My patient glared at me. Ropes of pain lashed him down, but his anger hit me with such force that I thought, What on earth did I say? In fact I hadn’t said anything yet, though my hand was already extended, dumbly, in greeting. I tucked it out of sight. Hi, I said slowly, glancing around the ER to see what might have incurred such wrath. There were no other likely targets. Just me, wrapped in a white coat. I’m Dr. Dajer.
Yeah, well listen, my unimpressed patient replied, am I going to get t-PA?
Mr. Simmons looked about 50. Graying temples and a square jaw framed his smoldering eyes. It was a face of clean, forthright lines--a face usually presented to the world atop a sleek business suit, not a wrinkled, ridiculous hospital gown. Before I could say Whoa, Excuse me, or Mind if we recheck our scripts and determine who is the doctor here? he grabbed me, verbally, by the lapels.
And don’t skimp. I have good insurance. I want t-PA. Now.
The little temper inside me flared. I don’t treat my patients according to their insurance, it fumed, and I really don’t care to be told how to practice medicine. That, of course, wouldn’t do. I stepped back and forced my face to adopt its detached, Teflon doctor’s expression.
Mr. Simmons, you just got here, I said evenly. How about if we take a moment and figure out what’s going on?
Well, I don’t have a moment, he muttered.
The ambulance crew had already filled me in. Mr. Simmons had been waiting to change trains on a subway platform when the elephant had come to kneel on his chest. His legs had turned to Jell-O, and his body warmth had receded like the tide, leaving a cold, sticky sweat. The rush-hour hubbub dissolved into a sickening fuzziness. They had found him helpless, clinging to a bench as if he were the last passenger on the listing deck of a doomed ocean liner.
Probably heart attack, Doc, the paramedics said when they rushed him in. Pain hasn’t let up at all.
The nurse handed me the electrocardiogram she’d performed the second he hit the bed. I took it almost reverently--it was the only window I had to what was going on inside Mr. Simmons’s chest. It would give me the most objective clue to the question that demanded an instant answer: Heart attack or no?
Before I could focus on the tracing, Mr. Simmons preempted me. Again.
I have a left bundle block, Doc. That ECG isn’t going to help you.
I glanced down at the pink graph paper. It was covered with boldly plunging lines recording the electrical activity within Mr. Simmons’s heart. Each heartbeat begins in a cluster of cells in the upper- right-hand corner of the heart; from there an electric wave spreads to the powerful pumping chambers via two trunk lines, or bundles. When the larger of these--the left one--malfunctions, the resulting ECG is so abnormal that the telltale tracings of a heart attack can be obscured. Mr. Simmons was right: he had textbook left bundle branch block. But the blockage in electrical conduction could be caused by something as simple as wear and tear on the heart’s wiring system. My window to his heart was sprayed over with graffiti.
I reluctantly put it aside.
How’s the pain, Mr. Simmons?
Bad, he replied. His eyes said the rest.
The only tests I could rely on now were that pain and his story.
Mr. Simmons, I said carefully, you know, t-PA, in a few cases per thousand, can cause severe hemorrhage. It’s not worth taking that risk unless I’m sure you’re having a heart attack. I need three minutes to ask you some questions.
Okay, he sighed.
The story was of a man who had escaped the talons of one disease only to fall into those of its offspring.
Twenty-five years ago I had Hodgkin’s disease, he began.
Hodgkin’s is a cancer of the lymph system, the network of capillaries that absorb water and protein from tissue and return them to the bloodstream. When Mr. Simmons came down with it, doctors had just gotten good at treating it with radiation.
I was lucky. If I’d gotten sick five years earlier, they said, I probably wouldn’t have made it. As it was, I did great. It wasn’t fun, but after that, no other problems--except a bit of high blood pressure. I was healthy.
But the body rarely gets something for nothing. For reasons still poorly understood, the same radiation that melted the tumor in Mr. Simmons’s chest can also accelerate the formation of atherosclerotic plaque, the tiny, fatty plugs that block arteries in the heart and cause about 1.5 million heart attacks in the United States each year.
I played racquetball three times a week, said Mr. Simmons with a wistful smile. I felt great. So then my doctor did a routine ECG during a checkup. It showed the left bundle block. He said it could mean decreased blood flow to that part of the heart. To be safe we did a stress test. Positive. But even while I was on the treadmill, pounding away, I felt no pain.
Mr. Simmons paused to swallow. He had to have told the story dozens of times already, but never, he knew, to a listener who had to act on the information faster.
