The Heart Healers (36 page)

I have imagined myself as a patient being the object of the controlled bedlam created by recording vital signs, starting intravenous lines, drawing blood, and recording an ECG, all while getting a brief history and performing a physical examination. Our goal is to get our patient out of the emergency room and on his way to the catheterization laboratory in less than half an hour.. Even as a cardiologist, I would be terrified by the experience, which to any ordinary eyes says that everybody in this room thinks I am about to die. When I was chief of cardiology, I recall watching a young ER resident physician wedge herself sideways into the middle of the tumult. Her job was to obtain a brief medical history and to conduct a cursory physical exam before the patient left the ER. I was deeply gratified to hear her voice rise above the cacophony with a reassurance, “I know this is a confusing blur to you right now. But each of us is doing something to help you. We know how to take good care of you. Now that you are here, you can feel confident that everything is going to turn out right.” With access to new technology that we never knew, the generation of young doctors still understood that compassion comes first.

As I left the ER, I stopped to introduce myself to the young ER resident. “The way you treated your patient made my day,” I said. From her reaction, I think I made hers, too.

*   *   *

IN THE CATH
lab Aaron Stein went into ventricular fibrillation as our multitalented interventional cardiologist Steve inserted his catheter. Steve defibrillated Aaron, and proceeded with angioplasty. He opened the culprit vessel with a balloon and placed a stent. Today angioplasty has so completely replaced thrombolysis as the primary treatment for acute myocardial infarction in major medical centers that our trainees may go for a year without seeing the use of clot-dissolving drugs in acute myocardial infarction.

Discharged from the hospital after his angioplasty, Aaron and I sat across a table to discuss what was next. Aaron had reached new levels of fury. He blamed his doctor for the stress test that precipitated his heart attack. He wanted to sue. I listened for a while, then leaned across the table, and gripped his fist.

“Aaron, look at me. Let’s agree that you will win the lawsuit. But what do you gain? You certainly don’t need the money. So you gain whatever joy there is in punishing the doctor. Balance that against your downside. First, let’s be clear: the doctor is a good man who made a big mistake when he delegated his responsibility to someone who was unqualified. But he did not cause the heart attack. Your ECG tells us that your heart attack was already in progress; the stress test made it obvious. But most important to you is that to win, you’ll endure a year or more of joyless, irritating conferences and depositions with lawyers. You’ll have to relive all the events with your expert witnesses. After that is done, you’ll have to participate in heated negotiations. If those break down, you’ll have to testify in a confrontational trial. What price victory?”

When Aaron cooled down, even though he had a slam-dunk lawsuit, he opted for personal peace. He did not sue. Although Aaron was able to put his doctor’s mistake behind him, I suspected that he was not done with either CAD or the complications of diabetes.

*   *   *

IN LESS THAN
a decade after Gruentzig’s first angioplasty in Zürich, randomized trials in over 5,000 patients had proven that angioplasty is an effective therapy for relief of angina (chest pain on exertion) and for reducing mortality in acute myocardial infarction (heart attack).

Industrial collaborators now competed to create better technology. Whereas the first angioplasty catheters were stiff, bulky, and difficult to manipulate, today an entire new set of slippery wires, flexible catheters, and low-profile balloons has led to catheters that can be steered into any location in the coronary tree. Whereas my generation had learned to insert our large-bore catheters through an artery deep in the leg, a new breed of interventional cardiologists frequently uses smaller diameter catheters inserted through a smaller diameter artery in the wrist, with less bleeding complications and shorter recovery times.

But as with the original cardiac surgeons, our success bred an unanticipated failure, which only became apparent as worldwide experience accumulated. Within six months of opening a vessel stenosed (partially obstructed) by an atheroma, about a third of the treated lesions narrowed right back to their original diameter, “re-stenosed,” and their angina returned. With some dismay, we realized that in the third of patients who suffered restenosis, we had returned full circle to where we had begun. In medicine, it’s always that way: where God has a temple, the devil has a chapel. If we were honest with ourselves, in a third of our patients, we had accomplished nothing.

