Turbulence is good?

It’s hard to believe that turbulence could be a good thing for the heart.

Consider how the word turbulent is defined: “characterized by conflict, disorder, or confusion; not controlled or calm.” Those traits don’t sound very heart-healthy.

But when it comes to the heart rhythm, it turns out that a turbulent response—to a premature beat—is better than a blunted one.  The more turbulent the better.

No, you haven’t missed anything, and turbulence isn’t another of my typos.  Until this past week, heart rate turbulence (HRT) was an obscure phenomenon buried in the bowels of heart rhythm journals.

What is Heart Rate Turbulence?

When you listen to the heart of a young, physically-fit patient you are struck, not just by the slowness of the heart beat, but also by the variability of the rhythm.  It isn’t perfectly regular, nor is it chaotic like AF.  Doctors describe this–in typical medical speak–as regularly irregular: the heart rate increases as the patient inhales and slows as they exhale.  This variability occurs as a result of the heart’s responsiveness to its environment.   The more robustly and quickly the heart responds the healthier it is.

Heart Rate Turbulence seeks to measure how quickly and vigorously the heart rate reacts in response to a single premature beat from the ventricle—a PVC.  Normally, after a PVC, the heart rate speeds for few beats, and then slows back to baseline over the next 10 beats.  The healthy heart responds with a more intense rise in heart rate and a quicker return to baseline. Using simple measurements of heart rate from a standard 24-hour ECG monitor, a propriety software program averages many of these responses and comes up with a measurement of Turbulence Onset and Turbulence Slope.

Why does the heart respond to a PVC this way?

Your heart rate at any moment is controlled by the balance of the two arms of this nervous system: the sympathetic nervous system releases adrenaline, which signals the heart rate and blood pressure to increase, while the parasympathetic nervous system, through activation of the vagus nerve, lowers heart rate and blood pressure.  The yin and yang of these two opposing feedback systems influences each and every heart beat. When at rest the vagal system predominates, the heart rate is low and variable. When under stress (physical or mental) the adrenaline system activates, and our heart rates are higher and less variable.

For activities like bike racing, running on a treadmill or, (in the days before drive-thrus), chasing down your food, adrenaline surges are both necessary and beneficial.  The benefit of these bursts are that they induce a physically-fit state in which the activity of the parasympathetic nervous system predominates.  That’s why athletic people have slower heart rates.

PVCs occur commonly—in both well and unwell patients. The prematurity of a PVC transiently decreases the BP.  This drop in BP causes the involuntary nervous system to release adrenaline.  This raises the heart rate transiently.  Immediately, the faster heart rate and higher BP feedback, and the involuntary nervous system now withdraws adrenaline while vagal nerve activity slows the heart rate back to baseline.

Background:

It’s well established that patients immersed in high-adrenaline states—low heart variability and higher resting rates–have more cardiac events, and a higher death-rate.

Also, previous studies done in patients with weakened hearts, or after a heart attack show that absence of heart rate turbulence strongly predicts dying from a cardiac cause, even after controlling for the usual cardiac risks.

Current data:

A recent study from researchers at the Washington University School of Medicine in Saint Louis has rekindled enthusiasm about this little-used, decade-old measurement of heart rate variability.  The researchers followed nearly 1300 patients with varying degrees of cardiac risk over 14 years.  Using data from routine 24-hour monitors, they reported that low-risk individuals with less turbulent responses to PVCs were 8 times more likely to die from heart disease over the 14 year follow-up period.  This strong correlation far exceeded the relationship of CRP—a known biomarker for inflammation.

Though provocative, this study had several weaknesses: It was an observational trial, not a randomized prospective clinical trial. Secondly, not only is 1300 patients a small sample size, but in this study, only seven percent of the 1300 had abnormal HRT responses.  FInally, these findings don’t tell us whether an impaired HRT can be treated, modified or prevented.

Why these recent findings are intriguing?

We need better ways to predict heart disease—especially in low risk individuals.  The sad (and not well known) fact about heart disease is that its first manifestation is often fatal or catastrophic. Nearly four in ten people find out they have heart disease when they die, or suffer a major heart attack.

That heart disease remains so undetectable is one of the major reasons why—despite breathtaking technological advances—it remains our number one killer. (Unhealthy lifestyles also contribute greatly to heart disease’s present status as top-killer.)   At the moment, we don’t have a reliable test to predict when, and if heart disease will strike.  It’s not for lack of trying; we submit patients to executive physicals, treadmill exercise tests, ultrasound exams and even radiation, all in the name of predicting heart disease.

Whether HRT can fill this void remains to be seen. It’s non-invasive, non-radiating and obtainable from a standard ECG recording.  In the present study, and previous ones on patients with diseased hearts, patients with abnormal HRT responses sustained cardiac events at much higher rates than expected—it had a positive predictive value.

Limitations of HRT:

HRT has been available for more than a decade, but yet, it hasn’t caught on.  In fact, the review article that I used for this piece was published in 2005. (It is a good reference for those who need more details.)

Measuring HRT is impossible in patients with AF, an atrial-paced rhythm or lack of PVCs.  This excludes up to 30% of heart patients.

An accurate assessment of HRT requires sophisticated filtering.

The reporting of HRT is complicated: we aren’t just reporting an ‘H’ or an ‘L’ for a lab value, but rather a dv/dt and slope.

Remaining Questions:

How much added value to the risk assessment does an abnormal HRT add?

Likewise, how strong is its negative predictive value: How safe are you if your HRT is normal?

Other than say, “Uh-oh,” at the moment, we don’t know what to do with an abnormal HRT.  Can an abnormal HRT be treated, or prevented?

And even if we could make the heart more turbulent after a PVC would this translate into better outcomes?

That’s a lot of questions.

Summary:

Heart rate turbulence, like its cousin heart rate variability, measures the heart’s responsiveness to its neural inputs. Young healthy hearts respond more robustly than diseased hearts.  In the diseased heart, a less turbulent response to a PVC predicts adverse cardiac outcomes.

Many more studies are needed to determine whether HRT will add to the risk-assessment of heart patients, or become a modifiable goal of therapy.

I am far from a HRT expert, but will at least offer this prediction:  An abnormal HRT will improve with a regular exercise program. (Well, it looks like that study has been done.)