What then? I asked.
Well, we talked it over and decided to go for an angiogram.
The heart has its own blood supply system: the coronary arteries, which wrap around the heart and supply it with oxygen. An angiogram provides an image of this network of fuel lines. To obtain it, a catheter is inserted at the groin into the femoral artery and then threaded up the pelvic artery into the aorta, the large blood vessel that emerges from the heart and distributes blood to the rest of the body. Then a substance that shows up on an X-ray screen is squirted into the coronary arteries where they branch off from the aorta. Blockages look like white kinks and bites taken out of a smooth black sausage.
Mr. Simmons said his angiogram showed just one kink, but it was at a crucial spot: the gateway to the right coronary artery, a blood vessel about the size of a soda straw that feeds roughly a third of the heart. There the plaque lay, so narrowing the artery that only a trickle of blood could flow through. To make matters worse, in Mr. Simmons’s case, as in only one out of seven people, the right coronary artery carried blood to a much larger part of the heart than normal. The result was that more than half of Mr. Simmons’s heart--including the area containing the left bundle- -was being held hostage by a few grams of calcium and fat. Its rough, ratty-looking surface was a prime breeding ground for a clot. It would take only a tiny one to choke off the vessel completely.
We decided to go with aspirin and a calcium blocker and see what happened, Mr. Simmons continued.
Aspirin--cheapest of wonder drugs--makes platelets, the blood’s clotting starters, less sticky. And calcium channel blockers, developed over the past decade, improve blood flow by dilating the coronary arteries. So in Mr. Simmons’s case, the aspirin kept platelets from clumping inside his narrowed right coronary artery while the calcium channel blocker kept it as open as possible.
I did fine for a year, Mr. Simmons went on. Then it started. I’d walk up a flight of stairs or be getting to the end of a racquetball game and the squeezing would come. Here. He closed a fist and pressed it into his left pectoral muscle.
The angina meant the narrowing in his right coronary artery had grown critical. Until 1977, Mr. Simmons’s only remaining option would have been a coronary bypass. In this technique, one of the long, sturdy, and easy-to-get-at veins in the leg is removed. One end of it is attached to a newly made opening in the aorta and the other to the coronary artery beyond the blockage. Unfortunately, bypasses require splitting the sternum and stopping the heart--major surgery from which it takes months to recover.
In 1977, Swiss cardiologist Andreas Gruentzig thought he had a better idea. He used the femoral-to-aorta-to-coronary conduit to slip a tiny balloon into a patient’s partially blocked coronary artery. Then he inflated the balloon, compressing the offending atherosclerotic plaque against the artery wall. As he had hoped, the squishy plaque stayed flattened, permitting much better blood flow. Today angioplasties are performed on over 200,000 Americans each year who need their coronary arteries unblocked. But clever as it is, balloon angioplasty doesn’t work on every plaque: sometimes the balloon cannot pass through because of a bend in the artery or because the vessel’s inner wall tears and a flap falls down, blocking the artery. And it’s much less likely to work on heavily calcified plaque.
In response, new angioplasty devices have proliferated in a species explosion not unlike those evolutionists so love to describe. Lasers, scoopers, spinning blades, diamond-tipped bits, and ultrasound probes--none thicker than a strand of spaghetti--have all joined the fray. The heaped-up, calcified plaque that had almost choked off Mr. Simmons’s right coronary artery was an ideal target for the Rotablator, a metal burr the size of a pencil point. Once inside the artery, it spins at 200,000 revolutions per minute and pulverizes the toughest calcified plaque with its microdiamond-studded tip. Mr. Simmons’s timing was right again. The Rotablator had just been approved by the FDA.
It worked like a charm, Mr. Simmons recalled. I was whacking that racquetball around two weeks later. No pain. Nothing. But the good times didn’t last long. Two months. The angina came back.
He fell silent for a moment.
And now here I am.
Unfortunately, Mr. Simmons has a lot of company. The reblockage rate six months after coronary angioplasty is about 30 percent. Because angioplasty techniques all involve fairly crude scraping, crushing, burning, or compressing, the body’s natural response is to form scar tissue that can easily replug a coronary artery’s few millimeters of breathing room. And over the long run, no matter how high-tech and individually tailored the treatment, the villains responsible for the obstruction--high cholesterol, diabetes, smoking, or, in Mr. Simmons’s case, high blood pressure and bad genes--get back to work.
Mr. Simmons had run the gantlet, only to be met by a brick wall.
How’s the pain now? I asked one last time.
