Heart: An American Medical Odyssey (34 page)

By this time, we had used nearly all the technology and medical procedures available for dealing with my disease. My doctors had equipped me with a small pump that kept me supplied with a steady dose of milrinone, or “rocket fuel,” to assist my weakened heart, but it was a short-term expedient and would soon lose its effectiveness. At this point, there were only two remaining possibilities. One was a transplant. But the demand far outstripped the supply of transplantable organs, and the average waiting period was twelve months. It was clear I would not live long enough to work my way up the transplant list.

There was one other possibility, which Dr. Reiner had mentioned to me earlier in the year: a left ventricular assist device (LVAD). At that time, my condition hadn’t deteriorated to the point where I was a candidate. Now I was there. Dr. Reiner arranged for us to visit with the surgical team at Inova Fairfax Hospital in Northern Virginia. The team, headed by Dr. Nelson Burton, briefed us on the LVAD that would be installed in my chest to assist my heart in providing an adequate supply of blood to my vital organs. They showed us a model of the device
and explained how it worked. One end would be connected to the bottom of my left ventricle and the other to the aorta. A small pump inside, operating at nine thousand RPM, would push blood from the ventricle through the aorta and the rest of the circulatory system. The pump itself is powered by a driveline that goes from the pump through your chest wall to a control element/computer worn on the outside of your chest, powered by batteries or a base power unit plugged into an electrical outlet.

When I first saw an LVAD, I was intrigued by the technology. Under ordinary circumstances, the idea of putting a device operating at nine thousand RPM into my chest, attached to my heart and to a driveline running through a hole in my chest wall would have seemed a little off-putting. But it was an option, and I was out of other options.

The LVAD was developed as a transition device to sustain a patient long enough to become eligible for a transplant. The original LVADs were not user friendly. They were so large that they were not portable. The patient’s bed would be wheeled into the room with the LVAD, and the patient hooked up to the device. Significant progress in recent years, however, had transformed the LVAD to a size that allowed its external elements to be worn on a harness or a vest so the patient could lead a more normal life. Some patients decided to live with the LVAD and not go to a transplant. If the LVAD surgery were successful, I would have the opportunity to decide at some future date if I wanted to go the transplant route.

Surgery was scheduled for July 8, 2010. Because it was expected to be difficult surgery, I checked into the hospital on July 6, two days early, so the doctors could attempt to stabilize my condition and improve my overall health as much as possible before the surgery. I was given additional doses of milrinone on July 6, but it wasn’t working. Indeed, it was becoming clear that my heart was failing rapidly and my liver and kidney functions were crashing. I have a vivid memory of that evening with my doctors and my family gathered together around my hospital bed, telling me they believed it was essential to implant the
LVAD on an emergency basis that night. I didn’t have two more days. After I heard from the doctors, I asked Lynne, Liz, and Mary, one by one, what they thought. It was unanimous. I looked around the room at everyone and said, “Let’s do it.”

Like a tornado, water entering a drain begins to rotate, forming a cone-shaped whirlpool triggered by the downward suction of the departing fluid. In the idiomatic and indelicate language of medicine, a patient who is “circling the drain” has entered the sinking spiral of accumulating medical issues. In the beginning, the problems gather slowly, but as the patient descends lower, the vortex spins faster and the complications come more quickly, leading inexorably to the patient’s demise. It’s not always apparent when someone enters the terminal spiral, but once it becomes obvious, it is almost impossible to stop.

The year 2009 was a tough one for Dick Cheney. There had been debilitating back pain requiring spine surgery, an episode of congestive heart failure, and in the final days of the year, a cardiac arrest resuscitated with a shock from his implanted defibrillator. Viewed individually, each of these events had a successful resolution; surgery fixed the back, diuretics resolved the CHF, the defibrillator restored a normal rhythm. In reality, however, these were not isolated incidents but rather a continuum of the same process. The vice president’s chronic cardiac disease led to a decrease in his overall physical fitness, which increased the likelihood of a back injury, the surgical repair of which provoked an episode of congestive heart failure, which in turn increased the chance of developing sudden cardiac arrest.

