Episode Transcript
[00:00:00] Welcome friends, to the Heart Rate Variability Podcast. This week in HRV Edition. Each week we explore the latest research and news from the world of hrv. Please remember the information in this podcast is for informational purposes only and not medical advice. Always consult your healthcare provider before applying any strategies we discuss. This week we explore seven new studies that shine light on the many dimensions of heart rate variability. We'll see how air pollution can alter HRV within minutes, how simply changing posture reveals differences in diabetic autonomic function, and and even tackle the chicken or egg question of whether poor sleep causes low HRV or vice versa. In the second half of the show, we'll dive into the heart Brain connection. A novel study links spiritual well being to how our brain senses heartbeats. 24 hour HRV emerges as a marker of consciousness in coma patients. A central review shows how heart disease remaps the brain's autonomic centers, and a meta analysis confirms HRV's power to predict mortality and heart failure. It's a packed episode, so let's let's get started.
[00:00:56] Let's begin with an environmental health study. This first study, published in ScienceDirect by Park and colleagues, titled Ultra Short Term Effects of fine particulate matter PM2.5 exposure on heart Rate Variability in Susceptible and Vulnerable Individuals, using real time personal monitoring, looks at the immediate impact of fine particulate air pollution, or PM2.5, on HRV. We know air pollution is a cardiovascular risk factor it contributes to heart disease over the long run. But this study asked, how quickly does polluted air affect our autonomic nervous system? To find out, researchers equipped participants with personal air monitors and HRV recorders that capture data on a minute by minute basis. They focused on PM2.5 exposure and immediate changes in HRV, even examining different time lags and the effects. The results were eye opening. Minute level spikes in PM2.5 led to significant drops in HRV almost immediately. In other words, breathing polluted air for just a few minutes can acutely reduce harm heart rate variability, indicating a rapid increase in sympathetic stress or withdrawal of vagal activity. What's more, these effects were more pronounced at night and in particular vulnerable groups, notably women and people with arrhythmias. HRV reductions were more substantial during nighttime exposures, perhaps because our baseline vagal tone is higher at night, making any interference more noticeable, and females and patients with cardiac arrhythmias showed greater autonomic sensitivity to pollution spikes. The pattern of HRV change was intriguing as well. HRV initially dropped, then rebounded briefly and then fell again with sustained exposure. It's almost as if the body tries to adapt after the first few minutes, but continued pollution overwhelms that adaptation, leading to a second phase of autonomic strain. And indeed, when people experience more prolonged bouts of high pollution, for example over three hours straight, the cumulative exposure led to pronounced autonomic impairment, a much larger and sustained HRV reduction compared to short exposure. This suggests there might be a dose time threshold around the two to three hour mark where the autonomic nervous system becomes especially taxed by pollution. The takeaway is that air quality isn't just an abstract long term concern, it's it has immediate physiological impacts that you can measure in real time. The authors highlight that using real time monitors for both pollution and HRV offers critical insights. For instance, one could imagine a wearable that alerts you when pollution is spiking, your HRV is dropping, prompting you to go indoors or turn on an air filter. This kind of personalized monitoring could help protect high risk populations, say someone with heart failure or asthma, by allowing proactive steps when the air becomes dangerous. Overall, this study drives home a clear point. Our environment can influence our autonomic nervous system within minutes. Next time you see a haze of smog or smoke, remember that your body is likely feeling it, even if subtly. And for those of us tracking hrv, it's a reminder that context matters. The day of mysteriously low HRV might just have been particularly polluted from environmental stressors. Let's turn to a more everyday influence on hrv. Your posture Our second study from Scientific Reports led by Taiade and team titled Effective Posture on Photoplithysmography Signals from the Posterior Tibial Artery in Adults with and without type 2 diabetes and investigated how simple changes in posture like sitting or standing affect HRV, especially in people with type 2 diabetes. Now, posture changes are something we all experience daily and they provoke well known autonomic responses. For example, when you stand up, your body usually increases heart rate and constricts blood vessels to maintain blood pressure. The researchers used that as a test to probe autonomic and vascular differences between healthy individuals and those with diabetes. They recruited two groups of adults, one one group of healthy controls and one group with type 2 diabetes 30 people in each around middle age. Each person had a PPG sensor placed over the posterior tibial artery at the ankle to record pulse waveforms, which were then measured in three positions lying supine, sitting and standing. From the ppg, they extracted not only heart rate and HRV from pulse interval timing, but also Features of the pulse waveform, such as amplitude and the presence of a dicrotic notch, which relates to arterial health. The first finding was that posture itself significantly affected the cardiovascular readings as expected. For example, pulse wave amplitude was highest when lying down and dropped when sitting. In fact, sitting produced the lowest amplitudes. Gravity and perhaps vessel pooling reduce how much blood the heart ejects to the ankles. When you're seated upright, the average pulse interval, the time between beats, shortened slightly from supine to standing, indicating that heart rate increased upon standing, a normal response. However, their data showed a nuanced trend. Sitting had the shortest average intervals. Many other metrics changed with posture, such as the standard deviation of pulse periods, an analog of hrv, which changed significantly in both groups as they changed position.
