I have written several times on Fighting Fatigue about the heart failure theory in ME/CFS patients. I have talked to a cardiologist regarding this but she wasn’t much help. I have also worn a halter monitor for 24 hours but this showed no irregularities in my heart either. If you want to read about the other articles I’ve written on heart problems in ME/CFS patients, please view the “Related Posts” links at the end of this post.
Thanks to Adrienne once again at the About.com website for CFS & Fibromyalgia for posting the links to these studies.
Both of these recent studies were published in Neuroendocrinology Letters: the studies were a CoQ10 Study and an Inflammation, Oxidative & Nitrosative Stress Study. Here is an excerpt from the CoQ10 study:
The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms may be caused by CoQ10 depletion. Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders. The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population.
In this study, the CoQ10 levels in the 58 CFS patients was significantly lower than that of the 22 healthy individuals tested. The researchers stated that lower C0Q10 is a predictor of chronic heart failure and may explain the link between ME/CFS & chronic heart failure. What really scares me from this research is where they state that ME/CFS patients dying from chronic heart failure is 25 years youngger than the general population who die from chronic heart failure.
So naturally, researchers are suggesting that CFS patients take CoQ10 supplements. If CFS patients are on cholesterol drugs, these will decrease the CoQ10 levels in the body so it is imperative to take CoQ10 supplements if on cholesterol drugs.
An excerpt from the second study states that:
There is evidence that disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways and a lowered antioxidant status are important pathophysiological mechanisms underpinning myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS). Important precipitating and perpetuating factors for ME/CFS are (amongst others) bacterial and viral infections; bacterial translocation due to an increased gut permeability; and psychological stress. Recently, Jason et al (2006) reported that the mean age of patients with myalgic encephalomyelitis/chronic fatigue syndrome dying from heart failure, i.e. 58.7 years, is significantly lower than the age of those dying from heart failure in the general US population, i.e. 83.1 years. These findings implicate that ME/CFS is a risk factor to cardio-vascular disorder.
This study was very hard for me to understand, so please click the following link (also posted above) to read the entire study: Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS.
Chronic fatigue syndrome (ME/CFS) involves a lot more than fatigue. On top of a few dozen possible symptoms, this disease is also linked to certain heart abnormalities. Does that mean you have to worry about developing heart disease? Not necessarily. However, they do point to the need to watch out for it.
We’re not sure about the cause and effect relationship of ME/CFS and heart abnormalities. We do know that the incident rate is higher in people with it than in the general population, and many researchers believe the association is more than incidental.
One study published in the journal Fatigue in 2016 reported a mean age of 58.8 years for deaths related to heart failure in people with ME/CFS. That’s about 25 years younger than the mean age of cardiac-related death overall.1 While no one can know for sure which factors may have contributed to this result, studies like this have long suggested that ME/CFS is inherently linked to insufficient heart function.
And the abnormalities don’t stop there. Other investigators have noted similar high rates of heart irregularities, including:
A lack of nocturnal heart rate variability (meaning the heart fails to slow as expected during sleep)2
A small left ventricle (the chamber of the heart that pumps blood to the rest of the body)3
Postural tachycardia (a condition where the heart rate speed up, often unevenly, when a person rises)4
Short QT interval (a genetic disorder which affects the electrical system of the heart and causes palpitations or sudden loss of consciousness)5
Abnormally low blood volumes6
A study conducted in 20117 looked into sleep patterns in people with ME/CFS in order to better understand the common symptom of unrefreshing sleep. What they found, surprisingly, was that people with ME/CFS had little variation in their heart rate from day to night, a condition known as low heart rate variability (HRV).
To understand this, feel your pulse and then breathe in and out slowly. You’ll notice that your heart rate changes slightly, faster when you breathe in and slower when you breathe out. That’s heart rate variability.8
A low night-time HRV suggests that there’s a problem with the nerve signals that regulate the heart’s natural pacemaker (called the sinus node). This is in line with the theory that ME/CFS is caused, at least in part, by flaws in the autonomic nervous system, which regulates automatic functions such as breathing, digestion, and heart rate.
Your heart has four chambers, and the ones that pump blood out to the rest of the body are called ventricles.
A 2011 study10
found that some people with ME/CFS have a smaller left ventricle. This is believed to explain the symptom of dizziness upon standing, which is called orthostatic intolerance (OI).
