Posts Tagged ‘Right Ventricle’

I get by with a little help from my HeartMate II

May 28, 2010

I’ve written about Left Ventricular Assist Devices (LVADs) before – these are small (and getting smaller!) machines designed to be attached to the Left Ventricle and give a weak heart a needed boost. Usually it is used as a “bridge to transplant” – to keep a heart going until a donor heart can be found – but more and more often they are being used as a temporary measure. The LAVD is being inserted and left in long enough for the heart to rest; if the natural pump improves the artificial one can be removed.  Robert Jarvik and a team from the University of Maryland are even developing LVADs that can be used on children and infants!

Henry Ford Hospital in Detroit Michigan has been studying LVADs and they have discovered that they help improve the right side of the heart, too. They also show that a newer model of LVAD, the HeartMate II, has a significantly lower risk of infection than its predecessor.

The HeartMate II is a continuous flow pump – unlike the earlier model, which tried to simulate the beating of the heart. Because of this, someone using a HeartMate II LVAD has almost no pulse!

A Cure for the Funky Heart?!?!

December 10, 2009

I’ve got Google Alerts searching for the appearance of certain Heart Defect words and phrases across the internet, and they deliver new information to my computer every night. The information is new to me, but not always new.

So imagine my surprise when I read this report from a 1981 edition of the Scandinavian Cardiovascular Journal. Obviously, the internet didn’t exist in 1981 (or exist in the form that we know today) so this couldn’t have been put on line then; apparently another organization recently uploaded it – and Google Alerts “hit” on the phrase Tricuspid Atresia.

In eight patients from 1976 until 1980, tricuspid atresia (TA) was corrected with valved xenograft conduits…


This is unreal – in this trial, eight patients with Tricuspid Atresia were given a conduit that ran from the Right Atrium to the Pulmonary Artery, or a conduit that connected the Right Atrium to the Right Ventricle and “jumped” the missing Tricuspid Valve. This is the first time I have heard of this… but it sounds as if it might work.

All patients suffered from transient right-heart failure postoperatively and eventually developed normalized cardiac function throughout the first two months after operation.

Holy cow, it did work! All eight went through a passing phase of right side heart failure that quickly stabilized, and in two months their hearts began to function normally!

X-ray examination showed normalization of the heart size in the majority of the patients, and in those with conduits between the right atrium and the right ventricle a considerable enlargement of the right ventricular chamber together with normalization of right ventricular contractility had developed. Arterial oxygen saturation, haemoglobin and haematocrit values had normalized in all patients.

“Normalization” is a word I like to read – especially when pertaining to Heart Defect, and for damn sure when it’s MY defect! There was one adverse outcome – one patient died of “intractable right ventricular failure, septicaemia and intravascular coagulation” – in layman’s terms,  there was blood poisoning, runaway blood clotting and the Right Ventricle failed for an undetermined reason.

Two patients with valved conduits between the right atrium and the right ventricle showed a normal unrestricted level of activity without medication, while patients with valved conduits between the right atrium and the main pulmonary artery were digitalized with an almost normal level of activity. Early repair with valved conduits of patients with TA is advocated.

But despite the success of this very limited trial, I can not find any information about followup trials. Today’s Tricuspid Atresia patients do not have this treatment option. Which begs the question:

What happened?

The obvious answer to why this isn’t being used today is “Something went wrong.” – but what? I’d certainly like to know. With 2009 technology, this trial could very well be worth repeating.


October 19, 2009

Trouble! Oh we got trouble! Right here in River City! – The Music Man

I don’t know if this was filmed in River City, but someone certainly does have Trouble (with a capital T!). Here’s a scan from EchoJournal, the online database of unusual ultrasound findings: This is a “apical TTE” – a TTE is a TransThoracic Echocardiogram, a test in which a small ultrasound scanner is pressed against your chest. “Apical” means the scanner head is located near the apex of the heart – the “point” located right at the bottom.

Right Ventricle pressures are usually relatively low. After all, the Right Ventricle sends blood to the lungs and back, so there is no need for a high pressure flow. But as this TTE shows, the pressure in this Right Ventricle is pretty high. The pressure is so high that the Ventricular Septum (the wall between the two lower chambers of the heart) actually bends into the Left Ventricle with each beat.

The readout screen also shows that the heart is beating 221 Beats Per Minute, so that Septum is bending a lot.

Trouble with a capital T, that rhymes with P, and that stands for pressure!