[00:05:02] But the more important finding was the difference between the healthy and diabetic groups. People with type 2 diabetes showed blunted and even opposite autonomic adjustments to posture compared to healthy controls. A key example is the LF HF ratio, a common HRV metric that reflects the balance between sympathetic and parasympathetic activity. In the healthy group, LF HF behaved normally. It increased from lying to sitting to standing, reflecting the expected rise in sympathetic tone when you stand up. But in the diabetic group, LF HF actually decreased when moving from the supine to the upright posture. In other words, in people with diabetes, standing up did not produce the usual dominance of low frequency sympathetic HRV power. If anything, their autonomic response was paradoxical or subdued. This points to possible autonomic neuropathy or dysregulation, a known complication of diabetes, where the nerves controlling heart and vessel reactions don't function normally. Indeed, other measures supported the idea that the diabetic group had autonomic impairment. For instance, their mean pulse intervals were consistently longer, slower heart rate than the healthy groups. And unlike healthy subjects, the diabetics did not have a statistically significant change in mean heart rate between lying, sitting, and standing. Their bodies weren't adjusting heart rate as much. On the vascular side, the PPG waveform also differed in shape. Healthy folks showed a sharp pulse upstroke and a distinct dicrotic notch, a sign of good arterial elasticity in all postures. In contrast, the diabetes group's pulses had a more gradual rise and less pronounced notch, indicating stiffer arteries and damping of the pulse wave. One quantified measure of this, the B A ratio of the pulse wave, was higher in diabetics and increased more when they stood up, consistent with the idea that changing posture in someone with stiffer arteries causes a bigger relative change in the reflection of the pulse wave. So what does all this mean? Practically, it means a simple orthostatic HRV test. Checking HRV in the supine versus standing position could reveal early autonomic dysfunction. For example, if a patient's LF HF ratio doesn't ramp up upon standing, the that might be a red flag for diabetic neuropathy affecting the autonomic nerves. It also highlights how wearable PPG devices like a smartwatch might one day be used for more than just resting HR or single HRV readings that could track your body's responses to routine postural changes as a window into your cardiovascular health. For someone with diabetes, such data might warn of developing autonomic complications even before they feel symptoms. And for all of us, it's a reminder that context again matters for hrv. Whether you're lying down, sitting or standing will alter your HRV readings, and comparisons should take posture into account. The study elegantly shows that the dance between our heart nerves and blood vessels changes with position, and when that dance looks offbeat, as in diabetes, it can tell a story about underlying health. Our third study asks a fascinating question when it comes to insomnia and hrv, which causes which We've long seen that people with chronic insomnia often have lower heart rate variability, likely due to stress, hyperarousal or poor restorative sleep. Still, it's been hard to untangle cause and effect. The study, titled what comes first? Heart rate Variability changes or Insomnia? A causal investigation using Mendelian randomization, published in Science Direct, was led by Yan Cui, Chen, Miao, Jiang, Wang and Wang. The team used a technique called Mendelian randomization, often described as nature's own randomized trial, to see whether low HRV leads to poor sleep or vice versa. It uses genetic variants as proxies for a risk factor here HRV or insomnia, and assesses whether those variants are also associated with the outcome, for example insomnia or hrv, because your genes are assigned at conception. If a gene related to HRV also influences insomnia risk, that suggests an underlying causal path from HRV to insomnia rather than just correlation. So the researchers pulled data from extensive genome wide association studies. This they took genetic summary data for three HRV measures, including a time domain measure and a high frequency HRV measure related to respiratory sinus arrhythmia and for insomnia using data from the Fingen study, which had about 5763 insomnia cases and approximately 445,000 controls. Then they performed two sample Mr. Analyses in both directions. HRV causes insomnia and insomnia causes HRV changes. The findings were quite clear in one direction. They found evidence that lower HRV may causally increase the risk of insomnia. In technical terms, genetic predispositions to higher vagal HRV, PVRs, AHF power and higher SDNN were associated with higher odds of insomnia with odds ratios around 1.4 and 1.9 respectively. That initially sounds counterintuitive. Higher HRV gene predicts more insomnia. But remember, genes associated with higher HRV in a general population might actually indicate a necessary high parasympathetic state that if dysregulated, leads to insomnia. The more straightforward interpretation offered by the authors is individuals genetically inclined to have altered notably lower HRV are more likely to develop insomnia over time. Importantly, when they looked in the reverse direction, there was no genetic evidence that a predisposition to insomnia is associated with either higher or lower hrv. In other words, they found no significant impact of genes linked to insomnia on HRV traits. This suggests the arrow of causality runs predominantly from autonomic dysfunction to to sleep problems rather than the other way around.
