) stated: ‘Entia non sunt multiplicanda praeter necessitatum’. This is recognised as Occam's Razor. Roughly interpreted, it proposes that it is better to have one hypothesis to explain five observations than five hypotheses to explain
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2 A common pathway: mechanical heterogeneity? |
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3 Principle of mechanoelectric feedback/coupling |
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4 Which factors are involved in mechanoelectric feedback? |
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4.1 Mechanoelectric effects in cardiomyocytes
4.2 Acute stretch and fibroblasts
4.3 Chronic stretch and cardiomyocytes
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5 Electrophysiological arrhythmic mechanisms and mechanoelectric feedback |
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5.1 Initiation: premature ventricular beats
5.1.1 Intracellular calcium abnormalities
5.1.2 ‘Triggered’ activity (Fig. 2 right hand side)
5.1.3 Electrophysiological heterogeneity (Fig. 2 left hand side)
5.2 Sustained arrhythmia formation
5.2.1 Excitability
5.2.2 Conduction velocity
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6 Clinical correlates, sudden death, and mechanoelectrical feedback |
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6.1 Correlates involving mechanical changes
6.1.1 Dilated heart, and poor ejection fraction: intramyocardial stress and strain
6.1.2 Systemic overload
6.1.3 Regional ventricular stress (dyskinesia — Fig. 2)
6.2 Correlates involving ECG changes
6.2.1 QT interval and U wave
6.2.2 QRS complex
6.3 Correlates derived from ECG analyses
6.3.1 Heart rate variability
6.3.2 Alternans
6.4 Correlates involving the autonomic nervous system
6.5 Correlates involving electrolyte disturbances
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7 Conclusions |
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