… but there is still a lot to be done

April 13, 2009

In my last post, I wrote about the amazing advances in Congenital Cardiac Surgery and how Heart Defect mortality rates have dropped 38% from 1979 to 1997. But there is still one defect we don’t have a good answer for yet: Hypoplastic Left Heart Syndrome, or HLHS.

Hypoplastic Left Heart Syndrome is not a singular defect, and could have any number of variations. But all of them feature a small (or nonexistent) Left Ventricle and a small Ascending Aorta.

If you look at a cutaway view of a normal heart, you will notice right away that while they are roughly the same size, the Right Ventricle has a larger volume than the Left Ventricle. The Right Ventricle has a smaller pumping muscle: a larger one isn’t necessary because the Right Ventricle only pumps blood to the lungs and back. But the Left Ventricle features a large, thick pumping muscle. When it contracts, the blood is really going places: out into the Aorta, and from there all over the body.

So if the Right Ventricle is content to just drive around the block, the Left Ventricle is at the airport boarding a flight to London. But in a heart with HLHS, the left Ventricle and its pumping muscle are tiny and the Aorta is barely functional. After all, the  root word for hypoplastic means “underdeveloped”. Because of this, a right sided heart defect (like Tricuspid Atresia, which is what I have) is more survivable than a left sided heart defect. 95% of children with HLHS who receive no treatment die within one week.

Even with surgery,  in the mid 1980’s only 28% of HLHS patients survived. (See the 5th Paragraph of the above link.) Until the late 1980’s an HLHS repair involved only two surgeries – The Children’s Hospital of Philadelphia (CHOP) didn’t begin to use the intermediate operation until 1989. (The entire link is informative, but page down to the section labeled “Discussion” for a look at how the three surgery procedure developed.) Current survival rates for the three stage surgical procedure are roughly 75%, with almost no data for long term survival.

This is completely unacceptable.

So what can we do about it?

1) Pass the Congenital Heart Futures Act. The Congenital Heart Futures Act, currently under review by two Congressional committees, will authorize more National Institutes of Health funding for Congenital Heart Defect (CHD) Research. Research is already going on – this January 2008 report from the National Institutes of Health (NIH) states that families with a Bicuspid Aortic Valve in their medical background are more likely to have an infant born with HLHS – but more funding means more and better tools, and more people trying to find a solution.

The Act will also create a CHD Patient Registry, maintained in one location and accessible to physicians. A properly administered registry will assemble a massive amount of data for study. The Centers for Disease Control will also develop educational programs concerning Congenital Heart Defects and their effects on patients and their families.

2) Identify Major Surgical Hubs. You aren’t going to allow a 200 bed community hospital to attempt the three surgery repair needed for HLHS. And it’s not that they are not careful, caring people… they do not have the experience. Identify the large national centers that perform many difficult medical procedures and create regional pipelines that move patients to these hospitals as quickly as possible.

3) Test new surgical theories. Gone are the days when new surgical procedures were developed through the “try it and see” method. With today’s faster computers, surgery can be simulated. A surgeon can “practice” on a computer before performing the actual operation, which give him the chance to anticipate any problems that may occur. By creating a computer simulation of an HLHS heart (multiple variations of HLHS can be programmed in, as can other defects) and using it to test new surgical theories, surgeons can explore “what if…?” theories without actually harming a patient.

4) Create a HLHS-only Registry. As a subset of the National CHD Registry, create a registry dedicated to gathering data only from patients with Hypoplastic Left Heart Syndrome. Small databases already exist and have been valuable in research: for example, researchers have used a HLHS database to  analyze the surgical approaches to HLHS to determine which ones work better. Research and better surgical procedures reduced HLHS deaths in California nearly 50% between 1990 and 2004. But such studies draw on limited databases for their information. Create a national database, and you open even more avenues for study.

5) Determine if HLHS has a genetic or an environmental origin. As noted in the January 2008 NIH report, families with an occurrence of a certain heart defect are more likely to have HLHS occur in the family later. That points to a genetic cause. But there is also evidence of an environmental factor – a “cluster” of twice as many HLHS cases than would be normally expected in a certain section of  Baltimore, Maryland. We need to devote the time and resources needed to determine what exactly causes HLHS: Is it a genetic predisposition?  Or is the environment the trigger? If it is genetic, can we learn how to prevent it? If it is environmental, what is the cause, and can we eliminate it? Or perhaps certain environmental conditions cause the genetic changes that eventually lead to HLHS.

These are just some of the things that we could do to improve Congenital Heart Defect survivability in general, and HLHS survival in particular. Quite often, we have to “think outside the box” to see the problem from an entirely different angle, and then perhaps we could find the answer.

Because every heart deserves to live a lifetime.