[00:09:55] Now real life is of course a two way street. If you have a terrible night's sleep, you'll likely see a dip in HRV the next day and chronic insomnia can wear down your vagal tone. But this study implies that there may be an underlying autonomic profile that precedes and predisposes to insomnia. It aligns with what some insomnia researchers theorize that many insomnia patients have an overactive sympathetic nervous system or blended parasympathetic activity even during the day, which could make it hard for their bodies to wind down at night. The authors go on to conclude that if low HRV is a causal risk factor for insomnia, then improving HRV might be a novel approach to treating or preventing insomnia. That could mean biofeedback or paced breathing exercises, stress reduction interventions, maybe even vagal nerve stimulation or exercise. Anything that can durably raise HRV might help with insomnia resilience. It's a really intriguing perspective. We often think of poor sleep leading to poor hrv, but here we see evidence for the inverse poor autonomic regulation setting the stage for poor sleep. At the very least, it underscores how closely our autonomic balance and sleep quality are linked. For those of us working on our HRV through meditation, relaxation or fitness, better sleep might be a bonus dividend. And for clinicians, it suggests that in a patient with difficult insomnia, assessing their autonomic state are they in chronic high alert mode could inform treatment. Maybe incorporating HRV biofeedback or other autonomic calming techniques into insomnia therapy. This episode of the Heart Rate Variability Podcast is brought to you by Optimal hrv. Optimal HRV is an app and platform designed to make a HRV tracking and training accessible for both clinicians and individuals. If you're a clinician or coach, Optimal HRV provides a complete toolkit. You can easily monitor your clients or patients HRV trends over time, run group reports and utilize clinically validated dashboards to see how their nervous system is adapting. The app comes with built in training resources including guided breathing exercises, videos on trauma, informed HRV use and educational content to help you integrate HRV into your practice. For the for individual users, Optimal HRV offers easy daily readings using a compatible sensor and translates your HRV into clear color coded wellness scores. It's like having a nervous system check in each morning with suggestions for self care when you need it. One of the standout features is the community and team function. You can securely share your HRV data with your healthcare provider, coach or even just an accountability buddy. That means your whole care team can stay informed and support your progress in real time. Optimal HRV was created by clinicians who wanted a heart centered, science backed tool that that anyone could use whether you're tracking your recovery, managing stress or improving patient outcomes. It's available now for iOS and Android and you can learn more and find additional resources like their books and training workshops on optimalhrv.com Optimize your nervous system health with Optimal HRV the smart way to measure what matters. Thank you to Optimal HRV for sponsoring this episode. Now back to the research. Our fourth story brings us into the realm of psychology and neuroscience, examining the link between our inner well being and physiological signals. The study titled Bayesian Modeling of Heartbeat Evoked Potentials and Heart Rate Variability as biomarkers of spiritual and mental well being. An exploratory study published in Cogent Psychology was led by Fatima Afzal, Ejaz, Ahmed Hassan and Yousuf. This exploratory study asked whether heart rate variability and brain measures of heartbeat perception serve as biomarkers of spiritual and mental well being. It sounds high concept and it is. The researchers were particularly interested in Something called heartbeat evoked potentials.
