Heart rate turbulence
Heart Rate Turbulence (HRT) is the return to equilibrium of heart rate after a premature ventricular contraction (PVC). 
It consists of a brief speed-up in heart rate, followed by a slow decrease
back to the baseline rate. An important feature of HRT is that PVCs occur naturally
in most adults, so that measuring the characteristics of a given
person's HRT offers a noninvasive way to evaluate his or 
her cardiac function without applying artificial external stimuli.
The measured values of HRT parameters have been shown to be a statistically
significant predictor of the likelihood of dying from cardiac disease after a patient suffers a heart attack. There are indications that HRT may help predict a person's risk from dying suddenly, and that HRT can predict death not only in patients who have suffered a heart attack, but those who have other cardiac diseases as well.
It should be noted that HRT has nothing to do with turbulence in fluid dynamics.

# History
The concept of HRT was officially introduced to the medical community by Georg Schmidt and colleagues from the Munich University of Technology in 1999 in the British medical journal Lancet.  While studying PVC characteristics, Schmidt and his colleagues had noticed that heart rate seemed to speed up after a PVC. To get a clearer picture, they listed the time from one heartbeat to the next (called RR intervals) and synchronized these lists to the time of the PVC beat and averaged the values in the list. A plot of this averaged RR interval list (called a PVC tachogram) not only confirmed their observation that heart rate sped up for a few beats after a PVC, but highlighted another less obvious feature, that heart rate then slows down beyond what it was before the PVC, before returning to the original heart rate.
If Schmidt et al had stopped there, it would have been an interesting observation to be found in the footnotes of an electrocardiography textbook. Instead, they reasoned that just as loss of variability in heart rate indicated patients more likely to be at high risk of dying after a heart attack, this phenomenon might also be an indicator of a healthy control of heart rate in such patients.  They proceeded to test this hypothesis using 24 hour electrocardiogram (Holter) recordings from one hundred survivors of heart attacks with frequent PVCs.  Greater turbulence seemed correlated with better prognosis. They then used this data to determine the optimal discriminating threshold between normal and abnormal HRT values, and came up with the values TS=2.5, TO=0%.  Now came the test.  Would HRT and these threshold values also work in the real world?   These thresholds were applied to Holter records from a total of 1191 patients who had experienced a heart attack. There were 162 deaths (13.6%) during the follow-up period of about 2 years. It turned out that patients with abnormal HRT were approximately 3 times more likely to die than those with normal HRT, beating out some other commonly used predictors. Thus the field of HRT was born.

# Mechanism of HRT
Everyone agrees that HRT is essentially a baroreflex phenomenon.  That is, a PVC interrupts the normal cardiac cycle, so the ventricles of the heart haven't had time to fill up to their normal level, before contracting and pumping their contents out. This results in a pulse (blood pressure) weaker than expected and triggers normal homeostatic mechanisms that try to compensate by constricting arteries and increasing heart rate (the turbulence onset part of HRT).  This is accomplished by the brain reflexively withdrawing the parasympathetic nerve signals and increasing the sympathetic nerve signals it sends to the heart. The compensatory constriction of the arteries and increased heart rate frequently cause blood pressure to oveshoot normal values (overcompensates), and activate the baroreflex in reverse.  This time, the brain reinstates parasympathetic nerve signals and decreases sympathetic nerve signals, which cause the heart rate to slow (the turbulence slope part of HRT).  
The exact quantitative contribution of the parasympathetic and sympathetic nervous flow to the heart  to HRT is unknown. The simplistic view assumes that HRT is solely dependent upon parasympathetic activity because atropine, a parasympathetic activity blocker abolishes HRT while a beta-blocker (sympathetic blocker) has no effect on HRT.  The contribution of the compensatory pause, the pause between the PVC and the next normal beat, to HRT is also unknown.  Some investigators believe that the compensatory pause produces a single beat blood pressure increase beyond normal only in compromised hearts, whereas other investigators have shown that the single beat surge occurs in normal hearts as well.  To date, no physiological parameter has been linked in a quantitative manner to turbulence slope, whereas turbulence onset was shown by researchers in Calgary, Canada to be linearly dependent upon duration of subnormal blood pressure in a well designed experiment.
Finally, the reason the size of HRT after a PVC predicts cardiac death is suggested by its mechanism.  Parasympathetic nervous activity to the heart is believed to be protective and sympathetic nervous activity, deleterious, to the heart.  Especially after a heart attack, sympathetic nervous activity tends to be increased.  A healthy HRT indicates the presence of a healthy amount of parasympathetic activity, countering sympathetic activity. To take a wider view, however, it may be that a healthy HRT is also an indication of a healthy brain, and is the reason small HRT also predicts a likelihood of death from non- cardiac causes as well as from cardiac causes.
  Raj SR, Sheldon RS, Koshman M, Roach DE. "Role of hypotension in heart rate turbulence physiology."
Heart Rhythm 2005 Aug;2(8):820-7

# Further reading
- The HRT website offers further information.
- Georg Schmidt, "Heart-rate turbulence after ventricular premature beats as a predictor of mortality after acute myocardial infarction. Lancet 1999; Vol. 353; No. 9162; 1390-96"
- Mari Watanabe, "Heart Rate Turbulence: a Review", Indian Pacing Electrophysiol. J. 2003;3(1):10