Gruentzig meticulously pursued his vision. He forged collaborations on steerable catheters with American manufacturers, including the company that would eventually become the multibillion-dollar conglomerate Boston Scientific. He practiced on the coronary arteries of cadavers, then later on living patients undergoing bypass surgery, but only in vessels that were already bypassed or about to be bypassed, or were small and inconsequential. Gruentzig presented his results at cardiology meetings but, like Werner Forssmann, encountered skepticism and derision. Nevertheless, he bided his time, waiting for the right opportunity to present itself, a living person on whom to demonstrate his technique.
He finally got his chance on September 16, 1977, when Adolph Bachmann, a thirty-seven-year-old insurance salesman, was transferred to the University Hospital in Zurich with chest pains. A coronary angiogram revealed a short obstructive plaque in the beginning portion of the left anterior descending artery. An emergency coronary bypass operation was scheduled for the following day, but Gruentzig persuaded Bachmann, who was afraid of open-heart surgery, and his doctors to allow him to perform balloon coronary angioplasty instead. The following morning, as a dozen cardiologists, surgeons, anesthesiologists, and radiologists looked on, Gruentzig threaded one of his balloon-tipped catheters into Bachmann’s femoral artery, up his aorta, and into the opening of his LAD. Two out of Gruentzig’s three balloons burst during preparations, but the third one remained intact. Two quick balloon inflations inside the coronary artery and blood began to flow normally down the vessel. The surgeons in the audience stared in disbelief. Gruentzig had restored blood flow to heart muscle without scalpel, saw, or heart-lung machine. It seemed impossible. Gruentzig was prepared to inject the LAD with Bachmann’s own blood to wash away any dislodged plaque, but he did not have to. Bachmann’s chest pains immediately subsided. A post-procedure angiogram showed almost complete resolution of the obstruction. (Ten years later, the artery remained open.) The only complication was a transient EKG abnormality that cleared up spontaneously.
At the American Heart Association conference in Miami that year, Gruentzig presented the results of his first four coronary angioplasties. True to his iconoclastic form, he presented his data (to raucous applause) wearing sandals. Afterward, Mason Sones, teary-eyed and by then battling lung cancer, told a colleague, “It’s a dream come true.”*
After years of working in obscurity, Gruentzig quickly became one of the most famous cardiologists in the world. In 1980, three years after the first coronary angioplasty, he moved his research enterprise to Emory University in Atlanta, Georgia. Over the next five years, he helped to popularize angioplasty in the United States by performing approximately twenty-five hundred procedures. He had so much faith in his technique that he once had a cardiology fellow perform a coronary angiogram on Gruentzig himself. Gruentzig climbed onto the cath table at 5:00 p.m., underwent the procedure, and then went to pick up his wife, arriving at the department’s Christmas party by 7:00. Incidentally, his coronary arteries were normal.
Gruentzig’s procedure ushered in the field of interventional cardiology. In 1980, Marcus DeWood and colleagues used coronary angiography to show that patients suffering heart attacks have arterial clots that obstruct coronary blood flow. This discovery quickly led to the development of clot-busting drugs and the refinement of angioplasty procedures for the treatment of acute myocardial infarction. In 2001, when I began my fellowship, coronary angioplasty was already a sprawling business. One evening, wearing bloodstained scrubs, I ran into Bert Fuller, the kindly chairman at Bellevue. He was sporting his usual maroon sweater and pants that were at least a size too small. We walked together, chatting about my cath lab experiences. Outside Bellevue, it had snowed, and the sidewalk was slushy. “How little we knew,” Fuller said, shaking his head as we waited in line in front of a truck to buy a cup of coffee. “When we started, cardiac catheterization was used only for unremitting chest pains. Now it has become routine.”
Today several million angioplasties are performed worldwide every year, one million in the United States alone. In 1994, the Food and Drug Administration (FDA) approved the release of coronary stents, tiny metallic coils that are used in the clear majority of angioplasties today to keep ballooned arteries open. In the early years of the twenty-first century, stents began to be coated with chemicals that prevent scar tissue from forming. The first drug that was used was rapamycin, an antibiotic discovered in a soil mold on Easter Island that stops cell division. Nowadays, most stents used in the United States are coated with rapamycin or a similar drug, which has nearly eliminated in-stent scarring.