[00:13:11] Heaps are subtle patterns in the EEG brain waves that occur in response to heartbeats. Essentially, they're a measure of how strongly and in what way the brain registers each heartbeat. Prior work suggests cheps relate to interoception, our sense of internal body signals, and even to emotional states. In this study, the team recruited 30 adults and had them fill out two surveys, one on spiritual well being, things like a sense of peace, purpose and faith measured by the Spirituality Index of well Being and one on mental well being, mood and life satisfaction measured by the Warwick Edinburgh Mental Wellbeing Scale. Then they recorded each person's EEG and ECG simultaneously under two eyes open and eyes closed, each for a few minutes. They computed heps from frontal EEG leads and also measured standard HRV parameters from the ecg. The idea was to see if people with higher spiritual or mental well being showed distinctive differences in their HEP or HRV data. They used Bayesian modeling to sift through combinations of these physiological features to predict well being scores. The most interesting result was that differences in heps brain responses to heartbeats between the eyes open and eyes closed states were significantly associated with spiritual well being. In fact, a model that combined the hep changes at two electrode locations, one at the forehead Fz and one over the left frontal area F7 was the best predictor of a person's spiritual well being score, explaining about 36% of the variance. That might not sound huge, but in this context it's quite notable that an EEG heart signal could account for over a third of the differences in a psychological spiritual metric across people. Specifically, people who had larger shifts in their HEP amplitude when they closed their eyes compared to eyes open tended to report higher spiritual well being. These HEP differences essentially reflect how the brain's processing of heart signals changes with a relaxed eyes closed state. Why would that link to spirituality? One speculation is that individuals with greater spiritual well being might have more attuned body awareness or more flexible heart brain interaction, which shows up as a stronger or more distinctive HEP pattern. Now, what about HRV itself? Interestingly, the study found that traditional HRV metrics were not strong predictors of either spiritual or mental well being in the sample. They looked at time domain measures SDNN, RMSSD, etc. And frequency measures HFLFLF, HF ratio, including something called the stress index, a metric derived from hrv. The only one that showed a hint of a relationship was the stress index si for spiritual well being. There was a weak trend that a lower stress index, which corresponds to higher overall hrv, correlated with higher spiritual well being, but it wasn't robust. The Bayesian analysis showed only modest support, and the credible interval on the effect touched zero. None of the HRV measures significantly predicted mental well being scores in plain terms. Unlike the HEP brain signals, the heart rate variability by itself didn't tell much about how spiritually or mentally well a person was, at least not in this small study.
[00:15:46] What does this all mean? The authors suggest that heartbeat evoked potentials could be a valuable tool for studying the mind body connection in contexts such as meditation, prayer or mental health interventions. If HPS indeed reflect a kind of heart brain communication efficiency or interoceptive awareness, then perhaps training practices that enhance interoception like mindfulness or contemplative prayer would strengthen HHEPs and that might relate to improvements in well being. It's early days though. This was an exploratory study with 30 participants, so more research will be needed to confirm and expand on these findings. But it's fascinating as a proof of concept. It's as if they found a neural signature, the brain listening to the heart, that correlates with a person's sense of spiritual fulfillment. For our purposes, it highlights that HRV isn't the only game in town when it comes to connecting heart and mind. Sometimes looking at the brain side of the heart brain equation like Hepps may reveal insights that HRV alone does not. It also reminds us that well being, whether spiritual or mental, is complex and multifaceted. You might be very calm, high hrv, but not necessarily high in life meaning or vice versa. By combining measures we might get a more holistic picture. It's a compelling direction for the field of psychophysiology, using both heart and brain data to quantify aspects of the human experience that often feel intangible. Next we move to the neurorehabilitation ward. Our fifth study, published in PubMed by Tang and colleagues, titled Long Term HRV Metrics, may assist in differentiating prolonged disorders of consciousness and emergence from minimally conscious state. A cross sectional study explores HRV as a vital sign for consciousness in patients recovering from severe brain injuries. These are patients who have survived severe brain injuries like traumatic brain injury or cardiac arrest, but remain in states of greatly reduced consciousness for example uws, which is what used to be called vegetative state, eyes open, cycles of sleep and wake, but no signs of awareness, or mcs, where there are intermittent minimal signs of consciousness. There's Also what's called EMCs emergence from MCS when a patient has just regained reliable communication or functional use of objects, essentially the step of waking back up to consciousness. Clinicians assess these patients using behavioral exams such as the Coma Recovery Scale Revised crsr. Still, misdiagnosis is common. Some patients who are actually minimally conscious can be misclassified as uws if they do not happen to show responses during an exam. This study aimed to determine whether long term HRV metrics differ between these groups and correlate with consciousness levels. They recruited 49 patients with prolonged DOC at least 28 days after brain injury. Each patient underwent a rigorous assessment. The CRSR was administered five times over a week to get a reliable picture of their best responsiveness. Based on those assessments, patients were categorized into three groups, 17 patients in UWS, 19 in MCS, and 13 in EMCs, the highest functioning of the three showing signs of emerging consciousness. Importantly, they also hooked each patient up to a 24 hour ECG monitor to continuously record their heart rhythms. From those recordings they computed a range of HRV measures, time domain indices like SDNN, standard deviation of NN intervals and SD ANN SD of 5 minute averages, and frequency domain indices like total power, ultra low frequency ulf, very low frequency vlf, low frequency LF, and high frequency HF power components. The differences they found were quite dramatic. Patients who had emerged from MCS to a minimally conscious state EMCs showed substantially higher HRV across many metrics than those still in MCS or UWS. For example, SDNN, which reflects overall variability, was was higher in EMCs than in MCS and in MCS than in UWS, with UWS the lowest.
