For decades, doctors have been aware of a relationship vs. Mitral Valve Prolapse & Anxiety Attacks. Lack of physiologic understanding caused many sufferers to be labeled “psychologic”.
In these patients who had frequent Panic Attacks, the primary etiologic factor was oft regarded to be an anxiety-infused mind driven by a“hysteria”.
We now know that Mitral Valve Prolapse (MVP) & Panic Attacks (PA) both occur with greater prevalence in pwHSD, & study of pwHSD teaches us the true primary-secondary relationships.
I did a study of HSD patients (N=50; all with Fibromyalgia). 67% had serial Panic Attacks with an average frequency of 4x/week. Of 39 examined by cardiac sonogram, 9% had MPV. 18% had recurrent syncope with 12 average lifetime events per person.
I presented this data in a paper published October 2019 in the Proceedings of 10th Interdisciplinary World Congress of Low Back & Pelvic Pain in Antwerp (also published on-line).
The problem with MPV evaluation is that the study is standardly done lying down, & in this posture the upper body blood-tower is less weighty during the diastolic phase of blood flow. IMO, this is reason MPV is not more commonly reported.
During the lying down posture, a lesser weight of blood-tower would be expected to cause reduced bio-mechanical forces against the mitral valve, & less likely to cause an imageable Sign of Mitral Valve Prolapse.
The most effective way to capture Mitral Valve Prolapse sonographic images would be with the patient seated upright. Perhaps, in the near future, such an exam will become available.
During diastolic phase, the heart is between contractions. If the mitral valve leaves are in proper anatomical approximation & function, they will maintain a water tight seal against back-flow of blood. Back-flow of blood would lower outflow from the heart & foster hypotension.
When the blood pressure dramatically falls, the brain, the most Oxygen-dependent organ in the body, sets in motion efforts to increase oxygen delivery to brain tissue:
Sympathetic nerve stimulation causes heart to race & to pump more blood. Sympathetic nerve stimulation causes lungs & breathing to speed up & to infuse body with oxygen laden blood; delivering increased amounts of oxygen to tissues.
Rapid breathing causes carbon dioxide to be blown off & baseline CO2 in blood is diminished. Decreased CO2 in blood changes ph of blood to alkaline, & Magnesium is bound to red blood cells; thereby depriving nerves of this relaxing substance.
The net effect of these physiologic changes is that the person suddenly feels horrible, with a sense of doom; as if death were imminent. This is called a “Panic Attack”.
As you can see, the cause of Panic Attack is organic; initiated as a body response. Unfortunately, historically, Panic Attacks have been regarded a Psychological disorders, initiated by the mind.
When the lack of adequate blood flow to the brain reaches critical values, the body has another trick to abort brain cell death. Unconsciousness is instituted, & fainting/syncope result.
In people with HSD, the elastic tissues of the body are more flexible. This includes the smooth muscle walls of blood vessels.
Whenever someone stands up, the blood column immediately falls toward center of earth. Normally, the smooth muscles of blood vessels of legs constrict to keep blood flowing in direction of the brain.
When soft tissues & blood vessel are super flexible, as in pwHSD, the blood column pools within the lower body. The body responds by falling down horizontally into a faint/syncope; so blood can be more rapidly pumped horizontally into brain.
If this phenomenon of sudden unconsciousness occurs serially & frequently, Postural Orthostatic Tachycardia Syndrome (POTS) is oft diagnosed.
Cardiologists often use a study called the tilt test to evaluate people for POTS. Patient lies on an exam table & table is suddenly flipped up. Autonomic blood pressure & pulse transducers measure these function throughout.
During the tilt test, when the patient assumes an upright posture, if blood pressure suddenly drops as pulse suddenly shoots up, then this confirms the diagnosis of POTS.
When body experiences suncope, it is not unusual for limbs to flail about wildly. This is normal. Some clinicians misinterpret this flailing as “seizures”, but Electro-Encephala-Grams (EEG) are negative. These are called “Pseudo-seizures”, & anti-seizure medications are useless.
Another heart-associated occurrence seen commonly in pwHSD is cardiac arrythmias. These are commonly tachy (speeded up) arrythmias. Cardiologists are not certain why these occur.
Perhaps craniotomy-cervical instability (CCI) causes impingement of proximate brain regions of medulla oblongata, wherein reside neural pacemakers originating impulses sent along sympathetic & parasympathetic (Vagus) tracts of autonomic nerves to heart.
My own observations of irregular rhythms of heart suggest that autonomic tracts are abnormally impinged & stimulated by scoliosis curves of thoracic spine. Scoliosis is common in pwHSD because vertebral disks are specialized ligaments.
When a pwHSD stands up it is often possible to trace their vertebral spines to note an S-shaped or reverse S-shaped scoliosis. I like to have X-rays taken both lying & standing to show the comparison.
It seems to me that pwHSD who have cardiac arrythmias more commonly have arythmias during daytime, when standing upright or sitting; when their scoliosis is expressed due to gravity compressing main upright post of body, the spine.
Recently, I had a patient with refractory cardiac arrythmias. Even after two procedures to ablate (burn & interfere with) nerves of heart that transit abnormal electrical pulses, arrythmias persisted.
When I examined the patient, he had a scoliosis throughout his thoracolumbar spine & which seemed to remit when he lay prone.
I was able to obtain X-rays of his spine lying & standing. There was a scoliosis standing. But when he lay supine, scoliosis persisted as a dramatic abrupt curve within the upper Thoracic spine at #2-3 vertebrae that looked deformed.
The patient had previously had a motor vehicle accident followed by chronic neck pain. The injured upper thoracic vertebrae were the obvious pain generators.
In this patient with a fixed scoliosis in his upper spine, laying down at night might be expected to stretch the fixed curve; thereby arousing impingements of contiguous sympathetic tracts & consequent cardiac arrythmias.
It might be interesting in his case to observe effects of Vagal stimulation (to over-ride sympathetic tone) by placing a TENS stimulator over the Vagus nerve within his neck-shoulder junction region; especially during nighttime hours.
CONCLUSION: hyper-elastic tissues in pwHSD can contribute to symptoms of cardiovascular conditions seen in this patient population.
Empirical observations suggest that dedicated efforts to correct functional scoliosis via specialized Physical Therapy might be efficacious.
Vagal nerve stimulation is hypothesized to therapeutically overcome Sympathetic overdrive responsible for Panic Attacks & cardiac arrythmias in this patient population.
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