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Guinea Pigs

By Eric Van De Graaff, MD November 02, 2009 Posted in: Heart Health

My seven-year-old daughter loves animals of all kinds. She loves snakes, spiders, bugs, birds—everything.  Her favorite are rodents of all varieties.  She has a hamster that she considers part of our family, but her infatuation with small furry animals extends to mice, voles, chipmunks and sewer rats.  She has previously told me that rodents are some of the best people she knows.

With considerable dissatisfaction she recently brought to my attention the various pejorative metaphors we humans extend to our furry friends.  “Are you a man or a mouse?”  “You dirty rat.”  “He squirreled away his savings.”  She especially didn’t like the use of “guinea pig” as an object of experimentation.  That got me thinking about guinea pigs and research.

Last week I saw a relatively young patient in whom I placed a defibrillator (implantable cardioverter defibrillator or ICD) about a year ago who came in because he had received a shock from his device.  We reviewed the recorded rhythm strips from his ICD and found that he had suffered ventricular fibrillation and would have died if he had not been saved by the electric jolt from his device.

By way of review, a defibrillator is somewhat like a pacemaker on steroids—it has all the functions of a pacemaker but can also deliver a whopping electrical shock directly to the inside of the heart.  It is meant to interrupt cardiac arrest in patients at risk for such.

This patient in particular has an interesting history.  He has a weak heart but has no coronary blockage (which is the usual cause of diminished heart strength) and our diagnosis for him is “dilated cardiomyopathy.”  We believe his heart muscle was damaged some time back during a viral infection, but there’s really no way to tell.

The use of defibrillators has been restricted in the past to patients with hearts that have been weakened by coronary artery blockage and heart attacks, so-called “ischemic cardiomyopathy.”  This changed with the publication of a landmark study in 2005 that showed that persons with dilated cardiomyopathy benefited from ICD implantation to a degree similar to those with coronary disease.  Shortly after the release of these data the Centers for Medicare & Medicaid Services (the branch of our complicated health care system that determines the practical applicability of new treatments) began promoting the use of ICDs in patients with dilated cardiomyopathy, and a couple years later my patient received his device.

For personal reasons I was particularly pleased to see publication of the research cited above since I was one of the principal investigators in the trial.  My team enrolled dozens of patients with weak hearts into the SCD-HeFT study and randomly assigned some of them to receive an ICD.

Since patients with cardiomyopathy of any type are at increased risk of cardiac arrest (as well as other problems such as congestive heart failure and heart attack), my group of patients had its share of fatalities.  Many of those fortunate to be assigned to the group receiving the ICD survived because they had the protection of the device.  Others, with no defibrillator, suffered cardiac arrest and didn’t make it.

You may look at this and think that we treated these patients as guinea pigs by randomly withholding the lifesaving technology, but you have to understand that, at the time, none of these patients would have otherwise received an ICD—it simply wasn’t an option for them based on the available science.

That’s the nature of clinical research.  We don’t know if something is helpful or not until we test it in people.  Think back to the experience with the rhythm medications in the CAST study.  Everyone believed drugs that blocked ventricular rhythm abnormalities were lifesaving in people who suffered heart attacks—until it was proven otherwise.

I look back on the volunteers in our study and recognize what they did for everyone else.  My patient is alive today because 2,521 patients in the SCD-HeFT study volunteered to test the theory that we could come up with a better way to prevent cardiac arrest.  You could even say that some of them—randomized to receive no ICD—effectively gave their lives to help us get this information.

So what does the future hold?  Hundreds of studies are underway at thousands of hospitals and clinics around the world.  Here are some that our cardiac research team is currently involved in:

ROCHE.  We have drugs that lower LDL cholesterol and know they protect us against heart attacks, but what about the idea of raising the protective HDL cholesterol?  Our office is studying a drug that may answer this question and serve as an important new avenue to decrease heart disease.

TRACER and TIMI-50.  Platelets are blood cells that form clots and can cause heart attacks and strokes.  We currently use drugs like aspirin and Plavix to block platelets, but these fail to offer complete protection in a large percentage of patients.  These two studies are looking at other options for platelet inhibition at the time of heart attacks.

ASCEND HF.  Congestive heart failure constitutes 20% of all hospitalizations for older individuals and continues to be associated with a high mortality rate.  We’ve relied on diuretic medication for years to drain unwanted fluid and see only mixed success.  We are now studying the effect of using a naturally occurring protein, nesiritide, to improve symptoms and outcomes in these patients.

PREMIUM PFO.  Experts have long suspected a link between migraine headaches and the presence of a small hole in the atrial septum of the heart called a patient foramen ovale (PFO).  Theoretically, small clots could traverse this opening and find their way to the brain, resulting in migraine symptoms.  This trial tries to determine if closing the PFO with a nonsurgical device improves symptoms in these patients.

RELYWarfarin has been the mainstay for over 50 years for decreasing risk of stroke in people with atrial fibrillation, but it’s difficult to dose and fraught with numerous drug and diet interactions.  We studied a newer compound called dabigatran as an alternative.  This study concluded recently and the positive results were printed in the New England Journal of Medicine.  After half a century we’re finally near to having an alternative to a medication originally developed as rat poison.

Every time you take a medication, submit to a surgical procedure, or undergo a test, remember that you’re able to do this only because thousands of people before you volunteered for the research needed to prove the therapy successful.  And the next time your doctor asks you to consider volunteering for a study, remember that guinea pigs are some of the best people I know.

Eric Van De Graaff, MD
Eric Van De Graaff, MD

Eric Van De Graaff, MD is a Heart & Vascular Specialist at CHI Health Clinic.

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