[00:19:00] Similarly, on the frequency side, EMCS patients had higher HF power, greater vagal activity, higher LF power, and higher VLF and ULF components than MCS patients, who in turn tended to have higher values than UWS patients. In fact, when they conducted statistical tests, several of these pairwise differences were significant, particularly EMCs greater than MCS and EMCs greater than UWS. They also reported that HRV measures correlated positively with the patients CRSR behavioral scores. In other words, the better a patient's clinical signs of consciousness, the richer their heart rate variability. These findings make intuitive sense if you consider that the autonomic nervous system and consciousness might share common neural networks. Consciousness isn't just a switch in the cortex. It involves broad brain networks, including some deep regions like the brainstem and hypothalamus, which also oversee autonomic control. In a vegetative state, those networks are severely disrupted. The person's body may still cycle through basic rhythms like sleep, wake and a fairly regular heartbeat.
[00:19:51] Still, the nuanced moment to moment variability driven by a dynamically reacting brain is lost as a patient recovers consciousness. The brain's integrative activity returns and with it comes more autonomic responsiveness. For instance, perhaps emotionally or cognitively driven changes in heart rate start to occur again. The study's authors suggest HRV could be used as a supplementary biomarker for consciousness. This is exciting because HRV is objective and continuous. You could monitor it even when a patient is alone in their room at night. It might help identify patients who are actually more aware than they outwardly appear. For example, imagine two patients, both unable to move or speak. If one has markedly higher 24 hour HRV, it could be a clue that their brain is more intact and they might be locked in or minimally conscious rather than unconscious. Of course, this would need further validation, but as a proof of concept, it's powerful. The heart can reflect the hidden presence of consciousness beyond clinical utility. It's also a poignant reminder of how entwined our physiological regulation is with our neural state. It's as if consciousness, the mind awakening brings the heart to life in a more variable, dynamic way. From a practical standpoint, I could envision future ICU or rehab unit protocols in which HRV is one of several measures, along with EEG imaging, et cetera, used to evaluate patients with disorders of consciousness. It also underscores the importance of the brainstem and autonomic pathways in the recovery of consciousness, something well known in neurology but beautifully illustrated here with HRV data. Up to now, we've looked at individual studies, but our sixth piece is a sweeping review article that ties directly into the theme of heart brain interplay. We've been exploring the review, titled the Brain Heart Effects of Cardiovascular Disease on the CNS and Opportunities for Central Neuromodulation, published in Nature Reviews Neuroscience, was led by Van Wepperin and Vasaghi. In this review, the authors synthesize a wealth of research on how conditions like heart failure and hypertension can lead to changes in the brain and autonomic nervous system, and how in turn, targeting the brain might help treat heart disease. We often talk about the brain affecting the heart, like stress causing palpitations or vagus nerve stimulation slowing the heart. But here the focus is on the other direction. When the heart is diseased, what happens in the brain? The review highlights that cardiovascular diseases, especially heart failure and chronic high blood pressure, induce structural and functional remodeling across multiple regions of the central nervous system. This includes areas such as the brainstem, which houses vital autonomic centers, the spinal cord, the hypothalamus and higher centers such as the amygdala and parts of the cortex involved in regulating autonomic output. In patients and animal models with heart failure, researchers have found, for example, changes in the medulla oblongata's baroreflex circuits and inflammation in gliosis supporting cell changes in areas like the paraventricular nucleus of the hypothalamus, altered activity in the insular cortex and amygdala, which can drive sympathetic tone and so on. Collectively, these changes tend to tilt the autonomic balance toward excessive sympathetic activity and reduce parasympathetic restraint. Clinically, this manifests as the well known sympathetic overdrive and heart failure patients have high resting norepinephrine levels, elevated heart rates and often low hrv. The review points out key molecular culprits behind these CNS changes and elevated angiotensin II signaling. Ang2 is not only a blood pressure hormone, it also acts in the brain to increase sympathetic drive. Chronic neuroinflammation pro inflammatory cytokines in the brain can disrupt normal neuron function, oxidative stress and activation of glial cells in these autonomic centers. All of these factors create a feed forward loop. A weaker heart leads to less baroreceptor firing and more Ang2, which triggers inflammation and oxidative stress in the brain's control centers, which then become hyperexcitable and crank up the sympathetic output, which then further strains the heart and blood vessels. It's a vicious cycle