Marek Malik, Dan Wichterle, Georg Schmidt.
Department of Cardiological Sciences, St. George’s Hospital Medical School, London, UK, Third Department of Medicine, First Medical School, Charles University, Prague, Czech Republic, Deutsches Herzzentrum and 1.Medizinische Klinik der Technischen Universität München, Germany
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Identification of cardiac patients at increased risk was originally
based on the measurement of left ventricular performance, on the assessment of the intensity of
arrhythmia triggers, and on the investigation of intra-myocardial conduction abnormalities1. More
recently, appreciation has emerged of the importance of cardiac autonomic and other reflex regulations.
Very recently, the importance of studies of myocardial refractoriness has been comprehended.
Established technologies to express autonomic and reflex modulations of cardiac function are based on
the assessment of heart rate variability2 and baroreflex
sensitivity3. While heart rate variability expresses
the degree of global modulations of sinus nodal periods in response to a gross variety of endogenous as
well as external stimuli, baroreflex sensitivity focuses on a more specific mechanism responsible for
cardiac modulations. When addressed using the conventional means of measurement, heart rate
variability and baroreflex sensitivity do not correlate very well and their risk predictive power is additive.
The conventional and most standardised way of assessing baroreflex sensitivity is based on the
phenylepherine administration and on the measurement of the relationship between blood pressure and
cardiac cycle increases. This investigation clearly tests the ability of cardiac cycles to adapt to extreme
baroreflex provocations. It is therefore not surprising that the measurement values obtained from the
phenylepherine test do not closely correlate with those obtained when expressing cardiac baroreflex
under more subtle conditions4.
In early 1999, a new technology to express the presence or absence of specific cardiac regulations has
been published based on the fluctuations of sinus rhythm cycles after a single ventricular premature
beat (VPB). These fluctuations are being termed the “heart rate turbulence” and the original publication
suggested two numerical quantifiers expressing the brief transient acceleration of sinus rhythm rate after
a VPB as well as the subsequent deceleration5. It has been shown in a fully prospective manner of data
analysis, that in both post-infarction patients at risk of early mortality, heart rate turbulence is blunted or
completely missing (Fig. 1).
Fig. 1: Preserved pattern of heartrate turbulence in a low-risk subject (left) and a blunted
pattern in a high risk subject (right).
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