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 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 [recently], heart rate turbulence was an obscure phenomenon buried in the bowels of heart rhythm journals.
What Is Heart Rate Turbulence (HRT)?
When you listen to the heart of a young physically-fit patient, you are struck not just by the slowness of the heartbeat, but also by the variability of the rhythm. It isn’t perfectly regular, nor is it chaotic like atrial fibrillation (AF). Doctors describe this — in typical medical speak — as regularly irregular: The heart rate increases as the patient inhales and slows as he or she exhales. 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.
HRT seeks to measure how quickly and vigorously the heart rate reacts in response to a single premature beat from the ventricle — a premature ventricular contraction (PVC). Normally after a PVC, the heart rate speeds for a 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 electrocardiogram (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 blood pressure (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.
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.
A recent study by researchers at the Washington University School of Medicine in St. Louis published in the Journal of Cardiovascular Electrophysiology has rekindled enthusiasm about this little-used, decade-old measurement of heart rate variability. The researchers followed nearly 1,300 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 eight times more likely to die from heart disease over the 14 year followup period. This strong correlation far exceeded the relationship of C-reactive protein (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 1,300 patients a small sample size, but in this study only seven percent of the 1,300 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 10 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 it remains our number one killer despite breathtaking technological advances. (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 if or when 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’s 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 percent of heart patients. An accurate assessment of HRT requires sophisticated filtering, and 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.
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.
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’m 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.)
*This blog post was originally published at Dr John M*