From a self-surgery in a tiny operating room in Eberswalde, Germany, cardiac catheterization has been transformed into a hugely profitable, multibillion-dollar industry. Unfortunately, Gruentzig never got a chance to witness this revolution. He and his second wife, a medical resident, died on October 27, 1985, when the private plane he was piloting crashed in a storm in rural Georgia. He was forty-six years old. That year was a tragic one for interventional cardiology. Smoking caught up with the field’s heroes. Mason Sones died of metastatic lung cancer; Charles Dotter, ironically, of complications of coronary bypass surgery.
*Obstructive plaque can stimulate “collateral circulation,” or the formation of new blood vessels. Oxygen-deprived cells downstream from the obstruction release chemical growth factors that signal primitive vascular cells to invade the hypoxic tissue, assembling into a plexus of new hollow tubes that link up into a complex network. This process, called angiogenesis, ensures that blood vessels permeate every region of the body. These new blood vessels—the heart’s attempt to repair itself—limit the damage caused by a heart attack.
*A few years later, Sones said that the era of angioplasty was “the best time in medical history to have been alive, and I am deeply grateful for the privilege.”
9
Wires
And pale and wan, and of all strength bereft,
…
My heart, as with an earthquake, then is cleft,
Which makes my pulse leave all its life behind.
—Dante Alighieri, from Sonnet IX
The old man shuffled slowly into my clinic room. He took off his hat and collapsed into a cracking vinyl chair. I had seen him before, last about two weeks ago. He had never looked this bad.
He leaned forward, a bearded, wispy-thin gentleman in a vintage suit whose bowler and neckerchief lent him an arcane, vaudevillian air. “The shortness of breath is getting worse,” he growled in a raspy voice, not unlike Bob Dylan’s. “The medications you prescribed aren’t helping.”
Jack, as he was called, had been a beneficiary of the pioneering heart surgeries of Walt Lillehei and others in the 1950s. A diseased valve was surgically repaired when he was a child. With no heart-lung machine, the surgeon used his little finger, wedged into the wall of the right ventricle, to free up the motion of the congenitally rigid valve.
Smoke flowing in cold air (From James N. Weiss et al., “Chaos and the Transition to Ventricular Fibrillation,” Circulation 99 [1999]. Reproduced by permission)
The procedure was successful, but over the years the valve leaked, eventually causing Jack’s heart to weaken and enlarge like a worn-out balloon. Now his heart was pumping much less efficiently than normal, about 30 percent of full strength. He was getting winded after only a few steps. Several weeks prior, he’d collapsed on the stairs leading to his third-floor walk-up and had to be carried up by neighbors.
Gripping my hands like a banister, Jack hobbled onto the exam table. I put the rubber buds of the stethoscope in my ears. His waterlogged lungs crackled like Rice Krispies in milk. With my fingertips, I made tiny craters in his edematous legs. I asked him to take off his shirt so I could listen to his heart. Then I noticed it, rolled up in a yellow vest, strapped to his chest like some sort of talisman. “What is this?” I asked.
He took it off and handed it to me. “My magnet,” he replied. It was wrapped in duct tape and must ha
ve weighed three or four pounds. I waved it at a cart sitting next to my desk. My arm wavered and then jerked gently as the magnet stuck to the metal.
“It’s heavy,” I said. He nodded. “Why do you have it?” I asked.
Magnetic fields dilate blood vessels, he explained. (I didn’t know.) In fact, they have a host of salutary effects on the body, he told me.
He had first heard about magnets a few years back on shortwave radio; he had been using them ever since to relieve headaches, heal minor cuts, and now support his failing heart. He even wore a magnetic belt—made with tiny domino magnets that he purchased from Radio Shack—to treat an abdominal hernia, which had gotten smaller. “Could it just be the pressure of the belt?” I asked.
“A plain belt didn’t work,” he replied.
