September 20, 2011 (San Diego, California) — Heart failure puts patients at a nearly 30% greater risk for major osteoporotic fractures than those without the condition, according to research presented here at the American Society for Bone and Mineral Research (ASBMR) 2011 Annual Meeting.
The bottom line for clinicians, Dr. Majumdar said, is that “heart failure should make you think about fracture.”
The study was honored by the ASMBR as the meeting’s “Highest-Rated Clinical Abstract.” The authors have disclosed no relevant financial relationships.
“Patients with heart failure are less likely to tolerate or survive a major fracture, such as hip, so prevention is key.” Dr Sumit Majumdar-lead author
But heart failure is really a loss of dynamic control within the autonomic nervous system. Dr Majumdar is doing a great service at the observational level at applying his study to bear onto a cross section of patients that have had fractures along with their deteriorating heart conditions. Dr Majumdar is not able to advocate cause and effect with this study, but he points, in a way, toward a better evaluation of the brain-bone-heart connection. This appears very similar to my query of heart-brain connections with seizures. Vagal nerve stimulation (VNS) has demonstrated its usefulness in decreasing seizures. Now the following article describes VNS usefulness in reducing the characteristics profiling heart failure. Its effectiveness pushes the question: can speculating about VGN manipulation toward pivoting the balance of the sympathetic/parasympathetic in the setting of bone fragility, reestablishing a more balanced sympathetic drive to a more balanced parasympathetic drive, creating a more normal performance profile within the autonomic nervous system be attempted toward reestablishing stronger bone density? If we heal the brain-heart traffic is bone-brain-heart healed too?
Depiction of an implanted CardioFit vagus nerve stimulation device showing the position on the right vagus nerve, the intracardiac pacing lead in the right ventricular apex with the implantable Cardiofigt neurostimulator in the right subclavicular region Courtesy of BioControl Medical Ltd, Yehud, Israel
“Autonomic imbalance characterized by sustained sympathetic overdrive and by parasympathetic withdrawal is a key maladaptation of the heart failure (HF) state. This autonomic dysregulation has long been recognized as a mediator of increased mortality and morbidity in myocardial infarction and HF.1,2 Sympathovagal imbalance in HF can lead to increased heart rate, excess release of proinflammatory cytokines, dysregulation of nitric oxide (NO) pathways, and arrythmogenesis. Diminished vagal activity reflected in increased heart rate is a predictor of high mortality in HF.3,4 Sustained increase of sympathetic activity contributes to progressive left ventricular (LV) dysfunction in HF and promotes progressive LV remodeling.5,6 Pharmacologic agents that reduce heart rate, such as beta-blockers and, more recently, specific and selective inhibitors of the cardiac pacemaker current If, have been shown to improve survival and prevent or attenuate progressive LV remodeling in animals with HF Electrical vagus nerve stimulation for the treatment of chronic heart failure”
Electrical vagus nerve stimulation for the treatment of chronic heart failure by Hani N Sabbah Cleveland Clinic Journal of Medicine August 2011 vol 78 Suppl 1 S24-S29
The critical term in the above Sabbah reference is autonomic dysregulation or autonomic imbalance which is the sympathetic/parasympathetic balance shifting off its delicate pivot point. Instead of the tipping point happening with heart failure acting at this junction I’ll introduce the term the pivoting point to characterize the chronic remodeling behavior involving sustained increase of the sympathetic drive at the same time as withdrawal of parasympathetic drive activity is happening. This type of sympathetic/parasympathetic pivoting appears to counteract the surging sympathetic overdrive component getting stabilized when beta-adrenergic receptor blockers are employed as pharmacological agents. So modulation of the parasympathetic activation appears as a potential re-pivoting therapy toward reestablishing better dynamic equilibration with a sympathetic/parasympathetic balance pivoting point as a treatment for chronic heart failure associated now with a increased osteoporosis risk as reported by Dr Majumdar.
The following is shamelessly paraphrased from the Sabbah article: ‘The imbalance of the sympathetic/parasympathetic autonomic regulation leads to increased heart rate , excess release of pro-inflammatory cytokines, dysregulation of nitric oxide pathways and arrythmogenesis. Diminished vagal activity in the setting of heart failure is a predictor of high mortality. With a sustained increase of sympathetic activity leads to a progressive left ventricular dysfunction and promotes left ventricular remodeling, which is a distended shape change of the ventricle volume. Pharmacolgical agents that reduce heart rate, such as beta-blockers and selective inhibitors of the cardiac pacemaker current If, have been shown to improve survival and prevent the remodeling of the progressive left ventricular distension. Heart failure treatments against hart failure gave prominence to beta-adrenergic receptor blockers, angiotensin-converting enzyme inhibitors and aldosterone antagonists. However modulating parasympathetic activity for treating heart failure can be directed at the cardiac vagal efferent activity by targeting the peripheral cardiac nerve stimulation to slow the heart down (bradycardia) plus the capacity to modify both the atrial as well as the ventricular contractile function. Vagal nerve stimulation was shown to prevent sudden cardiac death in dogs with myocardial infarction and to improve long-term survival in rats with chronic heart failure. Also in conscious rats vagal nerve stimulation has been shown to suppress arrhythmia’s with chronic heart failure secondary to myocardial infarction.
Here’s the gist. Physicians have attempted in the past few decades to influence this sympathetic-increased heart rate surge by throwing drugs at the pivoting point shift. My opinion is that they are onto half the solution at best. If a dynamic shift is happening inside the brain zones the heart-brain axis of control, singling out only the increased heart rate drive surge doesn’t deal with the compliment of the parasympathetic drive, what Nature already has in place- the ratcheting down of heart rate, slowing the beating pace down. So I will stress the approach that I found serendipity style last week. Remember I have been on this for twenty years but the progress is grindingly slow at times trying to pick out the appropriate traffic that is meaningful in the brain-heart axis. The reality is it’s very shallow but at least the approach of using AC/DC as a pivoting point evaluation gives a better assessment of brain-heart net interaction. What is the AC/DC pivoting point? Here’s my first crude explanation which with time will get smoother plus more accurate. As a clinician concerned with bone fracture going unreported following heart failure it must have been a shocking reaction that Dr Majumdar must have been really stunned to look at the X-rays post cardiac infarct to see vertebral (spinal cord) fractures that the patient was not even aware of! So it’s a clear risk that as the heart fails over time an entire remodeling process kicks in. The heart changes shape, it’s main pumping chambers distend as compensation pumping harder trying to keep up to demand. Here’s my point. As the heart size increases, Nature has this elaborate net of tracking to react. Tensegrity shape sensing kicks in as one of the repertoire of repairs, trying to stabilize the off balance now imposed onto the entire system of checks and balances. So first priority should be get the heart shape back into a normal elastic range of pumping motion, no? That’s where acceleration capacity/deceleration capacity as a metric, a window of dynamic performance is our best set on the pivoting point shift. Reestablish the balance while maintaining the focus on AC/DC proper balance. It is clear that right now that is the best option to track our ability to reconnect the brain-axis balance. But first we have to get a much better feel for it’s normal swings. That’s the hard part.
What I seem to be observing is a failed heart shape becomes a failed bone shape, all happening at the heart-brain axis of control.