'Smart" pacemakers may slow progression of heart failure..
- by IAN MC
- 2020-03-30 10:10:48
- General Posting
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- 11 comments
With all the current gloom and doom re. Covid-19 , it is good to read something positive about future pacemaker development. This was reported in the magazine published by the British Heart Foundation . ( This research may have been mentioned on here before but it still makes good reading ) :-
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" Normally your heartbeat speeds up when you inhale and slows down when you exhale, but pacemakers usually pace the heart at a regular rate. Now researchers at the Universities of Bath & Bristol have built a "smart" pacemaker that reads the body's own breathing signals to speed up and slow down the heart more like a natural heartbeat.
They tested the PM on rats with heart failure and found that within 2 weeks there was a 20% increase in blood pumped by the heart. The next step is to find out whether the same thing happens in humans.
Professor Julian Paton, senior author of the study said " Our findings give hope for heart failure patients and may revolutionise the design of pacemakers "
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I hope he is right. Anything which makes pacemakers more physiological in their action is a step in the right direction.
Ian
11 Comments
Interesting...
by crustyg - 2020-03-31 06:33:31
It's certainly an interesting article, although it skims over quite a lot of what is already known: 1) two vendors world-wide already have PMs on the market which use some form of input from breathing to drive rate response - I have one of them, 2) there is already a *lot* of evidence that RV apical pacing causes HF in some patients and there is good published work to show that CRT restores %LVEF in many of these patients - the implication being that anyone who paces a new patient with a simple RV apical lead can look forward to a *lot* of litigation in the future, which is why I wonder about the wisdom of RV leadless PMs. What I don't think we know yet is which patients will develop LV remodelling and reduced %LVEF at the outset.
Right now, where one applies the pacing stimulus is already a practical discussion point with existing technology (but it's not applicable or available to everyone). Whether applying some form of input to the PM's rate system to deliver beat-to-beat variability for patients with existing HF will be effective is an interesting question. Actually designing a study to test it will be difficult. Causes of HF and objective assessment of HF (i.e. not just the NY cardiology criteria - very subjective) will be important.
I'm also interested at a personal level, as I already have a very mild cardiomyopathy with proven raised RA pressure. Depending on how you define HF, I'm already there, although you wouldn't know it to look at my Strava profile. But this could be magical for patients with severe Left-sided HF who struggle to walk around at home or even breathe.
Thanks.
I'm confused
by AgentX86 - 2020-03-31 10:55:20
"Heart speeds up during inhale" and "slows on exhale" makes no sense to me. At a normal respiratory rate is about 16 breaths per minute and a heart rate of 60 (scale as you will) there about four heartbeats during each inhale/exhale. So that would be four "fast" beats followed by four "slow" beats. Does this make sense? Has anyone felt this? Has anyone seen this on an EKG? I'd think this would be something EPs would look for. Has anyone had an EP even mention this? Certainly eps would know about this.
I was slightly confused too , but .........
by IAN MC - 2020-03-31 11:22:39
............. a couple of minutes Googling produced stuff like this :-
"In humans inhalation is an active movement with the contraction of diaphragm and auxiliary muscles; it creates negative pressure and “sucks” air into the lungs. Exhalation is generally a passive movement as the air flows with the pressure gradient and thus no muscle work is essentially needed in its process. Because inhalation is an active and exhalation is a passive movement, breathing affects autonomous nervous system in such way that during inhalation there is an increase in sympathetic activity while during exhalation there is an increase in parasympathetic activity. As a result a heart rate increases during inhalation and decreases during exhalation, a phenomena observed as heart rate variability and commonly explained as respiratory sinus arrhythmia Corresponding neurochemical mechanisms of this interaction are documented in research of vagal feedback, vagal modulation and external vagus nerve stimulation. Such a sequence of active inhalations and passive exhalations, usually referred to as negative pressure ventilation, is common to all vertebrates with the exception of amphibians and some reptile species who use additional pumping mechanisms to force oxygen into lungs "
I bet you're even more confused now, I am !