He told me that ever since he started putting the magnet on his chest, his heart failure had improved. I reminded him that when we first met in the Bellevue Emergency Room a few months earlier, he was near death, literally drowning from the congestion in his lungs. “Just imagine where I would have been without the magnet,” he said.
I had heard of magnets being used to treat chronic pain—even here the evidence was sketchy—but never to treat advanced heart failure. I wasn’t sure what to say. “You should have told me,” I said finally.
“You never asked,” he replied.
He went on to say that I had given off a negative vibe whenever the subject of alternative medicine had come up. Remember when he had asked about milk thistle and taurine? (I didn’t.) Apparently, I had been dismissive, almost scornful. He had asked me to call Gary Null, one of his “natural healers,” to review his treatment protocol, but I never did. He had even considered switching doctors because I had seemed “too dogmatic.”
Heat rose to my face. Too dogmatic? Me? I remembered the book he had lent me, The Clinician’s Handbook of Natural Healing, which lay on my coffee table, unopened. Now I wished I had looked at it, if only to show him what an open-minded doctor I was.
“I’m not aware of any good evidence for alternative therapies for heart failure,” I stammered.
How did I know this without reading up on the current research? he demanded. I felt like a first-year fellow again, unprepared to argue my point. It didn’t matter to Jack that I was the doctor or that I had made it through most of a cardiology fellowship or that I was, in fact, planning on specializing in the treatment of congestive heart failure. Like me, he wanted evidence. He was using my own paradigm against me.
Chastened by his criticism, I offered an apology, which he accepted. Then he told me that besides milk thistle and taurine, he had been taking more than a dozen other unproven off-the-shelf supplements: carnitine, glutathione, goldenseal, corn silk, dandelion, black cohosh, dimethylglycine, coenzyme Q, thiamine, alpha-lipoic acid, stinging nettles, oil of oregano, echinacea, magnesium, selenium, and copper. None were recorded in the chart.
Once the genie was out, he could hardly hold back. He removed the soles of his shoes, embedded with tiny neodymium magnets that he had purchased for forty-five cents apiece at a thrift store. He handed me his glasses; two round magnets were attached to the frames. (That’s what those were!) A few years back, he said, he had had a serious lung infection, requiring treatment with several antibiotics for almost a year. He wasn’t using magnets at the time. He was never going to make that mistake again.
Could it just be random, I asked, this association between magnets and health? Knowing that Jack was well versed in philosophy, I brought up Karl Popper’s theory of science and the requirement of falsifiability. Suggest an ailment we can test, I said excitedly. We could conduct a small trial, on and off magnet therapy. He shrugged, unfazed. “I try to keep myself from analyzing it too much or talking myself out of the placebo effect,” he said.
When he got up to leave, he handed me a tiny magnet as a gift. “Keep it away from your wallet,” he advised. “It’ll erase your MetroCard.”
•
It was on Wednesdays that Jack would come to see me at the Bellevue cardiology clinic. Like many of my patients, he was a clinic veteran who had been through several cycles of fellows. “I know I’m getting older when the doctors are getting younger,” he quipped. The clinic was always packed. You’d get ten or twelve minutes per visit, max. You listened to the heart and lungs, went through the problem list, wrote a progress note, maybe wrote a prescription, and then it was off to see the next patient. No surprise, then, that Jack—and many other patients, I suspected—had adopted alternative medicine. I figured Dr. Null spent more time with Jack, listened to him, and showed that he cared. But did his natural remedies work? I took it as a challenge to prove to Jack that my way, informed by science, was better.
At a clinic visit a few weeks after Jack showed me his magnets, I spoke with him about his treatment options. “You have a weak heart,” I said, slowly moving my outstretched fingers, as if palming a basketball, to illustrate. I brought up the option of an implantable defibrillator. The beeper-sized device would be inserted in Jack’s chest to monitor his heartbeat and apply an electrical shock if the rhythm degenerated into something dangerous. It was like the paddles in the ER, but it would always be inside him. A special “biventricular” defibrillator would help to coordinate the contractions of Jack’s failing heart. It might relieve his breathlessness and decrease the frequency of hospitalizations. It might even prolong his life.