of heart and brain deterioration, but here's the hopeful the authors discuss emerging neuromodulatory therapies that aim to break this cycle by targeting the brain or nerves. Some examples include vagus nerve stimulation, which electrically stimulates the vagus nerve and may boost parasympathetic signals and dampens central sympathetic outflow. There's research on carotid barore receptor activation devices, implanted stimulators that trick the brain into thinking blood pressure is high, thereby reflexively reducing sympathetic tone. Also, renal denervation is indirectly mentioned as the kidneys and the brain share feedback loops for blood pressure. More futuristic approaches include deep brain stimulation, transcranial stimulation of specific autonomic related brain regions, or pharmacologically targeting central receptors such as angiotensin blockers that cross the blood brain barrier or anti inflammatory treatments specifically for the brain. The review essentially maps out a paradigm shift Treating heart disease isn't just about the heart it's it might require treating the neural feedback loop that has gone awry in the central autonomic network. One striking statement from the abstract maladaptive central autonomic remodeling and heart failure and hypertension drive sympathetic overactivity and cardiac dysfunction. It puts responsibility on the brain for a big part of heart disease progression. For those of us interested in hrv, it's validating. We often say low HRV is bad for heart patients. This review shows why low HRV reflected by high sympathetic drive occurs. It results from these central changes and directly contributes to worse outcomes. It also implies that by the time we see low HRV in a hypertensive or heart failure patient, their brain's autonomic control centers are literally changed in structure and chemistry. The silver lining is that some of those changes can be modulated. Indeed, there have been small trials where vagus nerve stimulation improved heart failure outcomes and even patients quality of life. The authors call targeting the CNS in cardiovascular disease an exciting avenue for new therapies. Stepping back the brain heart access concept reminds us that the heart and brain are are an interdependent unit. If one fails, the other suffers. For clinicians, managing a cardiac patient may involve managing stress, perhaps using centrally acting drugs, such as certain beta blockers or AC inhibitors that cross the blood brain barrier and in the future, using devices that directly adjust autonomic outflow. For researchers, it's a call to arms for interdisciplinary work cardiologists, neurologists, and bioengineers working together. And for patients, it underscores why symptoms like depression or cognitive fog can occur in heart failure. It's not just feeling down about an illness there are physical brain changes underway. Conversely, it might explain why aggressive treatment of blood pressure and heart failure, thus improving cardiac output, can sometimes improve mood and cognition. You're likely normalizing some of that brain physiology. In short, the review paints a holistic picture. The heart and brain dance together for better or for worse. And to truly heal one, we may need to tend to both. Our final study returns to a concrete clinical application using HRV to predict outcomes in heart failure patients.
[00:25:44] We already touched on how low HRV and high sympathetic tone are hallmarks of heart failure. But how strong is HRV as a predictor of mortality in these patients? To answer that, our seventh study, titled Heart Rate Variability as a Predictor of Mortality in Heart Failure, a systematic review and meta analysis published in Koreas was led by Yadav Waqas, Muhammad Lashari Sabra Dwayad and Rajput. They gathered 10 studies conducted between 2000 and 2024 and involving 10,544 heart failure patients and analyzed the association between HRV measures and mortality. The meta analysis synthesized both time and frequency domain HRV metrics, but the primary focus was sdnn, the standard deviation of normal to normal intervals, because many studies report it as a summary of hrv. The headline result? Heart failure patients with lower HRV had significantly higher mortality risk and this was consistent across the pool data in quantitative terms. The META analysis reported a pool defect size of approximately 1.99 for the association between HRV and mortality, roughly interpreting that patients in the low HRV category were approximately twice as likely to die during follow up compared to those with higher hrv, that is A substantial difference when they zoomed in on specific metrics. SDNN emerged as the strongest predictor among HRV measures. The pooled effect size for SDNN was about 1.75 with fairly high consistency. Some studies looked at frequency domain too, e.g. low LF or low HF power, and generally found those associated with worse outcomes. Still, the meta analysis suggests time domain SDNN is a simpler and very robust indicator. They also conducted subgroup analyses, one specifically for HFrEF patients, heart failure with reduced ejection fraction, the classic form of systolic heart failure, and one for mixed or broader heart failure populations. The association between low HRV and mortality held in both. In HFRF, the pooled effect is approximately 1.74, in mixed HF, approximately 1.99. There was heterogeneity in the data. Not