In this section we will present different interesting applications that are using HeartBeat products.

 

Treating depression and dementia patients  -

Dr. Ikenaga Dog Therapy project in Japan

 

Ikenaga Toyotake, M.D., Cardiologist, that is the president and owner of the

Ikenaga Group hospitals in Japan, is one of the pioneers of Animal Assisted Theraphy for mental health.

Dr. Ikenaga is also one of the pioneers in usiing HeartBeat products to monitor the physiological correlates of his therapy, making this intuitive way of treating depression and dementia in the elderly scientificaly sound and eligible for medical insurance and wellfare support.

 

The problem of the aging population and its increased burden on the healthcare system is a world wide phenomena. By 2015 there will be more people over the age of 65 than children under 5. By 2050, there will be an estimated 1.5B people age 65 or older. Without strong preparation around prevention, treatment, and rehabilitation, the so called “silver tsunami” will significantly increase the burden of global diseases associated with aging - chronic diseases such as cancer, diabetes, and cardiovascular diseases. The burden of disease will also include declining cognitive acuity and mental health. A lot of suffering from such chronic disease can be reduced by "Dynamic Medicine" approach that includes prevention, proactive intervention and continuous monitoring during everyday life anytime anywhere, as HeartBeat products offer.

 

Depression and Cardiovascular health

The correlation between depression and cardiovascular disease is well known although not completely understood. Early research findings have indicated there may be genetic factors that increase a patient’s risk of depression and risk of recurrent cardiac events after a heart attack. Patients with heart disease and depression also perceive a poorer health status, as manifested by Quality of Life (QoL) studies. Negative lifestyle habits associated with depression – such as smoking, excessive alcohol consumption, lack of exercise, poor diet and lack of social support – interfere with the treatment for heart disease. Depression has been proven to be such a risk factor in cardiac disease that the American Heart Association (AHA) has recommended that all cardiac patients be screened for depression.

 

Treating depression and dementia of elderly patients

 

For more than 10 years, Dr. Ikenaga started his pioneering work on treating depression and dementia symptoms of elderly patients that cannot communicate using Dog Therapy. The idea behind it was that in order to get these patient react the stimulus should create some positive emotional response and this can be elicited through interaction with animals, like dogs. His hope was that the patients that did not respond to human communication will show interest when a dog is introduced to their room. Using specially trained dogs, patients that have been completely apatic started to follow with their eyes the dog. Suring following meetings, patients showed more and more interest in the dog, until they finally wgere willing to touch it and even to hug it or hold it. This was a major step forward, but there was still the problem how to measure the progress and assess the treatment effectiveness.

At this point Dr. Ikenaga purchased the HeartWatch devices that provide realtime information to the therapist about the physiological reactions of the patient, even when the patient does not move or talk. Most patients are suffering from depression and dementia, so this new channel of communication is invaluable. The HeartBeat mobile App also allows the therapist to enter comments into the time line and correlate it with the cardiovascular data.

In this Newsletter we will continue to update our readers with this exciting use of HeartBeat.

Stay tuned!!

Endurance exercise and heart disease

 

On June 24, 2013 published John Mandrola, in theHeart.com online magazine a very interesting review of the literature about the realtionship between endurance training and heart disease.

His review, that is summerized below points out the exercise paradox: regular exercise is critical for good health, but certain individuals who are exposed to high levels of exercise develop disease of both the heart muscle and electrical system.

 

 

A study presented at EUROPACE 2013 sheds some light on the question of individual susceptibility to exercise.

 

ARVD (Arrhythmogenic Right Ventricular Dysplasia ) is a form of cardiomyopathy where fibrous and fatty tissue replaces normal myocardium, primarily in the RV. Disruption of the architecture of cell-cell coupling sets up a milieu favorable for arrhythmia. , ARVD might cause sudden death in young athletes.

 

What makes this disease especially interesting is its genetics. Mutations in the genes that code for connecting proteins, called desmosomes, are the culprit. These defects are passed down in an autosomal dominant pattern, but the genotype is variably expressed with incomplete penetrance. This means some patients might suffer early ventricular arrhythmia while others with the same genetic material live into old age. In other words, the genotype has many phenotypes.