Biventricular defibrillators then cost about $40,000 each. In the United States, where more than six million patients have heart failure and half a million new cases are diagnosed each year, if even a small fraction of patients like Jack received the device, the costs could reach billions. But apart from the money, a bigger question in my mind was whether the device was even right for Jack. He was probably going to live at least a year, but certainly no more than five. How did he want to die when his time came? Patients with heart failure mostly die in two ways: either by a sudden, “lights out” arrhythmia, in which the heart abruptly stops, or by progressive pump failure, in which the heart weakens to the point that it cannot deliver adequate blood and oxygen to the tissues. Pump failure is a horrible way to die. The symptoms it creates—nausea, fatigue, and unremitting shortness of breath—are some of the most torturous and feared in the human experience. Wasn’t a sudden arrhythmia a better way for Jack to go than struggling for breath as his lungs filled with fluid from congestive heart failure? Sure, a defibrillator would prevent sudden death. But it would also take away the sudden-death option, potentially directing the dying process down painful, winding paths. Of course, when Jack’s condition inevitably spiraled downward, he could always deactivate the device and prevent it from delivering a painful shock. However, in my experience, few patients ever did. Doctors rarely informed them of this option, and families, struggling to cope with the impending death of a loved one, were often reluctant to make that choice.
I did not go into these details with Jack, however. It was hard enough to fit any sort of discussion, let alone a drawn-out, morbid one, into a ten-minute office visit. I recommended he get a defibrillator. I wasn’t sure it was the right decision, but the device, I figured, would at least help him in the short run. But none of this mattered anyway, because Jack quickly waved off my recommendation. He didn’t want a defibrillator. With time, he was convinced, his magnets were going to work.
•
The heart is fundamentally an electrical organ. Without electricity, there would be no heartbeat. Electrical impulses stimulate special proteins in heart cells, causing them to draw together, resulting in contraction of the entire organ. Derangements in the rhythm of these impulses impair the heart’s ability to pump blood. By the early part of the twentieth century, this was understood, and the heart’s wires had been mapped. For example, physiologists knew that nearly every one of the three billion heartbeats that occur during a typical human lifetime begins with the spontaneous activation of cells in a region high up in the right atrium called the sinoatrial node, the
heart’s natural pacemaker. Through the flow of charged ions, the voltage of these cells periodically arrives at a threshold; this happens about once a second in a normal person at rest. That induces an electrical wave—an action potential—that spreads through the atria and travels down specialized conductive tissue—wires, really—into the ventricles, stimulating heart cells along the way. (Think of the pulse generated when you jerk the end of a rope up and down.) Just before the wave enters the ventricles, it passes through a narrow, relatively inert disk of tissue called the atrioventricular node. Here, the electrical impulse slows to a crawl for about a fifth of a second, giving the atria time to finish squeezing and filling the ventricles with blood. The wave then passes into the ventricles through thick bundles of tissue that rapidly and finely split into conductive filaments that extend through the ventricles like the roots of a tree. In this way, an impulse originating in one part of the heart quickly conducts through the entire organ, causing the right and left ventricles to contract almost simultaneously, ejecting blood into the lungs and the main body, respectively.
After a cardiac cell is stimulated, it enters a “refractory” period in which the cell becomes essentially quiescent; no electrical stimulus, no matter how intense, will elicit another response. This is a protective mechanism, preventing cardiac tissue from being rapidly and repeatedly activated. If the heart beats too fast, circulation can cease and the person will die.
There are several other layers of protection that ensure the stability of the human heartbeat. For example, if the sinoatrial node, the heart’s natural pacemaker, becomes dysfunctional, any number of backup pacesetters in the heart can take over. These regions normally have different electrical properties and activate more slowly than the sinoatrial node, so their activity is ordinarily suppressed (their cells are in a refractory state) when the sinoatrial node is firing normally. But if one of these regions speeds up because of damage or disease or adrenaline release, it can usurp the sinoatrial node’s pacemaking function.
Heart Page 14