every study showed the same magnitude of risk. Nevertheless, the direction was uniform. Low HRV meant higher risk. Importantly, the authors noted that HRV provided prognostic information beyond traditional risk factors such as left ventricular ejection fraction and NYHA functional class. This is key for clinicians. Even if you know a patient's EF, say 20%, and their symptom status, say NYHA Class III, measuring their HRV can further stratify their risk. For instance, two patients with EF 20%, if one has a high SDNN and the other a very low sdnn, the latter might be much more likely to have arrhythmic death. In fact, some of the studies in the review looked specifically at sudden cardiac death. They found HRV to be a strong predictor hazard ratios in individual studies of two to three for sudden death when HRV was low. That suggests HRV is capturing something about electrical stability and autonomic trigger potential for lethal arrhythmias. The conclusion of the meta analysis was bold. Impaired HRV is a robust predictor of mortality and heart failure and and SDNN in particular should be considered a reliable risk marker. They even call for standardization in HRV guided therapy trials. Standardization because different studies cut HRV at different thresholds and use different recording lengths. Having a consensus, for example, measuring a 24 hour SDNN or a 5 minute ultra short SDNN would help implement this clinically. And HRV guided therapy? That's an intriguing idea. It could mean using HRV to decide who gets an ICD defibrillator who needs more aggressive meds, or even to guide pacing therapies to improve hrv. Or it could mean actually trying to raise HRV through interventions and seeing if that improves outcomes. A bit like how beta blockers raise hrv. And we know beta blockers improve survival. Maybe HRV was part of the mechanism for now, if you're a clinician managing heart failure patients, this meta analysis encourages you to pay attention to hrv. It's easy to obtain with a holder monitor or even some chest strap and app technologies. If you see a heart failure patient with say, a 24 hour SDNN well under approximately 70 milliseconds, that's a red flag that they're in a high risk group. It might prompt closer monitoring, referral to electrophysiology for consideration of an ICD if appropriate, and optimization of their meds, particularly those that can improve autonomic balance, such as beta blockers and acs, which were likely not only treating the heart but also calming neurohumeral activation. On the patient side, one could view HRV as a motivational vital sign. Improving fitness, diet, stress management and adherence to therapy might raise their HRV and potentially improve prognosis. Though we don't have direct proof that raising HRV itself lowers mortality, it's logical, given it reflects a healthier state.
[00:30:00] This meta analysis basically adds weight to the idea that HRV is not just a wellness metric. It's a clinical prognostic marker, at least in the context of heart failure, but likely in other cardiac conditions too. It's gratifying to see the hard numbers that back up what many HRV enthusiasts have believed that there's a real signal in HRV measurements that can foretell meaningful outcomes. So let's zoom out. What does all this research actually mean for you? Let's break down the big picture, takeaways and actionable insights for individuals. One message is that your environment and lifestyle have immediate effects on your autonomic Health the pollution study reminds us to be mindful of air quality on heavy pollution days or smoky days. Consider reducing strenuous activities or using air filtration, especially if you have heart or lung issues as your body is under extra stress in those conditions. On the flip side, the Insomnia study offers hope that working on calming your nervous system might improve your sleep. So if you suffer from poor sleep, techniques like slow deep breathing, hrv, biofeedback, meditation or yoga things known to boost HRV aren't just fluff, they could address a root cause and help break the cycle of insomnia. We also saw that simply staying active and making posture changes are part of normal healthy physiology. They keep your autonomic reflexes sharp, so for general wellness, avoid being sedentary for too long. Even going from your desk to standing regularly could be a mini workout for your baroreflex. And interestingly, the Spiritual well being study hints that mind body practices that increase your awareness of internal signals like mindfulness or prayer or breathing exercises might not only make you feel better spiritually but potentially train your brain heart connection in positive ways. Lastly, if you have a health condition, consider tracking your HRV with an app like Optimal HRV or a reliable tool as an additional window into your body. As we heard, HRV tends to be higher in healthier states as people recover consciousness or when heart failure is better compensated. While as an individual you can't diagnose yourself from hrv, you might notice trends. For instance, if your HRV is consistently dropping over weeks, it could be a cue to check in with a healthcare provider or examine what in your life might be driving stress or illness. Think of it as one more vital sign to listen to. For clinicians, these studies collectively suggest HRV is a valuable biomarker across multiple domains of health. Firstly, consider