•  •  •

In January 2010, the vice president experienced a nosebleed that required cauterization at George Washington University Hospital. For more than a year, Mr. Cheney had been treated with warfarin (Coumadin), a
powerful anticoagulant used to prevent strokes in patients with atrial fibrillation. Warfarin is a synthetic derivative of dicoumerol, a naturally occurring blood thinner that was initially discovered in spoiled sweet clover animal feed and was developed seventy years ago at the University of Wisconsin (part of the name derives from “
W
isconsin
A
lumni
R
esearch
F
oundation’) and introduced in 1948 as rat poison. The drug has been used for decades as both a therapy and prophylaxis for clots in a variety of settings, including deep vein thrombosis, pulmonary embolism, the use of mechanical heart valves, and atrial fibrillation. Patients taking the strong anticoagulant must be closely monitored with blood tests and watch their diet, because foods like green leafy vegetables can decrease the effectiveness of the medicine, while other medications taken at the same time, such as antibiotics, can dramatically raise the effectiveness of warfarin. The major side effect of the medication is bleeding, which can be severe or even fatal.

Three weeks later, Cheney’s bleeding recurred. A nosebleed is a common ailment, particularly in the dry air of winter. The hemorrhage can be impressive, even in an otherwise healthy person who is not taking any medication. For a patient, such as the vice president, who is being treated with an anticoagulant like warfarin, bleeding, once started, can be hard to stop.

When she called, I told Mrs. Cheney to bring the vice president to the George Washington University Hospital emergency room right away.

“How do I get there?” she asked.

Nine years of Secret Service protection for the Cheneys had concluded just the day before, and Mrs. Cheney was going to have to drive the vice president into Washington by herself, something she hadn’t done in almost a decade. I gave Mrs. Cheney directions to the hospital and told her to come to the ER entrance, where we would meet them.

After calling the emergency room to let the attending physician on duty know that the Cheneys were on their way, I tracked down Dr. Nader Sadeghi, a GW ear, nose, and throat surgeon, and Dr. Jehan “Gigi” El-Bayoumi.

Gigi had taken over as Vice President Cheney’s internist after Ryan
Bosch left GW several months earlier and had quickly become indispensable to the Cheneys (and to me). She is an extraordinary physician and role model whose exceptional clinical skills are surpassed only by her astonishing compassion and personal care for her patients. Not surprisingly, she cares for many of DC’s political elite but somehow manages to deliver her remarkable VIP care to every patient, prominent or not, in her large practice.

Dr. Sadeghi examined Mr. Cheney, identified the problem vessel, which had already mostly stopped bleeding, applied a silver nitrate cautery, and packed the nostril with gauze. We watched the vice president for a while and considered keeping him in the hospital overnight for observation, but a few hours later, when there was no further bleeding, he was allowed to go home.

A little before 10:00 p.m., Mrs. Cheney called again, and now I could hear fear in her voice. Once again, the vice president was bleeding, now much more vigorously than earlier in the day. They were on their way back to the hospital. When Mr. Cheney arrived in the emergency room, blood was pouring from his nose, and a garbage can he had been bleeding into during the ride from Virginia was filled with clots. After manual compression failed to staunch the flow of blood, the vice president was rushed to the operating room, where, under general anesthesia, Dr. Sadeghi located and recauterized the bleeding artery but not before the loss of about one liter of blood (20 percent of his body’s total supply).

We had stopped Cheney’s Plavix after the first bleed three weeks earlier, and now we needed to stop the warfarin as well. These drugs, both of which impair the ability of blood to clot, had been prescribed in an effort to prevent a host of potentially lethal thrombotic events, such as recurrent DVT, stroke from atrial fibrillation, clotting of his stents, and recurrent heart attack. Unfortunately this last hemorrhagic event was severe: we needed to let the dust settle, and the troublesome vessel heal, before restarting one or both of these drugs.