Around the world, my laboratory and others set out to find the cause of restenosis. Detectives in search of clues, we went to the microscope. Initially we thought we would find reaccumulation of the cholesterol responsible for the original obstruction. Surprise! Instead of new cholesterol accumulation, we saw masses of scar tissue heaped up at the angioplasty site.

We reasoned that when we inflated the angioplasty balloon we caused microscopic injury to the coronary blood vessel that was too small to be seen by angiography. Restenosis seemed to be the body’s normal wound healing response in overdrive. So we spent millions of research dollars to discover compounds that markedly inhibited scar tissue formation following injury to the blood vessels of animals. To our dismay, when we tested these drugs in humans, we did not reduce the restenosis rate. I was completely baffled … we had done science step by perfect logical step. We identified scarring as the cause of restenosis, defined the mechanism of scar formation, and then found drugs that inhibited scarring in animals. And yet we had failed to prevent restenosis in man. Like maniacal architects, we drew and redrew our study design. Impossible. We had identified the cause of restenosis and yet we couldn’t prevent it. Where had we failed?

*   *   *

THE ANSWER TO
our conundrum arose from a completely unanticipated source. A new technology called intravascular ultrasound allowed us to see the coronary artery vessel wall in cross section (angiography shows the lumen of the vessel, not its wall). The new technology was a new set of eyes looking at the same problem. At the Washington Hospital Center in Washington, D.C., Dr. Martin Leon and his team of investigators saw the vessel lumen expand following balloon angioplasty, then slowly recoil back over a few months. Restenosis following angioplasty, it turned out, had two causes, not one. Both elastic recoil and scarring occurred after angioplasty. Each process made about equal contribution to restenosis. We had no silver bullet that could kill this two-headed beast.

*   *   *

IN 1986, JUST
nine years after Gruentzig’s landmark first angioplasty, two cardiologists in France independently found the solution to elastic recoil. Drs. Ulrich Sigwart and Jacques Puel used a hollow metal cylinder to prevent elastic recoil. They called the device a coronary stent. To visualize a stent, imagine a cylinder made of chicken wire. Crimp the cylinder on a collapsed balloon around the tip of a catheter. Inside a blood vessel, wedge the tip of the catheter against atheroma. Inflate the balloon inside the cylinder, forcing it against the vessel wall. When the balloon is deflated, the stent remains, a permanent scaffold for holding open that segment of the blood vessel.

Why do we call it a “stent”? Charles Thomas Stent was a nineteenth-century dentist to the Royal Household who created a formula for dental impressions. The new compound was so effective that his sons formed a company to sell Stent’s compound. Sixty years later during World War I, a Dutch plastic surgeon used Stent’s compound to stretch and fix skin grafts on facial wounds. He made the grammatical error of describing it as “stents mold,” without a capital letter. From a peccadillo came immortality. His method of stretching and fixation by “stenting” became widely employed even as Stent’s compound disappeared. Later, surgeons and cardiologists made the logical transition of “stenting” to tubes that stretched and fixed tissue in the body. Not many men have their name immortalized as a verb.

In the next year following its first description, Argentinean interventional vascular radiologist Julio Palmaz collaborated with San Antonio interventional cardiologist Richard Schatz to create a balloon-expandable stent for deployment in coronary arteries. Seven years later, after trials showed that stents cut the rate of restenosis almost in half, to 15 to 20%, the FDA approved stents. But answers create questions. Could we do even better? We had discovered that stents, just like balloons, induced the scarring response to injury. In eliminating elastic recoil we had precipitated even more injury.

And so once again, failure became success. We reasoned that stents could be coated with our drugs that had inhibited the scarring response but failed to prevent restenosis. Now the restenosis rate fell again, by more than half. We had failed twice, first with wound healing alone, then with recoil alone. Now we stood failure on its head, and proved that two wrongs can make a right. We created “drug-eluting stents.” Drugs coat the stent’s surface, inhibiting the scarring response, as the cylinder prevents elastic recoil. That bring us to today, where the restenosis rate has fallen to 5%.

Stents propelled us into today’s era of treatment of heart disease, with the catheterization laboratory as its centerpiece. As we will see in our final chapter, we have a fabulous array of devices. We can close holes in the heart, implant pacemakers, suck clots out of coronary arteries, replace and repair heart valves, and implant cells to restore cardiac function. It all began with Andreas Gruentzig in a Zürich kitchen, determined to find a way to open a coronary artery with a balloon.