incorporating HRV monitoring for your patients with chronic illnesses in cardiology. As the meta analysis showed, hrv, especially sdnn, can stratify risk and heart failure. It might be time to make HRV analysis a routine part of holder reports or even discharge planning. For HF patients, a low HRV could prompt more aggressive therapy or follow up in neurology and rehabilitation. Consciousness research suggests that HRV may help assess patients with severe brain injury. While we're not at the point of replacing behavioral exams, it's something to be aware of. Maybe in the icu, an unexplained rise in a coma patient's HRV could hint at neurological improvement for psychiatrypsychology practitioners, the Insomnia Mr. Study reinforces that the autonomic nervous system is a key player in mental health when treating anxiety or insomnia. Measuring HRV can provide objective feedback and therapies that increase HRV such as biofeedback and relaxation training should be part of the toolkit, not merely adjunctive. Also, keep in mind that HRV is context dependent. The posture study shows that factors such as body position, time of day and environment can influence HRV readings. So standardize conditions when possible or at least interpret readings with context in mind. Another insight not all calming techniques are equally effective in all situations. In this batch of studies we found, for example, that at night the body might respond more strongly to stressors like pollution. So we might advise patients that evenings should primarily be a time to cultivate a calm environment, good sleep, hygiene, clean air, et cetera. And for diabetic patients or those with suspected autonomic dysfunction, a simple orthostatic HRV test or even measuring heart rate response from lying to standing in your office might uncover neuropathy early. Overall, clinicians should view HRV as a cross cutting indicator. It's not just a cardiology number. It reflects autonomic regulation that can be pertinent in pulmonology, for example pollution, endocrinology, diabetes, neurology, brain injury, Ms. psychiatry, stress, PTSD and beyond. Encouragingly, HRV is cheap and non invasive to measure. The challenge has been knowing what to do with it. But as research like this accumulates, we're getting clearer thresholds and interventions. Perhaps in the near future guidelines will include HRV as a factor in care. Imagine if 24 hour SDNN less than 50 milliseconds double check patients beta blocker dose or consider autonomic function tests. For researchers, this week's studies showcase the expanding frontier of HRV research. We're seeing HRV applied in novel ways from using Mendelian randomization to establish causality to integrating HRV with et cetera EEG to provide a more complete picture of mind body interaction. The field is truly interdisciplinary now. One study was essentially an environmental epidemiology study air pollution. Another was a clinical meta analysis, another was a neurophysiology study using eeg and another was in the area of consciousness and rehabilitation. As researchers, it's an exciting reminder to think outside traditional silos. There are opportunities to collaborate. For example, an engineering researcher might draw on the posture study to develop more effective PPG algorithms to detect autonomic dysfunction. A neurologist might follow up on the HEP findings to see whether training programs such as meditation retreats produce measurable changes in heps and HRV along with improvements in well being. The Nature Reviews paper emphasizes mechanisms. It would be great to see more mechanistic studies that bridge animal models and human data to pinpoint how changes in, say, the amygdala or inflammation translate into the HRV metrics we record. Also, the idea of HRV guided interventions is ripe for exploration. We have consumer wearables and apps everywhere. Maybe researchers can run trials where one group of patients gets a tailored intervention when their HRV drops like an alert to do a relaxation exercise or an automatic medication titration and see if outcomes improve. Another research avenue is long term monitoring and big data. That pollution study with minute level data across day and night hinted at circadian patterns and multiphase responses. With more continuous data we might discover patterns. And of course, there's still work to do in standardizing HRV measures and establishing normative values across ages and conditions. In short, the horizon is broad. HRV research is venturing into genomics, digital health, neuromodulation, mental health and precision medicine. The common thread is the autonomic nervous system touching all organ systems. We as researchers should continue to push these boundaries. Every time we do, we uncover a bit more of how intimately the heart connects with everything we experience.
[00:35:58] As always, thank you for joining us on the Heart Rate Variability podcast. This week's studies underscore the remarkable versatility of HRV and as a lens on human health, reflecting the air we breathe, the sleep we get, the injuries we recover from, and the resilience of our hearts and minds. HRV research is not just about one number, but about understanding the dynamic rhythm of life in our bodies. We hope you found these insights as engaging as we did. Keep listening to your heart, take care of your brain, and we'll see you next time. Stay well.