He just shook his head. My three minutes were up.
The longer a coronary artery stays closed, the more heart muscle dies from lack of oxygen. Just the week before, headlines had pronounced t- PA--tissue plasminogen activator--the clot dissolver of choice over streptokinase. Naturally Mr. Simmons wanted t-PA. Both drugs exploit the body’s limited ability to break up clots by boosting levels of plasmin, a clot-busting protein. T-PA activates plasmin within the clot itself, while streptokinase increases levels of plasmin throughout the bloodstream, where it breaks down other, clot-building proteins. But the kicker is that treatment with t-PA, a genetically engineered copy of the body’s own clot buster, costs $2,300. Streptokinase, an enzyme produced from streptococcus bacteria, costs about $320. The study in question showed that with t-PA only 6 out of 100 heart attack patients died, versus 7 with streptokinase. In other words, for every 100 patients treated with t-PA, the extra life saved cost an additional $198,000. That aside, though, certain subgroups-- such as the elderly or those with a longer duration of pain--did less well with t-PA. And Mr. Simmons, with his atypical ECG and history of Hodgkin’s, was in a subgroup all by himself.
Listen, I began. First of all, both t-PA and streptokinase can cause serious bleeding complications, especially in the brain. Second, without a clear-cut ECG I’m not sure this isn’t just worsening angina. Third, if a clot is forming at the point of your angioplasty, it may be wiser to use streptokinase, which has a lower rate of reocclusion than t- PA.
Mr. Simmons took this all in. I probably hadn’t told him anything he didn’t already know.
So I’m calling Dr. Mansell. He’s our best cardiologist. He’ll be down right away.
Dr. Mansell has a manner like the television detective Columbo and a brain that can ferret out a heart attack through all the bundle branch blocks, misleading symptoms, and atypical stories in the world.
He arrived, studied the ECG, sat down at the foot of Mr. Simmons’s stretcher, and quickly covered the ground I had. He finally said, Still hurts, huh?
Yes, Mr. Simmons replied.
Like the pain you had before the angioplasty?
Dr. Mansell spread his hands, pretended to hesitate a bit, then turned to me.
I think it’s real. Strepto.
Instantly, like the crew of a racing yacht swerving into a new tack, the nurses and I jumped to our posts. I tore out the vial of streptokinase powder and filled it with saline solution, careful not to raise foam that would trap precious medication in the tube. The nurses hung IV pumps, started another line, and read out the protocol like battle commands from the quarterdeck.
Aspirin 162 milligrams.
Hydrocortisone 100 milligrams. Benadryl 25 milligrams.
Streptokinase 1.5 million units over one hour.
In four minutes the clot buster was flowing into Mr. Simmons’s vein. It usually takes streptokinase one to two hours to dissolve a coronary clot. In the meantime we would hold our breath like submariners in a World War II movie, clocking the time to impact, wondering if we had aimed our torpedoes true.
During the wait we controlled Mr. Simmons’s pain with intravenous nitroglycerin. Every ten minutes I asked him the same question. And each time I got the same answer. Medium. The pain’s about medium. Finally he said, Look, I’ll holler if it’s better, okay?
Okay, I replied. But you’re also supposed to holler if it’s worse, right?
The holler came 80 minutes after we started the streptokinase. Besides the first cry of a newborn baby, no sound in medicine is sweeter than a heart attack patient saying, The pain is gone. I couldn’t help breaking into a cheek-splitting grin. And so, to my surprise, did Mr. Simmons. His anger had evaporated, leaving behind a thoughtful, gentle man who’d weathered more than his share of medical storms.
I guess Hillary Clinton would be proud of you guys, he teased.
I saw him four days later, before his transfer back to the hospital where they’d done his angiogram. His heart attack was over, leaving behind only a slight, temporary rise in the enzymes that signal muscle-cell damage.
Now what? I asked him.
Well, I don’t see what else I can do except for the bypass, he answered. Can’t be running into emergency rooms getting my coronary artery unclogged for the rest of my life. He winked. Besides, what would Hillary say?
Three weeks later the bypass went off without a hitch. Mr. Simmons had pulled ahead again. Elated as I was when I heard the news, I couldn’t squelch the thought that bypass grafts can reocclude, too. Or that Hodgkin’s survivors sometimes develop a second tumor somewhere down the road. But then, bypass grafts can be angioplastied, and bone marrow transplants, gene therapy, and all kinds of new treatments are being unleashed against cancer. All Mr. Simmons has to do is keep his timing perfect.