Here's the kicker: It has been hypothesized that endurance exercise (remember the ARVD-association with athletes) might induce an ARVD-like disease (phenotype) in genetically susceptible individuals.

The study:

Researchers from Birmingham, UK and colleagues in Muenster and Aachen, Germany used genetically modified mice to look at the interaction between exercise and heart disease. They knew that many patients with ARVD harbor mutations in the domain of the desmoglein 2 (DSG2) gene. They were able to genetically engineer mice lacking parts of the DSG2 gene. Those mice with two copies of the deletion (homozygous) developed profound ARVD, whereas those mice with one copy (heterozygous) did not manifest disease.

The question then was whether heavy physical exercise could provoke a disease state in genotypically susceptible mice. So they made heterozygous mice swim. Training sessions were done six days a week for up to 90 minutes per day. The research team then looked at both structure and electrical findings in the exercised mice and compared the swimming mice with their wild-type littermates.

The exercised and genetically susceptible (heterozygous—one copy of mutation) developed dilated RVs and had easily provoked ventricular arrhythmias. There were no such findings in the wild-type littermates.

This simple but elegant experiment led the researchers to conclude that endurance training revealed an ARVD-like phenotype in otherwise-healthy and morphologically inconspicuous mice. During the slide presentation they suggested that these data support the idea that endurance training may be dangerous for carriers of mutations in junctional proteins.

 

Mandrola take is that in the study, exercising mice had genetic susceptibility to the disease, but no disease was manifest. The mice looked normal and did not develop changes of cardiomyopathy until exposed to endurance exercise.

 

We know some—but not all—athletes develop arrhythmias like AF. And we know AF, like ARVD, has strong genetic ties. Take the athlete who harbors a yet-described partial gene defect for AF. He has no signs of disease. His nonathletic brothers and sisters do not have AF. But he's an exerciser, and might it be that the exercise unmasked or induced the disease?

It's the same story with focal cardiomyopathy. We know from post–marathon and Ironman studies that athletes sustain enzyme elevations and transient functional impairments of the RV and LV. These defects resolve in most athletes, but some develop persistent scarring. The easy explanation is that those few athletes who develop scar had the highest dosage of exercise. But you know it's more than just dose of exercise and random chance. It's something about the athlete's genetic make-up.

Mark my words on this one: When we learn more about the genetic basis of disease, the personal genome if you will, we will better understand susceptibility not just to exercise, but to many other of life's exposures. Why do some smokers avoid cancer? Why do some heavy drinkers never develop cirrhosis? Why does an occasional mean person live to old age? The answer according to Mandrola might be found in the genes.

 

 

Reference:

Vloumidi E, Fortmueller L, Sakhtivel S, et al. Arrhythmogenic right ventricular cardiomyopathy-like phenotype induced by endurance training in heterozygous desmoglein-2 mutant mice. EUROPACE 2013; June 23, 2013; Athens, Greece. Abstract 83.

 

 

AF detection

 

The device described by Lewis et al is a finger probe similar to that used in general practice for pulse oximetry which uses the principle of photoplethysmography. The two studies by Wiesel et al. and that by Stergiou et al.

 

They considered a modified blood pressure monitor similar to those used by patients to monitor their blood pressure at home. This could either be used by people monitoring their own blood pressure to self-screen for AF or by primary care professionals to opportunistically screen patients. These devices benefit from the ability to modify thresholds of detection in order to achieve maximum sensitivity to optimise their value as screening devices.

 

In general, a screening test needs to have high sensitivity so it doesn’t miss cases. The higher the specificity, the fewer people who need to have the reference standard investigation.

 

The reference standard test in diagnosing AF, a 12-lead ECG, is readily available, non-invasive andrelatively inexpensive. Its main drawbacks are that it is more expensive, more obtrusive to the patient life and requires some skills from the care giver so cannot be used by patients at home.

 

 

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Applications

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