Dr Crusty... where are you ?
Ian
Elevated pulmonary artery systolic pressure
by marylandpm - 2020-03-31 11:58:49
I have been paced 100% since 6/01/2015. Have a RV appex lead and my EF has remained normal however I have now been labled in pulmonary heart failure. I don't think there is anything wrong with my lungs. ( I hope the elevated pressure is not doing damage. ) I have been trying to get hisbundle but since my EF is not low they won't do it. I think the RA problems are do to the RV apex pacing.
Sinus arrhythmia is caused by pressure changes in the chest cavity
by crustyg - 2020-03-31 16:50:40
You breathe in by reducing the pressure inside your chest - either by diaphragm pulling down, or by chest wall expanding outwards and upwards, or both.
This also increases the rate of venous blood returning to the heart, the RA fills more, and the RV produces a larger output and increases rate - slightly. As you breathe out, the venous return to the heart decreases slightly and the net effect is that your HR reduces slightly. So your beat-to-beat timing is not exact, and it's partly controlled by your breathing.
My guess is that the group attempting to replicate sinus arrhythmia with a PM hope/believe that this behaviour might in some way keep the heart muscle more healthy. My opinion is that they are muddling cause and effect: the beneficial effect (if there is one) is the small changes in heart muscle stretching from breath to breath, and the small changes in HR are merely a consquence - an epiphenomenon. Against my opinion is their rat heart research: a lot will depend on *how* they induced HF in their rats.
Elevated pulmonary artery systolic pressure
by AgentX86 - 2020-03-31 19:53:34
Yeah, as clear as mud. This sounds like a typical, journalism grad written, press release. I agree with crusty. Color me skeptical. But what do I know. I'm not an EP, just an EE.
Thank you for your response Crusty
by IAN MC - 2020-04-01 05:53:47
I, too, wondered how they induced heart failure in the laboratory rats and whether this would affect the outcome. I believe that the usual methods would be via a drug-induced tachycardia or some sort of surgical intervention , maybe by constricting the aorta.
I started life as a research chemist in the pharmaceutical industry and we used to have a definition of a drug as being " any chemical compound, which when injected into a rat, produces a published paper ".
Maybe there's a similar definition for " pacemaker "
That apart, I don't altogether share the cynicism re the validity of this work and hope something good comes from it. We won't know until they move from one species to another i.e. from rat to human guinea pig.
Ian
I am still hopeful for a positive outcome
by Gemita - 2020-04-01 07:29:37
Many new treatments come from humble beginnings and I am optimistic that they will find a breakthrough for this debilitating disease.
The treatment with medication to slow the progress of HF is often unpalatable and can cause worse symptoms than the condition being treated. I just hope the present crisis will not spell the end of future research for so many excellent charities who will be badly affected because of loss of revenue from cancelled charity events like the London Marathon.
I. Get it but how does this effect EF
by PacedNRunning - 2020-04-03 02:35:56
This would only work with people that have CI where the pacemaker controls your Sinus node. I have AV block and my RV lead follows my sinus node so as i breath in and out, if my rate sinus rate changes, my AV delay follows my SA node. But this sounds hopefully maybe?
T
How does this effect EF
by AgentX86 - 2020-04-04 21:09:30
I think the hypothesis, here, is that the more "natural" the heartbeat, the better it is for the patient. Since your SI node is normal and you're relying on it for pacing, I don't think this applies to you at all. RV-only pacing and RV/LV dyssynchrony and the associated cardiomyopathy, is a different problem (mostly solved by CRT or His pacing).
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Thank you Ian
by Gemita - 2020-03-30 14:06:16
for this information. It sounds a promising development and I hope it will be available in my lifetime(?) I agree anything that can more closely match the way our bodies work "naturally" can only be to our advantage. I attach the BHF link for further reading
https://www.bhf.org.uk/what-we-do/news-from-the-bhf/news-archive/2020/january/bionic-pacemaker-slows-progression-of-heart-failure.