Normally, when we get up from a seated or lying position, our blood pressure will go up for just a minute to counter gravity and keep the blood flowing to the brain. When you have OI, this doesn’t happen, and it makes you feel dizzy—or even faint—when you stand up.
This physiological anomaly could explain why what most people consider a small amount of exertion can wipe out someone with ME/CFS.
Postural tachycardia is similar to OI except that it involves the pulse rate rather than the blood pressure.
Tachycardia is the medical term for an abnormally rapid heart rate. Postural tachycardia simply means your heart rate speeds up abnormally whenever you rise, again, leading to dizziness or fainting.11
Postural tachycardia is about three times more common in people with ME/CFS than in the general population.
A QT interval is a term used to describe the space between certain up-and-down beats on an electrocardiogram (ECG) readout. A short QT interval means that your heart is beating normally but has less chance to recover after a heartbeat.12
A short QT interval is typically considered a genetic disorder and is associated with the increased risk of sudden cardiac death. While rare in the general population, a short QT interval is more common in people with ME/CFS.
Two studies conducted in 200913 and 201014 reported that people with ME/CFS had lower-than-normal blood volumes–basically, less blood.
Moreover, the lower the blood volume, the more severe the case of ME/CFS. Many scientists now believe that low blood volume contributes to many of the symptoms of ME/CFS simply by depriving cells of the oxygen needed to produce energy.6
While the studies suggest that abnormalities of the heart and nervous system contribute to the high rates of cardiac failure in people with ME/CFS, that doesn’t mean they’re the only factors. Other things, such as weight and sedentary lifestyle, may contribute as much or even more.
In the end, most of these studies are small and isolated and need far more investigation to considered conclusive. What they should highlight, however, is the increased need to monitor the cardiac health of people living with ME/CFS. This is especially true for those with severe symptoms as well as anyone who has risk factors for cardiac disease (including smoking, obesity, and a lack of exercise).
If you have ME/CFS, talk to your doctor about heart health, which of these abnormalities you may have, and what you can do to help prevent cardiac disease.
One of the most significant challenges to achieving a better understanding of ME/CFS results from the methodological limitations of the current research base. Issues related to external and internal validity and to reliability frequently have led to inconsistent results across studies, as well as other shortcomings. Despite these limitations, however, the committee was able to glean evidence of symptoms, signs, and objective measures for ME/CFS. The evidence with respect to major symptoms and manifestations is presented in this chapter, while that related to other symptoms and manifestations and to pediatric ME/CFS is reviewed in Chapters 5 and 6, respectively.
Studies on ME/CFS used different inclusion criteria and different sources of ME/CFS patients and control participants. The end result is heterogeneity in both patient and control cohorts, creating an unclear picture of the symptoms and signs of the disorder and its outcomes. Findings are based on samples with a large majority of middle-aged women (late 40s to early 50s) who are Caucasian and of higher educational status, perhaps limiting the generalizability of the studies. Very few studies focused on other population subsets, such as pediatric or geriatric patients, or included ethnic and racial minority patients. Some studies recruited patients from specialized ME/CFS treatment centers, while others used community-based samples.
These different sampling methods may result in patient groups that differ in demographic characteristics and symptom type and severity. Furthermore, those most severely affected by ME/CFS may be bedridden or homebound and may not have been included in any of these studies (Wiborg et al., 2010). Thus, there are selection biases in the studies’ sample composition.
In many cases, studies lacked properly matched controls to account for confounders. The majority of published studies compared a small number of ME/CFS patients with healthy controls. Control groups including people with other illnesses, sedentary individuals, or people who meet different case definitions of ME/CFS have not commonly been used. Because almost all controls were healthy and most were physically active, the findings from those studies do not shed light on which symptoms and signs distinguish ME/CFS from other disorders with some overlapping symptoms.
Some contradictory findings may also be due to the use of various scales, instruments, and measures for symptoms, some of which are imprecise, not comprehensive, or not validated. ME/CFS symptoms were derived mainly from patient self-reports, which raises questions about the internal validity of the study results. Moreover, relatively few studies were longitudinal, so little light has been shed on the natural history of ME/CFS (Jason et al., 2011b). There also were few studies of the early stages of the illness. This is understandable given that the diagnosis can be made only after 6 months of symptoms (see Chapter 3 and below), but nevertheless is a barrier to understanding the natural history of the illness.
A lack of replication and validation in many studies limits the ability to assess the study findings critically. Few attempts have been made to follow up on or replicate intriguing findings in the literature to date.