*   *   *

ABOUT A YEAR
after my friend Aaron Stein’s heart attack during an exercise test, he woke with slurred speech and profound confusion. He had a stroke. Aaron recovered with only modest impairment. He had to use a cane. He retained his conversational ability, but his stroke left him with a strange, selective memory loss. He could recall past events without difficulty, and still tell amusing stories, but could not accurately place them in time. Yet Aaron saw himself as defeated. He slept a lot more, and he admitted to crying episodes. Aaron was depressed. He had abandoned hope.

With his family, we focused on helping Aaron find meaning in life, on finding what he could still do. We suggested he could emphasize a life of the mind and the soul. Aaron returned to dedicated study of his Jewish heritage, a part of his life, which he had ignored since his teenage years. Aaron joined a small devout local temple. He was a natural leader and a counselor to others. The experience awakened a new Aaron. He became less impatient, less combative. He listened to other points of view. He mellowed. Our medical conversations became far less factual, far more philosophical.

But diabetes had a trump card even after our advances in cardiology had fueled his recovery from angina, heart attack, and stroke. Aaron was hit with a second heart attack. The additional loss of heart muscle led to congestive heart failure, leaving him barely able to handle the chores of daily living. His prior stroke and other illnesses disqualified him for cardiac transplantation. Now nine years into Aaron’s care, Steve tried different drugs, then different drug combinations. Now what? The new role for Steve and me was to help Aaron, for the first time in his life, confront his own mortality. He continued his religious pursuits and he entered trials of new experimental agents for heart failure. He would improve a little, then slip back, a pharmacologic Sisyphus. When we reached a point where there were no more new drugs, something remarkable happened. Aaron consoled us. It was, I imagine, not the first time a patient consoled a doctor.

One night at home, Aaron passed away silently in his sleep. In his case, however, the strangler in the backseat had become the old man’s friend. It is easy to imagine Aaron’s final years as a downward spiral to death. But to do so would completely miss the humanity of his last decade. A Greek myth tells us of Pandora (“all giving”), the first woman on earth, being given a chest by Zeus, who tells her never to open it. Consumed by curiosity, Pandora opens the box, allowing all evil emotions to escape into the world of mankind. She quickly closes the box, but it is too late. Everything has escaped, except for one emotion. Only Hope remained.

Hope fueled Aaron’s last years when little else remained. A group of us helped life’s journey to death by never abandoning it. Not hope that Aaron could become physically stronger or younger, but hope that he could every day become a better person. Aaron won that battle. He used his physical adversity to help him rediscover love of his family, of his fellow man, of himself. As he said, “You gave me time to become a mensch.” In turning an unending string of physical defeats into spiritual victory Aaron taught me that perseverance in the face of adversity brings special gifts. In living through denial, anger, and depression Aaron had come to acceptance.

At Aaron’s burial, my urge was not to cry, but to celebrate a life well lived. In Aaron’s faith, each mourner is invited to throw a symbolic shovelful of dirt onto the casket. As I did, I murmured to Aaron and myself, “Someday I want to write a book, and when I do I want to tell your story.”

PART IV

HOW TO CONQUER CORONARY ARTERY DISEASE

21

WHY DO ATHEROMAS FORM IN BLOOD VESSELS?

He who loves practice without theory is like the sailor who boards ship without a rudder and compass, and never knows where he may cast.

—LEONARDO DA VINCI, ITALIAN RENAISSANCE POLYMATH

WHEN WE SAW
that bypass surgery and angioplasty relieved exercise-induced chest pain (angina) and X-ray pictures showed blood flowing through previously obstructed coronary vessels, most of us believed that we would soon see people living longer. But a few dissenting voices questioned this logic. Dr. Thomas Preston is a University of Washington cardiologist whom I have known since our years together at a small Quaker college in Swarthmore, Pennsylvania. I no longer recall if Tom is a Quaker, most of us were not, but he embodies all their virtues: serious, intellectual, gentle, and polite, and in the Quaker tradition unafraid of standing alone.