•  •  •

During the evening of Sunday, February 21, three weeks after the nearly exsanguinating event, Vice President Cheney experienced about thirty minutes of chest burning. The Cheneys had been spending time on the Eastern Shore of Maryland, and I told them to go to the nearest emergency room, which was Memorial Hospital in Easton, for evaluation. After speaking with the ER doctor there, we decided that in view of the typical cardiac nature of his symptoms, it would be best to bring the vice president back to Washington and arranged to fly him the seventy-five miles by medevac helicopter.

When Cheney arrived at George Washington University Hospital, he was pain free, and his EKG was similar to his prior tracings. Although the first two sets of blood tests used to assess whether the heart muscle had sustained any damage were normal, the third set was mildly elevated, consistent with a small heart attack. The next morning we brought the vice president back to the cath lab to see what had changed.

The last time Cheney had undergone coronary angiography was nine years earlier, in March 2001, when he had developed chest pain caused by restenosis in the coronary stent that had been implanted four months earlier, during the presidential campaign. The procedures in 2000 and 2001 had been performed by accessing the femoral artery through a needle puncture at the top of his right leg. By 2010 we had largely abandoned the groin approach in favor of the radial artery of the wrist because of the increased patient safety and comfort when using this approach. My colleague Dr. Ramesh Mazhari joined me for the procedure, and through a two-millimeter puncture in Cheney’s right wrist, we advanced our catheters up through the arteries of his arm, under the clavicle, and down into the chest.

In March 2001, we had been criticized for not performing intracoronary radiation therapy (brachytherapy) when the vice president presented with chest pain and restenosis. The
New York Times
even published an article with the headline
“The New Treatment Cheney Did Not Get.” In that piece I was quoted as saying, “When you look at a technology in its infancy, I think it is often appropriate to be a little circumspect about applying it, especially using something like gamma radiation.”
Within a few years, brachytherapy would be shown to mostly only delay the onset of restenosis, not prevent it, and the technology would soon be relegated to the dustbin of abandoned devices by a new generation of “drug-eluting” stents coated with potent inhibitors to the formation of the scar tissue inside stents that causes restenosis.

Now, looking at Cheney’s coronaries for the first time in nine years, we noted that the diagonal stent we placed in 2000, and then ballooned again in 2001, was wide open, a very good thing as it supplied blood to a large portion of the vice president’s limited amount of remaining viable heart muscle and had likely helped keep him alive. Cheney’s coronary anatomy was remarkably similar to what we found almost a decade earlier, with the exception of a grape-sized aneurysm that had since formed in the left anterior descending, the other major artery supplying the still-contractile muscle. We surmised that a clot had probably formed in the aneurysm, eventually tumbling downstream (embolizing) and causing the small heart attack.

It wasn’t a coincidence that Vice President Cheney’s latest heart attack came less than a month after we stopped his anticoagulants. Blood thinners had precipitated the nosebleeds, but those drugs had also helped to prevent harmful clots like the one that caused this most recent event. If we didn’t restart the blood thinners, the vice president would be at risk of another heart attack, but if we did, he would be at risk for another bleed. The medical care of a complex patient like Vice President Cheney is often filled with such conundrums and catch-22s, and after much deliberation we decided to cautiously restart the Plavix.

A little more than one year after leaving office, Cheney had been through worsening heart failure, a sudden cardiac arrest, severe bleeding, and now his fifth heart attack. The vortex was spinning faster.

•  •  •

Although the clinical signs and symptoms of heart failure had been known for hundreds of years, there were only a limited number of options to improve a patient’s symptoms and nothing a physician could
do to alter its inevitably bad outcome until late in the twentieth century.

For three millennia, the practice of bloodletting, literally the therapeutic draining of blood from a patient, was used to treat a variety of ailments.
The Egyptians introduced the technique in about 1000 B.C., and it was continued until about a hundred years ago. When the Council of Tours in A.D. 1163 barred monks and priests from performing bloodletting, barber-surgeons (still identified by the familiar red and white barber pole) became the primary practitioners of the art.

Bloodletting was typically accomplished by incising a vein and was used to release what were thought to be evil spirits or bad humors and treat plethora (an excess of body fluid, that is, congestive heart failure), divert blood away from another actively bleeding site, decrease the body’s heat (treat an infection), and treat a variety of other maladies, including gout, “madness,” and seizures.